The Gravedigger’s Guide to Cardiology
Overview TOC
The Evaluation of Chest Pain ................................................................................................................. 2
TIMI SCORE (Thrombolysis in Myocardial Infarction) ....................................................................... 3
Non-ST Elevation Acute Coronary Syndrome ....................................................................................... 3
ST-Elevation Acute Coronary Syndrome ............................................................................................... 6
Reperfusion Therapy .............................................................................................................................. 8
STEMI/NSTEMI Discharge ................................................................................................................ 10
Mechanical Complications of AMI ...................................................................................................... 11
AMI Arrhythmias ................................................................................................................................. 12
Characeristics of MIs ............................................................................................................................ 14
Cardiogenic Shock................................................................................................................................ 15
Intraaortic balloon pump counterpulsation ........................................................................................... 15
Acute Heart Failure .............................................................................................................................. 16
Hypertrophic Cardiomyopathy ............................................................................................................. 17
Restrictive Cardiomyopathy ................................................................................................................. 18
Constrictive Pericarditis ....................................................................................................................... 18
Hyperensive Crisis................................................................................................................................ 18
Radiation-Induced Cardiac Injury ........................................................................................................ 20
Endocarditis .......................................................................................................................................... 20
Mitral Valve Prolapse ........................................................................................................................... 20
Mechanical Valves ............................................................................................................................... 21
Aortic Dissection .................................................................................................................................. 22
Congestive Heart Failure ...................................................................................................................... 22
Bradyarrhythmias ................................................................................................................................. 24
Tachyarrhythmias ................................................................................................................................. 27
Atrial Fibrillation .................................................................................................................................. 29
Atrial Flutter ......................................................................................................................................... 29
Permanent Pacemakers and AICDs ...................................................................................................... 30
Pregnancy Related Cardiology ............................................................................................................. 31
Contrast Nephropathy ........................................................................................................................... 31
Stopping Medications Before Interventions ......................................................................................... 31
Complications of Cardiac Catheterization............................................................................................ 32
Secondary Prevention of CAD at Strong.............................................................................................. 33
Pulmonary Hypertension ...................................................................................................................... 33
Cardiology Trials .................................................................................................................................. 34
ACS ECG Interpretation....................................................................................................................... 34
Cardiac Monitoring and Normal Values .............................................................................................. 35
Laboratory Values ................................................................................................................................ 35
Pharmacology of Inotropes and Vasoactive Medications .................................................................... 36
Cardiac Medications ............................................................................................................................. 39
Ward Lessons ....................................................................................................................................... 41
Patient Checklist ................................................................................................................................... 42
Physical Exam ...................................................................................................................................... 43
Admission Notes .................................................................................................................................. 43
Admission Orders ................................................................................................................................. 43
ACS algorithm ...................................................................................................................................... 53
Orders Set Examples ............................................................................................................................ 53
1
The Evaluation of Chest Pain
Rapid Evaluation
 HPI
o Chest discomfort type, location, quality, radiation, duration
o Associated symptoms such as nausea, vomiting, diaphoresis, dyspnea, dizziness
 PMH
o Known CAD
o Diabetes – assume cardiac disease until proven otherwise
o HTN
o HLD
o Cigarette smoking
o Stroke/TIA
o PVD
o Obesity
o Poor physical conditioning
 Physical Exam
o Pulmonary congestion
o Tachy or brady
o Irregular pulse
o S3 or S4
o Listen to carotids and femorals for bruits
o Check leg pulses
 Workup
o ECG – 1mm or more elevation in two contiguous leads or new LBBB (compare to an
old one)
Treatment
 Call cardiac fellow or page office for “Acute MI team”
 Start large 1-2 large bore IVs (18-20) guage and start saline IV at KVO
 Draw stat labs including CPK and isoenzymes
 Start O2 by nasal cannula
 NTG (SL or paste)
 Obtain cath consent
 Morphine or fentanyl in small doses to relieve pain and anxiety
 ASA 325mg
 Anterior MI
o Metoprolol 5 mg IV x3 doses approximately 5 minutes apart to total of 15 mg IV.
Watch for hypotension or bradycardia. May decide to avoid beta blocker in CHF, LV
failure
 Inferior MI
o Do not routinely use beta blocker
2
TIMI SCORE (Thrombolysis in Myocardial Infarction)
Non-ST Elevation Acute Coronary Syndrome
Definitions


Unstable Angina: new angina or departure from previous pattern of angina without ECG
changes or biomarker changes
NSTEMI: non-Q wave myocardial infarction (biomarker changes)
Pathophysiology
ACS result from an imbalance between oxygen supply and demand. Either ventricle may be involved
but the left ventricle is at higher risk for ischemia due to its greater muscle mass and greater afterload.


Factors which may decrease oxygen delivery
o Coronary atherosclerosis
o Coronary artery vasospasm
o Plaque rupture and thrombosis
o Anemia
o Hypoxemia
o Limited diastolic filling time (tachycardia)
o Hypotension
Factors with may increase oxygen demand
o Tachycardia and/or increased metabolic demands (i.e. infection, hyperthyroid)
o Heightened LV afterload causing increased transmural wall tension
 HTN
 LV cavity dilation
 Aortic dissection
 PE or pulmonary HTN in right heart
3
o Increased LV mass (hypertrophy)
o Increased contractility
Diagnosis


History and physical
o Substernal tightness, heaviness, squeezing
o Autonomic manifestations (nausea, vomiting, diaphoresis) are signs of instability
Data
o ECG
 ST elevation or depression
 T-wave flattening or inversion
 PVCs
 Conductive disturbance
 Normal ECG in up to 15% of those with UA
 70% of all ECG documented episodes of ischemia are clinically silent
o Cardiac Enzyme Markers
 Increased trop I/T
 Increased highly sensitive CRP (hsCRP)
Prognostic Factors


Short-term mortality
o UA: 2-3%
o NSTEMI: 5-7%
o STEMI: 6-9%
Long-term mortality
o NSTEMI: 10-12%
o STEMI: 9-11%
Treatment
Algorithm
Initial management for unstable angina/NSTEMI
 ASA (high dose)
 Heparin or enoxaparin
o LMWH is better than UFH
 BB
o Decreases demand and progression to AMI
o No decrease in mortality in NSTEMI
 Nitrates
 Possibly Glycoprotein Iib/IIIa inhibitor (abciximab)
o Decreased mortality, increased bleeding
o Most suited for high-risk patients
o Give if
 TIMI 3-4 or above
 Recurrent angina
 Elevated Troponin
4


 New ST depression
 Signs or symptoms of congestive heart failure
 Prior bypass grafting
 PCI within 6 months
 Sustained ventricular tachycardia
 Hemodynamic instability
o Has been shown to be beneficial only in those who will undergo PCI and may have
increased mortality in those who do not
o If no clear indication for PCI a small molecule such as eptifibitide or tirofiban is often
selected
Clopidogrel
o Usually indicated
o Hold if angiography is planned within 24 to 36 hours of presentation
o Hold if possible CABG
PCI?
o Low TIMI risk score (0-2)
 No further meds
 Stress testing for ischemia and risk stratifications
o High TIMI (5-7)
 Give glycoprotein IIb/IIIa inhibitor
 Stabilize for coronary angiography
o Intermediate TIMI (3-4) and no high risk markers
 Can undergo stress testing and risk stratification before angiography
 Cath if
 Recurrent angina/ischemia at rest or with low-level activities despite
medication therapy
 Elevated Troponin
 Recurrent angina/ischemia with symptoms of heart failure
 LVEF < 40%
 Sustained ventricular tachycardia
 PCI within 6 months
 Prior CABG
 Ischemia during provocative test
Reasoning



Reduce demand (decrease HR and afterload)
o Limit physical activity (bedrest)
o Control arrhythmias
o Control HTN
Increase oxygen supply
o Increase hemoglobin saturation or concentration
o Nitroglycerin
 Titrate to relieve chest pain and decrease BP 10-20%
o Calcium-channel blockers
 Revere coronary vasospasm
 Be careful of preload dependence
Antiplatelet Therapy
o ASA 325 mg qdaily
 RISC trial found to reduce the risk of death and acute MI by ~50% in patients
with NSTE-ACS
5





 Decreases risk of recurrent events by 25%
 ASA resistance in 5-10% of patients
Thienopyridines (Ticlopidine and Clopidogrel)
o Evidence
Glycoprotein 2b/3a Receptor Inhibitors
o Evidence
o Large-molecule agents
 Preferred for PCI with STEMI
 Continue 12 hours post PCI
 If CABG is required
 D/c medication
 Give 6-12 units platelet transfusion
o Small-molecule agents
 Used with ASA and heparin
 Initial stabilization of NSTE-ACS
 Dosing: initial bolus with infusion for 24-72 hours
 Most beneficial for those at high risk
 Continue for 12-24 hours post coronary intervention
 If CABG, d/c at least 4-6 hours prior
Antithombotic Therapy
o Unfractionated Heparin
 Heparin Sliding Scale
 Bolus 60 U/kg
 Cont infusion at 12 U/kg/hr
 Continue until revascularization or for 3-5 days if none planned
o Low-Molecular Weight Heparin
Direct Thombin Inhibitors
o Only recommended for those with HIT
Fibrinolytic Therapy
o May be deleterious in NSTE-ACS
ST-Elevation Acute Coronary Syndrome
“often troponins are the tip of the iceberg…”
Management Strategies for patients with STEMI
1. Quickly screen patients for indication and risk
2. Start thrombolytic therapy or send patient to cardiac catheterization lab for emergency
angioplasty and stenting
3. Open the infarct-related artery and its distal microvasculature with minimal incidence of
stroke by the fastest and most effective way
4. Prevent left ventricular remodeling (no left ventricular dilation)
5. Prevent another MI in the future (secondary prevention)
Factors suggestive of high risk patients
1. Hypotension (SBP < 100)
2. Congestive Heart Failure
3. Sinus Tachycardia (HR > 100)
4. Advanced Age
5. Female Sex
6. Diabetes Mellitus
7. Persistent ST Segment Elevation
6
8. Persistent Chest Pain
9. High BNP Level
10. Anemia
11. High WBC
12. Chronic Kidney Disease
The risk of dying within the next 24 hours is low if the SBP is greater than 100 and the HR is less
than 100 (but greater than 50 because this may be a sign of an AV block).
Thrombolytic Therapy
Indications
 Patient presents for chest discomfort < 12 hours after symptom onset
 Chest discomfort and ST-segment elevation of at least 1 mm in at least two limb leads and
2mm in 2+ contiguous precordial leads
 New LBBB
Contraindications
 Absolute
o Any prior intracranial bleeding
o Known structureal cerebral vascular lesion (AV malformation)
o Known malignant intracranial neoplasm
o Ischemic stroke within 3 months except ischemic stroke within 3 hours
o Active bleeding or bleeding diathesis (excluding menses)
o Significant closed head or facial trauma within 3 months
 Relative Contraindications
o History of chronic, severe, or poorly controlled hypertension
o Severe uncontrolled HTN on presentation (SBP > 180 mmHg, DBP > 110 mmHg)
o History of prior ischemic stroke > 3months
o Traumatic CPR (> 10 minutes) or major surgery (< 3 weeks)
o Non-compressive vascular puncture
o For streptokinase/anistrepplase: prior exposure (more than 5 days ago) or prior allergic
reaction to these agents
o Active peptic ulcer
o Current use of anticoagulants: the higher the INR, the high the risk of bleeding
Primary Coronary Intervention
Exclusion Criteria
1. Unprotected LM lesion > 60%
2. Infarct-related artery with TIMI 3 flow and lesion morphology extremely high risk for abrupt
closure (extremely long or severe angulated lesion)
3. Multivessel disease with TIMI-3 flow in infarct-related artery, now stable and pain free
4. Infarct-related artery supplies a small or secondary vessels supplying a small amount of
myocardium, risk may outweigh benefit
5. Inability to clearly identify infarct-related artery

Fibrinolytic Therapy
o Fibrinolysis should resolve chest pain and ECG changes
o Indications
 Pt presents < 12 hours after symptom onset
 If transfer to cath lab (at another hospital > 2 hr) unless
 Contraindication
7



 STEMI > 12 hours after onset with residual ST-segment elevation
 STEMI with hsf CABG
 Cardiogenic shock
o Give within 30 minutes of arrival in the ED
o 60-75% reperfusion rate
Catheterization
o 90-95% reperfusion rate
Reperfusion Arrhythmias
o Usually a transient accelerated idioventricular arrhythmia
o Usually do not require therapy
Medical Management
o ASA
o Beta-blocker
o Statin
o ACEI
o Thienopyridines (Ticlopidine and Clopidogrel)
 Clopidogrel is a reasonable alternative to aspirin for patients with
contraindications to aspirin, but there is no benefit of adding clopidogrel to
aspirin therapy in the management of acute myocardial infarction.
o Glycoprotein IIb/IIIa blocker
 An intravenous glycoprotein IIb/IIIa blocker in addition to aspirin and heparin
is indicated for patients with continuing ischemia, an elevated troponin level,
or with other high-risk features, including angina at rest with ST-segment
changes, congestive heart failure, diabetes, or patients in whom catheterization
and percutaneous intervention are planned
 Glycoprotein receptor blockade with such agents as eptifibatide is indicated for
patients with acute coronary syndrome who will undergo coronary
angiography and intervention. Early treatment likely improves outcomes of
percutaneous coronary intervention.
Reperfusion Therapy
Goals:
 Early patency of the infarct-related artery with improved ventricular remodeling, electrical
stability and myocardial salvage
 Shortest time to treatment
o Lytics: <30 minutes
o PCI: <90 minutes door to balloon
Thrombolytics
Administration
Dose
Streptokinase
Bolus and
infusion
1.5 million units
over 30-60
minutes
TPA
Bolus and
infusion
15 mg bolus, then
0.75 mg/kg for 30
min, then 0.5
mg/kg over 60
minutes (max
dose <= 100 mg)
Reteplase
Double bolus
Tenectaplase
Single bolus
Two 10 mg
boluses given 30min apart
Single bolus of
0.5 mg/kg (range
30-50 mg)
8
Half-life (min)
IV heparin
required
23-29
No
4-8
Yes
15
Yes
20
Yes
Mechanism of Action
 Conversion of plasminogen to plasmin which promotes degradation of fibrin clot
 Streptokinase has a more systemic lytic effect and is highly antigenic and can only be
administered once
Adjunctive Agents
 Heparin: Bolus of 60U/kg (maximum 4000Units) followed by a 12U/kg/hr infusion (goal
aPTT 50-70 seconds)
 Aspirin: improves efficacy of all lytics
Indications
 Typical chest pain for >30 minutes but <12 hours, relieved by sublingual NTG
AND
 ST segment elevation in >= 2 contiguous leads
o >=1 mm in limb leads
o >= 2 mm in precordial leads
OR
 ST depression in only V1 and V2 or >= 2 mm
OR
 New LBBB
Contraindications
Major
 Any previous history of hemorrhagic stroke
 Stroke, dementia or CNS damage with 1 year
 Head trauma or brain surgery within 6 months
 Known intracranial neoplasm
 Suspected aortic dissection
 Internal bleeding within 6 weeks
 Active bleeding or know bleeding disorder
 Major surgery, trauma, or bleeding within 6 weeks
 Traumatic CPR within 3 weeks (brief CPR is not a contraindication)
Relative
 Oral anticoagulant therapy
 Acute pancreatitis
 Pregnancy, or within 1 week postpartum
 Active peptic ulceration
 Transient ischemic attack within 6 months
 Dementia
 Infective endocarditis
 Active cavitating tuberculosis
 Advanced liver disease
 Intracardiac thrombi
 Uncontrolled hypertension (SBP > 180 or DBP > 110)
 Puncture of noncompressible blood vessel within 2 weeks
9
Factors which are not contraindications
 Menstruation
 Non-traumatic CPR lasting < 10 minutes
 Diabets
Post-Lytic Management
1. Has myocardial reperfusion occurred?
a. Complete or partial restoration of flow only occurs in 50-60% and rescue angiography
may need to be performed
b. Evaluation
i. Symptoms: Has the patient’s chest discomfort resolved or abated substantially?
ii. ECG: Has the degree of ST elevation improved by >50%
iii. Reperfusion arrhythmias: has accelerated idioventricular rhythm or sinus
bradycardia occurred in concert with symptoms and ECG improvements?
iv. Hemodynamics: Is the patient hemodynamically stable?
2. Is there vessel reocclusion?
a. Up to 20% of patient may reocclude the vessel with the first few hours
b. Evaluation
i. Symptoms: resurge of symptoms
ii. ECG: worsening of ECG
3. Hemorrhagic complications
a. Risk of major bleed with fibrin-selective agents (non-streptokinase) is 1.5-2%
b. Intracranial hemorrhage has a 50% mortality
i. New-onset HA, seizure, visual disturbance, new focal neuro deficit
ii. Order stat head CT and rapid neurosurgical consult
iii. Reversal of anticoagulant agents
c. GI bleed
i. Less common
ii. Aggressive supportive treatment
Catheterization
Patients may have pain post plasty. This can be due to embolic spasm and may be relieved by imdur
Bleeding from site
 Sandbag
 Call Interventional Fellow
 May need norepinephrine injection at site
STEMI/NSTEMI Discharge

Medications
o BB
o ASA
o Plavix
 9 months if no stent
 1 month post BMS
 1-2 years post DES
o DM control
o Statin
o ACEI if CHF
10

Non-medications
o Exercise
o Smoking cessation
o Nutrition/DM planning
Mechanical Complications of AMI
Essentially all mechanical complications are due to anatomic rupture of infracted tissue. There are 3
subtypes:
1. LV free-wall rupture (RV rupture is very rare)
2. Interventicular septal wall rupture
3. Papillary muscle rupture or dysfunction
LV free-wall rupture
 Type I (slit-like rupture)
o Early (within 24 hours)
o Anterior MI, single vessel disease
 Type II (erosion of myocardium)
o Early (within 24 hours)
o Posterior infarct, multi-vessel disease
 Type III
o Later (after 24 hours)
o Large anterior MIs
o Severely expanded and thinned myocardium
o May by sealed off by pericardium to form a pseudoaneurysm
Diagnosis
Acute form
Beck’s triad
 Elevated systemic venous pressure
 Systemic arterial hypotension
 Small quiet heart
Frequently decompensated into EMD or asystole leading to cardiac death
Subacute form (tamponade)
Transient hypotension
Syncope
Transient EMD
Bradycardia
Nausea and agitation
ECG with persistent and diffuse ST elevation
Echo with effusion, RV/RA compression, “shaggy” intrapericardial echo densitites
Management
 Decompensating patient
o Early pericardiocentesis to relieve tamponade
 Stable
o Open surgical drainage
Interventricular Septal Rupture
 First week post-MI in 1-3% of all Mis
 Results in shunt from left to right heart
11



Clinical Presenation
o RV overload
o Cardiogenic shock
o New load pansystolic murmur with thrill
Diagnosis
o Echo
o Right-heart cath (increased RV oxygen sat)
Management
o Stabilize
 Diuretics, vasodilators, inotropes
 IABP
 PPV
o Surgical repair
Acute Papillary Muscle Rupture or Dysfunction
 Clinical Presentation
o Usually 2-7 days after MI
o Sudden Onset CHF and/or hypotension
o Short systolic murmur in the apical area
 Management
o Temporizing measures
 Diuretics, vasodilators, intermittent PPV
 IABP
o Surgery
AMI Arrhythmias
Ventricular Premature Beats
A conservative approach is taken to management as their was an increase in mortality with treatment
in the CAST and SWORD trials.
Correct underlying electrolyte and metabolic disturbances.
Treatment only if hemodynamic compromise or serious arrhythmia
Ventricular Tachycardia
Accelerated Idioventricular Tachycardia
Ventricular Rhythm with a rate between 60-125
Usually resolves spontaneously
Treat if hemodynamic compromise, increased myocardial oxygen requirement, predisposition to
more lethal arrhythmias
Treat: overdrive the rhythm with a pacemaker or atropine
Non-Sustained and Sustained Ventricular Tacycardia
NSVT
Definition
 3+ ectopic ventricular beats
 Rate > 120 BPM
 Lasts less than 30 seconds
12
Classify as monomorphic or polymorphic
Monomorphic
Thought to be related to myocardial scarring
Tx: Require long term anti-arrhythmic and/or AICD
Polymorphic
May be related to ongoing ischemia
Tx: Resolve ischemia (cardiac cath, anticoagulation, decrease myocardial O2 demand)
Sustained Venticular Tachycardia
Sustained polymorphic V-tach within 48 hours postMI are associated with a hospital mortality of
20%
Treat if HD compromise or HR > 150:
Cardioversion
Correct electrolytes
Anti-arrhythmics (lidocaine, procainamide, amiodarone)
Ventricular Fibrillation
Primary VF
Occurs suddenly and unexpectedly in patients with no or few signs of LV dysfunction
Occurs early after MI (within first 12 hours?)
Secondary VF
Occurs in patients with severe cardiogenic shock and LV dysfunction
Bradycardia
Most often seen early after infarct
Likely due to increased vagal tone
Most often seen in posterior and inferior MI
Management often amounts to observation
First 6 hour: if HR < 40 and has ventricular premature beats, give atropine in small doses
After 6 hours: likely sinus node dysfunction or atrial ischemia rather than excessive vagal tone
If hypotension does occur and the bradycardia is unresponsive to atropine, then a pacemaker is
indicated
Atrioventricular Block/Intraventricular Block
First Degree Block
Almost always 2/2 disturbance above bundle of His. Complete heart block can only occur in those
with first degree block below the node.
Consider stopping beta-blockers if PR interval becomes greater than .24 seconds
Second Degree Block – Type I
10% of patients with AMI
Usually in inferior MI
Usually transient, resolving 3 days post infarction)
No treatment required unless other blocks also present or excessively slow rate
13
Second Degree Block – Type II
Usually develops below the bundle of His with a widened QRS
Block can progress suddenly to complete AVB and asystole
Treatment: pacemaker placement
Complete Block
Inferior block – often slowly progressing through the various degrees of block, usually stable escapre
rhythm, may be responsive to methylxanthine. May resolve spontaneously but mortality is high
Anterior – sudden, ominous and dramatic. Patients have unstable, wide QRS complex escape rhythm,
asystole can occur,
Treatment: supportive care, pacemaker insertion
RBBB
2% of MI
Can lead to complete AVB
LBBB
5% of MI
High mortality because of amount of myocardial damage needed to produce a LBBB is large
Paroxysmal Supraventricular Tachycardia (PSVT)
Vagal maneuvers
Adenosine (if not hypotension)
AV slowing medications (CCB and BB)
Atrial Fibrillation/Atrial Flutter
Atrial Flutter – rare, usually transient
Atrial Fibrillation – 10-15% in MI, may be marker of poor prognosis, treat with cardioversion, AV
blocking meds, procainamide and amiodarone
Characeristics of MIs
Anterior MI
2nd degree block type II
Complete heart block
Interventricular septal rupture
Type I and type III LV free-wall rupture
Wait 72 hours before discharge due to higher complication rate 2/2 rhythms
Anteroseptal MI
RBBB
Interventricular septal rupture
Wait 72 hours before discharge due to higher complication rate 2/2 rhythms
Posterior MI
Type II LV free-wall rupture
Inferior MI
2nd degree block type I
Complete heart block
14
Cardiogenic Shock
Diagnostic Criteria
BP < 90 mm Hg, or a decrease in the MAP by > 30 mm Hg, for at least 30 minutes, not improved
with fluid administration
Signs of hypoperfusion (cold extremities), altered mental status (restlessness or agitation)
Reduced urine output (<20 cc/hr)
Cardiac index of < 2.2 L/min/m2
Management Strategy Overview
Identify the patient with cardiogenic shock, even if the blood pressure is not yet low
Revascularize the patient with a percutaneous or surgical approach
Close follow-up and correct all non-cardiac problems such as respiratory, liver, kidney failure
Management in the ED
The presence of sinus tachycardia and borderline low BP (<100 mm Hg but >90 mm Hg) should
trigger the process of investigating carefully the causes of declining BP.
1. Does the patient still have ongoing ischemia as evidenced by chest pain or angina-equivalent?
2. Are there any rales in the lung ausculatation, suggestive of LV failure with pulmonary
congestion?
3. Does the patient have signs or peripheral hypoperfusion (cold extremities, agitation,
restlessness, or low-urine output < 20mL/h)
4. Are there any signs of mechanical complications from AMI – new murmur of mitral
regurgitation, muffled heart sounds of a pericardial effusion, VSD from ventricular septal
rupture
Work-up during pre-shock period
1. Frequent monitoring of HR and BP
2. Generous IV fluid challenge
3. Reassessment with ECG
4. STAT echocardiography
5. Comprehensive physical exam
6. Right heart catheterization
Electrocardiogram
Suspicion of early cardiogenic shock by ECG
1. Anterior wall MI or multisite MI with decreasing SBP (most common)
2. >20 mmHg decrease of BP in patient with history of prior MI
3. >20 mmHg decrease of BP in patient with inferior wall MI
4. Decreasing BP with clear lung due to right ventricular infarction
Intraaortic balloon pump counterpulsation
Indications for use:
 Cardiogenic shock
 Intractable angina
 Weaning patients from cardiopulmonary bypass
 Adjunctive therapy in high risk or complicated angioplasty
 Prophylaxis in patients with severe left main coronary artery stenosis or critical aortic stenosis
in whom surgery is pending
15
Hemodynamic Effects
A balloon pump works by sitting in the aorta and inflating during diastole and deflating during
systole. Inflation during diastole generates a pressure wave causing blood to flow back into the
coronary arteries. Deflation during systole generates a vacuum which reduces afterload.
Decrease systolic pressure
Increases diastolic pressure
Reduces heart rate
Decreases MCWP
Elevates cardiac output
Contraindications
Aortic regurgitation or significant AV shunting
Abdominal aortic aneurysm or aortic dissection
Uncontrolled sepsis
Uncontrolled bleeding disorder
Severe bilateral peripheral vascular disease
Bilateral femoral popliteal bypass grafts for severe PAD (can be carried out in patients with aortobifemoral bypass grafts)
Complications
Vascular
Limb ischemia
Vascular laceration necessitating surgical repair
Major hemorrhage
Arterial dissection with balloon placement into a false lumen
NonVascular
Cholesterol embolization (thrombocytopenia, livedo reticularis, eosinophilia)
CVA if balloon migrates proximal to the left subclavian artery
Sepsis (rare if used for less than 7 days)
Balloon rupture
Thrombocytopenia
Hemolysis
Groin infection
Seroma
Peripheral neuropathy
Acute Heart Failure
Clinical Presentation


Physical exam: rales, JVP, S3, peripheral edema, weight gain
CXR: pulmonary congestion
Heart failure may be a much more difficult diagnosis in a person with chronic heart failure without
evidence of pulmonary congestion on CXR or physical exam. The history is important and will
always include: fatigue, DOE, PND
What is the cause of the heart failure?
 Sodium intake/dietary changes
 Acute ischemia
16




Medication noncompliance
NSAIDs
Atrial fibrillation
Initiation of beta-blocker therapy
Management
Dependent upon hemodynamic status
 Normal blood pressure and predominant fluid overload
o Aggressive diuretic therapy
 Marginal blood pressure
o Diuresis
o Inotropes
o Vasoactive medications
Diuretics
Lasix bolus
Lasix gtt
 Indications
o Better titration to effect
 Dosing
o Bolus half of the usual outpatient dose
o Infuse 5-20 mg/hr
If there is no response a thiazide diuretic such as diuril, HCTZ or metolazone may augment response
Aggressively replete electrolytes. Add acetazolamide (diamox) for extreme contraction alkalosis.
Inotropes
Empiric therapy with dobutamine/dopamine or milrinone
Vasodilators
Nitroprusside and nitroglycerin
ACEI can be continued but may want to switch to short-acting (captopril) and decrease dose if also
using dobutamine and hypotensive response may be greater
B-Blockers
Decrease beta-blockers or if inotropic support is needed (dobutamine) stop them completely.
Hypertrophic Cardiomyopathy
Treatments
 AICD: improves survival
 Septal myomectomy: improves symptoms of outflow obstruction
 Avoidance of stenuous exercise
17
Restrictive Cardiomyopathy
Cardiac Amyloidosis
Epidemiology
Clinical Presentation
Diagnosis
 ECG
o Low voltage
 Echo
o Increased wall thickness
o Right sided heart failure with diastolic dysfunction with restrictive pattern
 Fat pad biopsy
 With the combination of a low voltage ECG and interventricular septal thickness is greater
than 1.98 cm, the diagnosis of cardiac amyloidosis can be made with a sensitivity of 72% and
a specificity of 91%
Treatment
Constrictive Pericarditis
Epidemiology
 Mediastinal radiation therapy may result in cardiac disease 10-20 years later
 TB exposure
Clinical Presentation
Physical Exam
 Elevated jugular venous pressure
 Prominent x and y descents
 Kussmaul’s sign
o Paradoxical increase in JVP with inspiration
o Rarely seen
Diagnosis
 CT Scan – direct visualization of pericardium
 Right and left heart catheterization
o Would show equalization of diastolic pressures in all four chambers
Treatment
 Pericardectomy
o Definitive treatment
o Surgical mortality is 6-19%
 Medical Mangement
o Appropriate for those with minor symptoms
o Edema
 Compression stockings
 Lasix can be cautiously started
 Patients are preload dependent
Hyperensive Crisis
Natural course of untreated hypertensive crises are renal failure, stroke, MI and death.
18
Hypertensive Emergency
 Diastolic pressure >130 mm Hg
 Evidence of end-organ damage
o Group 3 or 4 retinopathy (hemorrhage or papilledema)
o Cerebral edema or intracranial hemorrhage
o Left ventricular dysfunction
o Aortic dissection
o Acute renal disease
Hypertensive Urgency
 Diastolic pressure >120 mg Hg
 Lack of end-organ damage
 Fundoscopic changes can be seen
o Changes
 Arteriolar narrowing
 Vasospasm
 AV crossing abnormalities
o Definitions
 Acute damage to retinal vessels – accelerated malignant hypertension
 Retinal exudates – malignant hypertension
Hypertensive Encephalopathy
 Clinical Presentation: HA, irritability, alteration in consciousness, central nervous dysfunction
Therapy
 HTN Emergency
o Goal: reduce MAP by 20% but not more than 25% in the first hour or the diastolic
pressure to 100-110 over several hours
o Medications
 Nitroprusside (DOC) 0.25-10 mcg/kg/min gtt
 Pathophysiology: direct arteriolar and venous dilator. The arteriolar
dilation prevents the expected rise in vascular resistance when cardiac
output falls as a result of venodilation
 Labetalol 2 mg/min gtt or 20-80 mg IV bolus q10min
 Combined alpha and beta blocker. Use with caution in patients with
heart failure
 Nicardipine 2-10 mg/h IV
 CCB that provides gradual reduction in systemic pressure with little
overshoot
 Enalapril 1.25-5mg q6h
 IV ACEI, can be used in patients with acute left ventricular failure
 Esmolol 200-500 mcg/kg per min for 4 minutes, then 50-300 mcg/kg/min IV
 Fast on-fast off, used with aortic dissection and in postoperative period
 Loop diuretics
 Almost always needed to overcome the tendency for renal sodium
retention after MAP is lowered
 HTN Urgency
o Nifedipine 10mg by mouth, repeat in 30 minutes if needed
19
Radiation-Induced Cardiac Injury
Complication
Constrictive Pericarditis
Myocardial Fibrosis
Valve Dysfunction
Premature Coronary Artery Disease
Diagnostic Testing
CT scan
Diastolic Damage, biopsy?
TTE/TEE
Coronary angiography or nuclear perfusion
The relative risk of cardiovascular death is 3.1 at 10 years in patients with radiation therapy for
Hodgkin’s disease, most due to premature coronary artery disease.
Endocarditis
Epidemiology
Presentation
Physical Exam
Diagnosis
Treatment
 Medical management
 Surgical management
o Paravalvular extension
 40% of native valve endocarditis
 Usually extends near the interventricular septum and AV node and therefore
can cause conduction abnormalities
o CHF (moderate or greater carries 56% mortality with medical therapy alone)
o Severe valvular regurgitation with destruction
o Life-threatening instability
o Resistant bacterial infection or fungal infection
o Vegetations larger than 1 cm
o Recurrent distal embolization
Mitral Valve Prolapse
Epidemiology
 2% of population
 Most common cause of mitral regurgitation
 Increased prevalence in marfan’s disease
Presentation
 Palpitations or atypical chest pain/tightness/discomfort
 Symptoms of mitral regurgitation if severe
Physical Exam
 Midsystolic click (sudden tensing of mitral subvalvular apparatus as the leaflets prolapse into
the atria
 Valsalva and standing from squatting move the click closer to S1
20
Diagnosis
 TTE
Treatment
 For palpitations – stop caffeine and other stimulant use
Bicuspid Aortic Valve
Epidemiology
Presentation
Physical Exam
Diagnosis
 TTE
Complications
 Sudden cardiac death
 Congestive Heart Failure
 Severe Aortic Stenosis
Treatment
 Medical Management
o Serial echocardiograms
o Nifedipine – proven to delay need for valve replacement
o ACEI – may be beneficial but unproven
o Digoxin and diuretics for symptom relief
o Beta-blockade is contraindicated in severe aortic regurgitation
 Surgical Management
o Consider surgery in asymptomatic patients when LV end systolic diameter reaches 55
mm or EF < 60%
Mechanical Valves
May present with either:
 Thrombotic events
o Similar to heart failure behind valve or valve regurgitation
 Embolic events
o Similar to endocarditis
Thrombotic events
 Prophylaxis warfarin dosing goal is based on risk factors
o 2.5 to 3.5 for high risk
 Once thrombosis has occurred
o Hemodynamically unstable
 Surgery
 Thrombolytic therapy
o Hemodynamically stable
 Long-term medical management with appropriate anticoagulation
21
Warfarin Therapy


Goal INR of 2 to 3
Complications
o Anemia
 Check haptoglobin and lactate dehydrogenase as valves can shear RBCs
 Anemia in a patient who is therapeutic on warfarin usually signifies a
gastrointestinal lesion
Aortic Dissection
Epidemiology
 72% of older patients have history of hypertension
 Bicuspid aortic valve more common in younger patients
 In marfan’s patients, 50% have family history of dissection
Clinical Presentation
 Classic presentation: chest pain radiating to back
 6% are painless
Diagnosis
 TEE
 CT with contrast
 MRI
Classification Schemes
Treatment
 Ascending: surgical
 Descending: medical
Goals:
Lower HR to under 60
Goal MAP of 60-75
BB are first line
Esmolol: 200-500 mcg/kg/min x 4 min, then 50-300 mcg/kg/min
Labetolol: 20-80 mg iv q10min. total 300 or 0.5-2.0mg/min IV gtt
Then add on other agents
Nitroprusside: start at 0.25-0.50 mcg/kg/min. Maximum dose is 8-10 mcg/kg/min but no more than
10 minutes at this dosage level. Watch for thiocyanate toxicity
Nicardipine 2-10 and up to 15 mg/hour
Congestive Heart Failure
Treatment

Medical
o ACEI – proven survival benefit
22
o B-blocker
 Proven survival benefit for all classes of HF
 Do not initiate when patient is acutely decompensated or fluid overloaded
because there is a transient decrease in cardiac output.
 Carvedilol vs. others
o CCB – management of HTN or angina not adequately controlled on ACEI or BB


EP
o BiVenticular Pacing
 Indication: NYHA class III, LV enlargement, prolonged QRS complex, LVEF
< 35%
Surgical
o Mitral Valve Repair
 Improves short and intermediate hemodynamic outcomes in patients with
severe mitral regurgitation
 Not mortality benefit
Prognosis
 EF of 20% carries a one year mortality of 20%? (or one year survival). Same as metastatic
carcinoma
23
Bradyarrhythmias
Results from either a
1. Failure to initiate an impulse or a
2. Failure to conduct an impulse
And so the two most common causes of bradyarrhythmias are:
1. SA node dysfunction
2. AV conduction block
SA Node
 The SA node is cluster of fusiform cells located in the sulcus terminalis on the epicardial
surface of the heart at the right atrial-superior vena caval junction
 Is a relatively heterogeneous group of cells
 Typically contains fewer myofibrils, no intercalated disks, a poorly developed sarcoplasmic
reticulum and no T-tubules
 Fed by SA nodal artery which arises from the right coronary in 55-60% of people and the left
circumflex in 40-45% of people
SA Node Dysfunction
Broadly classified as extrinsic or intrinsic causes. In acute MI (typically inferior) the sinus
abnormalities are usually transient.
Causes of SA Node Dysfunction
Intrinsic
Extrinsic
Sick Sinus Syndrome
Carotid sinus hypersensitivity
CAD
Vasovagal stimulation
Inflammatory
Medications
 Pericarditis
 Beta-blockers
 Myocarditis
 CCB
 Rheumatic
 Antiarrhythmics
 Collagen vascular disease
 Adenosine
 Lyme disease
 Clonidine
Senile Amyloidosis
 Lithium
Congenital heart disease
 Cimetidine
Radiation therapy
 Amitriptyline
Post-surgical
 Phenothiazines
Chest trauma
 Narcotics (methadone)
Non-cardiac congenital diseases
 Pentamidine
Hypothyroidism
Sleep Apnea
Hypoxia
Endotracheal suctioning
Hypothermia
Increased ICP
Clinical Features
 1/3 to ½ will also develop a tachyarrhythmia
24

o tachycardia-bradycardia variant of SSS
o Require anticoagulation
Not associated with increased mortality except when it occurs with comorbidities
Electrocardiography
 Usually defined as HR < 40 but depends on individual characteristics
 A sinus pause of greater than 3 seconds is indicative of sinus node dysfunction
 First degree block
o Prolonged PR
 Second degree block
o Type I
 Progressive prolongation of PR until pause
o Type II
 No change in PR interval in beats before pause
 Third degree block
o Complete disassociation
 Tachycardia-bradycardia syndrome
o Brady alternating with tachy (most often atrial fibrillation)
 Chronotropic Incompetence
o Inability of heart rate to increase in response to demand from exercise or stress
Diagnostic Testing
 ECG
 Telemetry, holter, or event monitor
 Test for autonomic sensitivity
 Exercise testing (for ischemia or chronotropic incompetence)
 EP testing
Treatment
 Exclude extrinsic causes
 No good chronic medical therapy available
 Pacemaker
AV Conduction Disease
Pathophysiology
 AV node is subendocardial
 Located in posterior-inferior right atrium
 Located at the apex of the triangle of Koch
o Coronary sinus ostium posteriorly, septal tricuspid valve annulus anteriorly, and the
tendon of Todaro superiorly
 Vascular supply
o AV nodal artery
o 1st septal perforator of the left descending coronary artery
25
Causes of Atrioventricular Block
Autonomic
Metabolic/Endocrine
Infectious
Congenital
Inflammatory
Infiltrative
Neoplastic/Traumatic
Degenerative
CAD
Drug Related
Carotid sinus hypersensitivity
Vasovagal
Hyperkalemia
Hypermagnesemia
Hypothyroidism
Adrenal insufficiency
Endocarditis
Lyme
TB
Chagas
Syphilis
Diptheria
Toxoplasmosis
Congenital
Maternal SLE
Others
SLE
RA
MCTD
Scleroderma
Amyloidosis
Sarcoidosis
Hemochromatosis
Lymphoma
Mesothelioma
Melanoma
Radiation
Catheter ablation
Lev disease
Lenegre disease
Acute MI
BB
CCB
Lithium
Digitalis
Adenosine
Antiarrythmics
AV conduction dysfunction in acute MI
 Transiently develops in 10-25% of patients
 Most commonly first or second degree block
 Inferior MI
o Level of block is AV node
o More stable narrow escape rhythms
 Anterior MI
o Level of block is in distal AV nodal complex
o Wide, complex, unstable escape rhythms
o Worse prognosis, higher mortality
 Treatment
o Inferior MI often produces transient AV conduction problems
o Indications for pacing
 Persistent 2nd or 3rd degree block particularly if symptomatic
 Transient 2nd or 3rd degree block associated with BBB
26
First degree AV Block
Second degree AV Block
 Mobitz type 1 (Wenckebach)
o Progressive lengthening of PR interval until a QRS is dropped
o Decremental conduction of electrical impulses in the AV node
 Mobitz type 2
o Typically occurs in distal or infra-His conduction system
o Worse prognostically as may progress to higher grade
 Paroxysmal AV block
o Series of nonconducted p waves
o Indication for permanent pacemaker placement
 High-grade block
o Intermediate between 2nd and 3rd degree block
Treatment
 Exclude reversible causes
 Temporary and permanent pacemaker placement
Tachyarrhythmias
Atrial Premature Complexes (APCs)



Clinic
o Typically asymptomatic
ECG
o APCs reset the sinus node and there is a compensatory pause until the next sinus beat
Treatment
o Explanation and reassurance
o Beta-blockers
o Catheter ablation
Inappropriate Sinus Tachycardia


Etiology
o Often postviral dysautonomia which may last 3-12 months and then resolve
spontaneously
Treatment
o Hydration and salt-loading
o Careful titration of beta-blockers
Atrial Fibrillation

Treatment
o Acute Rate Control

27
28
Atrial Fibrillation
Treatment

Medical Therapy
o Rate Control
o Rhythm Control
 Antiarrhythmic drug therapy and attempts at restoring sinus rhythm should
thus be reserved for patients who are symptomatic and who do not tolerate the
rhythm well
o Anticoagulation

Surgical Therapy
Hospitalization and anticoagulation are not indicated in a patient with a brief episode of atrial
fibrillation, after spontaneous cardioversion. There is no indication for antiarrhythmic therapy in this
clinical situation, but it may be considered if atrial fibrillation recurs with symptoms of dyspnea,
fatigue, or intolerable palpitations.
Atrial Flutter
Diagnosis
 Saw-tooth waves most prominent in the inferior leads
Treatment
 Radiofrequency catheter ablation is the therapy of choice for recurrent atrial flutter
 90% success rate
29
Permanent Pacemakers and AICDs
Pacemaker
Threshold: An output from the pacemaker at which at which every impulse will stimulate the heart
muscle at a time which the heart muscle would not be expected to be refractory. Pacemakers are set
to 2-3 times the threshold
Ex. Threshold value of 1.5 volts, then pacemaker output set to 3 to 4.5 volts
Sensitivity: The voltage above which the pacemaker will consider a sensed electrical event as
significant.
Indications for permanent pacing:
 Class I evidence
o 3rd degree AVB with either
 HR < 40 bpm
 Pauses >3 seconds
 Required drugs that may cause further bradycardia
 Post AVJ ablation
 Neuromuscular disease causing AVB
o 2nd AVB with symptoms
o Intermittent 3rd degree AVB with chronic bifascicular or trifascicular block
o After AMI
 Transient infranodal advanced AVB with BBB
 Persistent and symptomatic 2nd or 3rd degree AVB
o Symptomatic sinus bradycardia or chronotropic incompetence including if associated
with necessary drug therapy exacerbating bradycardia
o Pause dependent VT with or without prolonged QT
o Syncope with carotid sinus massage induced pause >3 sec
 Class II evidence
o Asymptomatic 3rd degree AVB with HR > 40 bpm
o Asymptomatic type II 2nd degree AVB
o Asymptomatic type I 2nd degree AVB if EPS documented block below or in His
o Symptoms from first degree block
o Marked first degree AVB >0.3 sec with impaired LV ad CHF
o Syncope with chronic bifascicular or trifascicular block and no clear cause for syncope
found
o Chronic bifascicular or trifascicular block with HV >100 ms in asymptomatic patient
o Chronic bi and trifascicular block with non-physiologic block below His found at EPS
o After AMI
 Persistent 2nd and 3rd degree nodal AVB after MI
o Minimally symptomatic but HR <30 bpm
o High risk patients with congenital long QT
o Prevention of symptomatic, drug refractory atrial fibrillation
o Recurrent syncope with no clear cause but abnormal carotid sinus massage or with
abnormal sinus or AV conduction incidentally detected on EP study
o Neurocardiogenic syncope with significant bradycardia during tilt
o Medically refractory HOCM
Pacer Codes
Chamber being paced
A (atrial)
Chamber being sensed
A
Mode of pacing
I (inhibited)
Rate Modulation
30
V (ventricular)
D (dual)
O (none)
V
D
O
T (triggered)
D
O
Magnet application
Turns off sensing and paces at set “magnet rate”
ICD
Indications
 Class I
o Cardiac Arrest due to VF or VT without reversible cause
o Spontaneous sustained VT
o Syncope VF/VT at EPS when drug Rx is not tolerated, ineffective or not preferred
o NSVT, low EF, prior MI, VT at EPS not suppressed with class I antiarrhymics (from
MADIT study)
 Class II
o Cardiac arrest presumed to be VF when EPS is contraindicated
o Symptomatic VT in a patient awaiting heart transplant
o Familial conditions with high risk of cardiac arrest like LQT or HOCM
o NSVT, low EF, prior MI, VT at EPS
o Recurrent syncope of unclear etiology with abnormal LV and VT at EPS
Magnet Application
A magnet placed over the OCD will temporarily or permanently turn the ICD off except for
bradycardia pacing.
Pregnancy Related Cardiology

In young healthy women with cardiac chest pain consider spontaneous coronary artery
dissection 2/2 hormonal and vascular changes
Normal Dysfunction



A basal systolic murmur is present in 80% of pregnant women owing to increased flow across
the pulmonic and aortic valves.
The resting heart rate increases by 20% to 30% during pregnancy as compared to before
pregnancy
An S3 gallop is common because of increased early diastolic ventricular filling.
Contrast Nephropathy
Prevention
 Acetylcysteine 1200 mg po q12h x 4 doses, please give at least 1 dose prior to catheterization
and 2 doses post catheterization
Treatment
Stopping Medications Before Interventions

PCI
o ASA
o Clopidogrel
31

o Abciximab
o Eptifibatide
o Heparin
o Enoxaparin
o Direct thrombin inhibitors
CABG
o ASA
o Clopidogrel
o Abciximab
 D/C and give 6-12 units of platelets
o Eptifibatide
 D/C at least 4-6 hours prior
o Heparin
o Enoxaparin
 D/C 12-24 hours prior to CABG
o Direct thrombin inhibitors
Complications of Cardiac Catheterization



Major
o Death
 Approximately 0.1%
 High-risk groups
 NYHA class IV (10-fold increase in mortality)
 Left main coronary artery disease
 LVEF < 30%
 Valvular heart disease
 DM requiring insulin
 Cerebrovascular disease
 Pulmonary insufficiency
 Preexisting renal disease
o MI
o Stroke/TIA
 Especially high in those with AS who undergo retrograde catheterization of the
aortic valve
Local Vascular Complications
o Hemostasis at the access site
 Devices used
o Prior warfarin therapy
 Ideally INR < 1.5 but procedure is preformed with INRs of 2-3
o Hematoma formation
 Common, most resolve over days, intervention not usually required
o Retroperitoneal extension
o Pseudoaneurysm
 Pulsatile mass with a systolic bruit over catheter site
 Confirm by duplex US
 Most occur by day 3
o Arterial Thrombosis
 Lower extremity pain or paresthesia with reduced or absent distal pulses
 Urgent vascular surgery or thrombectomy may be required
Atheroembolism
32
Secondary Prevention of CAD at Strong







Weight control
Exercise (30-60 minutes at least 3-4 days/week)
Diet modification
Alcohol reduction
Medications
o ASA daily
o BB titrate for HR >50 or SBP >100
o Statin for LDL >100, cholesterol >160
o ACEI
o Plavix
Smoking cessation
Blood Pressure Control: <140/90 or <130/85 in DM, HF, or RI
Pulmonary Hypertension
Classification
 Primary
o Familial and idiopathic
 Secondary
o Chronic venous thromboembolism
o Scleroderma
o HIV infection
o Cirrhosis
o Anorexigen use (phen-fen)
Presentation
 DOE
 Palpitations
 Pre-syncope/syncope
Physical Exam
 Prominent P2 because of higher pulmonary pressures
 Tricuspid regurgitation murmur
 JVP
 RV heave
 Ascites/edema
Evaluation
 Pulse oximetry at rest and with exertion
 ECG
 CXR
 Spirometry
 Exercise Echo
Management
 Referral to a specialist

33
Cardiology Trials
RISC: ASA reduces risk of death and acute MI by 50% in patients with NSTEMI
Cardiac Resynchronization–Heart Failure (CARE-HF) study has suggested improved survival with
BiV pacers in select populations
CURE trial (Clopidogrel in Unstable Angina to Prevent Recurrent Events): all TIMI risk score groups
had a significant reduction in death, non-fatal MI, and stroke when given aspirin and plavix as
opposed to aspirin and placebo
ESSENCE trial (Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events):
Risk of death/MI post UA/NSTEMI was reduced in those treated with enoxaparin and aspirin as
opposed to UFH and aspirin
PROVE IT-TIMI 22 trial (Pravastatin or Atorvastatin Evaluation and Infection Therapy –
Thrombolysis in Myocardial Infarction 22): intensive statin therapy (atorvastatin 80mg) decreased
death or rehospitalization for recurrent ACS at 30 days as compared to pravastatin 40mg.
CAST/SWORD: Trials showing that antiarrhythmics for non-lethal arrhythmias post MI may
increase mortality
ACS ECG Interpretation
I High Lateral
II Inferior/Posterior
III Inferior/Posterior
ECG Leads
V1-V2
AVR
AVL
AVF Inferior/Posterior
V1 Septal
V2 Septal
V3 Anterior
Injury Related Artery
LAD – septal
V3-V4
Area of Damage
Septum, HIS bundle,
bundle branches
Anterior wall LV
V5-V6, I, aVL
High Lateral Wall
Circumflex
II, III, aVF
Inferior wall LV
Posterior wall LV
RV, inferior LV,
posterior wall LV
RCA – PDA
Posterior wall LV
Either CX or PDA
V4R, (II,III, aVF)
V1-V4(depression)
LAD – diagonal
RCA – Proximal
V4 Anterior
V5 Anterior
V6 High Lateral
Complications
Infranodal block and
BBBs
LV dysfunction, CHF,
BBBs, complete heart
block, PVCs
LV dysfunction, AV
nodal block in some
Hypotension, sensitive
to nitrates and MSO4
Hypotension, supranodal and infranodal
blocks, afib/flutter
LV Dysfunction
34
Management of Hemodynamics in the CCU
Variables
Variable
Cardiac Output
Cardiac Index
Stroke Volume
Stroke Volume
Index
Systemic
Vascular
Resistance
Pulmonary
Vascular
Resistance
Left Cardiac
Work Index
Arterial Oxygen
Content
Mixed Venous
Oxygen Content
Arterio-venous
Oxygen
Difference
Oxygen
Consumption
ABR
CO
CI
SV
SVI
Normal Range
4-6 L/min
2.5-3.5 L/min/m2
60-70 mL/beat
41-51 mL/beat/m2
Derivation
Meaning
SVR
PVR
LCWI
CaO2
CvO2
A-VO2D
VO2
Cardiac Monitoring and Normal Values
JVP/RA
PA systolic
PA mean
PAWP/LA
Cardiac Index
SVR
AVO2 difference (?)
0-8 cm
15-30 cm
9-16 cm
3-12 cm
2.6 – 4.2 (L/min/m2)
700-1600
2.9 – 5.3 mL/dL
Calculations
SVR = ((MAP – CVP)x79.9)/CO
MAP = DBP + 1/3 (PP)
AVO2 difference = (8.5 x 1.36 x Hgb x SaO2) – (1.36 x Hgb x Svo2)
Laboratory Values
Cardiac markers
Non-MI causes of elevation of Troponin
35
1.
2.
3.
4.
5.
6.
7.
8.
Defibrillator charge
Renal Insufficiency
LVH failure
Tachy-arhythmias
Myocarditis
Pericarditis
Pulmonary embolism
Assay interference (heterophil antibodies, RF, excess fibrin)
Pharmacology of Inotropes and Vasoactive Medications
Catecholamines
Derivatives of dopamine precursor
Act on:
 Alpha receptors
o Located in peripheral vessels
o Cause vasoconstriction
 Beta receptors
o Beta 1
 Located on cardiac tissue
 Increased intracellular cAMP => increased intracellular calcium =>positive
inotropic and chronotropic effects
o Beta 2
 Located in peripheral tissues and bronchial tree
 Increased intracellular cAMP => increased intracellular calcium =>relaxation
of smooth muscle => vasodilation
 Dopaminergic receptors
o Located primarily in splanchnic and renal circulation
o Vasodilation
Dopamine

Low dose (1-3 micrograms/kg/min)
o Dopaminergic receptor stimulation
o Increases renal and splanchnic blood flow
o Often used in cardiac failure in order to augment renal blood flow and facilitate
diuresis with lasix
36


Intermediate dose (3-10 micrograms/kg/min)
o Stimulates beta receptors by being a partial agonist itself and causing release of
norepinephrine from cardiac nerve terminals
o Commonly used in heart failure complicated by hypotension
o Results in an increase in cardiac output and increases heart rate and myocardial
oxygen demand which may worsen myocardial ischemia
High dose (>10 micrograms/kg/min)
o Alpha receptor stimulation
o Causes systemic vasoconstriction
o Supports blood pressure in shock states
Administer via a central catheter as extravasation will lead to skin necrosis. If this occurs promptly
inject phentalamine 10mg locally (alpha-adrenergic antagonist)
Dobutamine




Net effect
o Increased myocardial contractility
o Increased heart rate
o Varying degree of peripheral vasodilation
Use
o To increase CO in patients with depressed left ventricular function and clinical heart
failure and impaired cardiac output
o Frequently combined with other agents
 Low dose dopamine to augment renal perfusion
 Nitroprusside for venodilation
Dosing
o Initial 2 micrograms/kg/min
o Titrate to 10-15 micrograms/kg/min (target dose in CHF is 10)
o Tolerance develops after several days of continued use
Adverse Effects
o Arrhythmia
o Ischemia
Norepinephrine




Net effect
o Increases cardiac contractility
o Vasoconstriction
Use
o Profound hypotension and shock
Dosing
o 2-10 micrograms/min
Adverse Effects
o Arrhythmia
Epinephrine


Net effect
o Increased cardiac contractility
o Vasoconstriction
Use
o Cardiopulmonary arrest
37


o Shock
o Cardiopulmonary bypass
Dosing
Adverse Effects
o Arrhythmia
o Tachycardia
o Vasoconstriction
o Cardiac Ischemia
o Metabolic Acidosis that resolves with discontinuation
Isoproteronol

Phosphodiesterase Inhibitors
Pathophysiology
 Inhibit break down of cAMP by membrane bound phosphodiesterase enzymes
Milrinone




Net effect
o Increased CO via positive inotropy and vasodilation
Use
Dosing
Adverse effects
Vasodilators
Nitroprusside




Net effect in CHF
o Fall in right atrial and pulmonary wedge pressure
o Decrease in systemic vascular resistance
Use
Dosing
o Start with lowest dose and titrate up
Adverse effects
o Cyanide toxicity in patients with underlying hepatic and/or renal disease who receive
prolonged infusions
Nitroglycerin




Net effect
o Venodilation
Use
o Ischemic heart disease
o Acute pulmonary edema
Dosing
o Drip: 10 microgram/min
o Paste
o 0.4 mg SL
Adverse effects
o Headache
38
o Flushing
o Hypotension (response quickly to d/c and fluids)
Cardiac Medications
Atropine
Mechanism: Anticholinergic that increases firing of SA node and increases conduction through AV
node
Dosing
 Asystole, PEA: 1.0 mg IVP q3-5min to a total of 3.0 mg
 Bradycardia, symptomatic: 0.5-1.0 mg atropine q3-5min to total of 0.04mg/kg (approximately
3.0 mg in a 70kg patient)
 Third degree block: do not use
Adverse Effects
Notes: Heart transplants do not respond to atropine (lack parasympathetic innervation
Nitroglycerin
Mechanism: vasodilation
Dosing
 Initial 5-15 mg/min
 Titrate as necessary by 5 mg/min q5min to relieve pain with a maximum of 200 mg/min
Adverse Effects
 Headache: use Tylenol
 Nausea:
 Hypotension: volume expansion
 Tachycardia: volume expansion +/- alpha agonist
Aspirin
Mechanism: inhibits COX-1 platelet aggregation with 15 minutes
Dosing: ASA 81-325mg qdaily
Adverse Effects:
Reversal: None
Thienopyridines
Mechanism
 Noncompetitive inhibition of ADP binding to type 2 purinergic receptor
 Inhibits activation of glycoprotein Iib/IIIA complex
Ticlopidine
Dosing:
 Requires 3-6 days of use for full effect
 Ticlopidine 250 mg po BID
Adverse Effects
 2.5% risk of neutropenia
39

1 in 1500 – 5000 develop TTP-HUS within first 12 weeks of therapy
o Treatment is drug d/c and possible plasmaphoresis
Clopidogrel
Dosing
 Initial loading: Clopidogrel 300 mg
 Maintenance: Clopidrogrel 75 mg qdaily
Adverse Effects
 3-5% risk of major bleeding, esp in elderly
Glycoprotein IIB/IIIA Receptor Inhibitors
Mechanism: GPIIB/IIIA receptor binds fibrogen and is the mechanism for cross-linking platelets and
therefore the antagonists inhibit platelet aggregation
Classes
 Large-molecule agents (irreversible binders)
o Abciximab (ReoPro)
 Small-molecule agents and non-peptides (reversible binders)
o Eptifibatide (Integrilin)
o Tirofiban (Aggrastat)
Abciximab




Used with ASA and heparin
Dosing
Adverse Effects
o Bleeding from vascular access sites
o Severe thrombocytopenia (< 50000) seen in 0.5-1.5%
Monitoring
o Check platelet counts within 4 hours of starting transfusion and again at end of
transfusion
Eptifibatide
Tirofiban
Unfractionated Heparin
Mechanism: inhibits soluble clotting factors
Dosing
Adverse Effects
 Bleeding
 HIT
o DX:
40
o TX:
Low-Molecular-Weight Heparins
Mechanism: increase factor Xa activity and decrease IIa activity compared to UFH
Enoxaparin
Dosing
 CrCl > 30 ml/min: 1 mg/kg SQ BID
Adverse Effects
Dalteparin
Dosing
Adverse Effects
Direct Thrombin Inhibitors
Mechanism: bind factor IIa, not dependent on ATIII
Names
 Hirudin
 Lepirudin
 Argatroban
 Bivalirusin
Adverse Events
 Increased risk of bleeding
Statins
Except for lipitor and crestor, statins should be taken at night.
Intensive statin therapy should be used to ACS
Ward Lessons
Dr. Bis:
Spironolactone is a bad diuretic and only acts as a diuretic at high doses. At low doses it is purely
hormonal.
Atenolol is renal excreted. Use metoprolol for Cr 1.5 and up
Easiest way to create asystole is to give a patient with renal disease atenolol and diltiazem.
In patients with heart failure consider whether or not to give them a regular or heart-healthy diet. In
older patients who are not likely to change their diet after leaving the hospital it might be prudent to
41
give them a regular diet and adjust medications for it instead of having them discharged with a
mismatched regimen.
Beta-stimulant of choice is isoproterenol. Dobutamine is 2nd line.
New cardiomyopathy just about always buys itself a cardiac cath to r/o reversible disease (such as left
main disease).
Heart failure patients – old, frail, unchangeable, may be better on a regular diet than a heart healthy
diet
Rewarming often overshoots the temp. So if they are febrile, it doesn’t mean they are infected unless
there is also some other indication.
Patient Checklist
ACS



Risk Stratification
Medications
o ASA
o Beta blocker
o Plavix
o Statin
o ACEI
o Heparin
Procedures
o Fibrinolysis
o Echo
o Coronary angiography
Heart Failure





Underlying reason for CHF
Reason for CHF exacerbation
Timing of hospitalizations
Home weight
Medications
o Beta-blocker
o ACEI/ARB
 No benefit in using both
 If ACEI/ARB can not be tolerated (such as hyperkalemia) try a
Hydralazine/Nitrate combination
o Calcium-channel blocker
 If HTN not controlled by ACEI + beta-blocker
o Spironolactone
 Reduces mortality in Class III-IV heart failure and EF < 35%
o Digoxin
 Reduces symptoms and hospitalizations but not mortality
42
Physical Exam
Right sided MI - hypotension, clear lung fields, and elevated jugular venous pressure
Admission Notes
STEMI
NSTEMI back from cath
CV: NSTEMI anterior
ACS: BB, ASA
Symptom management: morphine, nitro
To cath: NPO, premeds (heparin gtt, infiximab, plavix)
NSTEMI/UA
Chest Pain
ECHO/ETT in AM
Admission Orders
Cardiology
ST-Elevation MI
Admit to: CCU
Diagnosis: STEMI
Vital Signs: Unit routine, continuous telemetry
Activity: Bedrest
Nursing:
 O2 2L, increase as necessary to maintain oxygen saturation > 93%
 Guaic all stools
 FSBG ACHS
Diet: NPO for prior to cardiac catheterization, then Heart Healthy Diet
IV Fluids: NaHCO3 3 Amps in 1 Liter D5W – administer 250 ml/H x 1 hour, then 80 mL/h x 6
hours, then saline lock.
HO:
 Call for SBP < 100 or >180
 Call for HR < 50 or > 100
Medications:
 ASA 81 mg po qday
 Clopidogrel 75 mg po qday (for stents)
 Metoprolol 50 mg po q12h (begin in AM). Hold for SBP < 100, HR < 50 and call MD
 Eptibatide 2 microgram/kg/min for 18 hours post-stent placement
 Enalapril 2.5 mg po q12h – begin in AM. Hold for SBP < 100
 Nitroglycerin 0.4 mg SL prn chest pain; may repeat in 5 minutes
 Morphine Sulfate 1-4 mg IV q5minutes prn chest pain, not to exceed 10 mg/h. Hold for
sedation, RR < 10 breaths/min, or SBP < 90.
43
Labs





ECG on admit and for recurrent
chest pain
Troponin I
CBC now and qday (keep Hct >
30)
Chem 7 now and qday
Mg now and qday




PT, INR, PTT
Lipid panel
UA
Type and screen
Discharge Planning:
 Meet with nutritionalist
 Smoking cessation
 Advice on activity and when it is safe to return to work
 Review of medications
 Discharge meds: BB, ASA, ACEI, Statin, Plavix
UA/NSTEMI
Admit to: CCU
Diagnosis: UA and NSTEMI
Vital Signs: Unit routine, continuous telemetry
Activity: Bedrest
Nursing:
 O2 2L, increase as necessary to maintain oxygen saturation > 93%
 Guaic all stools
 FSBG ACHS
House Officer:
 Call for SBP < 100 or >180
 Call for HR < 50 or > 100
Diet: NPO for prior to cardiac catheterization, then Heart Healthy Diet
IV Fluids: Saline lock. Hydrate if going for cardiac catheterization with HCO3 3 amps in
1 L D5W and run at 3ml/kg in hour prior to catheterization and 1 mL/kg for 6 hours postcath.
Medications:
 ASA 81 mg po qday
 Clopidogrel 300 mg po now and then 75 mg po qday
 Enoxaparin 1 mg/kg SQ q12h
 Metoprolol 50 mg po q12h – first dose now. Hold for SBP < 100, HR < 50 and
call MD
 Nitroglycerin 0.4 mg SL prn chest pain; may repeat in 5 minutes
 Morphine Sulfate 1-4 mg IV q5minutes prn chest pain, not to exceed 10 mg/h.
Hold for sedation, RR < 10 breaths/min, or SBP < 90.
Labs
 ECG on admit and for recurrent chest pain
 Troponin I
 CBC now and qday (keep Hct > 30)
 Chem 7 now and qday
 Mg now and qday
 PT, INR, PTT
 Lipid panel
 UA
44
Discharge Planning:
 Meet with nutritionalist
 Smoking cessation
 Advice on activity and when it is safe to return to work
 Review of medications
 Discharge meds: BB, ASA, ACEI, Statin, Plavix
45
Atrial Fibrillation
Admit to: Telemetry
Diagnosis: Atrial fibrillation
Vital Signs: Vitals q2h x 4, then decrease to q4h, continuous telemetry
Activity: As tolerated, teach patient to sit at side of bed for several minutes before
standing
Nursing:
 O2 2L per NC if oxygen saturation < 93%
House Officer:
 Call for SBP < 100 or >180
 Call for HR < 60 or > 140
Diet: If cardioversion is planned NPO 8 hours prior, else Heart Healthy Diet
IV Fluids: Saline lock.
Medications:
 ASA 81 mg po qday (if warfarin is not going to be prescribed)
 Rate control medications (see table)
 Warfarin (for CHAD2 score > 2) 5 mg po tonight, dose of warfarin to be adjusted
daily based on PT/INR
Medication
Dosing
Metoprolol/atenolol
Diltiazem
Digoxin
CHADS2
CHF
HTN
Age >= 75
Diabetes
H/O stroke or TIA
1
1
1
1
2
Labs
 ECG on admit and for chest pain
 TSH, T4
 Troponin I
 Iron panel
 CBC
 TTE/TEE
 Chem 7
 PT, INR, PTT
 CXR
 Lipid panel
 Mg

Discharge Planning:
 Cardioversion or rate control at 60-80 at rest and up to 115 with exercise
 Smoking cessation
 Advice on activity and when it is safe to return to work
 Review of medications
 Assessment for OSA
46
 FU with cardiology
Discharge meds: Warfarin or ASA
47
Congestive Heart Failure
Admit to: Telemetry
Diagnosis: Congestive Heart Failure
Vital Signs: Vitals on admit and q4h, then decrease to q4h, weight upon admission,
orthostatic BP each morning (to assess diuresis), continuous telemetry
Activity: Bedrest with bathroom privileges, up only with assistance. Fall precautions.
Nursing:
 O2 per NC to maintain oxygen saturation > 92%
 Daily weights
 Strict I/Os
House Officer:
 Call for SBP < 100 or >180
 Call for HR < 60 or > 140
Diet: 2 g sodium restriction, heart healthy diet, nutrition consult for teaching on lowsodium diet
IV Fluids: heparin lock.
Medications:
 ASA 81 mg po qday (if warfarin is not going to be prescribed)
 Lasix 80 mg IV now, then 60 mg IV BID (depends on home dose, may try
bumetanide or torsemide if lasix restistant)
 Chlorothiazide if not reaching goal diuresis (monitor potassium)
 Spironolactone for patients with NYHA class IV HF or renal insufficiency
 ACEI or ARB for HF with reduced LVEF
 Digoxin 0.125 mg po qday (consider if already on BB, ACEI, diuretic and
symptomatic)
 Hold BB until after resolution of volume overload
 Morphine may improve vascular resistance and symptoms in patients with
significant pulmonary edema, increased anxiety and work of breathing
 ABX if pneumonia is suspected




Labs

NYHA CLASSIFICATION OF HEART FAILURE
Class I: patients with no limitation of activities; they suffer no symptoms
from ordinary activities.
Class II: patients with slight, mild limitation of activity; they are comfortable
with rest or with mild exertion.
Class III: patients with marked limitation of activity; they are comfortable
only at rest.
Class IV: patients who should be at complete rest, confined to bed or
chair; any physical activity brings on discomfort and symptoms occur at
rest.
ECG on admit and for chest pain

Troponin I
48





CBC
Chem 7
CXR
Mg
TSH, T4





Iron panel
TTE/TEE
UA
Lipid panel
BNP
Discharge Planning:
 Obtain copy of prior echo
 Cardiology consult – repeat echo if significant decline or echo was remote
 How many exacerbation in past year?
 Counciling of monitoring daily weights
 Nutrition consult
 Smoking cessation
 Advice on activity
 Review of medications
 Assessment for OSA
 FU with cardiology
Discharge meds:
49
Syncope
Admit to: Telemetry
Diagnosis: Syncope
Vital Signs: Vitals on admit and q4h, if severe volume depletion is suspected consider
vitals q2-4 hours over first 12 to 24 hours to monitor volume repletion. continuous
telemetry
Activity: fall risk, up with assistance only
Nursing:
 O2 per NC to maintain oxygen saturation > 92%
 Daily weights
House Officer:
 Call for SBP < 100 or >180
 Call for HR < 60 or > 140
Diet: Regular
IV Fluids: heparin lock.
Medications:
 Heparin 5000 U SQ TID
 Docusate 250 mg po bid prn (hold for loose stools)
Labs









ECG on admit
Troponin I
CBC
Chem 7
CXR
Mg
TSH, T4
UA
Tox screen


bHCG
Other possible
o EEG
o BNP
o Stress test
o Holter monitoring
o EP studies
o Tilt-table test
Discharge Planning:
 Advance activity after first 24 hours
 Cardiology consult if warranted
 Neurology consult if warranted
 Pysch consult if warranted
 If orthostatic: education about sitting at side of bed, script for compression hose
Discharge meds:
50
Hypertensive Emergency
Admit to: ICU
Diagnosis: HTN Emergency
Vital Signs: Vitals on admit and q1h, BP q30 minutes (call HO with result) possible
continuous BP monitoring with an arterial line if refractory to initial management or
nitroprusside to be used.
Activity: bedrest
Nursing:
 O2 per NC to maintain oxygen saturation > 92%
 I/Os
 Neuro checks q2h
House Officer:
 Call for SBP >190 or DBP > 110
 Call for HR < 60 or > 140
 Call HO for nausea, vomiting headache, tinnitus, seizure, muscle spasm, delirium
while nitroprusside infusion is running
Diet: Low-sodium diet
IV Fluids: ½ NS TKO.
Medications:
 Sodium nitroprusside IV infusion. Begin at 0.1 microgram/kg/min and titrate
q15m to achieve 25% reduction in MAP within first 3-4 hours
 Docusate 250 mg po bid prn (hold for loose stools)
Alternatives to Nitroprusside
Labetalol 20 (40,60) mg IV bolus q 10-15
minutes or as continuous infusion
Fenoldapam IV infusion
Nicardipine IV infusion
Hydralazine IV
Contraindicated in CHF, bradycardia, heart
block, RAD
Dopamine antagonist, can be used in RI but
can raise intraocular pressure (CI in
glaucoma)
Vasodilator
Reflex tachycardia (CI in MI, increased
ICP and aortic dissection)
Nitroglycerin IV infusion
Labs






ECG on admit
Troponin I
CBC with smear
Chem 7
CXR
Mg





TSH, T4
UA
Tox screen
BHCG
CT of head
Discharge Planning:
51
 Graph planned BP goals for first day
 Assess each organ system for damage and recovery over time
 Consider assessment for secondary causes of HTN
 Neuro consult for stroke or intracranial hemorrhage
Discharge meds:
Aortic Dissection
Admit to: ICU
Diagnosis: Aortic Dissection
Vital Signs: Vitals on admit and q1h, Continuous BP monitoring via arterial line
Activity: absolute bedrest
Nursing:
 O2 per NC to maintain oxygen saturation > 92%
 I/Os
 Neuro checks q1h
 Check pulse in LE q1h and call if change
House Officer:
 Call for SBP >120 or DBP > 80
 Call for HR < 50 or > 80
 Call for UO < 30 ml/h
Diet: NPO
IV Fluids: ½ NS TKO.
Medications:
 Labetalol 5-10 mg IV now, then 1 mg/min continuous infusion. Titrate up to
achieve SBP 95-110 mmHg over first hour. Call HO if SBP goal can not be reach
(may add nitroprusside at 0.3 microgram/kg/min and titrate q15min until goal
achieved)
 Esmolol is an alternative to labetalol
 Morphine sulfate 1-4 mg IV q1h prn pain (hold for sedation or RR < 11)
 Docusate 250 mg po bid prn (hold for loose stools)
Labs












ECG on admit
Troponin I
CBC now and qday
Coag panel now and qday
Chem 7 now and qday
CXR
LFTs
Mg
TSH, T4
UA
Tox screen
BHCG


CT of chest & abd with contrast
TEE
52
Discharge Planning:
 Possible surgery
 Assess each organ system for damage and recovery over time
 Assessment for causes of dissection
 FU with cardiology
Discharge meds:
ACS algorithm
Is this cardiac?
Proper meds
History
Risk stratification with TIMI score
Review ECG
Where part of the heart is this occurring in?
What is the suspect vessel?
What are the complications?
Review trops and cardiac markers
Orders Set Examples
Patient with chest pain from afib, no ECG changes, no positive trops
Went to cath for unstable angina 4 days later
DIAGNOSIS 1. CHEST PAIN
DVT PROPHYLAXIS NOT INDICATED
NRT NOT INDICATED
PATIENT CONDITION SATISFACTORY
VITAL SIGNS Q4HRS DAILY UNTIL D/C
OXYGEN: NASAL CANNULA
HEART HEALTHY-4GM NA, MOD FAT
FOR CHEST PAIN : FOR CHEST PAIN
CALL HO/MLP : TEMPERATURE > 38.5 C
CALL HO/MLP : RESPIRATIONS < 10 > 30
CALL HO/MLP : PULSE < 50 > 110
CALL HO/MLP : SBP < 100 > 180
CALL HO/MLP : OXIMETRY < 92.0
TELEMETRY
ACETAMINOPHEN 650. MG PO Q4H PRN
DOCUSATE SODIUM 100. MG PO BID PRN
NITROGLYCERIN 0.4 MG SL Q5M PRN
ELECTROCARDIOGRAM Q8HRS DAILY X 24 HOURS
TROPONIN I, ULTRASENSITIVE STAT
FUROSEMIDE 20. MG PO ONCE EACH DAY
DIGOXIN 125. MCG PO ONCE EACH DAY
53
WARFARIN SODIUM 2.5 MG PO ONCE EACH DAY
CALCIUM CARBONATE/VITAMIN D 1. TAB PO BID
MAALOX 30. ML PO Q6H PRN
DIGOXIN 125. MCG PO ONCE EACH DAY
FUROSEMIDE 20. MG PO ONCE EACH DAY
NITROGLYCERIN 0.4 MG SL Q5M PRN MAY REPEAT X3 DOSES
DOCUSATE SODIUM 100. MG PO BID PRN
ACETAMINOPHEN 650. MG PO Q4H PRN
CALL HO/MLP : OXIMETRY < 92.0
COMPLETE BLOOD COUNT W/ PLTCNT ONCE DAILY X 3 DAYS
TROPONIN I, ULTRASENSITIVE
CK, SERUM
PROTIME, BLOOD
LIVER PROFILE, SERUM
LIPID PROFILE
ASPIRIN, ENTERIC COATED 325. MG PO ONCE EACH DAY
ACTIVITY AS TOLERATED
ELECTROCARDIOGRAM ONCE DAILY X 3 DAYS
METOPROLOL TARTRATE 12.5 MG PO BID
Pre-Cath Orders
NPO AFTER MIDNIGHT
COags
Post-Cath
CALL CARDIAC CATH FELLOW FOR:
Y
CONT DAILY UNTIL D/C
N/V, CHEST PAIN/ANGINA,
RESPIRATION RATE < 12,
UNCONTROLLED BLEEDING AT
SITE, HEMATOMA FORMATION,
MENTAL STATUS CHANGES,
SEVERE BACK PAIN
IF PULSE DROPS 10 BEATS/MIN
FROM BASELINE OR < 50
BEATS/MIN:
54
Y
FROM BASELINE OR < 50
BEATS/MIN:
AND BP DROPS 20MM FROM
BASELINE, GIVE 0.5MG
ATROPINE AND NOTIFY CARDIAC
CATHETERIZATION FELLOW
IF BP DROPS 20MM FROM
BASELINE OR SBP < 100
Y
BASELINE OR SBP < 100
GIVE 250CC NS BOLUS, PUT
PATIENT IN TRENDELENBURG
POSITION AND NOTIFY CARDIAC
CATHETERIZATION FELLOW
CHECK CATH INSERTION SITE
CHECK WITH EACH VS FOR
BLEEDING, HEMATOMA OR PULSE
LOSS
VITAL SIGNS
DAILY
Q15MIN FOR 1H
Q30MIN FOR 1H
Q1HR FOR 1H
Q4HRS UNTIL D/C
HOB NO MORE THAN 30 DEGREES
BEDREST - STRICT
RESUME DIET AND MEDICATIONS
ENCOURAGE PO INTAKE
MORPHINE SULFATE 2. MG IV X 1
NSTEMI went to cath
PANTOPRAZOLE 40. MG PO ONCE EACH DAY
NITROGLYCERIN 2% OINT. 1. IN. TRANSDERM. ONCE EACH DAY
55
NITROGLYCERIN 0.3 MG SUBLINGUAL Q5M PRN
DIPHENHYDRAMINE HCL 25. MG PO QHS PRN
ACETAMINOPHEN 650. MG PO Q4H PRN
ALPRAZOLAM 0.25 MG PO Q8H PRN X 7 DAYS
CLOPIDOGREL BISULFATE 600. MG PO X 1 STAT
CLOPIDOGREL BISULFATE 75. MG PO ONCE EACH DAY
ATORVASTATIN 40. MG PO ONCE EACH DAY
LISINOPRIL 10. MG PO ONCE EACH DAY
ASPIRIN, ENTERIC COATED 325. MG PO ONCE EACH DAY
METOPROLOL TARTRATE 25. MG PO Q12HRS
DOCUSATE SODIUM 100. MG PO BID
SENNA 1. TAB PO BID
Admission STEMI
A/P 81 yo F with no significant PMH developed CP while walking
1. CVS – STEMI
a. Will place on metoprolol 6.25 BID, asa 325 QDAY, Plavix 75 QDAY,
zocor 80 QDay
b. Telemetry
c. CXR
d. Trend cardiac enzymes
e. NTG prn CP
f. Check fasting lipid profile and LFTs
g. Avoid ACEI until renal function known
h. Other recs (integrillin and acetylcysteine) per cath protocol from cath
fellow
2. Renal – FU creatinine
3. PPX – heparin SQ when?
4. PMH/Home meds
5. Dispo
RAD CHEST SINGLE VIEW
NS IV CONT
ACETYLCYSTEINE 1200. MG PO BID X 48 HOURS
EPTIFIBATIDE DRIP 750. MCG/ML IV CONT
I&O
FOR CHEST PAIN : FOR CHEST PAIN
CALL HO/MLP : SBP < 100
CALL HO/MLP : PULSE > 110
CALL HO/MLP : TEMPERATURE > 38.0 C
CHECK CATH INSERTION SITE
VITAL SIGNS Q15MIN FOR 1 H , Q30MIN FOR 1H , Q4HRS DAILY UNT
TELEMETRY
56
HOB NO MORE THAN 30 DEGREES
BEDREST - STRICT
ELECTROCARDIOGRAM ONCE DAILY X 3 DAYS
PROFILE 8 (BASIC METABOLIC) ONCE DAILY X 3 DAYS
CBC, PLT AND DIFF ONCE DAILY X 3 DAYS
LIVER PROFILE, SERUM
SIMVASTATIN 80. MG PO ONCE EACH DAY
CLOPIDOGREL BISULFATE 75. MG PO ONCE EACH DAY
NITROGLYCERIN 0.3 MG SUBLINGUAL Q5M PRN
METOPROLOL TARTRATE 6.25 MG PO BID
ACETAMINOPHEN 650. MG PO Q4H PRN
ASPIRIN, ENTERIC COATED 325. MG PO ONCE EACH DAY
PROTIME, BLOOD
APTT, BLOOD
LIPID PROFILE NEXT AM
COMPLETE BLOOD COUNT W/ PLTCNT
PROFILE 8 (BASIC METABOLIC)
TROPONIN I, ULTRASENSITIVE Q8HRS DAILY X 24 HOURS
*CK ISOENZYME, SERUM Q8HRS DAILY X 24 HOURS
OXYGEN: NASAL CANNULA
WEIGHT
MAY BE OFF TELEMETRY FOR TESTS
TELEMETRY
I&O
HEART HEALTHY-4GM NA, MOD FAT
CALL HO/MLP : FOR CHEST PAIN
CALL HO/MLP : OXIMETRY < 91
CALL HO/MLP : SBP < 100 > 160 ; DBP > 100
CALL HO/MLP : RESPIRATIONS < 8 > 22
CALL HO/MLP : PULSE < 55 > 95
CALL HO/MLP : TEMPERATURE < 35 C > 38 C
VITAL SIGNS Q4HRS DAILY UNTIL D/C
PATIENT CONDITION SATISFACTORY
ADMIT PATIENT TO 736 ; DELEHANTY, JOSEPH M
FULL CODE
DIAGNOSIS 1. STEMI
ORDERS
BB are first line
Esmolol: 200-500 mcg/kg/min x 4 min, then 50-300 mcg/kg/min
Labetolol: 20-80 mg iv q10min. total 300 or 0.5-2.0mg/min IV gtt
Then add on other agents
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Nitroprusside: start at 0.25-0.50 mcg/kg/min. Maximum dose is 8-10 mcg/kg/min but no
more than 10 minutes at this dosage level. Watch for thiocyanate toxicity
Nicardipine 2-10 and up to 15 mg/hour
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