Anatomy
4 chambers:
▪ Atria (2)
▪ Ventricle (2)
4 Valves:
▪ Semilunar: Aortic, pulmonic
▪ Atrioventricular: Tricuspid,
Bicuspid/Mitral
Remember:
Stenosis – is a narrowing of
valves
Regurgitation – is the process
(backflow of blood)
Murmur – is the symptom
(assessment)
Coverings (epicardium):
Pericardium
▪ Fibrous
▪ Serous (parietal,
pericardial cavity,
visceral)
Myocardium
Endocardium
Major Veins
▪ Inferior & Superior Vena
Cava (unoxygenated)
▪ 4 Pulmonary Veins
(oxygenated)
Major Arteries
▪ Pulmonary arteries
(unoxygenated)
▪ Aorta (oxygenated)
Physiology
Action – Potential
The brief reversal of electric polarization (positive and negative) of the
membrane of a nerve cell (neuron) or muscle cell (ex: cardiac).
In the neuron an action potential produces the nerve impulse, and in
the muscle cell it produces the contraction required for all movement.
Action-Potential to Heart:
1. Cardiac Pacemaker Cells action-potential
2. Cardiac Myocyte action-potential
Depolarization
During depolarization, the membrane potential rapidly shifts from
negative to positive polarity. For this rapid change to take place
within the interior of the cell, several events must occur along the
plasma membrane of the cell such as sodium influx into the cell.
Repolarization
Is a stage of an action potential in which the cell experiences a
decrease of voltage (negative polarity) This phase occurs after the
cell reaches its highest voltage from depolarization.
Electrolytes: Determine action potential in the cell membrane
Sodium (Na+) Extracellular
Potassium (K+) Intracellular
Calcium (Ca++) Extracellular
Remember:
▪ It is important to know cardiac action potential
to understand knowledge involving cardiac
pharmacology. It is influenced by innervation of
the Autonomic Nervous System (Sympathetic
and Parasympathetic). However, it can initiate
and generate its own (automaticity) thru its
specialized pacemaker cells.
▪
Action potential activity within the heart can be
recorded to produce an electrocardiogram
(EKG).
Autonomic Innervation
The autonomic nervous system plays a key role in regulating
changes in the cardiovascular system and its adaptation to various
human body functions. The sympathetic arm of the autonomic
nervous system is associated with the fight and flight response, while
the parasympathetic division is responsible for the restorative
effects on heart rate, blood pressure, and contractility.
How?
Sympathetic Nerves: Binding of catecholamines (e.g.
norepinephrine, epinephrine) to adrenergic
receptors in the heart (Beta 1)
Cholinergic Nerve (Vagus): Binding of acetylcholine
to muscarinic/cholinergic receptors in the heart (M2)
Cardiac Conduction system
Cells in the cardiac conduction system can generate electrical impulses
and then distribute the signal throughout your heart. While all cells in
your heart can conduct electricity, the cells in this system conduct it at
very specific speeds. This is how different parts of your heartbeat at just
the right time. The parts of the cardiac conduction system are (in order,
starting where electricity is generated):
▪
▪
▪
▪
▪
The sinoatrial (SA) node.
The atrioventricular (AV) node.
The Bundle of His.
Bundle branches.
Purkinje fibers.
Cardiac output:
Cardiac output (CO) is the amount of blood the heart pumps in 1
minute, and it is dependent on the heart rate, contractility, preload,
and afterload.
Normal CO: 4-8 liters per minute, depending on the person’s size.
Basically, total blood volume circulates to heart in 1 full minute
as a cardiac output (CO)
Remember: Cardiac output
Cardiac Output is just simply what you want from heart to produce in order
to nourish nutrients and O2 in each body system.
Persistent decrease CO means abnormal heart and subsequent problem
to brain, kidneys, heart, liver tissues, etc.
Cardiac CO: Heart Rate (HR) x Stroke Volume
Heart Rate (HR): Heart rate is the speed of the heartbeat measured by the
number of contractions (beats) of the heart per minute (bpm) propagated
by conduction system.
Stroke Volume (SV): Volume of blood pumped by the ventricles
with each heartbeat. Approximately 70 ml.
Preload: aka “Filling Pressure”. Is the pressure that stretches the right
or left ventricle during relaxation or before it contracts to produce
cardiac output.
Afterload: is a pressure against which the heart must overcome to eject
blood during contraction. Ex: aortic pressure
Illustration:
Ejection fraction: The measurement of the percentage of blood leaving
the heart each time it contracts.
EF= SV X 100%
EDV
Example: CHF (Systolic vs diastolic heart failure)
Blood Pressure:
Is the pressure of the blood in the circulatory system (Heart and Blood
vessels), often measured for diagnosis since it is closely related to the
force and rate of the heart (Cardiac Output) and the diameter and elasticity
of the arterial walls (Vascular resistance). 120/80 mm Hg are considered
within the normal range.
Systolic vs. Diastolic Blood Pressure:
The first number, called systolic blood pressure, measures the pressure in
your arteries related to heart activity (Cardiac output)
The second number, called diastolic blood pressure, measures the
pressure in your arteries (Vascular resistance) when the heart rests.
Mean arterial pressure (MAP):
The average pressure in your arteries throughout one cardiac cycle, which
includes the series of events that happen every time your heart beats.
What is a normal MAP?
In general, most people need a MAP of at least 60 mmHg or greater to
ensure enough blood flow to vital organs, such as the heart, brain, and
kidneys. Consider anything between 70- and 100-mm Hg to be normal.
A MAP in this range indicates that there’s enough consistent pressure in
your arteries to deliver blood throughout your body.
What is a high MAP?
A high MAP is anything over 100 mm Hg, indicates that there’s a lot
of pressure in the arteries. This can eventually lead to blood clots
or damage to the heart muscle, which must work a lot harder.
Associated conditions are MI, kidney failure and heart failure.
What is a low MAP?
Anything under 60 mm Hg is usually considered a low MAP. It
indicates that your blood may not be reaching your major organs.
Without blood and nutrients, the tissue of these organs begins to fail,
leading to permanent organ damage. They include septic shock and
other forms of circulatory shock.
Formula:
Illustration: Blood pressure
Heart sounds:
S1, S2, S3, S4
Acute Coronary Syndrome (ACS)
Acute coronary syndrome (ACS) encompasses a range of cardiac events,
including stable angina, unstable angina & acute myocardial infarction
(with or without ST segment elevation). Clients with ACS require
immediate treatment. ACS is a sequelae of coronary artery disease (CAD).
Assessing a patient with ACS:
Risk Factors of CAD:
▪ Hereditary/Familial, Age, Gender
▪ Hyperlipidemia (Atherosclerosis)
▪ Hypertension (Arteriosclerosis)
▪ Diabetes Mellitus
▪ Smoking
History of present illness:
▪ Presence of Chest Pain (Angina)
Characteristics:
✓ Substernal
✓ Relieved by Nitrates
✓ On exertion
3/3: Typical Angina
2/3: Atypical
0/3: non-Angina
Associated signs and symptoms:
▪ Shortness of breathing
▪ Nausea/vomiting
▪ Dizziness/Syncope
▪ Lightheadedness
▪ Anxiety
▪ Sweating (diaphoresis)
▪ Fatigue
A cardiac chest pain (angina)
or discomfort, often described
as aching, pressure, tightness
or burning. Pain may spread
from the chest to the shoulders,
arms, upper abdomen, back,
neck or jaw.
▪ Cool clammy skin
Note: If the patient is complaining of chest pain, it is important to
determine what causes the symptom. A chest pain can be for
instance, pleuritic, positional, or upon touch (tender)
Ruling out (approach to chest pain)
Skin
Wounds, burns, herpes zoster etc.
Subcutaneous
Cellulitis, abscess
Sprain, strain, rhabdomyolysis, costochondritis
(most common cause of chest pain in ER)
Pleuritic (Upon Breathing): Pleurisy, Pulmonary
embolism, Pulmonary Tumor, Pneumothorax,
Pneumonia
Musculoskeletal
Pleural Space
Pericardium
Positional & pleuritic: pericarditis, myocarditis
Heart
Ischemic: Acute coronary syndrome
Esophagus
Epigastric: GERD, Esophagitis, GI ulcers
Trachea
Tracheitis
Aorta
Aortic dissection (chest pain with tearing
sensation in the back), thoracic aortic aneurysm
(tenderness) if ruptures, may radiate in the back
downwards.
Note: Always remember that ACS is a result of CAD that overtime
results from the risk factors mentioned. It will cause the buildup of
fatty deposits (plaques) in and on the walls of coronary arteries, the
blood vessels delivering oxygen and nutrients to heart muscles.
When a plaque deposit ruptures or splits, a blood clot forms. This clot
blocks the flow of blood to heart muscles. When the supply of
oxygen and nutrient to cells is too low (ischemia), cells of the
myocardium can be injured and eventually die if no prompt treatment
is done. The death of cells resulting in damage to muscle tissues is a
severe type of ACS known as myocardial infarction.
Differentiating ACS
Differentiating ACS
Asymptomatic
CAD
Stable angina
Unstable
angina
NSTEMI
STEMI
Chest Pain
On exertion
On rest
On rest
On rest
On rest
Relief
With rest
With nitrates
With nitrates
With nitrates
(-)
(-)
(-)
(-)/(+) ST
depression
With
nitrates
ST
elevation
(-)
(-)
(-)
(+)
(+)
<50%
Upto 70%
Upto 90%
Upto 90%
Upto 100%
EKG (ST
changes)
Cardiac
Markers
Occlusion
Asymptomatic CAD and Stable Angina:
Stable plaque with no platelets
and coagulation involved
Unstable angina and non-ST elevation MI (NSTEMI):
Unstable plaque with platelet
aggregation involved; results
to subendocardial injury
ST elevation MI (NSTEMI):
Unstable plaque with platelet
aggregation and coagulation
involved results to transmural
injury
EKG Changes:
Cardiac Markers In order rising:
Myoglobin:
Troponin:
CPK:
AST:
LDH:
0 - 85 ng/ml
< 0.6 ng/ml (most specific & most sensitive)
12 - 70 U/ML (m)
10 - 55 U/ml (f)
10 - 50 IU/L
100 - 190 U/L
Algorithm: Considering the patient is having chest pain, risk
factors of CAD, history of present illness, associated signs
and symptoms
1
EKG
If ST elevation
Stat Heart
Catheterization
2
Cardiac Markers:
Troponin
CK-MB
If Troponin (+)
Urgent Heart
Catheterization
If Troponin (-)
and EKG (-)
CK-MB can be (+)
but not cannot be
a specific indicator
of ACS
If 1-2 vessels
involved: Stenting
(Percutaneous
coronary
intervention: PCI)
If 3 or more:
CABG
Serial Monitoring:
Q6 hours X 2 more
If negative (-)
Stress Test and
Echo (evaluation)
or outpatient work
up
Heart catheterization is a procedure in which a
thin, flexible tube (catheter) is guided through a
blood vessel to the heart to diagnose or treat
certain heart conditions (PCI or stenting)
Remember: Door-to-balloon is a time (1-1.5
hours) measurement in the treatment STEMI.
The interval starts with the patient's arrival in the
ER and ends when a catheter guidewire crosses
the culprit lesion in the cardiac cath lab.
If Stress test (+)
Remember:
If no access to heart catheterization,
may do thrombolysis. However, patient
will be at highest risk for bleeding
Routine Heart
Catheterization
Stress Test: (Non-Pharmacologic)
Heart Catheterization: Percutaneous Coronary Intervention (PCI)/
Balloon angioplasty:
Inflation of a balloon within the coronary artery to crush the plaque into the
walls of the artery. Angioplasty is often combined with the permanent
placement of a small wire mesh tube called a stent to help prop the artery
open and decrease its chance of narrowing again. PCI is an interventional
type of heart catheterization.
Preparation:
▪ Check dye allergy
▪ Check for intake of Metformin
▪ Check for intake of antiplatelets
▪ Check BUN, creatinine
▪ NPO 6-8 hours
Risk:
▪ Re-narrowing of artery
▪ Blood clots
▪ Bleeding
▪ Heart attack
▪ Coronary artery damage.
▪ Acute Kidney Disease
▪ Stroke
▪ Arrhythmias
Remember:
Check BUN, creatinine, and
intake of metformin (anti
diabetic) to patients receiving
contrast dye. Kidney primarily
excretes these materials
Metformin:
Withheld until 48 hrs. after
procedure). Induces toxic
accumulation of lactic acid.
Aggravates renal failure
Standard Management: Pharmacology (MONA-BASH-C)
Understanding Hemostasis/Clot formation vs AntiHemostatic (Antiplatelet, Anticoagulants,
Thrombolytics/Fibrinolytics):
Hemostasis involves three major steps:
▪ Vasoconstriction
▪ Platelet Plug (primary hemostasis)
▪ Blood coagulation (secondary hemostasis): Involves Clotting
Factors (CF) until the formation of Fibrin (non-water soluble)
Coagulation Cascade
Extrinsic Pathway
Intrinsic Pathway
Common Pathway
PTT
Physiologic anti-clot
mechanisms:
▪ Antithrombin mainly inhibits
thrombin by binding to
heparin like molecule
▪ Protein C pathway degrades
CF5, CF8
▪ Tissues factor and Protein S
inhibit extrinsic pathway
▪ Tissue Plasminogen activator
breaks down plasminogen to
form plasmin which degrades
fibrin. (D-dimer is the
biproduct)
Vit K
dependent
PT/INR
Antiplatelets: Bleeding risk LOW
▪ Prevents formation of new clots
▪ Prevent further increase in size of existing clots
Example:
▪ Aspirin (ASA)
▪ Clopidogrel
▪ Abciximab
▪ Eptifibatide
▪ Tirofiban
▪ Cilostazol
▪ Dipyridamole
▪ Prasugrel
▪ Ticlopidine
▪ Ticagrelor
Remember: NCLEX Tips
▪ Check for signs of bleeding
▪ Monitor platelet count
Hold medication if <50,000
Inform HCP if <150,000
▪ Monitor HGB, hold if <7 g/dl
▪ Activated charcoal for ASA
toxicity
▪ Hyperventilation (Respiratory
Alkalosis is a sign of ASA
toxicity
Anticoagulants: Bleeding risk MODERATE
▪ Prevents formation of new clots
▪ Prevent further increase in size of existing clots
Heparin
▪ Enhances antithrombin activity
▪ Unfractionated (IV): Inhibits CF2, CF10
▪ Low molecular weight/LMW (SQ): Inhibits CF10
Example:
Enoxaparin
Fondaparinux
Remember: NCLEX Tips
▪ Check for signs of bleeding
▪ Monitor platelet count
Hold medication if <50,000
Or if less than 50% of baseline (HIT)
▪ Monitor HGB, hold if <7 g/dl
▪ Check for PTT only for Unfractionated (IV)
heparin (not > 70 sec: bleeding risk),
LMWH does not need checking of PTT
▪ No massage to SQ injection site
▪ No Fondaparinux within 6 hours post
operative patients with spinal anesthesia
▪ Generally, not given with other blood
thinners (antiplatelets) unless prescribed by
HCP. Heparin is not given with other oral
anticoagulants like apixaban, rivaroxaban
and the likes due to high bleeding risk.
▪ Heparin antidote: Protamine Sulfate
Heparin-induced thrombocytopenia
(HIT):
Is a serious complication of taking
heparin. With HIT, your immune system
causes your platelets to clot in the
presence of heparin, resulting in your
platelet levels dropping. Without
treatment, the clotting puts you at risk of
developing life-threatening blood clots.
HIT usually happens from 5 days to 2
weeks after first dose of heparin.
It can cause DVT, PE and less often
ACS and CVA. Treatment Options for
HIT are blood thinners that rarely cause
HIT like Fondaparinux (SQ), Argatroban
(IV), Dabigatran (PO)
Warfarin
▪ Vitamin K inhibitor
▪ Anticoagulant of choice to patients with ESRD
▪ Anticoagulant of choice to patients with valvular disease
▪ Takes effect usually up to 5 days
Remember: NCLEX Tips
▪ Check for signs of bleeding
▪ Monitor HGB, hold if <7 g/dl
▪ Check for INR (not > 3.5 sec: bleeding risk)
▪ Consistent intake of green leafy vegetables (rich in Vit
K). It does not need to be increased or decreased.
▪ Antibiotics can affect Vit K due to its effect to intestinal
bacteria.
▪ Can be given with Heparin (bridging) until therapeutic
INR level is achieved usually up to 5 days
▪ Warfarin antidote: Vitamin K
Remember: Anticoagulation Therapy
Heparin (IV Drip)
PTT: 25 – 35 sec (less sensitive)
(1.5 – 2X is therapeutic)
Risk for Bleeding: > 70 secs
Warfarin (Coumadin):
INR: 0.9 - 1.18
(Up to 3X is therapeutic)
Risk for Bleeding: > 3.5 secs
Direct Acting Oral Anticoagulants:
Apixaban (PO), Rivaroxaban (PO), Edoxaban (PO)
▪ Inhibits CF10, non-Vitamin K inhibitor
▪ Anticoagulant of choice to patients without ESRD
▪ Anticoagulant of choice to patients without valvular
disease
▪ Takes effect immediately
▪ Alternate to Warfarin
▪ Lower risk of bleeding than warfarin
Argatroban (IV), Bivalerudin (IV), Dabigatran (PO)
▪ Inhibits CF2, non-Vitamin K inhibitor
▪ Takes effect immediately
▪ Alternate to Heparin
Remember: NCLEX Tips
Note: No need for too many blood works as compared
to Heparin
▪ Check for signs of bleeding
▪ Monitor renal function (BUN and creatinine)
▪ Do not give with any forms of heparin together (higher
risk for bleeding)
Thrombolytics/Fibrinolytics/Tissue Plasminogen Activator (TPA):
Bleeding risk HIGH
▪ Dissolves clots (Fibrinolysis) by catalyzing the conversion of
plasminogen to plasmin, the primary enzyme involved in dissolving
blood clots.
▪ This treatment is used in facilities without an interventional cardiac
catheterization laboratory or when one is too far away to transfer the
client safely.
Alteplase
▪ Intravenous (IV): 1 hour
▪ Catheter assisted: up to 72 hours
▪ Most often used fibrinolytic in the treatment of acute coronary
syndrome (ACS), pulmonary embolism (PE), and acute stroke
(CVA)
▪ Non antigenic, therefore seldom associated with any allergic
reactions compared to Streptokinase (produced from
streptococcus)
Remember: NCLEX Tips
▪ Check for signs of bleeding
▪ Do not give with other blood thinners
▪ No IM and SQ injections, No ABG blood draws
▪ Given in a compressible site in case of bleeding. Not
given central line (non-compressible)
Contraindications:
▪ Prior intracranial hemorrhage
▪ Arteriovenous malformation (AVM): aneurysms
▪ Ischemic CVA within 3 mos.
▪ Suspected aortic dissection
▪ Active bleeding
▪ BP >180/110 (may indicate hemorrhagic CVA)
▪ Recent surgery in 2 weeks
▪ Significant head trauma within 3 mos.
General signs of bleeding:
▪ Intracranial hemorrhage: Headache, altered mental status,
decrease LOC
▪ Epistaxis
▪ Gum bleeding
▪ GIB: Abdominal pain/discomfort, Upper GI: coffee ground
emesis, hematemesis; Lower GI: black tarry stool,
hematochezia
▪ Hemoptysis
▪ Petechiae, easy bruising (hematoma), purpura,
Note: easy bruising is expected to a patient getting blood
thinners. Bruising accompanied by other forms of bleeding like
epistaxis, hematuria and GIB must be investigated (inform
HCP). Bruises in unusual places such as back, abdomen and
upper thighs may be concerning because most people don’t
frequently bump those body parts (inform HCP).
▪ Hematuria
▪ Vaginal bleeding
Remember: Hypovolemic shock
The symptoms include:
▪ Anxiety, confusion
▪ Low or no urine output
▪ Pale skin
▪ Tachycardia
▪ Low Blood pressure
▪ Dyspnea
▪ Weak pulse
▪ Clammy skin
▪ Decrease O2 saturation
General Patient Teachings: Blood Thinners
▪ Monitor for signs of bleeding
▪ Monitor blood works for specific blood thinners
▪ Combination of some blood thinners must be prescribed by
physician.
▪ Antiplatelet and anticoagulants should be stopped at least 5-7
days prior to the surgery to reduce the chance of intraoperative
and postoperative bleeding or consult prescribing physician.
▪ Avoid EGOS (Risk for bleeding)
E: Vitamin E
G: (4Gs: Herbal Remedies)
Ginkgo biloba
Ginger
Garlic
Ginseng
O: Omega 3
S: St. John’s Wort
▪
▪
▪
▪
▪
No contact sports
Prevent constipation (increase fiber and oral fluid intake)
Prevent trauma resulting from falls
Avoid rigorous toothbrushing, flossing
Avoid use of razors
Infective Endocarditis
Risk: Preexistent disorders
Prosthetic valves
Cong. heart defects
Rheumatic heart disease
Intravenous drug use
Causative Agents:
▪ Streptococcus viridans (most
common but not virulent)
▪ Staph aureus (common and
virulent)
▪ Staph epidermidis
Remember:
Inflammatory type of
Endocarditis is called Libman
Sacks Endocarditis: related to
SLE.
Remember:
High risk groups with prosthetic
valves for example should have
antibiotics before dental
procedures.
▪
▪
▪
▪
Splinter hemorrhages: Thin,
red to reddish-brown lines of
blood under the nails due to
product of Ag-Ab complexes
forming emboli. It runs in the
direction of nail growth.
Janeway lesion: non-tender,
small erythematous or
hemorrhagic macular lesions
indicative of infective
endocarditis also due to Ag-Ab
complexes.
Osler’s nodes: Painful, red,
raised lesions on the hands and
feet caused by immune
deposition from Ag-Ab
complexes.
Roth spots: Retinal
hemorrhages with white or pale
centers due dysfunction of the
retinal capillaries from Ag-Ab
complexes or inflammatory
reactions.
Myocarditis
Causative Agents:
▪ Coxackie virus
▪ Parasitic/protozoal
(Trypanoma cruzi):
Severe case “Chagas
disease” needs heart
transplant
Pericarditis
Remember: Anatomy
Pericardial cavity:
< 50 ml fluid: normal
> 50 ml fluid: abnormal
(Pericardial effusion)
> 150 ml fluid: cardiac
tamponade
Causes:
▪ Idiopathic
▪ Coxackie virus
▪ Dressler’s syndrome
(Post AMI)
▪ Uremia (Urea irritates
pericardium)
Classic sign:
▪ Chest pain on lying
(relieved by sitting up)
▪ Pericardial friction rub
Treatment of choice:
▪ Pericardiocentesis
Complication:
Cardiac Tamponade
Beck’s Triad
▪ Narrowed pulse pressure
(Hypotension)
▪ Muffled/distant heart
sound
▪ Distended neck veins
Rheumatic Heart Disease (RHD)
Rheumatic fever:
An inflammatory disease (autoimmune) that can involve the heart, joints, skin or
brain. These diseases are closely associated with one another. (e.g. Rheumatoid
arthritis, rheumatic heart disease, scarlet fever, impetigo, pharyngitis) and are
usually triggered by Streptococcal infections (group A beta-hemolytic
streptococcus, aka GABHS)
Remember: Diagnostic criteria
▪ Acronym JONES (major criteria) CAFÉ PAL (minor criteria)
▪ Throat cultures for (+) GABHS, elevate Anti- streptolysin titer
Kawasaki disease (Mucocutaneous lymph node syndrome)
Kawasaki disease (KD):
Is a systemic vasculitis of
childhood that presents with
≥5 days of fever,
nonexudative conjunctivitis,
lymphadenopathy, mucositis,
hand and foot swelling, and
a rash.
Diagnosis: CRASH & Burn
4/5 of the given criteria
+ Fever ≥5 days
Treatment:
IV Immunoglobulin along
with aspirin is the
recommended initial
treatment for Kawasaki
disease, with the primary
goal of coronary disease
prevention.
Remember:
IVIG creates high plasma
oncotic pressure, and signs
of fluid overload and
pulmonary edema develop if
it is given in large quantities.
Therefore, the child should
be monitored for
symptoms of CHF
Congestive Heart Failure (CHF)
Remember: Anatomy and physiology is
the key
Right sided: Resistance to right side d/t
failure causes backflow to both large veins
(vena cavas). Excess fluids pool in GI
tract, liver, extremities (U/L)
Left sided: Resistance to left side d/t
failure causes backflow to lungs through
pulmonary veins. Excess fluids cause
pulmonary edema.
Assessing a patient with CHF:
Causes of CHF:
Note: Etiology does not change the manner of treatment in CHF
▪
▪
▪
▪
▪
▪
▪
Cor Pulmonale (Chronic lung disorders)
Pulmonary hypertension
Pulmonary stenosis
Acute coronary syndrome
Cardiomyopathy
Aortic stenosis
Hypertension
Right CHF signs and symptoms:
▪
▪
▪
▪
▪
▪
▪
▪
▪
▪
Jugular vein distention (JDV)
Headache
Syncope
Dizziness
Swelling in legs and feet
(peripheral edema)
Weight gain
Abdominal discomfort
Nausea/vomiting
Hepatosplenomegaly
Ascites
Remember:
Instruct the patient to seek
immediate care if gaining 2 or
more pounds in 1 day or 5 or
more pounds in 1 week
Left CHF signs and symptoms:
▪ Shortness of breathing on
exertion
▪ Orthopnea
▪ Paroxysmal nocturnal
dyspnea
Pulmonary edema
▪ Crackles “wet lungs”
▪ Hypoxemia
▪ Pink frothy sputum
▪ Shortness of breathing even
at rest
Remember:
Sudden shortness of breath,
irregular heartbeat, or chest
pain are signs of CHF
exacerbation, therefore a
priority and needs immediate
care.
Acute Exacerbation: Consider patient is manifesting sudden
shortness of breath, irregular heartbeat, or chest pain
▪ Chest X-Ray
▪ BNP (B-Type Natriuretic
Peptide
▪ EKG
▪ Cardiac markers (CK-MB,
Troponin)
(+) CHF
▪ Chest X-Ray (+) Infiltrates
▪ Elevated BNP
(+) ACS: Ischemic CHF
▪ EKG: (+) STEMI
▪ Troponins (+)
Remember: Normal BNP
<125 pg/mL (0 - 74 YO)
<450 pg/mL (75 - 99 YO)
Brain (or b-type) natriuretic
peptide (BNP) is secreted in
response to ventricular stretch
and wall tension when cardiac
filling pressures are elevated.
The BNP level is used to
differentiate dyspnea of
heart failure from dyspnea of
noncardiac etiology.
Remember:
It is important to evaluate or
rule out acute coronary
syndrome. Majority of CHF is
caused by CAD-Acute coronary
syndrome. EKG and cardiac
markers most specifically
troponin are gold standards. If
determined, additional
treatment approach is
necessary such as MONABASH and heart
catheterization. PCI (stenting) if
needed.
Remember:
Echocardiography confirms
and distinguishes between 2
types of CHF namely diastolic
(filling failure) from systolic
(pump failure) by checking
ejection fraction.
Remember: Ejection Fraction
(EF) A normal EF is 50-70%. A
measurement under 40% may
be evidence of CHF or
cardiomyopathy and may
indicate severity and may need
a long term management such
Implantable Cardioverter
Defibrillator (ICD) to prevent
serious arrhythmias
Pharmacologic treatment: According to classification
Class 1: No restrictions to activity
Class 2: Mild SOB on exertion (slight limitation)
Class 3: SOB on ADL (marked limitation)
Class 4: SOB at rest
1
2
3
4
Remember:
Patient with Class 4 CHF may be on
hospice status that needs palliative care.
Inotropes are indicated as a palliative
treatment. Home infusion of milrinone
through a central line is becoming more
common as a palliative measure for endstage heart failure. It requires venous
access a PICC line as the medication is a
vesicant and can cause extravasation if
infused through a peripheral IV. Monitor
the central line insertion site for infection,
ensure infusion pump, monitor daily
weights.
Helpful Mnemonics: UNLOAD FAST
Low Na diet:
Remember: Diuretics
Potassium Sparing (SEAT):
▪ Spironolactone
▪ Eplerenone
▪ Amiloride
▪ Triamterene
Potassium Wasting (BF):
▪ Bumetanide
▪ Furosemide
DASH (Diet Approach to Stop HTN)
▪ All foods high in sodium (>400 mg/serving)
should be avoided.
▪ Do not add salt or seasonings containing
sodium when preparing meals
▪ Do not use table salt
▪ Avoid high-sodium foods (e.g., canned
soups, processed meats, cheese, frozen
meals)
▪ Limit milk products to 2 cups daily
Venous thromboembolism (VTE)
Deep vein thrombosis vs
Pulmonary embolism
DVT occurs when a blood clot
(thrombus) forms in one or more
of the deep veins in your body,
usually in your legs. Pulmonary
embolism (PE) is a DVT that
breaks loose and travels through
the bloodstream to the lung
vasculature. Death from PE is
often attributed to a missed
diagnosis. Early identification of
risk factors can have a positive
effect on client outcome.
Assessing a patient with VTE: (DVT and PE)
Causes of DVT: Virchow’s Triad
Immobile conditions such as brain
trauma, major surgeries, long
flights, or drive of >3-4hrs, etc.
Smoking, IV
catheterization,
hypertension, chronic
inflammation, sepsis
Genetic predisposition
(coagulation disorders)
Cancer, contraceptives,
pregnancy, nephrotic
syndrome, etc.
Signs and symptoms of DVT:
Remember:
A 2 cm increase in size, larger
than the other extremity is a
significant finding. It may be a
sign of DVT along with other
manifestations. A measuring
tape is a necessary
equipment in suspecting DVT.
Diagnostic evaluation of DVT:
Duplex ultrasonography
is the standard imaging test to
diagnose DVT.
D-dimer blood test: Measures
a substance in the blood that is
released when a clot breaks up.
Indicated for suspicion of DVT.
D-dimer is the degradation
biproduct of fibrin after exposed
to plasmin. Normal levels 220 to
500 ng/mL.
Note: If D-Dimer is elevated or DVT is detected, the following
diagnostic exam is indicated to check for presence of PE.
Computed tomographic
angiography (CTA): A special
type of X-ray test that includes
injection of contrast material
(dye) into a vein. This test can
provide images of the blood
vessels in the lungs. Standard
imaging test to diagnose PE.
Note: If CTA is not available and contraindications are observed
may do V/Q scan
Ventilation-perfusion (V/Q)
scan: A specialized test that uses
a radioactive substance to show
the parts of the lungs that are
getting 02 (ventilation scan) and
getting blood flow (perfusion
scan). Used when CTA is not
available or when
contraindicated.
Pulmonary angiography:
Special type of X-ray test that
requires insertion of a large
catheter to femoral vein & into the
pulmonary arteries, followed by
injection of contrast dye through
the catheter. Most accurate test
to diagnose PE but requires
time and safe precautions are
observed due to its
invasiveness.
Signs and symptoms of PE:
Signs and symptoms:
▪ Shortness of breath (SOB)/
Dyspnea
▪ Pleuritic chest pain on
inspiration or coughing
▪ Tachycardia
▪ Tachypnea
▪ Hypoxemia
▪ Apprehension, anxiety
▪ Syncope
▪ Cough
▪ Diaphoresis
▪ Cold clammy skin
▪ Fever (rare sign of severe PE)
▪ Hypotension (sign of
impending circulatory failure)
Mechanism:
Preventing VTE (DVT and PE):
VTE PROPHYLAXIS/
TREATMENT
Pharmacologic
Mechanical
Unfractionated
Heparin (IV Drip)
Graduated compression
stocking/ted hose
Low molecular weight heparin
(LMWH): SQ
Intermittent pneumatic
compression device
Oral anticoagulants (Vit K
antagonist, Direct Acting)
IVC filter
Thrombolytics
Thrombectomy/
Embolectomy
Remember: Heparin Dosing and
indication
Most central lines require IV heparin
flushes to maintain patency and prevent
clotting by using single-dose vials of 2–
3 mL of 10 units/mL or 100 units/ml. A
dose of 1000–10,000 units is given
for cases of thromboembolism.
Remember: LMWH (Enoxaparin)
Comes in a prefilled syringe. To
ensure complete medication
delivery, the air bubble should not be
expelled prior to injection.
▪ Right or left side of abdomen, 2
inches from umbilicus
▪ Insert the needle at a 90-degree
angle into a pinched-up area of
skin.
▪ Discourage the client from
rubbing the site.
Anti-embolism stockings:
Anti-embolism stockings improve
blood circulation in the leg veins by
applying graduated compression.
When fitted properly and worn
consistently, the stockings
decrease VTE risk. The stockings
should not be rolled down, folded
down, cut, or altered in any way. If
stockings are not fitted and worn
correctly, venous return can be
impeded.
Intermittent pneumatic
compression device or
sequential compression device
(SCD):
A mechanical prophylactic
treatment to reduce the incidence
of VTE by enhancing the blood flow
in the deep veins of the legs,
thereby reducing venous stasis.
SCD utilize sleeves with separated
areas or pockets of inflation, which
works to squeeze on the
appendage in a “milking action.”
The most distal areas will initially
inflate, and the subsequent pockets
will follow in the same manner.
An inferior vena cava filter:
A device that is inserted
percutaneously, via the femoral vein.
The filter traps blood clots
(embolus from DVT) from lower
extremity and prevents them from
causing PE. Prescribed when
clients have recurrent emboli or
anticoagulation is contraindicated.
Clients should report any metallic
implants (e.g., vascular filters/coils)
to the health care team prior to
radiologic imaging.
Surgical or catheter
embolectomy:
Performed in patients with massive
pulmonary embolism. Embolectomy
is used for patients with persisting
shock despite supportive care and
who have an absolute
contraindication for thrombolytics
Thrombectomy:
Involves removal of the clot in a
patient with DVT.
Spectrum of PE: Overview
D/C Home
Signs/Symptoms
Right Heart Strain
Hypotension/VS
LMWH – Oral anticoagulants (Vit K antagonist, Direct Acting)
Asymptomatic
None
None
Stable
LMWH – Oral anticoagulants (Vit K antagonist, Direct Acting)
Symptomatic
Yes
None
Stable
Medical Unit
Heparin (IV drip) - LMWH – Oral anticoagulants
Sub-massive
Yes
Massive
Stable
Thrombolytics or Thrombectomy if with chronic right heart strain
Yes
ICU
Yes
Yes
Unstable
EKG Interpretation
Steps
1. Identify PQRST
2. Determine PR Interval, QRS complex (time)
3. Check rhythm
4. Determine heart rate
1. Identify PQRST
2. Determine PR Interval, QRS complex (time)
Normal values:
PR Interval: 0.12-0.20 secs
Abnormal: ≥ 0.24 secs
QRS comp: 0.6-0.12 secs
Abnormal: > 0.12 secs
Example:
PR:
QRS:
3. Check rhythm.
What is a regular rhythm?
What is irregular rhythm?
Remember:
Checking rhythms is important in counting the heart rate. One cycle of PQRST
represents the other in a regular rhythm. In contrast, one cycle may not
represent the other in an irregular rhythm.
Regular rhythm:
Irregular rhythm:
Common regular rhythm
(R-R Intervals):
▪ Sinus Rhythm
▪ Sinus Tachycardia
▪ Sinus Bradycardia
▪ Supraventricular
Tachycardia(SVT)
▪ Atrial Flutter (variable)
▪ 3rd degree AV block (CHB)
Common irregular rhythm
(R-R Intervals):
▪ Premature Atrial Contractions
▪ (PACs)
▪ Premature Ventricular
Contractions (PVCs)
▪ Atrial Fibrillation
▪ 2nd degree AV block (Type 1)
4. Determine the heart rate.
1. Six (6) seconds strip method:
Applicable for both regular and irregular rhythm. Count the number of QRS complexes
over a 6 second interval. Multiply by 10 to determine heart rate.
10 R waves or QRS complexes in a 6 second strip in a regular rhythm
multiply by 10 is 100 bpm. 10 QRS X 10 = 100 bpm
5 R waves or QRS complexes in a 6 second strip in an irregular
rhythm multiply by 10 is 50 bpm. 5 QRS X 10 = 50 bpm
2. 1,500 method: Applicable ONLY for regular rhythm. Since R-R intervals are all the
same or constant in all cycles, one R-R represents the other. Determine the heart rate
by counting the number of smallest boxes between R-R. (Most accurate in calculating
HR)
Smallest boxes: 1500 mm/min ÷ 15 = 100 bpm
Note:
1mm = 1 smallest box
1 sec = 25 smallest boxes
60 sec (1 min) = 1,500 smallest boxes (1,500 mm)
Overview of Common Arrhythmias:
Common Arrhythmias:
1.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
2.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
3.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
Types:
4.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
5.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
6.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
7.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
Types:
8.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
Types:
9.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
10.
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
PQRST
P wave:
PR Interval:
QRS complex:
Rhythm:
Rate:
Interpretation:
How to distinguish types of AVB?
PR ≥ 0.24 secs
Consistent PR
Inconsistent PR
1° AVB
2° AVB (II)
2° AVB (I)
3° AVB
1P:1QRS
≥2P:1QRS
Irregular
Rhythm
Regular
Rhythm
Management of arrhythmias: continued
1. Sinus Bradycardia
2. Sinus Tachycardia
3. Atrial fibrillation, Atrial Flutter
4. SVT
5. PVC
6. Ventricular Tachycardia, Ventricular Fibrillation
7. AV Blocks