CHAPTER 1
BASIC INFORMATION
I.
II.
Introduction to Internal Medicine
III.
Normal Laboratory Values and Conversion Factors
1. Complete Blood Count
2. Blood Chemistry
3. Urine Studies
4. Equivalent Values
IV.
Intravenous Fluids
1. Intravenous Fluids and Common Indications
V.
Commonly Used Drips
1. Formulation and Computation of Basic Drips
2. Other Commonly Used Drips
Core Skills in Internal Medicine
1. Electrocardiography
2. Chest Radiograph Interpretation
3. Arterial Blood Gas Interpretation
4. Thoracentesis
5. Paracentesis
6. Foley Catheter Insertion
7. Intravenous Line Insertion
1
SECTION 1
INTRODUCTION TO INTERNAL MEDICINE
I. INTRODUCTION
Internal Medicine (IM) can be quite overwhelming because of the complexity of cases and long work hours. Despite these
inherent toxicities, it remains one of the most rewarding fields in Medicine. Students and practitioners alike enjoy the
intellectual stimulation and experience of translating theoretical knowledge into direct patient care. As basic IM principles
cannot be dissociated from the cases we encounter, it is imperative for every practitioner to acquire the core
competencies and skills of an internist. The approach to patient encounter and chart writing are discussed in the
succeeding parts.
II. HISTORY AND PHYSICAL EXAMINATION
Complete history and physical examination are central to hypothetico-deductive reasoning in clinical medicine. Starting
from the chief complaint, problems are elicited from the in chronological order. After completing the details for acute
complaints, probe into the patient’s past medical history, including present medications and pre-morbid functional
capacity. Diseases in the family such as hypertension, diabetes, heart disease, early cardiac death and other
heredofamilial diseases should be elicited as part of the family medical history. History of allergic reactions to drugs and
food should always be elicited. Dietary habits, smoking history, alcohol intake and illicit drug use should also be included
in the personal and social history. Likewise, female patients should be asked about details on menstruation and
pregnancy.
The comprehensive history is followed by the systematic physical examination (PE). This starts with a general survey
followed by checking the patient’s vital signs. Permission should always be asked from the patient before doing any
maneuver, especially the more intrusive ones. A complete PE is carried out with special focus on certain procedures
pertinent to the identified problems of the patient.
III. WRITING THE ORDERS
With the information obtained from the history and PE, a prioritized problem list is then created, with the most urgent
conditions listed first. Based on the problem list, the management list is then outlined.
The orders for the patient usually contain the following:
Diet
Fluids and Drips
Monitoring
Diagnostics
Therapeutics
Transfusions
Dietary preparations (i.e., general liquids, soft diet, full diet) and specific dietary prescriptions
(i.e., low-salt, low-fat, low-purine, DAT)
Main IV lines (i.e., plain saline, D5-containing fluids) and side drips (i.e., vasopressors,
electrolyte solutions)
BP, HR, RR, temperature, peripheral O2 saturation, neurologic vitals, etc.)
Frequency by which these parameters are checked (i.e., q hourly, q4h, q shift)
Prioritized list of diagnostic procedures such as imaging, blood tests and special procedures
Medications with corresponding doses, frequency of dosing, duration and side effects to
watch out for
Blood products, the amount to be transfused, rate of transfusion and interval between
transfusions
Pre-medications and side effects to watch out for
Anticipatory measures: diuretics for possible congestion, anti-pyretics for febrile transfusion
reactions
2
DATE/TIME
6/10/2015
7:30am
PHYSICIAN’S ORDER SHEET
Gen Med
Diagnosis: Community acquired pneumonia, moderate risk
Hypertension, stage I, controlled
Diet: Low salt, low fat diet; limit oral fluid intake <1.5L day
IVF: PNSS 1L x 10 hours
Side drip1: MgSO4 2g in 250cc D5W x 24 hours
Dx:
Chest X-Ray (PA and lateral views)
Complete blood count
Tx:
1. Ceftriaxone 2g IV q24h
2. Azithromycin 500mg/tab 1 tab OD for 3 days
3. Losartan 50mg/tab 1 tab PO OD
Monitor VS q4 with temp and O2 sat
Monitor I&O q shift and record
Refer to dietary for dietary prescription and advice
Watch out for desaturation and BT reaction
Jaime Aherrera MD
Lic. No. 123456
IV. PRESENTING THE CASE
A. General data – begin with the name, followed by the age, sex, chief complaint, reason for admission, and date of
admission or referral
“Juan dela Cruz, 28 years old male, admitted yesterday morning for dyspnea.”
B. History of present illness – review of systems and pertinent information from the past medical, family medical,
personal/social, and obstetric (if applicable) histories
C. Significant diagnostic findings and their interpretations, including pertinent normal findings to rule out the
differentials being considered by the team
D. Hospital course – emphasize the developments or important events that happened to the patient
E. Case summary – two or three sentences
F. Assessment/problem list
G. Plan – based on the assessment/problem list; detailed and specific. Orders for the patient should have their bases
and the expected laboratory findings or trends should be known
H. Entertain clarifications or questions from the audience
3
SECTION 2
CORE SKILLS IN INTERNAL MEDICINE
ELECTROCARDIOGRAPHY
I.
THE STANDARD 12-LEAD ELECTROCARDIOGRAM (ECG)
A. Limb leads
Standard limb (Bipolar) leads: I, II, III
Augmented limb (Unipolar) leads: aVF, aVR, aVL
B. Chest leads
V1
II.
4th ICS, right parameter border
V2
4th IC, left parasternal border
V3
Between V2 and V4
V4
5th ICS, left midclavicular line
V5
5th ICS, left anterior axillary line
V6
5th ICS, left midaxillary line
THE P-QRST WAVES, SEGMENTS AND THE CARDIAC CYCLE
4
III.
BASIC STEPS IN ECG READING
Step 1: Determine rate
Step 2: Determine rhythm
Step 3: Measure intervals
Step 4: Determine axis
Step 5: Look for chamber enlargements
Step 6: Check for arrhythmias and other abnormalities
STEP 1: DETERMINE HEART RATE
Regular Rhythm
Heart Rate =
1500_____________
# of small squares from R to R
Irregular Rhythm
Heart Rate = # of QRS complexes within 30 large boxes x 10
STEP 1: DETERMINE RHYTHM
Regular Sinus Rhythm
Rhythm is determined by the sinus node, which fires at 60-100 bpm
P-wave is normally upright in lead II (and usually in leads I, aVL and aVF)
Each p-wave is followed by a QRS complex, and each QRS complex is preceded by a p-wave
The distances between the R-R intervals should be equal
Sinus Tachycardia and Bradycardia
Tachycardia: HR >100bpm
Bradycardia: HR <60bpm
Sinus Arrhythmia
SA node discharges irregularly (sinus node rate varies with the respiratory cycle)
Rate: normal
Rhythm: varies with respiration, variation in the P-P interval and R-R interval >120 msecs
P-waves, PR interval and QRS: normal
5
STEP 3: MEASURE INTERVALS
Normal Values
Wave/Interval
P-wave
PR interval
QRS duration
QT interval (QTc)
Description
Atrial depolarization
Conduction within the AV node
Ventricular activation
Ventricular activation and recovery
Normal Values
< 0.12 sec or <120 msec (<3 small boxes)
0.12-0.20 sec or 120-200 msec (3-5 small boxes)
< 0.11-0.12 sec or <110-120 msec (<3 small boxes)
0.35-0.43* (males) and 0.45* (females)
*may vary depending on reference
*Source: Kasper DL, et al. Harrison’s Principle of Internal Medicine, 19th edition
Corrected QT-interval (QTc) using the Bazett’s formula
Done to adjust for abnormal heart rates (HR <60 or >100 bpm)
QT actual
Corrected QT interval =
R-R interval in sec
STEP 4: DETERMINE AXIS
Computation of Frontal Axis
Deduct negative deflections form positive deflections in QRS complexes to derive the values for leads I and aVF.
If lead I is a negative integer, subtract the computed axis from 180 to get the final axis.
Note that the value for aVF in the denominator is the absolute value, while that in the numerator takes the sign
(positive or negative) into consideration. This is why a predominantly negative deflection in aVF will make the axis
negative.
____90 aVF____
Axis =
| I | + | aVF
Interpretation
Normal Axis
-30o to 100o
Right Axis Deviation (RAD)
100o to 180o
Left Axis Deviation (LAD)
-30oto -90o
Extreme Axis Deviation
-90o to -180o
“Eyeballing” method – can be used to estimate axis
INTERPRETATION
Normal
LEAD I
QRS pointing UP
LEAD aVF
QRS pointing UP
Left Axis Deviation
QRS pointing UP
QRS pointing DOWN
Right Axis Deviation
QRS pointing DOWN
QRS pointing UP
Extreme Axis Deviation
QRS pointing DOWN
QRS pointing DOWN
STEP 5: LOOK FOR CHAMBER ENLARGEMENTS
A. Atrial Enlargement
Right Atrial Enlargement (RAE)
Left Atrial Enlargement (LAE)
Peaked P-wave with > 2.5mm amplitude (> 2.5 small boxes)
in leads II, III or aVF
“P-Pulmonale” or peaked P-wave from pulmonary causes
Broad P-wave (> 120ms or > 3 small boxes)
Biphasic P wave in V1 with a broad negative component
Often notched P-wave in one or more limb leads
“P-Mitrale” or M-shaped P-wave
6
B. Left Ventricular Hypertrophy (LVH)
SOKOLOW-LYON CRITERIA
[S in V1] + [R in V5 or v6] > 35 mm (>35 small boxes)
OR
CORNELL CRITERIA
S in V3 + R in aVL:
Female > 20mm
Male > 28mm
R in aVL>11mm
C. Right Ventricular Hypertrophy (RVH)
Relatively tall R wave in lead V1 (R > S wave) with right axis deviation
R in V1 > 0.7mV
R/S in V1 > 1 with R > 0.5 mV
R/S in V5 or V6 < 1
IV. ARRYTHMIAS
JUNCTIONAL AND IDIOVENTRICULAR RHYTHMS
A. Junctional (Atrioventricular) Rhythm
Pacemaker: AV junction with a ventricular rate of 40 to 60 bpm
P wave: may appear before, after, or buried within the QRS complex
Rhythm (RR-interval): regular
QRS complex: narrow (<0.12 sec)
B. Idioventricular Rhythm
Pacemaker: Hiis-Purkinje system (HPS) with a ventricular rate between 15 to 40 bpm
P wave: absent
Rhythm (RR interval): regular
QRS complex: wide (>0.12 sec)
7
DISORDERS OF SINUS RHYTHM
A. Sinus Pause
Temporary cessation of sinus node activity
May be synonymous with sinus “arrest” – which pertains to a prolonged sinus pause (definition is arbitrary)
Difference from sinus exit block: the supposed P-P interval of the dropped beat is not a multiple of the normal P-P
interval
B. Sinus Exit Block
Failure of impulse transmission
No visible P-QRS-T complex for >1 cycle, wherein the P-P interval of the pause is a multiple of the normal P-P
interval (differentiating it from sinus pause)
ATRIOVENTRICULAR (AV) BLOCKS
A. First Degree AV Block
Prolonged PR interval
(>0.20 sec or >5 small
boxes)
P-wave is followed by a
QRS complex
B. Second Degree AV Block, Mobitz Type I (Wenckebach)
PR interval progressively
lengthens,
then
the
impulse is blocked (P is
not followed by QRS,
resulting in a dropped
beat)
8
C. Second Degree AV Block, Mobitz Type II
PR
intervals
of
conducted beats are
constant
in
length,
however,
beats
are
dropped with no warning
PR intervals may be
normal or prolonged
D. High Grade AV Block
2 out of every 3 or more
impulses from the atria
are blocked by the AV
node and fail to reach
the ventricles
PR
intervals
are
constant (in contrast to
complete heart block)
E. Third Degree (Complete) AV Block
P and QRS waves occur
regularly
but
are
independent of each
other
No
consistent
relationship
between
atrial and ventricular
activity (AV Dissociation)
PP intervals and RR
intervals are constant
9
ATRIAL ARRHYTHMIAS
A. Premature Atrial Contractions (PAC)
Premature
P-waves
(earlier than the next
expected sinus P-wave)
P-wave has a different
morphology compared to
the sinus P-wave since
this P-wave is coming
from a different atrial
focus
QRS is usually narrow
B. Atrial Fibrillation (AF)
Description:
Rapid,
erratic
electrical
discharge from multiple
atrial ectopic foci
Rate: atrial rate >350
bpm; ventricular rate
varies
Rhythm:
irregularly
irregular
P-waves: no discernable
P-wave
QRS: usually normal
C. Atrial Flutter
Description: Re-entrant
circuit within the atria,
with variable conduction
of impulses through the
AV node to the ventricles
Rate: atrial rate is 250350 bpm; ventricular rate
varies
Rhythm:
variable
(depending
on
conduction)
P-waves:
saw-tooth
appearance
QRS: usually normal
D. Wandering Pacemaker
Description:
impulses
originate from different
foci in the atrium
Rate: normal
Rhythm: irregular
P-waves:> 3 different
forms
PR interval: variable
QRS: normal
10
E. Multifocal Atrial Tachycardia (MFAT)
Rate: Fast; Irregular
atrial rate (> 100)
Rhythm: irregular
P-wave: >3 different
forms
PR interval: variable
QRS: normal
SUPRAVENTRICULAR TACHYCARDIA (SVT)
Arrhythmia has such a
fast rate that the P
waves may not be seen
Rate: 150-250 bpm
Rhythm: regular
P
waves:
frequently
buried in preceding T
waves
QRS: normal, but may
be wide if abnormally
conducted
through
ventricles
(aberrant
conduction)
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
Most common form of
SVT
Narrow QRS tachycardia
with a short RP interval –
P-waves buried in the
QRS complex
May have a “pseudo-S”
wave (which is actually a
retrogradely conducted
P wave) in inferior leads
or “pseudo-R prime” in
V1
VENTRICULAR ARRHYTHMIAS
Wide QRS tachycardias (>120 ms or 3 small squares): usually ventricular in origin
Differentials for wide QRS tachycardia
o Ventricular tachycardia (VT): more common
o Supraventricular tachycardia (SVT) with aberrancy
When faced with a wide-complex tachycardia and the morphology is in question, it is safer to treat as ventricular
tachycardia (the more life-threatening differential)
A. Premature Ventricular Contractions (PVC)
Prematurely
occurring
QRS complex which is
wide and bizarre-looking
Usually no preceding Pwave
T wave opposite in
Bigeminy: PVCs alternate with sinus beats
deflection to the QRS
11
complex
Trigeminy: PVC occurs after every 2 sinus beats
Couplet: two successive PVCs (if three successive PVCs, it is already considered unsustained VT)
B. Ventricular Tachycardia (VT)
1. VT According to Morphology
a. Monomorphic Ventricular
Tachycardia
Rapid, bizarre wide QRS
complex (appearance of
all the beats match each
other in each lead)
No P-wave
Ventricular
focus
produces
a
rapid
sequence of PVC-like
wide
ventricular
complexes
b. Polymorphic Ventricular
Tachycardia (Torsades de
Pointes)
Beat-to-beat variations in
appearance
Baseline
rhythm
demonstrates long QT
interval
Presents
with
an
oscillating
pattern
mimicking the “turning of
the
points”
stitching
pattern
2. VT According to Duration
a. Sustained: ventricular tachycardia that lasts for more than 30 seconds
b. Non-sustained: ventricular tachycardia that self-terminates within 30 seconds (presence of at least >3
successive PVCs is considered VT)
3. VT Based on Symptoms
a. Pulseless VT: no effective cardiac output (no pulse, no BP)
b. Unstable VT: with pulse, but unstable BP
cardioversion
defibrillate (treat as ventricular fibrillation)
12
C. Ventricular Fibrillation (VF)
Associated with coarse or fine chaotic undulations
No P-wave
No true QRS complexes
PACEMAKER RHYTHM
A. Ventricular Paced Rhythm
RR interval is regular
QRS complex is wide with an LBBB morphology
Pacemaker spike (“blip”) is followed by a wide QRS complex (good capture)
B. Atrial Paced Rhythm
Atrial pacing appears on the ECG as a single pacemaker stimulus followed by a P wave
PR interval and configuration of the QRS complex are similar to those seen in a sinus rhythm
C. Dual Pacemaker (Atrial and Ventricular)
13
V. OTHER ABNORMAL FINDINGS
ISCHEMIA
Findings suggestive of ischemia(should be in 2 or
more contiguous leads)
ST segment depression > 1mm (> 1 small box)
Deep T-wave inversions > 5 mm (> 5 small
boxes)
For example, if there are ST segment
depressions of >1mm in lead V5 and V6: then
we can say that there is lateral wall ischemia. If
ST segment depressions occur in V3 to V6:
then we can say there is anterolateral wall
ischemia.
The Contiguous Leads
II, III, aVF
I, aVL
V1, V2
V3, V4
V5, V6
V1 – V3
V3 – V6, I, aVL
V5, V6, II, III, aVF
Almost all leads
V3R, V4R (right-sided
leads)
Inferior wall
High lateral wall
Septal wall
Anterior wall
Lateral wall
Anteroseptal wall
Anterolateral wall
Inferolateral wall
Diffuse, massive
Right ventricular wall
INFARCTION
A. Findings suggestive of injury or infarction
Significant ST elevation:manifestation of myocardial necrosis; the earliest sign of acute infarction
> 1 mm ST elevation in contiguous limb leads, or
> 2 mm ST elevation in contiguous chest leads
B. Pathologic Q-Waves
Indicate myocardial necrosis
Significant Q-wave: > 0.04 secs duration and > 25% of the R wave amplitude
Ignored in lead V1 unless with abnormalities in other precordial leads
Ignored in lead III unless with abnormalities in leads II and aVF
C. Classification as to Timing of Myocardial Infarction
CLASSIFICATION
(A) Normal
(B) Acute MI
(C) Recent MI
(D) Old MI
TIMING
Minutes to hours
Hours to days
Days to months
ECG FINDINGS
ST elevation + peaked or inverted T-waves + Q waves
Q-waves +ST elevation + T-wave inversion
Q-waves + Isoelectric ST-segment + T-wave inversion
D. Posterior LV wall involvement
Posterior wall ischemia, which is usually associated with lateral or inferior involvement, may be indirectly
recognized by reciprocal or “mirror-image” ST depressions in leads V1 to V3
The posterior LV wall electrical activity is not represented in a typical standard surface ECG
The anteroseptal leads (V1 to V3) are directed form the anterior precordium pointing towards the internal surface
of the posterior myocardium
E. Reciprocal Changes
Pertains to ST-depression in leads opposite those demonstrating ST-elevation
“Ischemia at a distance”
Anterior MI: reciprocal change in inferior wall
Inferior MI: reciprocal change in I, aVL, or anterior wall
Lateral MI: reciprocal change in V1 or inferior wall
14
PULMONARY EMBOLISM (PE)
McGinn-White sign: S1Q3T3 pattern (large S-wave in lead I, Q-wave in lead III, and inverted T-wave in lead III)
indicating acute right heart strain
Sinus tachycardia: most commonly cited abnormality
T wave inversion on leads V1-V4: another most commonly cited abnormality (due to RV strain)
Right bundle branch block
Low amplitude deflections
ELECTRICAL ALTERNANS
Beat to beat variation in the QRS amplitude
Seen in massive pericardial effusion and/or cardiac tamponade
BUNDLE BRANCH BLOCKS
V1
V6
Normal
RBBB
LBBB
15
A. Left Bundle Branch Block (LBBB)
QRS duration >0.12 sec (complete LBBB)
If <0.12 sec, then it is considered incomplete LBBB
Broad, notched, or slurred R-waves in leads I, aVL,
V5 and V6
Small or absent initial R-waves in right precordial
leads (V1 and V2) followed by deep S-waves
Absent septal Q-waves in leads I, V5 and V6
B. Right Bundle Branch Block (RBBB)
QRS duration >0.12 sec (complete RBBB)
If <0.12 sec, then it is considered incomplete RBBB
Slurred S-wave in leads I and V6
RSR pattern in V1 (“bunny ears”)
PERICARDITIS
Acute Pericarditis
A. Stages of Pericarditis
Stage 1: Widespread ST elevation and PR depression with reciprocal changes in aVR (first two weeks)
Stage 2: Normalization of ST changes; generalized T wave flattening (1 to 3 weeks)
Stage 3: Flattened T waves become inverted (3 to several weeks)
Stage 4: ECG returns to normal (several weeks onwards)
16
B. Pericarditis versus Myocardial Infarction
PERICARDITIS
Diffuse ST elevations which are concave upward
MYOCARDIAL INFARCTION
ST elevations which are convex upward
ST elevation
T-waves
Q-waves
Reciprocal Change
PR depression
T-wave usually not inverted unless ST is
isoelectric
Usually absent
Unusual
Usually present
T-waves may begin to invert before ST
becomes isoelectric
Present
Common
Absent
WOLFF PARKINSON WHITE (WPW) PATTERN
Pre-excitation pattern: atrial impulse activates the
ventricle earlier than would be expected if the
impulse traveled by way of the normal AV
conduction system
o Triad of WPW: PR interval <120 msec,
QRS >120 msec, (+) delta wave (slurred
upstroke or initial portion of QRS complex)
o Secondary ST-T wave abnormalities
opposite that of the delta wave and QRS
forces
ARRHYTHMOGENIC RV DYSPLASIA (ARVD)
Epsilon wave: a small positive deflection (‘blip’)
buried at the end of the QRS complex, representing
delay in depolarization of the right ventricular (RV)
free wall and outflow tract
Epsilon waves, found in 50% of patients with
ARVD, are due to the slowed intraventricular
conduction, hence the terminal notch in the last 1/3
segment of the QRS complex (which represents
the right ventricular activation)
BRUGADA ECG PATTERN
Type 1
Type 2
Prominent coved ST-elevation displaying J-point amplitude or ST-elevation >2mm,
followed by a negative T-wave
>2 mm J-point elevation, >1 mm ST-elevation and a saddleback appearance, followed by
a positive or biphasic T-wave
Type 3
17
DEXTROCARDIA (“Right Sided Heart”)
Absent R-wave progression in the chest leads (dominant S-waves throughout)
Predominantly negative P-wave, QRS complex, and T-wave in lead I
Low voltage in leads V3-V6 (because these leads are placed on the left side of the chest)
Accidental reversal of the left and right arm electrodes may produce a similar ECG pattern in the limb leads but
with normal QRS morphology in the precordial leads
OTHER ECG FINDINGS
Non-specific ST-T wave changes
Poor R wave progression
Low voltage complexes
Electrolyte abnormalities
T-wave inversion, ST segment depression/elevation not fulfilling the
criteria for ischemia or infarction (as outlined above): flattened or
slightly inverted T-waves, ST segments slightly above or below the
isoelectric line
R-wave in leads V1-V3 is < 3 small boxes
Normal R-wave in V4-V6
QRS complexes <5 small boxes in limb leads or < 10 small boxes in
chest leads
Example: COPD, anasarca, obesity, myocarditis, moderate-sized to
massive pericardial effusions
Hypokalemia
Prominent U wave + flattened T wave
Hyperkalemia
Peaked T-waves > 10 mm, wide QRS, sine
wave pattern
Hypocalcemia
Prolonged QT interval
Hypercalcemia
Shortened QT interval
CHEST RADIOGRAPH INTERPRETATION
I. BASIC STEPS IN READING CHEST X-RAYS (CXR)
Step 1: Identify general data
Step 2: Determine view (PA, AP, lateral, decubitus)
Step 3: Assess quality of film
Step 4: Assess anatomy and determine abnormalities
18
STEP 1:
IDENTIFYING GENERAL DATA OF THE PATIENT
Patient name
Date/Time CXR was taken
Diagnosis of patient
Indication for CXR
STEP 2:
DETERMINING THE VIEW
Postero-Anterior View (PA)
Scapula winged out, ribs and clavicles more angulated
Arms at an angle with the body, with hands at waist
Mongolian hat sign appreciated
(formed by the C7 and T1 spinous + transverse
processes)
Heart not magnified
Antero-Posterior View (AP)
Scapula not winged out; clavicles more horizontal
Arms parallel to body
Mongolian hat sign not appreciated
Heart and other structures magnified
STEP 3: ASSESSING THE QUALITY OF THE FILM
Inclusion
Inspiratory Effort
Exposure
Obliquity
Apices of the lungs to the costophrenic angles should be adequately visualized
One should count >8 intercostal spaces, 6-8 anterior ribs, 9-11 posterior ribs
Upper four thoracic vertebrae should be visualized
Medial ends of both clavicles equidistant from midline
The spinous process of the thoracic vertebra should be in the midline
STEP 4: ASSESSING ANATOMY AND ABNORMALITIES
A. General Structure
Soft tissues and bones: soft tissue swellings, rib fractures, breast shadow, osteopenia/osteoporosis
Trachea and mediastinum: carinal angle, tracheal position, mediastinal widening, masses
Vessels: aortic knob and pulmonary arteries
Diaphragm: right hemidiaphragm is usually higher than the left
B. The Heart
Assess CT ratio: >0.50 in PA view suggests cardiomegaly
Cardiomegaly cannot be definitively ascertained on AP films, due to the possibility of magnification effects
CHAMBER
Left ventricular
enlargement
Right ventricular
enlargement
Left atrial enlargement
Right atrial enlargement
PA FILM
Apex displaced inferiorly and laterally
(drooping apex)
Apex displaced superiorly and
laterally (uplifted apex)
Prominence of left atrial appendage
Loss of cardiac waistline
Widening of carinal angle (>70o)
Double density sign on right cardiac
border
Bulging right heart border (height >1/2
of right cardiac silhouette and width
1/3 of right hemithorax)
LATERAL FILM
Obliteration of retrocardiac
space
Obliteration of retrosternal
space
Posterior displacement of the
left mainstem bronchus on
lateral film
N/A
C. The Lungs
CP angle: blunting suggests minimal pleural effusion
Pleura: check for pneumothorax, lesions
Parenchyma: check for opacities, densities, infiltrates
Lobes of the lungs:
19
o
o
Right Lung (3 lobes): Right upper lobe (RUL) + right middle lobe (RML) + right lower lobe (RLL)
Left lung (2 lobes): Left upper lobe (LUL) + lingula + left lower lobe (LLL)
II. COMMON CHEST X-RAY PATHOLOGIES
Aortic Aneurysm
Atelectasis
Bronchiectasis
Consolidation
COPD/Emphysema
Fibrosis
Fungus Ball
Hamartoma
Pericardial Effusion
Pleural Effusion
Pneumomediastinum
Pneumoperitoneum
Pneumothorax
Pulmonary edema
Pulmonary Metastasis
Mediastinum >30% of thoracic diameter, or mediastinum >8-10 cm
Density in the area of the collapsed lung
Displacement of interlobular fissures (direct sign)
Surrounding structures deviated to the side of the collapsed lung (ipsilateral
mediastinal shift)
Crowding of vessels/bronchi
Ipsilateral diaphragmatic elevation
Appears as “bunches of grapes” (ring shadows)
Tram-track lines
Inhomogenous opacities
Prominent air bronchogram sign
Hyperaerated lungs
Flattened hemidiaphragms
Tubular heart
Occasionally, bullae
Decreased lung volume
Shift of mediastinum and surrounding structures towards fibrotic area
Blurred heart border or diaphragm with indistinct vascular markings in the areas
of fibrosis
Homogenous round opacity with a crescent sign
Popcorn ball lesion
Generalized enlargement of the cardiac shadow (“water bottle sign”) with
normal vascular markings
Blunting of costophrenic angles
Meniscus sign
Presence of gas between the mediastinal structures
Presence of gas underneath the diaphragm
Hyperlucent pulmonary area
Loss of vascular markings beyond the visceral pleural line
Mediastinal structures deviated to contralateral side (tension pneumothorax)
Prominent hilar vessels (hilar fullness) in a bat-wing distribution
Cephalization of vessels
Kerley B lines
Cannon ball lesions
ARTERIAL BLOOD GAS (ABG) INTERPRETATION
I. BASIC STEPS IN ABG INTERPRETATION
Step 1: Determine the primary acid-base disorder and whether compensation is appropriate
Step 2: Check for secondary acid-base disorders
Step 3: Compute for anion gap and / when needed
Step 4: Check oxygenation status
20
CHAPTER 2
CARDIOLOGY
I. Introduction to Cardiology
II. Approach to Patients with Cardiovascular Conditions
1.
2.
3.
Cardiovascular History
Cardiovascular Physical Examination
The Cardiac Diagnosis
III. Common Conditions in Cardiology
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Atherosclerosis and Dyslipidemia
Hypertension
Heart failure
Chronic Stable Angina Pectoris
Acute Coronary Syndrome
A. Non-ST Elevation Acute Coronary Syndrome
B. ST-elevation Myocardial Infarction
Rheumatic Fever
Valvular Heart Disease
Pericarditis
Cardiac tamponade
Cardiomyopathy
Atrial Fibrillation
Peripheral Artery Disease
CorPulmonale
37
SECTION 1
INTRODUCTION TO CARDIOLOGY
CARDIOLOGY FORMULAS
SV = EDV – ESV
EF = SV
EDV
CO = HR X SV
STROKE VOLUME (SV)
Volume of blood pumped with each heart beat
Normal range is 55-100mL (for a 70kg man, normal
is ~70mL)
SV = stroke volume (mL/beat)
EDV = end diastolic volume (N: 65-240 mL)
ESV = end systolic volume (N: 16-143 mL)
EJECTION FRACTION (EF)
Most useful index of LV function
Fraction of blood ejected by the LV during systole
EF = ejection fraction
CARDIAC OUTPUT (CO)
Volume of blood being pumped by the heart per
minute
Normal CO = 5.0 – 5.5 L/min
CO = cardiac output (L/min)
HR = heart rate (bpm)
BLOOD PRESSURE (BP)
SVR = systematic vascular resistance (resistance
to blood flow through vascular system)
BP = CO x SVR
BODY SURFACE AREA (BSA)
BSA = Weight (kg) x Height (cm)
3600
Better indicator of metabolic mass than body
weight
BSA = body surface area (m 2)
CARDIAC INDEX (CI)
CI = CO
BSA
SV = EDV – ESV
Marker of cardiac function in relation to BSA, thus
relating heart performance to the size of the
individual
Normal CI = 2.6 – 4.2 L/min/m2
If CI < 1.8 L/min/m2 suspect cardiogenic shock
MEAN ARTERIAL PRESSURE (MAP)
Defined as the average arterial pressure during a
single cardiac cycle
SBP = systolic blood pressure in mmHg
DBP = diastolic blood pressure in mmHg
Normal MAP = > 60mmHg
can sustain organ
perfusion (normally 70-110 mmHg)
38
PULSE PRESSURE (PP)
Represents the force that the heart generates each
time it contracts
PP = SP – DP
PP = pulse pressure: usually about 30-40 mmHg
SP = systolic pressure (mmHg)
DP = diastolic pressure (mmHg)
Normal PP: if PP < 25% of the systolic value (eg, Low stroke volume, blood loss, aortic stenosis, tamponade)
Wide PP: may reach up to 100mmHg (eg., exercise, atherosclerosis, aortic regurgitation, AV malformation,
hyperthyroidism, aortic dilatation / aneurysm, fever, anemia, pregnancy, anxiety, beri-beri)
Maximum HR = 220 – Age
Target HR = Maximum HR x
MAXIMUM HEART RATE
Highest HR an individual can achieve without
severe problems through exercise-induced stress
TARGET HEART RATE
A specific age-based pulse rate to be maintained
0.85
during aerobic exercise to ensure optimal
cardiovascular function
39
SECTION 2
APPROACH TO PATIENTS WITH CARDIOVASCULAR CONDITIONS
CARDIOVASCULAR HISTORY
I. CARDINAL SYMPTOMS OF CARDIOVASCULAR DISEASE
Chest pain or discomfort
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), wheezing
Palpitations, dizziness, syncope
Cough, hemoptysis
Fatigue, weakness
Pain in extremities with exertion (claudication)
II. COMMON CAUSES OF CHEST PAIN
CONDITION
Cardiac Causes
DURATION
QUALITY
Angina
2-10 mins
Pressure, tightness,
squeezing,
heaviness, burning
Unstable Angina
10-20 mins
Similar to angina but
often more severe
Similar to angina
Acute MI
> 30 mins
Similar to angina but
often more severe
Similar to angina
Variable
As described for
angina
As described for
angina
Aortic Stenosis
Pericarditis
LOCATION
Retrosternal
Radiation to
neck, jaw,
shoulders or
arms (left)
Retrosternal or
toward apex
Left shoulder
and trapezius
radiation
Hours to days
Sharp
Sudden onset of
unrelenting pain
Tearing or ripping
sensation; knife-like
Sudden onset
Pressure
Variable
Pressure
Substernal
Variable
Pleuritic
Unilateral, often
localized
Sudden onset;
several hours
Pleuritic
Unilateral on
side of
ASSOCIATED FEATURES
Precipitated by
exertion, exposure to
cold, psychologic
stress
Similar to angina but
occurs with low levels
of exertion or at rest
Unrelieved by
nitroglycerin
May be associated
with evidence of heart
failure or arrhythmia
Late-peaking systolic
ejection murmur
radiating to carotids
Relieved by sitting up
and leaning forward
Pericardial friction rub
is present
Vascular Causes
Acute
Aortic
Syndrome
(Dissection)
Pulmonary
Embolism
Pulmonary
Hypertension
Anterior chest,
often radiating to
the back,
between
shoulder blades
Often unilateral,
on the side of
embolism
Associated with
hypertension and/or
underlying connective
tissue disorder (e.g.,
Marfan syndrome)
Dyspnea, tachypnea,
tachycardia,
hypotension
Dyspnea
Signs of increased
venous pressure
Pulmonary Causes
Pneumonia
Pleuritis
Spontaneous
Pneumothorax
or
Dyspnea, cough,
fever, rales,
occasional pleural
friction rub
Dyspnea
Decreased breath
40
pneumothorax
sounds ipsilaterally
Non-Cardiopulmonary Causes
Esophageal
Reflux
10-60 mins
Burning
Substernal,
epigastric
Esophageal
Spasm
Peptic Ulcer
2-40 mins
Retrosternal
Prolonged
Pressure, tightness,
burning
Burning
Gallbladder
Disease
Prolonged
Aching or colicky
Costochondritis
Variable
Aching
Herpes Zoster
Variable
Sharp or burning
Emotional/
Psychiatric
Variable; may
be fleeting
Variable
Epigastric.
Substernal
Epigastric, RUQ,
substernal
Sternal
Dermatomal
distribution
Variable; may
be retrosternal
Worsened by
postprandial
recumbency
Relieved by antacids
Can closely mimic
angina
Relieved by food
intake or antacids
May follow meals
Precipitated by fatty
meals
May be reproduced
by localized or
pinpoint pressure on
exam
Vesicular rash
Situational factors
precipitates
symptoms
Often with history of
anxiety/depression
CARDIOVASCULAR PHYSICAL EXAMINATION
I. COMMON FINDINGS ON INSPECTION
FINDING
Central Cyanosis
Peripheral Cyanosis
Differential Cyanosis
Homan’s Sign
Kussmaul’s Sign
Abdominojugular Reflux
REMARKS
Cyanosis due to right-to-left shunting, allowing deoxygenated blood to reach
systemic circulation
Cyanosis due to reduced extremity blood flow due to small vessel
vasoconstriction
Isolated cyanosis affecting the lower extremities but not the upper (seen in
large PDA)
Posterior calf pain on active dorsiflexion of the foot against resistance
(suggestive of DVT)
Rise or a lack of JVP with inspiration, associated with constrictive pericarditis
Normally, the venous pressure should fall by at least 3 mmHg with inspiration
Pressure over the upper abdomen (RUQ) for at least 10 seconds
Positive response: sustained rise of >3 cm in JVP for at least 15 seconds after
release of the hand
II. COMMON FINDINGS ON PALPATION
FINDING
Cardiac Findings
Normal LV Apex
LV Enlargement
RV Enlargement
Peripheral Pulses
PulsusParvus et Tardus
Bifid Pulse
PulsusParadoxus
REMARKS
Located in the left 5th ICS, mid-clavicular line
Normal apex is a localized systolic outward thrust, less than 2.5 cm in
diameter
Apical impulse is shifted laterally & downwards
Sustained systolic lift / heave in the left parasternal area
A weak and delayed pulse that suggest severe aortic stenosis
Two systolic peaks can be appreciated, described in hypertrophic obstructive
cardiomyopathy (HOCM), with inscription of percussion and tidal waves
Refers to a fall in SBP > 10mmHg with inspiration, seen in patients with:
41
PulsusAlternans
pericardial tamponade, massive pulmonary embolism, hemorrhagic shock,
severe obstructive lung disease, tension pneumothorax)
Beat-to-beat variability of pulse amplitude seen in severe LV systolic heart
failure
III. COMMON FINDINGS ON AUSCULTATION
A. Heart Sounds
HEART SOUND
First Heart Sound (S1)
Second Heart Sound (S2)
Third Heart Sound (S3)
Fourth Heart Sound (S4)
REMARKS
Coincides with closure of the mitral valve and tricuspid valve (Systolic
Pressure)
Caused by the closure of the aortic and pulmonic valves (Diastolic Pressure)
Indicates end of systole (or beginning of diastole)
Best heard at the base; splitting is normally heard
Variations include:
- Widened Interval: RBBB, severe MR
- Narrowly Split or Singular S2: Pulmonary arterial HPN
- Fixed Splitting: ASD secundum
- Paradoxical Splitting: LBBB, RV apical pacing, severe AS, HOCM, MI
Coincides with early diastole or rapid ventricular filling
It is caused by the flow of blood during rapid ventricular filling
Best heard after S2
Coincides with late diastole or atrial systole (atrial contraction/slow ventricular
filling)
Diminished ventricular compliance increases resistance to ventricular filling
More common in chronic LCH or active MI
B. Common Auscultatory Areas of the Heart
AREA
LOCATION
Aortic Area
From the 2nd to 3rd ICS at the right sternal border
Pulmonic Area
From the 2nd to 3rd ICS at the left sternal border
Tricuspid Area
From the 3rd to 5th ICS at the left sternal border
Mitral Area
Near the apex of the heart at the 5th ICS in the left mid-clavicular line
C. Grading of Murmurs
GRADE
Grade 1
Grade 2
Grade 3
Grade 4
Grade 5
Grade 6
D. Common Murmurs
POSSIBLE DIAGNOSIS
Pulmonic / Aortic Stenosis
Aortic Regurgitation
Tricuspid or Mitral
Regurgitation
VOLUME
Faint; needs concentration
Faint but can be heard readily by an experience observer
Moderately loud
Loud
Very loud; heard with stethoscope lightly pressed on the skin
Exceptionally loud; heard with stethoscope slightly above the chest wall
Tricuspid or Mitral Stenosis
Mitral Valve Prolapse
DESCRIPTION OF MURMUR
Systolic ejection murmur
Early diastolic murmur
Holosystolic (pansystolic) murmur if chronic
Early systolic murmur if acute
Murmur of TR usually increases with inspiration (Carvallo sign)
Late diastolic murmur / rumble
Systolic click with mid-to-late systolic murmur
E. Other Sounds
SOUND
Opening Snap (OS)
Pericardial Knock
Tumor Plop
DESCRIPTION
High-pitched and occurs after a very short interval following S2
From the 2nd to 3rd ICS at the left sternal border
From the 3rd to 5th ICS at the left sternal border
THRILL?
No
No
No
Yes
Yes
Yes
42
THE CARDIAC DIAGNOSIS
I. COMMON DIAGNOSTIC TESTS IN CARDIOLOGY
DIAGNOSTIC
Chest Radiograph (CXR)
12 Lead ECG
Holter Monitoring
Stress Testing
Electrophysiology Study (EPS)
Transthoracic
Echocardiography (TTE)
Transesophageal
Echocardiography (TEE)
Cardiac Magnetic Resonance
Imaging (MRI)
Computed Tomography
Angiography (CTA)
Nuclear Imaging
Intravascular Ultrasound
Coronary Angiography
Cardiac Catheterization
II. MAKING A CARDIAC DIAGNOSIS
COMPONENT
1. Underlying Etiology
2. Anatomic Abnormalities
3. Physiologic Disturbances
4. Functional Disability
REMARKS
Widely used to visualize the heart and lungs
Graphic recording of electric potentials generated by the heart to detect
arrhythmias, conduction disturbances and ischemia
Continuous ECG rhythm pattern for 24 hours or more to document
paroxysmal rhythm abnormalities
Non-invasive tool to evaluate the cardiovascular system’s response to stress
under controlled conditions:
o Exercise stress test: least invasive, makes use of a treadmill
o Pharmacologic stress test: drugs are used to induce stress (e.g.,
dobutamines)
Electrophysiological test of the heart involving intracardiac catheters with
electrodes probing the endocardium to test conduction pathways and
electrical activity
Uses ultrasound waves to visualize heart chambers and valves
Using Doppler studies, it can visualize blood flow through the heart
Echocardiography that uses a specialized probe with an ultrasound
transducer introduced into the esophagus to more accurately visualize
posterior structures
Differentiates soft tissues better than CT and allows comprehensive exams
for assessment of size, morphology, function and tissue characteristics
Displays vessels in the body (e.g., coronaries, aorta)
May also be used to detect calcium in the coronary arteries
Uses radioisotopes (Technetium, Thallium) taken up by viable myocardial
cells to assess myocardial perfusion, viability & function (ischemic
myocardium takes up less isotope)
Percutaneous procedure that uses catheters to visualize the lumen and the
interior wall of blood vessels
Determines the patency and configuration of the coronary artery lumen by
injecting contrast material into the coronary arteries
Uses invasive monitoring and blood sampling through a catheter inserted into
the heart to determine function, pressures, oxygenation, flow and volume of
blood within the chambers and great vessels
IMPORTANT QUESTIONS
Congenital, hypertensive, ischemic or inflammatory?
Which chambers are involved? Are they hypertrophied, dilated or both?
Which valves are affected? Are they regurgitant and/or stenotic?
Is there pericardial involvement?
Has there been a myocardial infarction?
Is an arrhythmia present?
Is there evidence of congestive heart failure or of myocardial ischemia?
How strenuous is the physical activity required to elicit symptoms?
Example:
Ischemic Heart Disease, Chronic Stable Angina Pectoris, CCS 3
Congestive Heart Failure NYHA FC III, in Sinus Rhythm
43
SECTION 3
COMMON CONDITIONS IN CARDIOLOGY
ATHEROSCLEROSIS AND DYSLIPIDEMIA
I. THE LIPID PROFILE
A. Total Cholesterol
TC = HDL + Non HDL
TC = HDL + [LDL + VLDL]
TC = HDL + LDL + TG
5
TC = total cholesterol in mg/dL
HDL = high density lipoprotein in mg/dL
LDL = low density lipoprotein in mg/dL
VLDL = very low density lipoprotein in mg/dL (estimated by dividing TG
level by 5)
TG = triglycerides in mg/dL
B. Individual Components
1. High Density Lipoproteins (HDL)
Removes cholesterol from peripheral tissues via the reverse cholesterol transport
Low HDL values < 40 mg/dL increased risk for heart disease
2. Non-High Density Lipoproteins (Non-HDL)
Includes low density lipoproteins (LDL) and very low density lipoproteins (VLDL)
Lower non-HDL cholesterol is desirable and is associated with a lower risk of heart disease
Value can be estimated from other lipid values when non-HDL level is not directly available:
NonHDL = TC – HDL
NonHDL = LDL + VLDL
NonHDL = LDL + TG
5
If VLDL values are not given, it can be
estimated by dividing triglyceride levels by 5
Non-HDL
are
ApoB-100
containing
atherogenic lipoproteins
C. The Lipoproteins
Composed of varying proportions of cholesterol, triglycerides and phospholipids
LDL and HDL carry most cholesterol
LIPOPROTEIN
REMARKS
Delivers
dietary
triglyceride
to peripheral tissues
Chylomicron
Delivers cholesterol to the liver in the form of chylomicron remnants
Delivers hepatic triglycerides to peripheral tissues (TG > cholesterol
VLDL
esters)
Secreted by the liver
Formed in the degradation of VLDL
IDL
Delivers triglycerides and cholesterol to the liver, where they are
degraded into LDL
Delivers hepatic cholesterol to peripheral tissues
LDL
Formed by lipoprotein lipase modification of VLDL in the peripheral
tissues
HDL
Mediates reverse cholesterol transport (from periphery back to the liver)
II. THE ACC/AHA 2013 GUIDELINES ON THE TREATMENT OF BLOOD CHOLESTEROL
Statin therapy is recommended for individuals at increased atherosclerotic cardiovascular disease (ASCVD) risk
who are most likely to experience a net benefit (benefit>harm)
There is insufficient evidence to support continued use of specific LDL-C and/or non-HDL-C treatment “targets”
Appropriate intensity of statin therapy should be used to reduce risk in those most likely to benefit
44
Non-statin therapies (e.g., fibrates, niacin), whether alone or in addition to statins, provide little benefit in risk
reduction
A. Four Major Statin Benefits Groups (ASCVD risk reduction outweighs risk of adverse events)
1. Acute coronary syndrome or history of MI
1
Patients with clinical ASCVD
2. Stable or unstable angina
3. Coronary or other arterial revascularization
4. Stroke, TIA or PAD
2
Primary elevations of LDL-cholesterol > 190mg/dL
3
Patients 40-75 years + LDL 70-189 mg/dL + Diabetes (without clinical ASCVD)
4
Patients 40-75 years + LDL 70-189 mg/dL + Estimated 10-year ASCVD risk > 7.5%
(without clinical ASCVD or diabetes)
B. Pooled Cohort Equations for ASCVD Risk Reduction
For the fourth group, risk prediction is done by using the pooled cohort equations for ASCVD risk prediction
(developed by the Risk Assessment Work Group)
Calculator is not appropriate for those with known ASCVD
Calculator is available online at http://tools.cardiosource.org/ASCVD-Risk-Estimator/
Computes for hard ASCVD events, including:
o
o
o
Non-fatal MI
Death due to coronary heart disease (CHD)
Fatal or non-fatal stroke
Data includes:
o Age, sex and race
o Total cholesterol and HDL levels
o Systolic BP
o Treatment for hypertension
o Diabetes
o Smoking history
C. Major Recommendations for Statin Therapy for ASCVD Prevention
Clinical ASCVD
LDL > 190 mg/dL
Age > 75
High Intensity Statin
(Class I)
Moderate Intensity Statin
(Class II)
Diabetes + 40-75
10 year ASCVD risk >
7.5% and Age 40-75
Moderate Intensity
Statin if risk is 5 to
<7.5%
(Class IIa)
High Intensity Statin if 10
year ASCVD Risk > 7.5%
(Class IIa)
*
45
D. Intensity of Statin Therapy
HIGH-INTENSITY THERAPY
Daily dose lowers LDL by > 50%
MODERATE-INTENSITY THERAPY
Daily dose lowers LDL by 30 to <50%
Atorvastatin 10-20 mg
Rosuvastatin 10 mg
Atorvastatin 40-80 mg
Simvastatin 20-40 mg
Rosuvastatin 20 mg
Pravastatin 40 mg
Lovastatin 40 mg
Fluvastatin XL 80 mg
Pitavastatin 2-4 mg
INDICATED FOR
Primary Prevention
For 40-75 yrs + LDL 70-189
For 40-75 yrs + LDL 70-189 mg/dL:
mg/dL:
With diabetes* , or
With diabetes and >
With 5 to <7.5% 10-year risk
7.5% 10-year risk*
(without ASCVD or MI)
> 7.5% 10-year ASCVD risk
For LDL-C >190 mg/dL:
(without ASCVD or DM);
moderate-to-high intensity
> 21 years + primary
LDL-C > 190 mg/dL (risk
Individuals in whom high-density statin
estimation is not
therapy would be recommended but
required)
have characteristics predisposing them
to statin-associated adverse effects**
Secondary Prevention
< 75 years + clinical
> 75 years or safety concerns +
ASCVD
clinical ASCVD
LOW-INTENSITY THERAPY
Daily dose lowers LDL by < 30%
Simvastatin 10 mg
Pravastatin 10-20 mg
Lovastatin 20 mg
Fluvastatin 20-40 mg
Pitavastatin 1 mg
Individualized (e.g., patients who
recover
from
mid-to-moderate
muscle symptoms with higher
doses of statins)
*For patients 40-75 years old with LDL 70-189 mg/dL and DM, moderate- (class I recommendation) or high-intensity (class Iia
recommendation if risk for ASCVD is >7.5%) may be considered, depending on the risk-benefit ratio.
**Multiple or serious comorbidities, including impaired renal or hepatic function; history of previous statin intolerance or muscle disorders;
unexplained alanine aminotransferase (ALT) elevations > 3 times the upper limit of normal (ULN); patient characteristics or concomitant use of
drugs affecting statin metabolism; age > 75 years
E. Monitoring
Fasting lipid profile within 4-12 weeks after initiation or dose adjustment and every 3-12 months thereafter
Indicators of anticipated therapeutic response to the recommended intensity of statin therapy (focus is on
the intensity of the statin therapy as an aid to monitoring):
o High-intensity statin therapy: LDL-C reduction of > 50% from the untreated baseline.
o Moderate-intensity statin therapy: LDL-C reduction of 30% to <50% from the untreated baseline.
III. MANAGEMENT
A. Non-Pharmacologic Management (ACC/AHA 2013 Guide for Lifestyle Management for Reducing CV Risk)
1. Diet
High in fruits and vegetables, whole grains; low fat; limit sweets
DASH diet (Dietary Approaches to Stop Hypertension):
o Rich in fruits, vegetables, whole grains, and low-fat dairy foods
o Meat, fish, poultry, nuts and beans
o Limited in sugar-sweetened foods and beverages, red meat, and added fats
2. Physical Activity
3-4 sessions a week, lasting 40 minutes per session
Moderate-to-vigorous intensity physical activity
46
B. Pharmacologic Management
DRUGS
Statins
Ezetimibe
Cholestyramine
MECHANISM OF ACTION
HMG-CoA reductase
inhibitor
Inhibits melavonate:
cholesterol precursor
Cholesterol absorption
inhibitor
Bile acid sequestrant
Prevents intestinal
reabsorption of bile
acids, this forcing liver
to use cholesterol to
make more bile acids
as replacement
LABORATOTY FEATURES
1st line of treatment
20-60% LDL reduction
Doubling of dose: 6%
additional lowering of
LDL
15-20% LDL reduction
Modest LDL reduction
Can increase
triglycerides
Fibrates
(Gemfibrozil,
Fenofibrate)
Upregulates lipoprotein
lipase which increases
hydrolysis of VLDL and
chylomicrons
35-50% fasting
triglyceride reduction
Niacin
Enhances activity of
lipoprotein lipase,
leading to decreased
VLDL and triglyceride
levels
Reduces hepatic VLDL
secretion into
circulation and
increases HDL
significantly
Only agent proven to
raise HDL levels
Omega-3-Fatty
Acids (“Fish Oil”)
Probucol
Unclear, but it is
thought to decrease
catabolism of
chylomicrons and
increase affinity of LDL
uptake
Increases rate of LDL
catabolism with strong
anti-oxidant properties
ADVERSE EFFECTS
Myositis / myopathy
Reversible elevation of
AST / ALT
May increase AST /
ALT
Bad taste, GI
discomfort
Decreased absorption
of fat-soluble vitamins
Contraindicated if
triglycerides >200
mg/dL (relative) or 500
mg/dL (absolute)
Myositis (increased
risk if with concomitant
statin use)
Increase in AST / ALT
Most common: nausea
Flushing
Hyperuricemia
Impaired glucose
tolerance
Primary use: lower
triglyceride levels (by
reducing triglyceride
synthesis in the liver)
Bad / fishy taste
Dyspepsia
Reduces LDL levels
Can reduce HDL levels
Can reduce HDL
QT interval
F. Potency Equivalence of Statins
DOSE OF AGENTS (mg)
PERCENT REDUCTION
Rosuvastatin
Atorvastatin
Simvastatin
Pravastatin
Total Cholesterol
LDL-C
10
20
22%
27%
10
20
40
27%
36%
5
20
40
32%
42%
10
40
80
37%
48%
20
80
42%
54%
Stained doses on same rows are equipotent
(e.g., Rosuvastatin 10 mg is equivalent to atorvastatin 40 mg and both reduce LDL by 48%)
47
HYPERTENSION
I. DIAGNOSIS OF HYPERTENSION
Two or more elevated readings on at least 2 clinic visits over a period of one to several weeks
Definition – adults with:
o SBP > 140 mmHg, or
o DBP > 90 mmHg
II. CLASSIFICATION OF HYPERTENSION
A. Classification as to Etiology
Primary / Essential (most common)
Secondary Hypertension
B. Clues for Suspecting Secondary Hypertension
Age of onset <20 or >50 years
No family history of HPN
DBP >100-120 mmHg
Sudden increase in BP in a patient with stable Stage I HPN
Poor BP control, despite good compliance
Systemic findings (e.g. weight loss/gain, potassium abnormalities)
C. Classification as to Stages
CLASSIFICATION
Normal
Pre-hypertension
Stage 1 Hypertension
Stage 2 Hypertension
Isolated Systolic Hypertension
D. Definition of Terms
VARIATION
White Coat Hypertension
Resistant Hypertension
Orthostatic Hypotension
SYSTOLIC (mmHg)
<120
120-139
140-159
> 160
> 140
DIASTOLIC (mmHg)
and <80
or 80-89
or 90-99
or > 100
and <90
DESCRIPTION
At least three separate clinic-based measurements >140/90 mmHg and at least
two non-clinic-based measurements <140/90 mmHg in absence of any evident of
target organ damage
Defined as high BP uncontrolled with three drugs or controlled with at least four
anti-hypertensive drugs (including a diuretic)
Fall in SBP >20 mmHg or in DBP >10 mmHg in response to assumption of the
upright posture from a supine position within 3 minutes
III. THE EIGHT JOINT NATIONAL COMMITTEE (JNC-8): MANAGEMENT OF HYPERTENSION
A. Simplified Algorithm
Age > 60
Age < 60
Any Age
(+) Diabetes
(-) CKD
Any Age
(+/-) Diabetes
(-) CKD
BP Goal
<150 / <90
BP Goal
<140 / <90
BP Goal
< 140 / <90
BP Goal
< 140 / <90
Initial Drug
Thiazide, or ACEI
or ARB, or CCB
Initial Drug
ACEI or ARB
48
B. Summary of the JNC-8 Recommendations on Management of Hypertension
RECOMMENDATION
No. 1
PATIENT POPULATION
Patients > 60 years old
Patients > 18 years old with
CKD
INITIATE THERAPY WHEN
SBP > 150 mmHg or
DBP > 90 mmHg
DBP > 90 mmHg
SBP > 140 mmHg
SBP > 140 mmHg or
DBP > 90 mmHg
GOAL BLOOD PRESSURE
SBP < 150 mmHg and
DBP < 90 mmHg
DBP < 90 mmHg
SBP < 140 mmHg
SBP < 140 mmHg and
DBP < 90 mmHg
No. 2
No. 3
Patients < 60 years old
No. 5
Patients > 18 years old with
DM
SBP > 140 mmHg or
DBP > 90 mmHg
SBP < 140 mmHg and
DBP < 90 mmHg
RECOMMENDATION
No. 6
PATIENT POPULATION
Non-black population
(including those with DM)
No. 4
No. 7
No. 8
No. 9
INITIAL ANTIHYPERTENSIVE AGENT OPTIONS
Thiazide-type diuretic
Calcium channel blocker (CCB)
Angiotensin-converting enzyme inhibitor (ACEI)
Angiotensin receptor blocker (ARB)
Thiazide-type diuretic
Calcium channel blocker (CCB)
Angiotensin-converting enzyme inhibitor (ACEI)
Angiotensin receptor blocker (ARB)
General black population
(including those with DM)
Patients > 18 years old with
CKD (regardless of race or
DM status)
The main objective of hypertension treatment is to attain and maintain goal BP:
If goal BP is not reached within a month, increase the dose of the initial drug or add
a second drug (thiazide-type diuretic, CCB, ACEI or ARB)
If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list
Do not use an ACEI and an ARB together in the same patient
If goal BP cannot be reached using only the drugs in recommendation 6 because
of a contraindication or the need to use more than 3 drugs to reach goal, other
classes can be used
IV. MANAGEMENT OF HYPERTENSION
A. Screening for Hypertension:
Us Preventive Services Task Force recommends screening for high blood pressure in adults > 18 years old
Screening:
o Every 2 years if BP < 120/80 (normal)
o Yearly if BP 120-139 / 80-89 (pre-hypertensive)
B. Non-Pharmacologic Management: Lifestyle Management for Hypertension
ASPECT
GOAL
Weight Reduction
Attain and maintain BMI < 25 kg/m 2
Dietary Salt Reduction
< 6 g NaCl/day
Adapt DASH-type Dietary Plan
Diet rich in fruits, vegetables, and low-fat dairy products
Reduced content of saturated and total fat
Moderation of Alcohol
For those who drink alcohol, consume:
Consumption
o < 2 drinks/day in men
o <1 drink/day in women
Physical Activity
Regular aerobic activity (e.g., brisk walking for 30 mins/ day)
C. Common Drugs for Hypertension
CLASS
Diuretics
Thiazide diuretics
MECHANISM OF ACTION
Selectively of Na/Cl
symporter
which
ADVERSE EFFECTS
Sexual impotence
Hypokalemia
REPRESENTATIVE
DRUGS WITH DOSE
RANGE
mg/day (doses per day)
Hydrochlorothiazide
6.25-50 mg OD
49
acts on the distal
convoluted tubules,
leading to enhanced
NaCl excretion
Dyslipidemia
Hyperuricemia
Hyperglycemia
Loop diuretics
Acts on the thick
ascending limb of
the Loop of Henle
Hypokalemia
Metabolic alkalosis
Ototoxicity
Hypocalcemia
hypomagnesemia
Potassium-Saving
diuretics
Spironolactone
antagonizes action
of aldosterone
Triamterene &
amiloride inhibit NaK exchange
mechanism
Hyperkalemia
Gynecomastia (only
for spironolactone)
Metolazone
2.5-5
mg OD
Indapamide 1.5mg
OD
Furosemide 40-80
mg OD
Bumetanide 0.5-2
mg OD
Ethacrynic Acid 25100 mg BID
Spironolactone
12.5-100 mg OD
Amiloride 5-20 mg
OD
Eplerenone 25-100
mg OD-BID
Triamterene 25-100
mg OD
Beta Blockers (BB)
Cardioselective BB (B1)
Non-Selective BB (B1/B2)
Vasodilating BB (A1/B)
Selectively inhibits
B1-Receptors (less
pulmonary effects)
Inhibits both B1 and
B2 receptors
Bronchospasm
Bradycardia
AV block
Metabolic syndrome
Glucose intolerance
Sleep disturbance
Depression
Combined A1 & Badrenergic receptor
blockade
Nebivolol: additional
nitric
oxide
potentiating effect
Atenolol 25-100 mg
OD
Metoprolol 50-400
mg/day
Metoprolol XL 50200 mg OD
Bisoprolol
2.5-20
mg OD
Esmolol IV
Propanolol 40-180
mg BID-TID
Others:
Pindolol,
Timolol, Nadolol
Cardvedilol 6.25-25
mg BID
Nebivolol 5-10 mg
OD
Others: Labetolol
Calcium Channel Blockers (CCB)
Dihydropyridine
Blocks L-type
calcium channels
Vascular effect >
AV-node effect
Tachyarrhythmia
Edema
Headaches
Blocks
L-type
calcium channels
AV node effect >
vascular effect
AV block (2nd and
3rd degree)
Non-Dihydropyridine
Trifascicular block
Severe LV
dysfunction
Drugs Acting on the Renin-Angiotensin-Aldosterone-System (RAAS)
ACE-Inhibitors
Inhibits ACE
Result: angiotensinI is not converted to
angiontensin-II
Cough
Angioedema
Hyperkalemia
Renal agenesis
Amlodipine 2.5-10
mg OD
Felodipine
2.5-20
mg/OD
Nifedipine
30-120
mg/day
Diltiazem 120-360
mg/day
Verapamil 120-480
mg/day
Captopril 25-150 mg
BID-TID
Enalapril
2.5-20
mg/day
Lisinopril
5-20
mg/day
Perindopril 2.5-10
50
Angiotensin Receptor
Blockers
Competitive
antagonism
angiotensin-II
Directly
rennin,
enzyme
RAAS
Direct Renin Inhibitor
with
inhibits
the
first
in
the
Hyperkalemia
Renal agenesis
Less cough and
angioedema
Angioedema
Hyperkalemia
Cough
Hyperuricemia
mg/day
Ramipril 2.5-10 mg
OD
Candesartan 8-32
mg OD
Irbesartan 150-300
mg OD
Losartan 25-100 mg
OD
Olmesartan
5-40
mg OD
Telmisartan 20-80
mg OD
Valsartan
80-320
mg OD
Aliskiren 75-300 mg
OD
Other Anti-Hypertensives
Alpha Blockers
Blocks
the
postsynaptic
A1receptors found in
capacitance
&
resistance vessels
Central Sympatholytics
Activation
receptors
CNS
Direct Vasodilators
Release of nitric
oxide, leading to
arterial vasodilation
of
in
A2the
Postural
hypotension
Reflex tachycardia
Sedation
Xerostomia
Impotence
CNS side effects
Rebound HPN on
withdrawal
Reflex tachycardia
Headache
Hypotension
Lupus-like
syndrome
(for
hydralazine)
Hypertrichosis (for
minoxidil)
Prazosin
1-5
mg/day
Terazosin
1-5
mg/day
Doxazosin 1-8 mg
OD
Clonidine
75-150
mcg BID-TID
Methyldopa
250500 mg BID-TID
Hyrdrazaline 25 mg
TID
Minoxidil
2.5-80
mg/day
V. MANAGEMENT OF UNCONTROLLED HYPERTENSION
A. Differentiation Between Types of Uncontrolled Hypertension
Usual BP
Actual Target
Organ Damage
Management
Monitoring
SEVERE HYPERTENSION
180-220 / 110-130 mmHg
None (asymptomatic)
Long-acting oral medication can
simple be restarted (usually
occurs in chronic hypertensives
who stopped taking medication)
Require outpatient follow-up
within 24-72 hours
HYPERTENSIVE URGENCY
>220/130 mmHg
None
HYPERTENSIVE CRISIS
> 220/130 mmHg
Present
(brain,
heart,
kidney, retina or vessels)
Short-acting oral medications
Immediate reduction of BP
with intravenous medication
Require outpatient follow-up
within 24 to 72 hours
Admit for monitoring (ICU)
51
B. Common Intravenous (IV) Drugs for Hypertensive Emergencies
DRUG
DOSE
5-15 mg/hr as continuous infusion
Nicardipine
Starting dose 5 mg/hr, increase q1530 mins by 2.5 mg until goal BP
achieved
Nitroglycerin
5-200 ug/min
5 ug/min increase q5 mins
0.3-10 ug/kg/min, increase by 0.5
Nitroprusside
ug/kg/min q5 mins until goal BP
achieved
Esmolol
0.5-10 ug/kg/min as bolus
500-300 ug/kg/min as infusion
Labetalol
0.25-0.5 mg/kg; 2-4 mg/min until goal
BP is reached, thereafter 5-20 mg/hr
CONTRAINDICATIONS & SIDE EFFECTS
Liver failure
Can cause headaches
Liver/kidney failure
Can cause cyanide toxicity
2nd or 3rd degree AV block, systolic
heart failure, bradycardia, COPD
2nd or 3rd degree AV block, systolic
heart failure, bradycardia, COPD
C. Recommended Treatment of Hypertensive Emergencies Based on End-Organ Involvement
TYPE OF EMERGENCY
TIMELINE, TARGET BP
THERAPY*
HPN Crisis with
Several hours
Labetalol,
Nitroprusside,
Retinopathy or Acute
Nicardipine
Target MAP: decrease by 20% t0 25%
Renal Insufficiency
HPN Encephalopathy
Immediate
Labetalol,
Nicardipine,
Nitroprusside
Target MAP: decrease by 20% to 25%
Acute Aortic Dissection
Immediate
Nitroprusside + Metoprolol,
Labetalol
Target SBP < 110 mmHg
Acute Pulmonary Edema
Immediate
Nitroprusside
+
Loop
Diuretic, Nitroglycerin
Target MAP: 60-100 mmHg
Acute Coronary Syndrome
1 hour
Nitroglycerin, Labetalol
Target MAP: 60-100 mmHg
Acute Ischemic Stroke and
1 hour
Labetalol,
Nicardipine,
BP > 220/120 mmHg
Nitroprusside
Target MAP: decrease by 5%
Cerebral Hemorrhage and
1 hour
Labetalol,
Nicardipine,
SBP > 180 mmHg or MAP >
Nitroprusside
Target SBP: < 180 mmHg and MAP 130
130 mmHg
mmHg
Several hours
Phentolamine
(after
Cocaine intoxication
benzodiazepines),
Target SBP: < 140 mmHg
Nitroprusside
Labetalol + MgSO4 and oral
Severe preeclampsia/
Immediate
anti-HPN, Nicardipine
eclampsia
Target BP: < 160/105 mmHg
Emergency Delivery of
Fetus
*Those underlined: first-line therapy
VI. HYPERTENSION AND PREGNANCY
Four categories of hypertension in pregnancy:
1. Pre-eclampsia: severe progressive multisystem disorder diagnosed by hypertension accompanied by any one
of the following:
o Proteinuria
o BP of 160/110 mmHg or higher despite bed rest
o Thrombocytopenia
o Impaired liver function
o Progressive renal insufficiency
o Pulmonary edema
o New-onset cerebral or visual disturbance
2. Chronic hypertension: hypertension predating pregnancy
3. Chronic hypertension with superimposed preeclampsia
4. Gestational hypertension: BP elevation after 20 weeks gestation in the absence of the additional systemic
features listed above
52
HEART FAILURE (HF)
I. ETIOPATHOGENESIS
A clinical syndrome consisting of a constellation of clinical symptoms (dyspnea & fatigue) and signs (edema and
rales) that lead to frequent hospitalization, a poor quality of life, and a shortened life expectancy.
Etiologies:
o Coronary artery disease (CAD): most common cause of HF in industrialized countries (60-75%)
o Hypertension: cause of HF in 75% of patients
o Idiopathic cardiomyopathy: 20-30% of depressed EF HF
o Pulmonary heart disease: cor pulmonale, pulmonary vascular disorders
o High output states: thyrotoxicosis, nutritional disorders (beriberi), excessive blood flow requirements,
chronic asthma
II. CLASSIFICATION / STAGES OF HEART FAILURE (HF)
A. Classification Based on Function / Ejection Fraction (EF)
TYPE
EJECTION
DESCRIPTION
FRACTION
Progressive disorder initiated by an
Systolic Heart
Depressed HF
index event (e.g., MI, volume
Failure or HF with
< 40%
overload, chronic anemia) that leads
reduced EF (HfrEF)
to a decline in the pumping capacity
of the heart
Proposed
mechanisms
include
Diastolic Heart
diastolic dysfunction and extraFailure or HF with
Preserved EF
cardiac mechanisms such as
preserved EF
> 40-50%
increased vascular stiffness and
(HfpEF)
impaired
renal
function
(still
undefined and evolving)
Occur when the body’s requirements
Normal at first, then for oxygen and nutrients are
High-Output Heart
may decrease over increased and the demand outstrips
Failure
time
what the heart can provide
COMMON EXAMPLES
CAD (e.g., MI)
Dilated cardiomyopathy
Valvular heart disease
Pathologic
hypertrophy
(HOCM, HPN)
Aging, fibrosis
Restrictive cardiomyopathy
Thyrotoxicosis
Beriberi
Chronic anemia
Systemic
arteriovenous
shunting
B. American College of Cardiology / American Heart Association (ACC/AHA) Stages of Heart Failure
STAGE
DESCRIPTION
EXAMPLES
At
high
risk
for
HF
but
without
structural
heart
Patients
with
HPN,
CAD, DM or patients using
A
disease or HF symptoms
cardiotoxins or with family history of cardiomyopathy
Structural heart disease but without signs or Patients with previous MI, LV systolic dysfunction, or
B
symptoms of HF
asymptomatic valvular disease
Structural
heart
disease
with
previous
or
Patients with known structural heart disease with
C
current symptoms of HF
shortness of breath, fatigue, reduced exercise tolerance
Refractory
HF
requiring
specialized Patient who have marked symptoms at rest despite
interventions
maximal therapy (e.g., patients with recurrent
D
hospitalizations or cannot be safely discharged without
special interventions)
C. New York Heart Association (NYHA) Functional Classification
NYHA
DESCRIPTION
Symptoms
occur
with greater than ordinary
I
physical activity
Symptoms occur with ordinary physical activity
II
III
IV
Symptoms occur with less than ordinary
physical activity
Symptoms may be present even at rest
COMMENTS
No limitation of physical activity
Can climb > 2 flights of stairs with ease
Slight limitation of physical activity
Can climb 2 flights of stairs but with difficulty
Marked limitation of physical activity
Can climb <1 flight of stairs
Unable to carry on activity without symptoms
Dyspnea at rest
53
III. CLINICAL MANIFESTATIONS
A. Symptoms
Fatigue and Shortness of
Breath
Orthopnea/Nocturnal Cough
Paroxysmal Nocturnal
Dyspnea
Cheyne-Stokes Respiration
Others
B. Signs
General Appearance and
Vital Signs
Cardiovascular
Pulmonary
Abdomen
Extremities
Cardinal symptoms
Due to pulmonary congestion
juxtacapillary J-receptors are activated
cardiac dyspnea
Redistribution of fluid from splanchnic and lower extremity into the central
circulation on recumbency
Severe dyspnea that awakens patient from sleep 1-3 hours after patient retires
Increased pressure in the bronchial arteries
In 40% of advanced HF: series of apnea
hyperventilation
hypocapnia
Diminished sensitivity of the respiratory center to arterial PCO2
GI: anorexia, nausea, early satiety, abdominal fullness which may be due to
congested liver and/or bowels
CNS: confusion, disorientation, sleep and mood disturbance may be due to
reduced cerebral perfusion
Uncomfortable when lying flat, labored breathing
Normal or low BP
Cardiac cachexia
Although essential, frequently does not provide information on the severity of
HF
JVP may be > 8 cm H2O
Sinus tachycardia due to increased adrenergic activity
Point of maximal impulse displaced due to cardiomegaly
S3 (protodiastolic gallop) at the apex: usually in volume overloaded patients
S4: usually in diastolic dysfunction
Crackles: transudation of fluid from intravascular space to alveoli
Expiratory wheezes: cardiac wheezing caused by peribronchial cuffing from
congestion
Pleural effusions: often bilateral; if unilateral, more often on the right
Hepatomegaly with pulsation (if with significant TR)
Ascites: increased pressure in the hepatic veins
Jaundice: impairment of hepatic function due to congestion
Peripheral edema: ankles and pre-tibial region
Indurated and pigmented skin: long standing edema
Peripheral vasoconstriction: cool extremities
IV. DIAGNOSIS OF HEART FAILURE
The diagnosis of HF is straightforward when the patients presents with classic signs and symptoms
Key to diagnosis is a high index of suspicion
A. Framingham Criteria for Heart Failure
MAJOR CRITERIA
MINOR CRITERIA
Paroxysmal nocturnal dyspnea (PND) or orthopnea
Ankle edema
Neck vein distention
Night cough
Rales
Dyspnea on exertion
Cardiomegaly
Hepatomegaly
Acute pulmonary edema
Pleural effusion
S3 gallop
Vital capacity decreased by 1/3 from maximal
capacity
Increased venous pressure > 16 cm H2O
Tachycardia > 120 bpm
Hepatojugular reflux
Major or Minor Criteria: Weight loss > 4.5 kg in 5 days in response to treatment
The diagnosis of HF requires simultaneous presence of at least:
1 Major Criteria, or
1 Major Criterion + 2 Minor Criterion
54
(use of minor criteria acceptable only if they cannot be attributed to another medical condition, such as pulmonary HPN, chronic lung disease, cirrhosis, ascites, nephrotic
syndrome)
B. Diagnostics in HF
DIAGNOSTICS
2D Echocardiography with
Doppler
12-L ECG
Chest Radiography
Cardiac Biomarkers (BNP)
Complete Blood Count
Serum Electrolytes, BUN,
Crea, AST, ALT
FBS, OGTT
Lipid Profile
FT4, TSH
DESCRIPTION
Most useful test, evaluation of ejection fraction (EF)
Semi-quantitative assessment of LV size, function, wall motion abnormalities,
valvular defects
Assess cardiac rhythm, LV hypertrophy, prior MI
A normal ECG virtually excludes LV systolic dysfunction
Assess the cardiac size and shape and state of pulmonary vasculature
Identify non-cardiac causes of symptoms
Relatively sensitive markers for the presence of HF
Increase with age and renal impairment
Look for anemia, signs of infection, and bleeding (may precipitate / worsen HF)
Assess for electrolyte disturbances, beginning cardiorenal syndrome, ischemic
hepatitis or chronic passive congestion of the liver
Assess for diabetes
Assess for dyslipidemia
Assess for thyroid hormone abnormalities
V. MANAGEMENT OF HEART FAILURE
A. Non-Pharmacologic Management and Basic Principles
Sodium restriction: limit Na+ intake to 2-3 g/day in all patients with HF; and to less than 2 g/day in patients with
moderate to severe HF
Fluid restriction: generally unnecessary unless with hyponatremia (< 130 mEq/L) and volume overload
Caloric supplement: for those with cardiac cachexia
B. Pharmacologic Management for Prevention and Treatment of Chronic Heart Failure
DRUG CLASS
DESCRIPTION / MECHANISM
DOSE
Cornerstone of modern HF treatment
Captopril 25-50 mg TID
Interferes with RAAS by inhibiting
the conversion of angiotensin I to
Enalapril 2.5-10 mg BID
ACE-Inhibitors
angiotensin II
Ramipril 2.5-10 mg OD
Inhibits kininase which may lead to
Lisinopril 5-20 mg OD
increase in bradykinin (ACE-I
induced cough)
Angiotensin Receptor
Use if ACEI intolerant (e.g., cough,
Valsartan 40-160 mg BID
Blockers
angioedema)
Candesartan 8-32 mg OD
Losartan 25-50 mg OD
Another cornerstone of modern HF
treatment
Carvedilol 3.125-25 mg BID
Beta Blockers
Interferes with sustained activation of
Bisoprolol 1.25-10 mg OD
the adrenergic nervous system,
Metoprolol succinate 25-200 mg OD
particularly the deleterious effects of
B1 activation
Inhibits action of aldosterone in
Aldosterone Antagonist
collecting duct
Spironolactone 25-50 mg OD
May also be used for fluid retention
Eplerenone 25-50 mg OD
(diuretic)
For symptomatic LV dysfunction +
Digoxin
atrial fibrillation
Digoxin 0.125-0.375 mg OD
Add-on to standard therapy
Reduces HR by inhibition of the
Ivabradine 5-7.5 mg BID
Ivabradine
“funny channel” (If) in the SA node
Primarily used for symptomatic
55
stable angina
May be used for HF with systolic
dysfunction in patients with sinus
rhythm and HR > 70 bpm
C. Management of Fluid Retention in Chronic HF
DRUG CLASS
DESCRIPTION / MECHANISM
Act on the loop of Henle by reversibly
Loop Diuretics
inhibiting the reabsorption of Na+, K+, Cl in
the thick ascending limb
Reduce the reabsorption of Na+ and Cl in
Thiazide and Thiazidethe first half of the distal convoluted tubule
Like-Diuretics
Tend to lose their efficiency with moderate
to severe renal insufficiency (Crea > 2.5
mg/dL)
Interfere with action at the vasopressin
Arginine Vasopressin
receptors
Antagonists
Primarily used for treatment of
hyponatremia by stimulating free-water
excretion and improving plasma
Na+concentration
D. Indications for Use of Drugs in HF
CLASS
ASYMPTOMATIC LV
DYSFUNCTION (NYHA I)
ACEI/ARB
Yes
Diuretic
No
B-Blocker
Yes, if Post-MI
Aldosterone
Yes, if Recent MI
Antagonist
Digoxin
May be considered*
DOSE
Furosemide 20-40 mg OD-BID
Bumetanide 0.5-1.0 mg ODBID
Hydrochlorothiazide 25 ODBID
Indapamide 2.5 mg OD
Metolazone 2.5-5.0 mg OD
Tolvaptan 15 mg OD
Satavaptan 25 mg OD
SYMPTOMATIC HF
(NYHA II)
yes
Yes, if with fluid retention
Yes
Yes
WORSENING HF
(NYHA III-IV)
Yes
Yes
Yes
Yes
END-STAGE HF
(NYHA IV)
Yes
Yes
Yes
Yes
May be considered*
Yes
Yes
*Digoxin may be considered for patients with NYHA-I for rate control in AF or when improved from more severe HF and in sinus rhythm
E. Devices Used in HF
Cardiac resynchronization therapy (CRT) or biventricular pacing: device used to restore synchrony of the
left ventricle in patients with HF and a widened QRS complex
Implantable cardioverter-defibrillator (ICD): device to treat tachyarrhythmias for primary / secondary
prophylaxis against sudden cardiac death
VI. ACUTE DECOMPENSATED HEART FAILURE (ADHF)
A. Distinctive Phenotypes
ACUTE
DECOMPENSATION
Typical
Pulmonary Edema
Low Output
Cardiogenic Shock
PRESENTATION
Normo-hypertensive
Usually not volume overloaded
Severe pulmonary congestion with hypoxia
Hypoperfusion with end-organ dysfunction
Low pulse pressure, cool extremities
Cardiorenal syndrome, hepatic congestion
Hypotension, low cardiac output, end-organ
failure
Extreme distress, pulmonary congestion,
renal failure
MANAGEMENT
Vasodilators, diuretics
Vasodilators, diuretics, opiates
O2 non-invasive ventilation
Inotropic therapy
Vasodilators
Hemodynamic monitoring
Inotropic therapy
Mechanical circulatory support
56
B. Parenteral Therapy for Acute Decompensated HF
DRUG CLASS
SAMPLE DRUGS
Inotropic Therapy
Dobutamine (2-20 mcg/kg/min)
Others: Milrinone, Levosimendan
Vasodilators
Nitroglycerine (10-20 mcg/kg/min)
Others: Nesiritide, Nitroprusside, Serelaxin
Furosemide (20-240 mg/day)
Diuretics
Bumetamide (0.5-5 mg/day)
Others: Torsemide, Metolazone, Chlorthalidone, Spironolactone, Acetazolamide
CHRONIC STABLE ANGINA PECTORIS (CSAP)
Patients with ischemic heart disease (IHD) fall into two large groups:
Chronic artery disease (CAD) who commonly present with chronic stable angina pectoris (CSAP)
Acute coronary syndromes (ACS), discussed in the next section, are composed of:
o Non ST-segment elevation acute coronary syndrome (NSTE-ACS)
o ST-segment elevation acute myocardial infarction (STEMI)
I. ETIOPATHOGENESIS
Inadequate supply of blood flow and oxygen to a portion of the myocardium causing inadequate perfusion of
myocardium supplied by an involved artery
Most common cause: atherosclerotic disease of an epicardial coronary artery
Obesity, insulin resistance, and T2DM are increasing and powerful risk factors for IHD
II. CLINICAL MANIFESTATIONS
A. Angina
Typical history involves a man >50 years old or woman >60 years old who complains of chest discomfort:
o Described as heaviness, pressure, squeezing, smothering or choking
o Crescendo-decrescendo in nature
o Usually lasts 2-5 minutes
o Associated with physical exertion or stress
o Radiation to either or both shoulders/arms, but does not radiate to the trapezius muscles
o Relieved within 5-10 minutes by rest and/or sublingual NTG
o Levine’s sign: hand placed over sternum with a clenched fist to indicate discomfort
B. Canadian Cardiovascular Society Classification of Angina
CCS CLASS
DESCRIPTION
I
Angina occurs with greater than ordinary physical activity
II
Angina occurs with ordinary physical activity
III
Angina occurs with less than ordinary physical activity
IV
Angina may be present even at rest
III. DIAGNOSIS
A. Non-Invasive Diagnostics
DIAGNOSTIC TEST
ECG
Stress Testing
2D Echo
EXPECTED FINDINGS
May be normal at rest
ST-segment and T-wave changes, LV hypertrophy, intraventricular
conduction disturbance (which may be non-specific)
Most widely used for both diagnosis of IHD and estimating prognosis
Involves recording the 12-lead ECG before, during and after exercise
Used to assess left ventricular function in patients with CSAP and
patients with a history of a prior MI, pathologic Q waves or clinical
evidence of CHF
Assess for wall motion abnormalities, ejection fraction, presence of
thrombus, etc.
57
B. Indications for Coronary Angiography
Patients with CSAP who are severely symptomatic despite medical therapy and considered for revascularization
Patients with troublesome symptoms that present diagnostic difficulties in whom there is a need to confirm or R/O
the diagnosis of IHD
Patients with known or possible CSAP who have survived cardiac arrest
Patients with CSAP or evidence of ischemia on noninvasive testing with clinical or laboratory evidence of
ventricular dysfunction
Patients at high risk of sustaining coronary events on noninvasive testing, regardless of symptoms
IV. MANAGEMENT OF CSAP
A. Pharmacologic Treatment for Angina
DRUG CLASS
EXAMPLES
Anti-Ischemic Drugs
Nitrates
B-Blockers (BB)
Calcium
Channel
Blockers (CCB)
MECHANISM OF ACTION
COMMENTS
None of the longacting nitrates are
as effective as SL
NTG for the acute
relief of angina
Used for
symptomatic relief
May be
discontinued with
the disappearance
of chest pain
Common side effect
limiting their use:
headache
At least 8 hour
nitrate-free interval
is recommended to
avoid nitrate
tolerance
Isosorbide Dinitrate
(ISDN) 10-40 mg BIDTID
Isosorbide Mononitrate
(ISMN) 30-240 mg OD
NTG 0.3-0.6 mg SL, as
needed up to 3 doses,
5 mins apart
NTG Transdermal
Patch 0.2-0.8 mg/hr OD
(remove at bedtime for
12-14 hrs)
Systemic venodilation
with reduction in LV
end-diastolic volume
and pressure, thereby
reducing myocardial
wall tension and O2
requirements
Dilation of epicardial
coronary vessels
Increased blood flow
in collateral vessels
Metoprolol 50-100 mg
BID-QID
Metoprolol XL 50-200
mg OD
Carvedilol 3.125-50 mg
BID
Atenolol 50-100 mg OD
Bisoprolol 5-20 mg OD
Reduced myocardial
O2 demand by
inhibiting increases in
HR, arterial pressure
and myocardial
contractility caused by
adrenergic activation
Cornerstone
therapy for angina
Shown to improve
life expectancy
following acute MI
Coronary vasodilators
that produce variable
and dose dependent
reductions in
myocardial O2
demand, contractility,
and arterial pressure
Indicated in patients
with:
o Inadequate
responsiveness to
the combination of
BB and nitrates
o Adverse reactions
to BB
o Angina history of
asthma or COPD
o Sick sinus
syndrome or
significant AV
conduction
disturbances
o Prinzmetal’s angina
o Symptomatic
Non-dihydropyridines
Verapamil 80-120 mg
TID-QID
Diltiazem 30-90 mg
TID-QID
Dihydropyridines
Amlodipine 2.5-10 mg
OD
Felodpine 2.5-10 mg
OD
58
peripheral arterial
disease
Other Pharmacologic Agents for Angina
Inhibitor of the IF ion channel (principal determinant of
Ivabradine
the SA node)
2.5-7.5 mg BID
Slows the heart rate through a mechanism that is not
associated with negative inotropic effects
Dilates peripheral and coronary resistance vessels via
Nicorandil
ATP-sensitive K+ channels
10-20 mg BID
Possess a nitrate moiety that promotes venous and
coronary dilation
B. Other Drugs for Stable Angina Pectoris
DRUG CLASS
EXAMPLES
Aspirin
75-162 mg OD
Antiplatelets
Clopidogrel
75 mg OD
Statins
Rosuvastatin
10-20 mg OD
Atorvastatin
10-80 mg OD
Simvastatin
10-40 mg OD
C. Coronary Interventions
INTERVENTION
Percutaneous
Coronary
Intervention (PCI)
Coronary Artery
Grafting (CABG)
Bypass
MECHANISM OF ACTION
Irreversible inhibitor of
platelet cyclooxygenase
activity, interfering with
platelet activation
Oral agent that blocks
ADP receptor-mediated
platelet aggregation
Act
as
HMG-CoA
reductase inhibitor
Exhibit
pleiotropic
effects:
plaque
stabilization and antiinflammatory effects
Only works in
patients who are in
sinus rhythm
Has anti-anginal
efficacy similar to
BB, nitrates & CCBs
COMMENTS
Chronic administration
has been shown to
reduce coronary events
May be substituted for
aspirin in those with
aspirin hypersensitivity
or those who cannot
tolerate aspirin
Can
lower
LDL
cholesterol (25-50%),
raise HDL cholesterol
and lower triglycerides
High intensity statin
therapy should be given
for
patients
with
established IHD who
are less than 75 years
old, in the absence of
contraindications
DESCRIPTION
Balloon dilatation usually accompanied by coronary stenting
Most common indication: persistent or symptom-limiting angina pectoris,
despite medical therapy, accompanied by evidence of ischemia during a
stress test
Indicated for those with three-vessel CAD or two-vessel CAD with
involvement of the left anterior descending artery (LAD) or stenosis of the
left main coronary artery
ACUTE CORONARY SYNDROMES (ACS)
Operational term that refers to a spectrum of conditions compatible with acute myocardial ischemia and/or
infarction due to an abrupt reduction in coronary blood flow
Patients with ACS are composed of:
o Non-ST segment elevation acute coronary syndrome (NSTE-ACS):
Non-ST segment elevation myocardial infarction (NSTEMI)
Unstable angina (UA)
ST elevation acute myocardial infarction (STEMI)
59
I. UNIVERSAL DEFINITON OF MYOCARDIAL INFARCTION
A. Criteria for Acute MI
“Acute MI” should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute
myocardial ischemia. Under these conditions, any of the following criteria meet the diagnosis for MI:
Detection of a rise and/or fall in cardiac biomarkers (preferably cardiac troponins/cTn), with at least one value
above the 99th percentile with at least one of the following:
o Symptoms of ischemia
o New or presumed new significant ST-segment and/or T wave changes or new LBBB
o Development of pathologic Q waves on the ECG
o Imaging evidence of new loss of viable myocardium or new wall motion abnormality
o Identification of an intracoronary thrombus by angiography or autopsy
Cardiac death with symptoms suggestive of myocardial ischemia & presumed new ischemic ECG changes or
new LBBB (Type 3)
PCI-related MI (Type 4a)
Stent thrombosis associated with MI (Type 4b)
CABG-related MI (Type 5)
B. Criteria for Previous Myocardial Infarction (any of the following):
Pathologic Q waves with or without symptoms in the absence of non-ischemic causes
Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract in the absence of a
non-ischemic cause
Pathologic findings of previous MI
II. UNIVERSAL CLASSIFICATION OF TYPES OF MYOCARDIAL INFARCTION
TYPE OF MYOCARDIAL INFARCTION
DESCRIPTION
(MI)
Related to atherosclerotic plaque rupture, ulceration, fissuring, erosion or
Type
Spontaneous MI
dissection with resulting intraluminal thrombus in one or more of the
1
coronary arteries that leads to decreased myocardial blood flow or distal
platelet emboli with ensuing myocyte necrosis
A condition other than CAD contributes to an imbalance between
MI secondary to
myocardial oxygen supply and/or demand, e.g., coronary endothelial
Type
Ischemic Imbalance
dysfunction,
coronary
artery
spasm,
coronary
embolism,
2
tachyarrhythmias/bradyarrhythmias,
anemia,
respiratory
failure,
hypotension, and hypertension with or without LVH
MI resulting in Death
Cardiac death with symptoms suggestive of ischemia and presumed new
Type
when Biomarkers are
ischemic changes (or new LBBB), but death occurring before blood
3
Unavailable
samples could be obtained
MI associated with PCI defined by elevation of cTn values to >5x the 99th
percentile of the upper reference limit in those with normal baseline values
or a rise in cTn values >20% if baseline values are elevated and are stable
or falling; AND either:
MI related to PCI
Symptoms suggestive of myocardial ischemia
Type
New ischemic changes on the ECG or new LBBB
4a
Angiographic loss of patency of a major coronary artery or a side
branch or persistent slow flow or no flow or embolization
Imaging demonstration of new loss of viable myocardium or new
regional wall motion abnormality
MI
associated
with stent thrombosis is detected by coronary angiography
Type
MI related to Stent
or autopsy in the setting myocardial ischemia and with a rise and/or fall in
4b
Thrombosis
cardiac biomarkers with at least one value >99th percentile of the upper
reference limit
MI associated with CABG – defined by elevation of cardiac biomarker
values >10x the 99th percentile of upper reference limit in patients with
Type
MI related to CABG
normal baseline values; AND either:
5
New pathologic Q waves or new LBBB, or
New graft or new native coronary artery occlusion on angiogram,
60
or
Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality
NON-ST ELEVATION ACUTE CORONARY SYNDROME (NSTE-ACS)
I. ETIOPATHOGENESIS
Most commonly caused by an imbalance O2 supply and demand, resulting from a partially occluding thrombus
forming on a disrupted atherothrombotic coronary plaque on eroded coronary artery endothelium
A. Four Basic Pathophysiologic Processes:
Most common cause: plaque rupture or erosion with superimposed non-occlusive thrombus
Dynamic obstruction (e.g., coronary spasm as in Prinzmetal’s variant angina)
Severe mechanical obstruction
Increased myocardial O2 demand (e.g., tachycardia) and/or decreased supply (e.g. anemia)
B. Definition of Terms
TERM
Unstable Angina (UA)
NSTEMI
Prinzmetal Variant Angina
DEFINITION
Angina or equivalent ischemic discomfort with at least one of the following:
Occurs at rest (or with minimal exertion), usually lasting >10 minutes
Severe and of new onset (e.g., within the prior 4-6 weeks) of at least
CCS III severity
Occurs with crescendo pattern (e.g., distinctly more severe, prolonged
or frequent than previous episodes)
Clinical features of UA plus evidence of myocardial necrosis (elevated
cardiac biomarkers)
Ischemic pain that occurs at rest but not usually with exertion,
associated with transient ST-segment elevation
Due to transient, focal spasm of an epicardial coronary artery
II. CLINICAL MANIFESTATIONS
A. Typical Chest Pain
Chest discomfort is typically severe and has at least one of the following features:
o Occurs at rest (or with minimal exertion), lasting >10 minutes
o Relatively recent onset (within prior 2 weeks)
o Occurs with a crescendo pattern (e.g., more severe, prolonged or frequent)
B. Symptoms & Signs of NSTE-ACS
SYMPTOMS
Chest pain radiating to the neck, left
shoulder, and left arm
Dyspnea
Diaphoresis
Anxiety, restlessness
SIGNS
Pale cool skin
Sinus tachycardia
S3 or S4
Basilar rales
Hypotension
III. DIAGNOSIS OF NSTE-ACS
A. 12-Lead Echocardiogram (ECG)
ST-segment depression, transient ST-segment elevation or T-wave inversion
T-wave changes: sensitive for ischemia but less specific (unless new & deep T-wave inversions > 0.3 mV)
If initial ECG is not diagnostic – serial ECGs should be done to detect ischemic changes if patient remains
symptomatic with a high suspicion for ACS
B. Cardiac Biomarkers
Elevated levels distinguish patterns with NSTE-ACS from UA
61
Serial cardiac troponin I or T levels should be obtained at presentation and 3-6 hours after symptom onset to
identify a rising and/or falling pattern of values
Additional levels should be obtained beyond 6 hours in patients with normal levels on serial examination when
ECG and/or clinical presentation confer an intermediate or high index of suspicion for ACS
1. Advantages and Disadvantages of the Common Cardiac Biomarkers
CARDIAC TROPONINS
Powerful tool for risk stratification
Greater sensitivity and specificity than
Advantage
CK
Detection of recent MI up to 2 weeks
after onset (remain elevated 7-10 days
after MI)
Low sensitivity in very early phase of
MI (<6 hours after symptom onset)
and requires repeat measurement at
8-12hours if negative
Disadvantage
Limited ability to detect late minor
reinfarction
Minor troponin elevations can be
caused by azotemiz/CKD, CHF,
myocarditis or pulmonary embolism
2. Timing of Cardiac Markers
CARDIAC BIOMARKER
Troponin-T
Troponin-I
CK-MB
TIME TO DETECTION
3-12 hrs
3-12 hrs
4-8 hrs
PEAK
24 hours
24 hours
24 hours
CK-MB
Rapid,
cost-efficient,
accurate assays
Ability
to
detect
early
reinfarction
Loss of specificity in setting
of skeletal muscle disease of
injury, including surgery and
IM injections
With contemporary troponin
assays, CKMB is not useful
for diagnosis of ACS
DURATION
5-14 days
5-10 days
2-3 days
C. Risk Stratification: TIMI SCORE for NSTE-ACS
Prognostication scheme, which categorizes patients based on risk of all-cause mortality, new or recurrent MI, or
severe ischemia requiring urgent revascularization
COMPONENTS
Age > 65 years
> 3 CAD factors
Known CAD (> 50% stenosis)
Aspirin use in the [ast 7 days
Severe angina in last 24 hours
Elevated cardiac markers
ST deviation > 0.5mm
POINTS
1 point
1 point
1 point
1 point
1 point
1 point
1 point
INTERPRETATION
Risk Total Score:
0-7 points
High Risk Score:
> 3 points
(13% mortality)
IV. MANAGEMENT OF NSTE-ACS
A. Standard and Anti-Ischemic Therapy
THERAPY
Non-Pharmacologic
Nitrates
DESCRIPTION
Bed rest with continuous ECG monitoring
Supplemental oxygen if O2 sat <94%
Avoid in:
SL nitrate (ISDN 5 mg/tab) q5
SBP <90 mmHg or >30 mmHg
mins x total of 3 doses
below baseline
IV NTG in first 48 hours (5-10
Severe bradychardia <50 bpm
mcg/kg/min, max 200
Tachycardia >100 bpm in
mcg/kg/min) for persistent
absence of symptomatic HF
ischemia, HF or HPN
Suspected RV infarction
Decrease in angina symptoms
Those who received sildenafil
for the past 24 hours (may
potentiate hypotension)
62
Beta-Blockers (BB)
Nondihydropyridine Calcium
Channel Blockers
ACE Inhibitors
Not given in patients with:
Signs of acute HF
Low output states (SBP <90,
Started within 24 hours
HR <50)
Metoprolol succinate,
PR interval > 0.24 secs, 2nd or
carvedilol or bisoprolol
3rd degree AVB without a
pacemaker
Active asthma or reactive
airway disease
Recommended for recurrent ischemia after appropriate use of BB and
nitrates
For those with contraindications to beta-blockers
Verapamil or diltiazem
Given orally within 24 hours in patients with congestion and/or LVEF <
40%
ARBs may be given if patient intolerant to ACE inhibitors
Captopril 6.25-12.5 mg PO q8
B. Anti-Platelet Therapy
Initial treatment should begin with aspirin
In the absence of a high risk of bleeding, patients with NSTE-ACS should also receive a P2Y12 inhibitor for up to
12 months (at least 12 months if patient is to undergo PCI with stenting): clopidgrel, ticagrelor, prasugrel
THERAPY
DESCRIPTION
Platelet cyclooxygenase inhibitor
Aspirin
Dose: 165-325 mg loading dose, then 80-162 mg OD maintenance dose
indefinitely
Thienopyridine
Clopidogrel
Inactive prodrug that is converted into an active metabolite that causes
irreversible blockade of the platelet ADP P2Y12inhibitor
Dose: 300-600 mg loading dose, then 75 mg OD
Non-thienopyridine
Novel, potent, reversible platelet ADP P2Y12inhibitor
Ticagrelor
May be used in patients who are treated either by an invasive or conservative
strategy
Dose: 180 mg loading dose, then 90 mg BID
Thienopyridine
Also a platelet ADP P2Y12 antagonist, but achieves a more rapid onset and
higher level of platelet inhibition than clopidogrel
Approved for ACS patients following angiography in whom PCI is planned (it
Prasugrel
has not been found to be effective in patients treated by a conservative
strategy)
Contraindicated in patients with prior stroke / TIA or a high risk of bleeding
Dose: 60 mg loading dose, then 10 mg OD (if patient is to undergo early
invasive management)
C. Anticoagulation Therapy
THERAPY
Unfractioned
Heparin
(UFH)
Enoxaparin
Fondaparinux
DESCRIPTION
Mainstay of therapy
Target aPTT 50-70 seconds (ratio of 1.5-2.5)
Dose: 60 U/kg IV bolus (maximum 4,000 U), then 12 U/kg infusion (1000
units/hour) for 48 hours or until PCI is performed (most trials continued therapy
for 2-5 days)
Superior to UFH in reducing recurrent cardiac events, especially in patients
managed conservatively
Dose: 30 mg IV loading dose, then 1 mg/kg SC q12 for the duration of
hospitalization or until PCI is performed
Indirect factor Xa inhibitor
63
Equivalent in efficacy to enoxaparin, but with lower risk of major bleeding
Dose: 2.5 mg SC OD for duration of hospitalization or until PCI is performed
D. Statins
High intensity statin therapy should be initiated or continued
Early administration of statins (e.g., Atorvastatin 80 mg/day) has been shown to reduce adverse outcomes
E. Conservative versus Early Invasive Strategy
Conservative strategy (low risk patients): anti-ischemic therapy and antithrombotic therapy followed by “watchful
waiting” (close observation)
Early-invasive strategy (for high risk patients): following treatment with anti-ischemic and antithrombotic agents,
angiography is carried out within 48 hours, followed by coronary revascularization (PCI or CABG)
CONSERVATIVE MEDICAL MANAGEMENT
EARLY INVASIVE MANAGEMENT
(Ischemia-Guided Strategy)
(Revascularization)
Low risk score (TIMI 0 or 1)
Recurrent angina or ischemia at rest or with lowlevel activities despite intensive medical therapy
Low risk troponin-negative female patients
Elevated cardiac biomarkers (TnT or Tnl)
Patient or physician preference in the
absence of high-risk features
New or presumably new ST segment depression
CHF symptoms, rales, MR
Reduced left ventricular function (LVEF < 40%)
Sustained ventricular tachycardia
PCI < 6 months or prior CABG
High-risk findings from noninvasive testing
Hemodynamic instability
Mild-to-moderate renal dysfunction
DM
High TIMI risk score > 3
IV. PRINZMETAL’S VARIANT ANGINA
Syndrome of severe ischemic pain that usually occurs at rest and associated with transient ST elevation
Caused by focal spasm of an epicardial coronary artery (most commonly the right coronary artery)
Diagnostic hallmark: coronary arteriography demonstrates transient coronary spasm
Main therapeutic agents: nitrates and calcium channel blockers
Aspirin may increase severity of ischemic episodes
ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
I. ETIOPATHOGENESIS
Acute plaque rupture is central to the pathogenesis of STEMI
Occurs when coronary blood blow decreases abruptly after a thrombotic occlusion of a coronary artery previously
affected by atherosclerosis
II. CLINICAL MANIFESTATIONS
Diagnosed similarly as NSTE-ACS (e.g., clinical features, increased cardiac biomarkers) but with ECG findings
evolving in a temporal pattern (see ECG Reading in Chapter 1)
III. DIAGNOSIS AND RISK STRATIFICATION FOR STEMI
A. Killip Scoring for STEMI
CLASS
DESCRIPTION
No rales or signs of pulmonary or venous congestion
Class
Normal BP
I
Class
II
Moderate HF, bibasal rales
Normal BP
S3 gallop
Tachypnea or signs of right-sided CHF (venous or hepatic
congestion)
Severe HF
RISK OF MORTALITY
0-5%
10-20%
64
Class
III
Class
IV
(+) mid-basal rales and pulmonary edema
(+) S3 and S4
Normal BP
Shock with SBP <90 mmHg & evidence of peripheral
vasoconstriction
Peripheral cyanosis
Mental confusion and oliguria
35-45%
85-95%
B. TIMI Risk Score for STEMI
TIMI risk score for STEMI: predicts 30-day mortality
Designed for risk assessment early after patient presentation and thus does not incorporate noninvasive and
invasive data
COMPONENTS
POINTS
INTERPRETATION
Historical
Age 65-74
2 points
Age > 75
3 points
Risk Total Score:
DM, Hypertension, Angina
1 point
0-14 points
Examination
SBP < 100 mmHg
3 points
High Risk Score:
HR > 100 bpm
2 points
> 5 points
Killip II-IV
2 points
(12%
mortality)
Weight < 67 kg
1 point
Presentation
Anterior ST elevation or LBBB on ECG
1 point
Time to Treatment > 4 hours
1 point
IV. MANAGEMENT OF STEMI
A. Pre-hospital Management of STEMI
Major components:
o Recognition of symptoms
o Rapid deployment of an emergency medical team capable of performing resuscitative maneuvers
o Expeditious transportation
o Expeditious implementation of reperfusion therapy
Most out-of-hospital deaths from STEMI are due to sudden ventricular fibrillation
Majority of deaths occur within 24 hours of the onset of symptoms (over half occur in the 1st hour)
B. Reperfusion Therapy: Primary Goal of Management
Reperfusion Therapy (fibrinolysis or PCI) should be administered to all eligible patients with STEMI with
symptom onset within the last 12 hours
o Primary PCI: recommended method of reperfusion when it can be performed in a timely fashion
o Fibrinolysis: administered at non-PCI-capable centers
FIBRINOLYSIS / THROMBOLYSIS
INVASIVE STRATEGY (PCI)
Generally preferred if:
Generally preferred if:
Early presentation (< 3 hours of symptom onset)
Available PCI laboratory with surgical backup
o Medical contact-to-balloon or door-to-balloon
Invasive strategy is not available:
< 90 minutes
Delay to invasive strategy:
o Door-to-balloon minus door-to-needle < 1 hr
o Prolonged transport
High risk STEMI (cardiogenic shock, Killip > 3)
o Door-to-balloon minus door-to-needle
time >1 hr
Contraindications to fibrinolysis
o Medical contact-to-balloon or door-toLate presentation (symptom onset > 3 hours)
balloon time >90 minutes
Diagnosis of STEMI is in doubt
Fibrinolytic agents:
Percutaneous coronary intervention (PCI) or
o Streptokinase
percutaneous transluminal coronary angioplasty
o Tissue plasminogen activators
(PTCA): balloon angioplasty and stenting
Adjunct anti-platelet therapy with fibrinolysis:
Aspirin continued indefinitely
Anti-platelet therapy during Primary PCI:
65
Clopidogrel for at least 14 days up to 1
year
o
o
Aspirin indefinitely after PCI
One P2Y12-receptor inhibitor continued for 1 year
for those who receive a stent:
Clopidogrel
Prasugrel (not used if + prior stroke/TIA)
Ticagrelor
Adjunctive
anticoagulant
therapy
with
fibrinolysis: given for a minimum of 48 hours or
until revascularization is performed (same dose
as in NSTE-ACS)
Anticoagulant therapy during primary PCI:
o Unfractioned heparin (UFH)
o UFH
o Enoxaparin
o Bivalirudin
o Fondaparinux
Fibrinolysis is still reasonable if symptom onset is within 12-24 hours as long as there is evidence of ongoing
ischemia (although primary PCI is preferred for this population)
CONTRAINDICATIONS TO FIBRINOLYSIS
ABSOLUTE CONTRAINDICATIONS
RELATIVE CONTRAINDICATIONS
Previous intracranial hemorrhage
History of chronic, severe, poorly controlled HPN
Structural cerebral vascular lesion (e.g.,
Significant HPN at initial evaluation (SBP > 180
AVM)
mmHg or DBP > 110 mmHg)
Malignant intracranial neoplasm
History of previous ischemia stroke > 3 months
Ischemic stroke within 3 months except
Dementia
acute ischemic stroke within 4.5 hours
Intracranial pathology not covered in absolute
Suspected aortic dissection
contraindications
Active bleeding / bleeding diathesis (except
Traumatic or prolonged (>10 minutes) CPR
mense)
Major surgery (<3 weeks)
Closed-head or facial trauma within 3 months
Recent (within 2-4 weeks) internal bleeding
Intracranial/intraspinal surgery within 2
Noncompressible vascular punctures
months
Pregnancy
Severe
uncontrolled
hypertension
Active peptic ulcer
(unresponsive to emergency therapy)
Oral anticoagulant therapy
For streptokinase, previous treatment within
the previous 6 months
AVM: Arteriovenous malformation
CPR: cardiopulmonary resuscitation
C. Other Routine Medications for STEMI
THERAPY
Beta Blockers
RAAS Inhibitors
Statins
DESCRIPTION
Should be initiated in the first 24 hours, except if
with signs of HF, low output state, increased risk for
cardiogenic shock, or other contraindications (PR
interval > 0.24, 2nd or 3rd degree AVB, active
asthma, reactive airway disease)
ACE-inhibitors should be initiated in the first 24
hours to all patients with anterior wall STEMI, HF or
EF < 40%
ARB may be used for those intolerant to ACEinhibitors
High intensity statin therapy should be initiated or
continued
D. Supportive Care
THERAPY
Activity
DESCRIPTION
First 12 hours: bed rest
Next 12 hours: dangling of feet at bedside and
sitting in a chair
2nd and 3rd day: ambulation in the room with
increasing duration and frequency to a goal of 185
cm (600 ft) at least 3x a day
2 weeks: resumption of work and sexual activity
66
Nothing or only clear liquids (due to risk of emesis
and aspiration) for the first 4-12 hours
Use of stool softener
Many require sedation during hospitalization to
withstand period of enforced inactivity
Diet
Sedation
E. Secondary Prevention and Long Term Management
THERAPY
DESCRIPTION
Smoking
Complete cessation
BP Control
BP <140/90 or <130/80 if CKD or DM
Lipid Management
High dose statins
<7% of total calories as saturated fats and <200 mg/day total cholesterol
Physical Activity
30 minutes of moderate intensity aerobic exercise, 3 to 4 days per week
Weight
BMI 18.5 – 24.9 kg/m2
Management
Waist circumference: women <35 inches, men <40 inches
DM Management
HbA1c <7%
Anti-platelets
Aspirin or P2Y12-receptor inhibitors
RAAS Blockers
ACEI in stable high-risk patients (anterior MI, previous MI, Killip > II, EF <40%)
Beta Blockers
Continued indefinitely
IV. USUAL COMPLICATIONS OF STEMI
COMPLICATION
FREQUENCY
Ventricular
1-3% in those who
Septal
Rupture did not undergo
(VSR)
reperfusion
Ventricular Free
Wall Rupture
Papillary Muscle
Rupture
0.8-6.2%
1% (posteromedial
more
frequently
affected
than
anterolateral
muscle)
DESCRIPTION
Bimodal peak (within 24 hours & 3-5 days; can range from 1-14 days)
Presents with chest pain, SOB and hypotension
Holosystolic murmur, S3, accentuated 2 nd heart sound, pulmonary
edema, RV and LV failure, cardiogenic shock
Bimodal peal (within 24 hours & 3-5 days; can range from 1-14 days)
Presents with angina, pleuritic or pericardial chest pain, syncope,
hypotension, arrhythmia, nausea, restlessness, hypotension and
sudden death
JV distention (29%), pulsus paradoxus (47%), electromechanical
dissociation and cardiogenic shock
Bimodal peak (within 24 hours & 3-5 days; can range from 1-14 days)
Abrupt onset of dyspnea, pulmonary edema, and hypotension
Soft murmur in most cases, no thrill, variable signs of RV overload,
severe pulmonary edema, cardiogenic shock
Hypercontractile LV, torn papillary muscle or chordae tendinae, flail
leaflet and severe MR on echo with color flow
RHEUMATIC FEVER (RF)
I. ETIOPATHOGENESIS
Multi-system disease resulting from autoimmune reaction to infection with Group A Beta-Hemolytic
Streptococcus
In RF, antibodies against M-proteins of certain strains of Streptococcus cross-react with tissue glycoproteins in
the heart, joints and other tissues (“molecular mimicry”)
II. CLINICAL MANIFESTATIONS
Latent period of 3 weeks (ranges from 1 to 5 weeks) between the precipitating infection and the appearance of
the clinical features of ARF with the exception of chorea and indolent carditis which may follow prolonged talent
period lasting up to 6 months
Most common clinical presentation: polyarthritis and fever
A. Major Manifestations
Carditis
(up to 60%)
Pancarditis involving the pericardium, myocardium and endocardium
Hallmark is valvular damage
67
Migratory
Polyarthritis
(75%)
Sydenham’s
Chorea (<10%)
Erythema
Marginatum
Subcutaneous
Nodules
B. Minor Manifestations
Clinical
Laboratory findings
Characteristic manifestation is mitral regurgitation
Typically migratory over a period of hours
Most often asymmetric and affecting large joints (ankles, wrists, knees, elbows)
Highly responsive to salicylates and NSAIDs
Involuntary jerking movements mostly affecting the head and upper limbs
Commonly occurs in females and in the absence of other manifestations
Usually resolves completely within 6 weeks
Evanescent pink macular eruption with round borders and central clearing
Usually concentrated on the trunk, sometimes on the limbs, but almost never on the
face
Painless small lumps found over extensor surfaces of joints
Usually a delayed manifestation (2-3 weeks after onset)
Commonly associated with carditis
Arthralgia (joint pains), fever
Elevated acute phase reactants (ESR/CRP), prolonged PR interval on ECG
C. Supporting Evidence of a Preceding Streptococcal Infection within the last 45 days
Elevated or rising anti-streptolysin-O or other streptococcal antibody, or
A positive throat culture, or
Rapid antigen test for group-A Streptococcus, or
Recent scarlet fever
III. DIAGNOSIS
A. The Revised Jones Criteria: Diagnosis of Rheumatic Fever (RF) and Rheumatic Heart Disease (RHD)
DIAGNOSTIC CATEGORIES
CRITERIA
Primary episode of RF
Evidence of preceding group-A streptococcal infection; PLUS:
2 major criteria, or
1 major + 2 minor criteria
Recurrent RF in a patient Evidence of preceding group-A streptococcal infection; PLUS:
without established RHD
2 major criteria, or
1 major + 2 minor criteria
Recurrent RF in a patient with Evidence of preceding group-A streptococcal infection; PLUS:
established RHD
2 minor criteria
Rheumatic chorea
Other major manifestations or evidence of group-A streptococcal infection not
Insidious onset rheumatic required
carditis
Chronic valve lesions of RHD
(patients presenting for the 1st
time with pure MS or mixed Do not require any other criteria to be diagnose as having RHD
MV disease and/or AV
disease)
B. Criteria for Echocardiographic Diagnosis of Rheumatic Heart Disease (RHD) in Individuals <20 years of age
Definite RHD (either A, B, C or D)
A. Pathologic MR + > 2 morphologic features of RHD of the mitral valve (MV)
B. MS mean gradient >4 mmHg
C. Pathologic AR + > 2 morphologic features of RHD of the aortic valve (AV)
D. Borderline disease of both the MV and AV
Borderline RHD (either A, B, C)
A. > 2 morphologic features of RHD of the MV without pathologic MR or MS
B. Pathologic MR
C. Pathologic AR
Normal Echocardiographic Findings (all of A, B, C and D)
A. MR that does not meet all four Doppler criteria (physiologic MR)
B. AR that does not meet all four Doppler criteria (physiologic AR)
68
C. An isolated morphologic feature of RHD of the MV (e.g., valvular thickening), without any associated pathologic
stenosis or regurgitation
D. Morphologic feature of RHD of the AV (e.g., valvular thickening), without any associated pathologic stenosis or
regurgitation
Definitions of Pathologic Regurgitation & Morphologic Features of RHD
Pathologic MR: all of the following – seen in 2 weeks; in at least 1 view, jet length 2 cm; peak velocity > 3 m/s;
pansystolic jet in at least 1 envelope
Pathologic AR: all of the following – seen in 2 views; in at least, jet length > 1 cm; peak velocity > 3 m/s’
pandiastolic jet in at least 1 envelope
Morphologic features of RHD in MV: anterior MV leaflet thickening > 3 mm; chordal thickening; restricted
leaflet motion; excessive leaflet tip motion during systole
Morphologic features of RHD in AV: irregular of focal thickening; coaptation defect; restricted leaflet motion;
prolapse
IV. MANAGEMENT OF RHEUMATIC FEVER
A. For Acute Management
Penicillin:
o PO: Pen V 500 mg BID or Amoxicillin 50 mg/kg daily x 10
days
o IM: single dose of 1.2 M units Benzathine Penicillin G
Aspirin 4-8 g/d in 4-5 divided doses up to 2 weeks
May add prednisone 1-2 mg/kg/day up to 4 max of 3 weeks
Carbamazepine or valproic acid
For Infection
For Arthritis / Mild Carditis
For Moderate-Severe Carditis
For Severe Chorea
B. For Prophylaxis of Rheumatic Fever
Primary prophylaxis for RH: to treat group-A streptococcal URTI and eradicate the organism to prevent an initial
attack of acute RF
Secondary prophylaxis for RF: to prevent colonization and/or infection in patients who had a previous attack of
RF to prevent recurrence of RF
1. Drugs Available for Secondary Prophylaxis
Benzathine Penicillin G 1.2 M units q 2-4 weeks (best)
Penicillin VK 250 mg/cap BID
Erythromycin 250 mg/cap BID (if allergic to Penicillin)
2. Duration of Secondary Prophylaxis
CATEGORY
RF without Carditis
RF with Carditis, but no residual
valvular disease
RF with persistent valvular disease
DURATION OF PROPHYLAXIS
5 years after last attack or until 21 y/o (whichever is longer)
10 years after last attack or until 21 y/o (whichever is longer)
10 years after last attack or until 40 y/o (sometimes lifetime)
VALVULAR HEART DISEASE (VHD)
I. STAGES OF PROGRESSION OF VHD
CLASS
STAGE A
STAGE B
(At Risk)
(Progressive)
General Definition
+
+
Risk
Symptoms
Severity
Mild-to-Moderate
Individual Valvular Heart Disease Staging
AS
At risk
Asymptomatic
Progressive
STAGE C
(Asymptomatic Severe)
STAGE D
(Symptomatic Severe)
+
Severe
+
+
Severe
Asymptomatic Severe
C1: normal LVEF
C2: low LVEF
Symptomatic Severe
D1: high gradient
D2: low flow, low gradient, low
LVEF
69
D3: low flow, low gradient,
preserved LVEF (paradoxical lowflow severe AS)
AR
At risk
Asymptomatic
Progressive
MS
At risk
Asymptomatic
Progressive
MR
At risk
Asymptomatic
Progressive
TR
At risk
Asymptomatic
Progressive
Asymptomatic Severe
C1: normal LVEF
C2: low LVEF or dilated
LVEF
Asymptomatic Severe
Asymptomatic Severe
C1: normal LVEF
C2: low LVEF & dilated
LVEF
Asymptomatic Severe
Symptomatic Severe
Symptomatic Severe
Symptomatic Severe
Symptomatic Severe
II. INDIVIDUAL VALVULAR HEART DISEASES (VHD)
A. Aortic Stenosis (AS)
Most common cause: degenerative calcification of aortic cusps in adults
Most common congenital defect: bicuspid aortic valve (BAV)
Symptoms (dyspnea, angina, exertional syncope) are rarely present until valve orifice <1 cm 2
Death usually at 7th-8th decades, and may depend on the presence of symptoms:
o If with syncope I angina: death in 3 years
o If with dyspnea: death in 2 years
o If with CHF: death in 1.5-2 years
Physical Exam
Diagnostics
Therapy
Pulsus parvus et tardus: weak and late pulse
Low pitched midsystolic ejection murmur at 2nd R ICS
Murmur may be transmitted to the apex, resembling murmur of MR (Gallavardin
effect)
CXR / ECG: LVH (with strain pattern on ECG)
2D Echo: calcified aortic valve with restriction in opening
Avoidance of strenuous activity and competitive sports
Diuretics for CHF
Caution with the use of nitrates and afterload unloaders (ACEI/ARBs) as these
may precipitate hypotension
Statins for slower progression of leaflet calcification
Intervention: Transcatheter Aortic Valve Implantation (TAVI), aortic valve
replacement (surgery)
B. Aortic Regurgitation (AR)
Physical Exam
Diagnostics
Therapy
Austin Flint murmur: soft low-pitched rumbling mid-to-late diastolic murmur
De Musset sign: jarring of the body & bobbing of the head with each systole in
severe AR
Quincke’s pulse: visible capillary pulsations at the root of the nail with pressure
Traube sign: booming pistol shot sound over femoral arteries
Duroziez sign: to and from murmur when femoral artery is compressed
Water hammer (Corrigan’s) pulse: bounding and forceful pulse, rapidly
increasing and subsequently collapsing
Others: widened pulse pressure, absence of A2 in severe AR
ECG: LVH usually with ST depression and T wave inversion in I, aVL, V5-6 (lateral
leads)
2D Echo: mosaic color flow across the aortic valve during diastole
Diuretics, ACEI and vasodilators for CHF
Intervention: aortic valve replacement (surgery)
70
C. Mitral Stenosis (MS)
Rheumatic heart disease is the leading cause
Poor prognosis for those >65 y/o, marked cardiac output depression, RV dysfunction and pulmonary
hypertension
Loud S1 and accentuated P2
Physical Exam
Apical diastolic rumble and murmur
Opening snap
CXR: LAE, RAE, RVH
Diagnostics
ECG: LAE, RAE, RVH; atrial fibrillation in severe cases
2D ECHO: doming motion of the mitral valve (anterior leaflet) during diastole
For fluid retention: sodium, restriction, diuretics
For rate control: beta-blockers, non-dihydropyridine calcium channel blockers,
digoxin
Therapy
For secondary prophylaxis of rheumatic heart disease: penicillin
For prevention of stroke: warfarin (target INR 2-3)
Intervention: percutaneous transseptal mitral commisurotomy (PTMC) or mitral
valve replacement therapy (surgery)
D. Mitral Regurgitation (MR)
Physical Exam
Diagnostics
Therapy
Soft S1; S4 in acute severe MR
Apical holosystolic murmur radiating to axilla (characteristic finding)
Hyperdynamic LV with brisk systolic impulse and laterally displaced apex beat
CXR: LAE, LVH
ECG: LAE, LVH; atrial fibrillation in severe cases
2D ECHO: mosaic color flow across the mitral valve during systole
For fluid retention: sodium, restriction, diuretics
For acute MR:vasodilators (decreases afterload and helps reduce severity of MR)
Intervention:mitral valve repair or replacement (surgery)
E. Mitral Valve Prolapse (MVP, Floppy Valve Syndrome, Barlow’s Syndrome)
More common in women 15-30 years old
More severe in men and >50 years old
Most patients are asymptomatic
Frequent finding in heritable connective tissue disease
Apical mid- or late non-ejection systolic click (characteristic finding)
Physical Exam
High pitched late crescendo-decrescendo murmur after systolic click
Murmur is accentuated by standing and strain phase of Valsalva, diminished by
squatting and isometric exercises
CXR / ECG: usually normal; but may have biphasic or inverted T in II, III, aVF
Diagnostics
(inferior leads) on ECG
2D ECHO: systolic displacement of MV leaflets (prolapse) at least 2 mm into LA
superior to mitral plane
IE prophylaxis for patients with prior endocarditis
Therapy
Symptoms: beat-blockers for palpitations; warfarin if with AF
Intervention: mitral valve repair or replacement (surgery) if with severe MR
F. Tricuspid Stenosis (TS)
Generally rheumatic in origin; does not occur in isolation and usually associated with MS
Almost always accompanied by severe TR
Symptoms of right-sided CHF (ascites, edema, hepatosplenomegaly)
Physical Exam
Opening snap of TV ~0.06 sec after PV closure
Diastolic murmur at LLSB, augmented during inspiration and reduced during
expiration & strain phase of Valsalva
Diagnostics
ECG: RAE, RVH
2D ECHO: restriction in opening of the TV
Therapy
Salt restriction, bed rest and diuretics
Interventions: surgery
71
G. Tricuspid Regurgitation (TR)
Physical Exam
Diagnostics
Therapy
Distended neck veins, hepatomegaly, ascites, (+) hepatojugular reflux
Prominent RV pulsation along left parasternal region
Carvallo sign: blowing holosystolic murmur at LPSB intensified by inspiration
ECG: RAE, RVH
2D ECHO: mosaic color flow across tricuspid valve during systole
Isolated TR is usually tolerated and does not require surgery
Intervention: valve annuloplasty or replacement for severe cases
H. Pulmonic Regurgitation (PR)
Most common acquired abnormality is regurgitation from severe pulmonary arterial HPN
Graham Steell murmur: high-pitched, decrescendo, diastolic blowing murmur along left sternal border
Intervention: percutaneous pulmonic valve replacement for severe PR
PERICARDITIS
I. ETIOPATHOGENESIS
Most common pathology affecting the pericardium and classified clinically and etiologically
May be infectious, non-infectious (MI, uremia, neoplasia, myxedema, cholesterol, chylopericardium, trauma, aortic
dissection, post-irradiation, acute idiopathic, sarcoidosis) or presumably related to hypersensitivity or
autoimmunity (rheumatic fever, collagen valvular disease, drug-induced, post-cardiac injury)
II. CLINICAL MANIFESTATIONS
A. Acute Pericarditis (< 6 weeks)
Pain resembles that of acute MI
Chest pain: severe, pleuritic, may be retrosternal or left pericordial and may be referred to neck and, arms or
left shoulder
Pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine
PE may reveal pericardial friction rub (85%): high-pitched and is described as rasping, scratching or grating
and heard most frequently at end-expiration with patient upright and leaning forward
B. Chronic (Constrictive) Pericarditis (> 6 months)
Results when the healing of an acute fibrinous or serofibrinous pericarditis or the resorption of a chronic
pericardial effusion is followed by obliteration of the pericardial cavity with formation of granulation tissue
Weakness, weight gain, fatigue, increased abdominal girth / ascites and edema
Common in the Philippines: tuberculosis, malignancy and radiation-induced
Kussmaul’s sign: increase in systemic venous pressure with inspiration (in normal conditions, there should
be a decrease in pressure with inspiration)
Pericardial knock: early diastolic sound in the left sternal border
III. DIAGNOSIS AND MANAGEMENT
DIAGNOSTICS
Cardiac biomarkers
ECG
ACUTE PERICARDITIS
Modest increase
Subepicardial inflammation displays:
Stage 1: Diffuse SST-elevation
with upward concavity and PR
segment depression
Stage
2:
ST
segments
normalize
Stage 3: T-wave inversions
Stage 4: ECG returns to
CHRONIC (CONSTRICTIVE
PERICARDITIS)
May
be
normal-minimally
increased
Low voltage QRS complexes
Diffuse flattening or inversion
of T-waves
Atrial fibrillation in 1/3 of
patients
72
normal (weeks or months)
This is in contrast with ECG findings in
AMI
wherein ST-elevations are
convex, QRS changes occur and Twave inversion is seen within hours
before the ST-segments become
isoelectric
Pericardial thickening
Septal bounce
Dilation of the IVC and hepatic
veins
Normal ventricular systolic
function
Flattening of the LV posterior
wall
Pericardial thickening (more
accurate)
Pericardial
resection
/
pericardectomy
Sodium restriction & diuretics
Anti-Koch’s for TB patients
Steroids (uncertain benefi)
Pericardial fluid or thickening
Differentiate pericarditis from
MI: assessment of wall motion
Echocardiography
CT/MRI
Pericardial fluid collection
Pericardial thickening
Bed rest
NSAIDs, colchicine
Pericardiocentesis
if
with
tamponade
Management
CARDIAC TAMPONADE
I. ETIOPATHOGENESIS
Accumulation of fluid in the pericardial space causes increased intracardiac pressures causing limited ventricular
filling and decreased cardiac output
Three most common causes are neoplastic disease, idiopathic pericarditis and renal failure
II. CLINICAL MANIFESTATIONS
Dyspnea, orthopnea and fatigue
Beck’s triad: hypotension, neck vein engorgement and muffled heart sounds
Tachycardia, tachypnea and pulsus paradoxus (>10 mmHg decrease in SBP during inspiration)
A. Diagnostics for Cardiac Tamponade
DIAGNOSTICS
12-L ECG
Chest Radiograph
2D Echocardiography
COMMENTS/EXPECTED FINDINGS
Low voltage QRS complexes with electrical alternans
Multi-chambered cardiomegaly “water-bottle” sign
Large pericardial effusion
Right atrial and right ventricular diastolic collapse
B. Differentials for Cardiac Tamponade
CHARACTERISTIC
CARDIAC
TAMPONADE
Clinical Features
Pulsus Paradoxus
+++
Jugular Veins
Prominent y-descent
+++
Prominent x-descent
Kussmaul’s sign
Third Heart Sound
Pericardial Knock
-
CONSTRICTIVE
PERICARDITIS
RESTRICTIVE
CMP
RV MI
EFFUSIVE
CONSTRUCTIVE
+
+
+
+++
++
++
+++
++
+
+++
+
+
-
+
+
+++
+
-
+++
++
+
-
73
Electrocardiogram
Low ECG voltage
Electrical Alternans
Echocardiography
Thick pericardium
Pericardial effusion
RV size
Exaggerated
Respiratory Variation
CT-MRI
Thick pericardium
Equalization of Diastolic
Pressure
Cardiac Biopsy Helpful?
++
++
++
-
++
-
-
++
+
+++
Usually small
+++
+++
Usually normal
+++
Usually normal
-
++
Enlarged
+++
++
+++
+++
+++
-
++
++
No
No
Sometimes
No
No
CMP: Cardiomyopathy; RVMI: right ventricular myocardial infarction
IV. MANAGEMENT
Emergency pericardiocentesis
Tube pericardiostomy with pericardial window (for recurrent, infectious, malignant and other chronic causes)
CARDIOMYOPATHY (CMP)
Heterogenous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that
usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of
causes that frequently are genetic
It excludes cardiac dysfunction that results from other structural heart diseases such as CAD, valvular disease or
severe hypertension
DILATED
RESTRICTIVE
HYPERTROPHY
CARDIOMYOPATHY
CARDIOMYOPATHY
CARDIOMYOPATHY
Cardiac enlargement,
Endomyocardial scarring or
Disproportionate
resulting in impaired systolic
myocardial infiltration
hypertrophy, typically
Pathophysiology
function, HF, arrhythmia,
resulting in restriction of
involving the interventricular
emboli
ventricular filling
septum more than the free
wall
Ejection Fraction
Usually <30%
25-50%
>60%
LV Dimension
Dilated >60mm
>60mm (may be decreased)
Often decreased
LV Wall Thickness
Decreased
Normal or increased
Markedly increased
Atrial Size
Increased
Increased; may be massive
Increased
Valvular Regurgitation
Related to annular dilation
Related to endocardial
Related to valve-septum
involvement
interaction
Common First Symptoms
Exertional intolerance
Exertional intolerance, fluid
Exertional intolerance; may
retention early
have chest pain
Congestive Symptoms
Left before right
Right often predominates
Left-sided congestion may
develop late
Viral, parasitic
Amyloidosis
Most common abnormality
Common examples
Peripartum
Loeffler’s
found at autopsy in young
Alcohol, MAP, cocaine
Endomyocardial
competitive athletes who die
Chemotherapy
suddenly
Normal LVEF: > 50%
Normal LV dimension: < 55mm
ATRIAL FIBRILLATION (AF)
I. TYPES OF ATRIAL FIBRILLATION
TYPE
Lone AF
First Diagnosed AF
DEFINITION
AF in a patient <60 years old with the absence of clinical findings of other
cardiovascular disease, related pulmonary disease, or cardiac abnormalities
Every patient who present with AF for the first time, irrespective of duration or
74
Paroxysmal AF
Persistent AF
Long-standing Persistent AF
Permanent AF
presence / severity of symptoms
Self-terminating, usually within 48 hours
Paroxysms may continue for up to 7 days
48 hour time point is important: after this, likelihood of spontaneous conversion
is low
Anticoagulation must be considered
AF episode either lasts >7 days or require termination by cardioversion
Lasted for > 1 year when it is decided to adopt a rhythm control strategy
Presence of arrhythmia is accepted by the patient – rhythm control interventions
are not pursued
II. STROKE PREVENTION IN AF
Efficacy of stroke prevention with aspirin is weak and the risk of major bleeding with aspirin is not significantly
different from oral anticoagulants (OACs)
Usually has two scoring systems:
o CHA2DS2-VASc Score: to determine the risk of having a stroke in the presence of AF
o HAS-BLED: to determine the risk of bleeding (since patients with AF will be given anticoagulants)
A. CHA2DS2-VASc Score
Estimates the risk of ischemic stroke in patients with non-rheumatic / non-valvular atrial fibrillation
Better than CHADS2 in identifying “truly low risk” patients with AF
Components and corresponding points:
VARIABLE
SCORE (POINTS)
C
Congestive HF / left ventricular dysfunction
1
H
Hypertension (>140/9 mmHg)
1
A2
Age > 75years
2
D
Diabetes
1
S2
Prior stroke / TIA / thromboembolism
2
V
Vascular disease (prior MI, PAD, aortic plaque)
1
A
Age 65-74
1
Sc
Female sex
1
RISK
0: 0%
1: 1.3%
2: 2.2%
3: 3.2%
4: 4.0%
5: 6.7%
6: 9.8%
7: 9.6%
8: 12.5%
9: 15.2%
B. HAS-BLED Score
Bleeding risk score to aid in decision-making for thromboprophylaxis (to balance the risk of stroke versus risk of
major bleeding)
High risk for bleeding: HAS-BLED score > 3 (regular monitoring and correction of potentially reversible risk factors
for bleeding)
VARIABLE
SCORE (POINTS)
Hypertension (SBP > 160 mmHg)
1
Abnormal renal / liver function
1
Renal: Chronic dialysis or renal transplantation or creatinine > 200 umol/L
1
Liver: CLD, bilirubin >2x ULN with AST / ALT / Alk Phos >3x ULN
Previous Stroke
1
Bleeding history or predisposition (bleeding diathesis, anemia, etc)
1
Labile INR (unstable or high INR)
1
Elderly (age >65)
1
Use of Drugs predisposing to bleeding (e.g., antiplatelets, NSAIDs)
1
Alcohol use (>8 drinks per week)
1
CLD: Chronic Liver Disease
ULN: Upper Limit of Normal
III. MANAGEMENT OF ATRIAL FIBRILLATION
A. Drugs for Rate Control:
B-blockers: metoprolol, bisoprolol, atenolol, esmolol, propranolol, carvedilol
Non-dihydropyridine CCB: verapamil, diltiazem
Digitalis / Digoxin
Others: amiodarone, dronedarone
75
B. Pharmacological Cardioversion:
If with structural heart disease: Amiodarone
If without structural heart disease: Flecainide, Ibutilide, Propafenone
C. Electrical Cardioversion:
Used for patients with recent-onset AF (<48 hours) and with hemodynamic instability
IV. ANTICOAGULATION FOR STROKE PREVENTION
POPULATION
Valvular AF (RHD, prosthetic valves)
Non-Valvular AF + <65 years old + Lone AF
Non-Valvulvar AF + CHA2DS2-VASc Score 0
Non-Valvular AF + CHA2DS2-VASc Score 1
Non-Valvular AF + CHA2DS2-VASc Score > 2
ANTITHROMBOTIC THERAPY FOR STROKE PREVENTION
Warfarin only
No antithrombotic therapy
No antithrombotic therapy
Class Iia: consider oral anticoagulant therapy (NOAC/warfarin)
Class I: start oral anticoagulant therapy (NOAC or warfarin)
A. Warfarin (Vitamin-K Antagonist)
Considered for patients with AF with >1 stroke risk factor(s) provided there are no contraindications
Superior to antiplatelets in preventing stroke
Usual INR target: 2.0-3.0
B. Non-Vitamin K Oral Anticoagulants (NOACs)
Non-inferior to warfarin, but with better safety profile
Broadly preferably to warfarin in the vast majority of patients with non-valvular AF
Assessment of renal function is mandatory for all NOACs, especially for Dabigatran
Do not require dose adjustment on the basis of a specific coagulation test (in contrast to INR in warfarin)
Do not have specific antidotes, and management of bleeding is supportive
Not recommended in patients with severe renal impairment (creatinine clearance < 30 mL/min)
DRUG
MECHANISM OF ACTION
DOSE
Oral direct thrombin inhibitor
150 mg BID
150 mg BID superior to warfarin
with same risk as warfarin to cause
110 mg BID for> age > 80,
Dabigatran
major bleeding
concomitant interacting drugs,
HAS-BLED > 3, creatinine
110 mg BID non-inferior to warfarin
clearance 30-40 mL/min
with fewer major bleeds (compared
to warfarin)
Oral direct factor Xa inhibitor
20 mg OD
Rivaroxaban
Non-inferior
to
warfarin
in
15 mg OD if: HAS-BLED > 3,
preventing stroke
creatinine
clearance
30-49
mL/min
5 mg BID
Apixaban
Oral direct factor Xa inhibitor
2.5 mg BID if : age > 80 years,
weight < 60 kg, or creatinine >
133 umol/L
PERIPHERAL ARTERY DISEASE (PAD)
I. ETIOPATHOGENESIS
Clinical disorder characterized by stenosis or occlusion in the aorta or arteries of the limbs
Atherosclerosis is the leading cause of PAD in patients >40 years old
II. CLINICAL MANIFESTATIONS
A. History and Symptoms
More than half of patients with PAD are actually asymptomatic, though some may present with slow gait
Most common symptoms: intermittent claudication (pain, ache, cramp, numbness, or sense of fatigue in the
muscles which occurs during exercise and is relieved by rest)
Other symptoms are rest pain or feeling of coldness or numbness in the feet and toes
76
B. Physical Examination
Decreased or absent pulses distal to obstruction
Bruits over narrowed artery
Muscle atrophy, hair loss, thickened nails, smooth and shiny skin
Reduced skin temperature
Pallor, cyanosis,, ulcers or gangrene
III. DIAGNOSIS
DIAGNOSTICS
ABI Assessment by Doppler
Other Non-Invasive Tests
COMMENTS / EXPECTED FINDINGS
ABI: ratio of ankle to brachial artery pressure
o >1.0: normal individuals
o <0.9: in patients with PAD
o <0.5: signifies severe ischemia (at risk for critical limb ischemia)
Segmental pressure measurements: presence of pressure gradients between
sequential cuffs signify stenosis
Segmental pulse volume recordings: amplitude of pulse volume contour
becomes blunted in significant PAD
Duplex ultrasonography: images and detects stenosis
Transcutaneous oximetry
Treadmill testing: assesses functional limitations objectively
IV. MANAGEMENT
A. Non-Pharmacologic Management
Goals: reduce the risk of associated CV events, improve limb symptoms, prevent progression to critical ischemia,
and preserve limb viability
Risk factor modification: cigarette smoking cessation, BP control
Supportive: feet care, elastic supports should be avoided, regular exercise (walk until nearly maximum
claudication discomfort is experience, and then rest until symptoms resolve before resuming ambulation)
Revascularization is usually indicated for patients with disabling, progressive or severe symptoms despite medical
therapy and for those critical limb ischemia
B. Physical Examination
Antiplatelet Therapy
Anticoagulant Therapy
ACE-Inhibitors
Statins
Cilostazol
Pentoxifylline
Aspirin and clopidogrel dual therapy is not more effective than aspirin alone in
reducing CV morbidity and mortality in patients with PAD
Not indicated to improve outcomes in patients with chronic PAD
Reduce CV risks in patients with PAD
Target LDL <100 mg/dL
Increases claudication distance by 40-60% and improves measured quality of
life
Contraindicated in patients with CHF
Increases blood flow to the microcirculation and enhances tissue oxygenation
COR PULMONALE
I. ETIOPATHOGENESIS
Often referred to as “pulmonary heart disease”
Defined as altered RV structure and/or function in the context of chronic lung disease and is triggered by the
onset of pulmonary hypertension
Acute Cor Pulmonale
Acute RV dilatation and failure occurs (e.g., massive pulmonary embolism) but RV does
not hypertrophy
Chronic Cor Pulmonale
More slowly evolving and progressive pulmonary hypertension leads to both RV
hypertrophy and dilation
II. CLINICAL MANIFESTATIONS
Dyspnea: most common symptom and occurs due to increased work of breathing
77
Tussive or effort-related syncope happens due to inability of RV to deliver adequate blood volume to the LV
Abdominal pain and ascites: happens due to backflow from right-sided HF
Orthopnea and PND: uncommon and occurs only with concurrent LV failure
RV heave: points to RV volume and pressure overload
Carvallo’s sign: increase in the intensity of the holosystolic murmur of tricuspid regurgitation with inspiration
Cyanosis: a late finding and is secondary to low cardiac output
III. DIAGNOSIS
DIAGNOSTICS
12-L ECG
Chest Radiography
2D Echocardiography
Spirometry
CT scan
COMMENTS / EXPECTED FINDINGS
P pulmonale (p waves > 2.5 mV in leads II and/or V1)
Right axis deviation and RV hypertrophy
Enlargement of main pulmonary artery, hilar vessels & descending right
pulmonary artery
Right-sided chamber enlargement with dysfunction; pulmonary hypertension
Identifies obstructive and restrictive parenchymal diseases
Identifies thromboembolic diseases, interstitial diseases
IV. MANAGEMENT
Target the underlying pulmonary disease
to decrease the underlying pulmonary valvular resistance and lessen
RV afterload
Non-invasive mechanical ventilation, bronchodilators and correction of respiratory acidosis
Correction of infection, anemia and polycythemia and other extra-cardiac problems
Pulmonary vasodilators: modest reduction of pulmonary pressure and RV afterload
78