Cardiology In-Training Objectives

1. Diagnose a venous stasis ulcer.

• Diagnosis: Venous ulcers are diagnosed by clinical examination.
• Location: distal lower leg, particularly the medial aspect of the ankle
o May result from a minor trauma, a medical procedure, or stasis
dermatitis flare.
• Form: irregular border and surrounding hyperpigmentation, and the skin and
subcutaneous tissues are thickened, resulting in lipodermatosclerosis (a
fibrosing dermatitis of the subcutaneous tissue),
• Patients often have varicose veins and peripheral edema.
• Duplex U/S based on the duration of reversed (retrograde) flow (>500 ms for superficial or
perforator veins, >1000 ms for deep veins)

2. Diagnose atrial septal defect.

• Classic Hx is a female 20 - 40y/o with a CC of fatigue, dyspnea on exertion. EKG
reported with atrial fibrillation. Physical exam with a pulmonary outflow murmur or
Fixed splitting of the S2. Parasternal impulse.
• What is the Diagnosis? ASD
• Another presentation may be a young patient presenting with a TIA. Physical
examination fixed splitting of the S2. What is the Dx? Paradoxical Emboli secondary to
ASD.
• Ostium secundum defects (75% of cases), located in the mid portion of the atrial septum and
are usually isolated anomalies.
• Diagnosis: Echocardiography is the primary test for the diagnosis of ASDs. Agitated saline
contrast injection in a peripheral vein during TTE may help identify an atrial-level shunt.
3. Diagnose cardiac tamponade.
• Classical Hx is a male patient 40-50 y/o Male who comes
to the ED with a CC of due to SOB and Dyspnea at rest.
V/S presented with BP <110/80. Physical exam with clear
lungs and (+) JVD. Cardiac Monitor shows this image.
• Becks Triad: JVD + Hypotension + Diminished Heart
Sounds
• ECG: Low Voltage QRS Complexes and Electrical
Alternans (related to a swinging motion of the heart
within the pericardial fluid).
• CXR: cardiac silhouette is typically enlarged
• Diagnosis: Echocardiogram
o Early diastolic collapse of the Right Atrial and Ventricular Collapse During
Diastole and Plethoric IVC
Pulsus Paradoxus: Abnormally
large inspiratory decreases in
Systolic BP > 10mmHg

4. Diagnose critical aortic stenosis on the basis of physical findings.

• Decreased or absent A2
• High-pitched late peaking murmur
• Delay in the carotid upstroke (pulsus tardus) that may be accompanied by a
decreased pulse amplitude due to low cardiac output (pulsus parvus).
5. Diagnose Eisenmenger syndrome.
• Clinical Hx is usually a 30-40 y/o patient who comes to clinic with a CC of fatigue,
Dyspnea on Exertion, Syncope and or Angina. May be presented with a prior
Cardiac Hx while infant which was never Tx. Physical examination may reveal a
Machine Like Holosystolic Murmur. Resulting in hypoxemia, erythrocytosis and
cyanosis
• It is caused by reversal of right-to-left congenital shunt caused by VSD, PDA, or, less
commonly, ASD leading to Severe pulmonary artery hypertension.
• Physical Exam: Right ventricular or parasternal lift on precordial palpation, loud P2.
Central cyanosis and digital clubbing which involves all extremities
• Eisenmenger PDA: Clubbing and oxygen desaturation affecting only the feet
a. Dx: Echocardiogram next step

6. Diagnose hypertrophic cardiomyopathy on the basis of physical findings.

• Systolic ejective crescendo-decrescendo murmur at LLSB
a. Increases with Decreased Preload (Valsalva, Squat) and Afterload (Nitrate)
• Enlarged apical impulse
 • An S4 is frequently present, especially in younger patients.
• Rapid Carotid Upstroke rapid and may be difid pulsus bisferiens

7. Diagnose ischemia-induced papillary muscle dysfunction.

o Classical Hx is a patient with Acute MI with a new systolic murmur which
disappears with administration of Nitroglycerin If dysfunction.
o If papillary muscle rupture in the setting of MI patient will be Hypotensive in
pulmonary edema and Systolic Murmur will be persistent with Inspiration.
o Diagnosis is typically confirmed by Transthoracic echocardiography (color
flow), which usually demonstrates a flail segment of the mitral valve.

8. Diagnose ischemic cardiomyopathy. (MC cause of HF in developed countries)

• Ischemic cardiomyopathy (I-CMP) defined LVEF ≤35 to 40% secondary to CAD.
• I-CMP has to be suspected in patients who have signs and symptoms of heart failure
(decreased exercise tolerance, dyspnea on exertion, JVD, lung crackles and LE
 edema) plus risk factors for coronary artery disease (Diabetes, HTN, Tobacco use,
hyperlipidemia).
• ECG may show of prior or ongoing ischemia (ST elevations/depressions, Q waves,
LBBB)
• Next Step:
a. Stress Test: If NO evidence of Unstable Angina
i. To determine if viable myocardial tissue
b. Cardiac Catheterization: If evidence of ongoing Unstable Angina

9. Diagnose mitral valve prolapse.

• Symptoms do not reliably indicate mitral valve prolapse, patients are mostly
asymptomatic, and symptoms are not specific.
• May present with palpitations, dyspnea, exercise intolerance, and dizziness or with
complications such as endocarditis and arrhythmias.
• Examination shows:
o non-ejection click (single or multiple) with Mid or Late Systolic Murmur
▪ Murmur increases with decreased preload decreases Valsalva
• Diagnosed by echocardiography with visualization of a displaced coaptation level of
the anterior and posterior mitral leaflets 2 mm or more above the mitral annulus.

10. Diagnose myocarditis.

• Classical Hx will be a young patient who comes to the clinic with a CC of 2 months Hx of
fatigue, SOB, Chest Pain and DOE. May be also asymptomatic or may present with fever.
He recently suffered an URI weeks ago. Labs reported with positive troponin levels and
ECG with anterolateral ST segment changes. What is the Dx?
• Spectrum of Myocarditis can range from subclinical to fulminant Heart Failure
• In the developed world MC associated with viral infections such as Lyme Dz,
Coxsackievirus, Adenovirus, and Parvovirus B19. In South America, Chagas is the most
common cause
• Labs: May present with (+) Cardiac Enzymes and EKG with ST segment changes (transient).
• Dx: MRI with Gadolinium Enhancement (aids in Dx)
a. Gold Standard for definitive Dx endomyocardial biopsy
i. Indicated if: ventricular arrhythmia, high-grade AV block (type II or III)

11. Diagnose pulmonary valve stenosis.

• Pulmonic Stenosis is rare. almost always associated with Hx of repaired on unrepaired
congenital heart disease.
• Patients are only symptomatic if moderate to severe PS.
• Physical Exam: late-peaking SEM at the LUSB with wide S2 split
• ECG: Normal when RV systolic pressure <60 mm Hg; if RV systolic pressure >60 mm Hg
RA enlargement, right axis deviation, RV hypertrophy
• Echo: Confirms the Dx identifying pressure gradient right ventricular outflow tract.
a. Peak Pressure gradient 36-64 mm Hg is considered moderate
b. Peak Pressure gradient >64 mm Hg is considered severe.

12. Diagnose Takotsubo cardiomyopathy.

• Classical Hx is a woman who comes to ED with a CC of Chest Pain and Fatigue.
Recently her husband passed away. ECG done remarkable
for ST segment changes and Cardiac Enzymes (+). Cardiac
Catheterization done and remarkable for non obstructive
CAD and Ventriculogram reveals bellow image. What is
the Diagnosis?
• Diagnosis is usually made by an echocardiogram or
ventriculogram showing a typical pattern of apical
ballooning and dysfunction. A global LV akinesis/dyskinesis with a classic
circumferential pattern involving the entire apex (most common) or the midventricular
or basal segments would be suggestive of stress cardiomyopathy.
• Pathognomonic of Takotsubos CMP usually patient will experience recent traumatic
personal event and Cardiac Catherization will show Absence of significant coronary
disease.

13. Diagnose torsades de pointes as a complication of long QT syndrome.

• Long QT syndrome: is one of the most common

inherited arrhythmias and is defined by the
presence of a prolonged QTc interval (>440msec
in men and >460msec in women) accompanied by
unexplained syncope or ventricular arrhythmia.
• Risks is greatest with a QTc interval >500ms
• Prolonged QTc interval alone is not sufficient for a diagnosis of long QT syndrome.
• Drugs prolonging QT
 o antipsychotics, TCAs, Antihistamines, some antiarrhythmics, Macrolides,
quinolones (Moxifloxacin), antifungals, class Ia, class III antiarrhythmics.
• Treatment: Inherited long QT syndrome may be treated with B-blockers, if not
responding to the latter may select ICD

14. Identify high-risk patients requiring coronary angiography.

• High risk patients with high pre-test probability for CAD are provided medical
management for CAD and warrant a coronary angiography
• Unstable patients are referred for immediate angiography

15. Manage an idioventricular rhythm.

• ECG shows a regular wide complex rhythm at 92/min with no clearly discernible atrial
activity, findings consistent with accelerated idioventricular rhythm (AIVR).
o rate is almost always less than 120/min and usually less than 100/min
• AIVR is postulated to result from abnormal automaticity in the subendocardial Purkinje
fibers.
• It is observed in up to 15% of patients who undergo reperfusion of an infarct-related
artery.
• Accelerated idioventricular rhythm is a common complication following coronary
reperfusion, generally benign and transient, and does not require intervention when it
occurs within 24 hours of reperfusion.

16. Manage anticoagulation therapy in a patient with a mechanical prosthetic valve.

• Lifelong oral anticoagulation with warfarin is recommended for all patients with a
mechanical prosthesis. Target INRs are:
o 2.5 for an aortic prosthetic valve without thromboembolism risk factors
o 3.0 for aortic prosthetic valve with thromboembolism risk factors, or any mitral
prosthesis
• All patients with mechanical prosthetic valves of any type, and most patients with
bioprostheses, should receive aspirin therapy.
17. Manage aortic dissection.

• First Step is to asses level of dissection using DeBakey

or Stanford (easier) classification as guides
management.
o Stanford Type A: Ascending Aorta
o Stanford Type B: Descending Aorta
• Dx: CTA Thoracic
o If unable to perform TEE

• Treatment:
• Stanford Type A: Surgery
• Stanford Type B: B-Blockade (Esmolol, Labetalol).
For hypertension that does not completely
respond to β-blockers, may use IV nitroprusside or
nicardipine if needed.
o Goal is to control HR and BP with target HR<60 and Systolic BP 100-120
o Surgery considered if evidence of end-organ ischemia, persistent severe
hypertension or pain, propagation of the dissection, aneurysm expansion, and
aortic rupture.

18. Manage atrioventricular nodal block after an acute inferior myocardial infarction.
o Atrioventricular Block after inferior MI is common as in Inferior MI usually supply to
RCA is affected and by consequence blood supple to AV and SA nodal artery is
compromised
o Treatment is to OBSERVE in inferior MI
o In contrary in Acute Anterior MI: Mobitz type 2 block may progress to complete heart
block and necessitates permanent pacing.

19. Manage chronic stable angina.

➢ All patients should undergo and be treated with risk factor modification,
cardioprotective medications, and antianginal medications.
o Engage in physical activity, weight loss, tobacco cessation, dietary changes,
diabetes mellitus control and blood pressure goal of <130/80 mmHg.
➢ Cardioprotective medications:
o Aspirin: low dose reduces risk of MI as effective as high dose but less risk of
bleeding.
o Clopidogrel: use for aspirin intolerant patients.
o Statins: recommended high statin as it decreased LDL by 50% or more.
 o ACE inhibitors: indicated in concomitant DM, hx of MI, CKD, Left ventricular
dysfunction EF <40%.
➢ Antianginal Medications:
o First line Therapy:
▪ Aspirin, high statin therapy and Beta Blockers.
▪ All Beta Blockers equally efficacious. Goal HR: 55-60/min.

Medications to reduce the frequency and severity of angina pectoris comprise:

• First Step:
o B-Blocker
o Long Acting Nitrate

• Continued Symptoms
o Increase B-Blocker Dose
o Increase Long Acting Nitrate
Dose

• Continued Symptoms
o Add Calcium Channel
Blockers
• Remember Ca Channel
Blockers Contraindicated in
patients with left ventricular
systolic dysfunction or
advanced atrioventricular
block.
• If on max doses of B-Blocker +
Ca-Channel Blocker + Nitrates
• Ranolazine, non-
nitrate, anti-anginal
effects not depend on
HR or BP reduction

If despite max therapy continues with Symptoms may consider referral for Coronary
Angiography for possible PCI vs CABG if suitable.

20. Manage Mobitz I second-degree heart block (Wenckebach).

• Progressive prolongation of PR interval until there is a Dropped Beat.
 • It generally carries a benign prognosis.
• Irregular R-R interval
• Frequently improves with exercise or increased sympathetic tone.
• Permanent pacemaker rarely needed, unless hemodynamically unstable

21. Manage peripheral artery disease.

• PAD is defined as Ankle Brachial Index (ABI) of 0.90 or below
o ankle-brachial index greater than 1.40 is uninterpretable, and a toe-brachial
index should be obtained for diagnosing peripheral arterial disease.
• Treatment:
o Cardiovascular Risk Reduction:
▪ Cessation of cigarette smoking
▪ A moderate or high-intensity statin is indicated in all patients with
PAD.
▪ Adequate BP control with goal of < 130/ 80mmHg.
▪ Antiplatelet therapy with aspirin or clopidogrel (as monotherapy)
▪ Annual Influenza vaccination
▪ Intensive diabetes control (goal of hemoglobin A1c should be ≤7%)
• meticulous attention paid to foot care.
o Supervised exercise rehabilitation
o Cilostazol
▪ Contraindicated in patients with heart failure NYHA Class III
▪ Phosphodiesterase inhibitor with antiplatelet and vasodilator activity.

o Endovascular or surgical revascularization is indicated for patients with

significant disability due to claudication who have had an inadequate
response to exercise or pharmacologic therapy.

22. Manage progressive angina.

▪ Always in angina asses therapy and if not at max dose increase
medication.
▪ If B-Blocker or Long Acting Nitrate @ Max Dose => Choose Ca Channel
Blocker
▪ If on Max doses of B Blocker + Ca Channel Blocker + Nitrates =>
Ranolazine
 ▪ Initial medical therapy in patients with ACS/UA: Oxygen if sat < 90% or if
respiratory distress present, nitroglycerin, beta blockers, statin therapy,
antiplatelet therapy with aspirin and a platelet P2Y12, anticoagulation.
▪ Early risk stratification
• TIMI score
o 0-2 low risk
o 3-4 intermediate risk
o 5-7 high risk
o Patients with intermediate and high risk have been shown to
benefit from early invasive strategy.
▪ May consider referral to Coronary Angiography

23. Manage recurrent atrial flutter.

• Atrial Flutter is an organized macro-reentrant tachycardia with discrete regular

atrial activity on ECG, usually with a rate of 250/min to 300/min
• Catheter ablation is the definitive treatment of typical atrial flutter.
• A rhythm control strategy is favored in atrial flutter because rate control may be
difficult and often requires high doses of more than one AV nodal blocker.
• Oral anticoagulation in patients with atrial flutter is approached in the same manner
as in patients with atrial fibrillation.
24. Manage venous ulceration.
• Diagnosis is usually made clinically, although duplex ultrasonography can be helpful in
evaluating venous reflux and obstruction, or if the diagnosis is unclear.
• Tx is directed towards three main areas:
o Reducing peripheral edema
o Creating a wound environment that is conducive to healing
o Treating any secondary infection that may present
• The mainstay of venous ulcer treatment consists of compression therapy, which
improves venous flow, reduces edema, and promotes fibrinolysis.
• Skin grafting may improve ulcer healing and is indicated in those who do not exhibit
appropriate wound healing after 12 months of medical care.
• Topical agents and systemic antibiotics do not promote healing. Only use if there are
signs of infection.
25. Predict the auscultatory findings in mitral stenosis.
• A tapping LV impulse in the precordium, a loud S1, an increased pulmonic component of
S2, a diastolic opening snap, and a diastolic rumble or low-pitched murmur at the apex
• Best in the left lateral decubitus position (at the apex).
• The opening snap, which is due to forceful opening of the mitral valve, occurs when the
pressure in the left atrium is greater than the pressure in the left ventricle.
• Interval between S2 and opening snap is short in severe mitral stenosis

26. Prevent recurrent supraventricular tachycardia.

• Class II agents (β-blockers) and class IV agents (nondihydropyridine calcium channel
blockers) are frequently used to slow heart rates in patients with supraventricular or
atrial arrhythmias; however, they should be avoided in patients who have atrial
fibrillation with pre-excitation (eg, WPW).
• For recurrent AVNRT despite drug therapy or intolerance of drug therapy, select
catheter ablation therapy. Avoid stressors like caffeine, alcohol, tobacco. Eat balance
diet and exercise.

27. Prevent sudden cardiac death.

• Primary prevention for the general population (w/o known cardiac disease):
o Management of risk factors for CHD (eg, Lipids, BP, glucose), otherwise no
additional screening is recommended.
o A heart healthy lifestyle, including physical activity, a heart healthy diet, and
abstinence or cessation of cigarette smoking, is recommended for the primary
prevention of SCD.
• Primary prevention for patients with known cardiac disease (eg, prior MI,
cardiomyopathy, or heart failure) who are at increased risk of SCD.
o Standard medical therapies that lower the incidence of SCA
o Heart failure:
▪ ACE-I, BB, Aldosterone Antagonist, Hydralazine, Nitrates
▪ ICD (if EF < 35%) and CRTD (if EF <35% and QRS >150)
o Hypertophic Cardiomyopathy:
▪ prior cardiac arrest
▪ massive myocardial hypertrophy (wall thickness ≥30 mm)
▪ family history of sudden cardiac death
▪ ventricular tachycardia
▪ unexplained syncope
• Secondary prevention of SCD
 o Management of survivors of SCA includes the identification and treatment of
acute reversible causes, evaluation for structural heart disease and/or primary
electrical diseases
o Usually with an ICD, is appropriate for most SCA survivors.

28. Recognize the indications for abdominal aortic aneurysm screening.

• U.S. Preventive Services Task Force guidelines recommend a one-time ultrasonographic
screening in men aged 65 to 75 years who are active or former smokers.
• risk factors for development of AAA are age, sex, smoking, and family history.
• Management:
o AAA <4 cm, U/S every 2-3 years
o AAA: 4.1-5.4 cm U/S every 6-12 months
o Surgery: If AAA > if 5.5 cm in diameter or increasing > 0.5 cm within a 1-year
interval

29. Select appropriate endocarditis prophylaxis.

• Prophylaxis is recommended for patients with
o Prosthetic cardiac valve
o Prosthetic material used for cardiac valve repair, including annuloplasty rings
and chords.
o Previous episode of infective endocarditis
o Congenital heart disease
▪ unrepaired cyanotic congenital heart disease
▪ completely repaired congenital heart defect with prosthetic material or
device during the first 6 months after the procedure
▪ repaired congenital heart disease with residual defects
o Valvulopathy following cardiac transplantation

• Antimicrobial prophylaxis is recommended for procedures involving incision or biopsy

of the respiratory tract mucosa, such as bronchial biopsy, tonsillectomy, and
adenoidectomy. In addition, recommended in periodontal procedures.
o Prophylaxis should be administered prior to dental procedures that involve
manipulation of gingival tissue or the periapical region of the teeth or
perforations if the mucosa.
o Prophylaxis is not recommended prior to nondental procedures
▪ Ex: TEE, GU procedures, GI procedures, inguinal hernia repair.
• Alternatives: (30-60 minutes prior to dental procedure)
o Amoxicillin 2gm PO
o Ampicillin 2gm IM or IV
 o Cefazolin 1gm IM or IV
o Cephalexin 2gm IV
o Ceftriaxone 1 gm IM or IV
o Allergic to Penicillin
▪ Clindamycin 600mg PO IM or IV
▪ Azythromycin/Clarithromycin 500mg PO

30. Select the appropriate cardiac stress test for a patient with a permanent pacemaker.
• Patients with abnormal baseline ECGs that may interfere with the interpretation of the
exercise stress test (for example, left bundle branch block [LBBB], left ventricular
hypertrophy with ST-segment abnormalities, or a paced rhythm) should undergo
Pharmacologic Stress Testing.
o Vasodilator nuclear perfusion stress imaging (Adenosine or Dipyrimadole)
▪ Contraindicated in Hx of Asthma/COPD or allergy to Theophylline.
o Dobutamine stress echocardiography
▪ Indicated if Hx of Asthma/COPD or allergy to Theophylline.
▪ B-Blockers must be held before the test

31. Treat a right ventricular infarction.

• Classical Hx if a Male patient who comes with CC of Chest Pain. V/S Hypotensive
MAP <65. Physical examination JVD and Clear Lung Fields.
• Nitrates given and led to worsening of Hypotension
o Patients with RV infarction are very preload sensitive (due to poor RV
contractility) and preload lowering agents such as nitrates worsen BP.
o Nitrates are contraindicated because they may worsen hypotension by
reducing preload.
• Treatment:
o Aggressive IVF resuscitation
o Use of inotropes like dopamine or dobutamine
o Reperfusion, particularly with primary percutaneous coronary intervention,
should be initiated as soon as possible.

32. Treat an acute myocardial infarction with a statin.

a. High-intensity statin ASAP after the diagnosis of ACS is made: Atorvastatin 40-80
mg daily or Rosuvastatin 20 or 40 mg daily regardless of baseline LDL-C level, and
should continue indefinitely.

33. Treat obstructive hypertrophic cardiomyopathy.

• Avoid strenuous exercise and abstention from competitive sports.
• Avoid dehydration, excessive alcohol intake, and situational exposures that may result in
vasodilation and decreased preload (for example, saunas, hot tubs) because these may
provoke greater LVOT obstruction.
• Beta-Blockers are 1st line for patients, should be initiated with nonvasodilating β-
blockers titrated to maximum tolerance; carvedilol, labetalol, and nebivolol should be
avoided.
o Verapamil or diltiazem may be used in patients in whom β-blockers are not
tolerated or are contraindicated.
o 3rd line is Disopyramide if symptoms persist related to LVOT obstruction.
• Diuretics must be used cautiously and only if symptoms of dyspnea cannot be managed
with other therapy. Because of their propensity to exacerbate LVOT obstruction,
nitrates and phosphodiesterase type 5 inhibitors should not be used.
• Digoxin should be avoided in patients with atrial fibrillation because the positive
inotropic effects may worsen the LVOT gradient.
• For patients with persistent, severe, drug-refractory symptoms or Outflow tract
gradient >50mmhg or or in patients with recurrent syncope not related to arrhythmia:
Surgery or Septal ablation
• ICD implantation if:
o massive myocardial hypertrophy (wall thickness ≥30 mm)
o Abnormal blood pressure response to exercise
o Recent, unexplained syncope
o Nonsustained ventricular tachycardia on ambulatory electrocardiography
o family history of sudden death due to HCM
o Sustained ventricular tachycardia or resuscitated sudden death event

34. Treat venous insufficiency.

- Chronic venous insufficiency is a clinical diagnosis, but venous duplex Doppler
ultrasonography can be used if the diagnosis is in doubt and in those considering
intervention
- Conservative measures: Exercise, leg elevation, lifestyle changes (weight loss)
gradient compression stockings (20-50 mm Hg depending on the stage of
disease) are first-line therapies
o Skin care is also part of management
▪ Daily use of topical moisturizers may reduce skin breakdown and
prevent infection
o Sclerotherapy, thermocoagulation, or laser therapy for:
▪ Presence of bothersome spider veins and small varicose veins
o Venous ablation, stripping or excision for:
▪ confirmed reflux and persistent symptoms despite conservative
therapy
35. Treat ventricular arrhythmias in a patient with an implantable cardioverter-
defibrillator.
• In a patient with ventricular arrhythmia and ICD, despites ICD the patient should be
provided with external shock
• β-Blockers are first-line therapy for ventricular arrhythmia, although antiarrhythmic
therapy with sotalol or amiodarone or catheter ablation is often required for recurrent
VT.
• Amiodarone is among the most effective and commonly used antiarrhythmic drugs, is
frequently used to treat patients with recurrent VT or atrial fibrillation.
• Quinidine, Lidocaine may be beneficial in patients with recurrent ventricular
arrhythmias and/or ICD shocks after appropriate therapy with β-Blockers and
antiarrhythmic.
Additional Objectives from Prior Years:

1. Diagnose an acute ventricular septal defect.

• Acute VSD likely secondary to septal rupture after an MI
• Physical exam: loud holosystolic murmur located at the left sternal border that
often obliterates the S2 and may be palpable.
• Echocardiography: a moderate left-to-right shunt
• Cardiac Cathereization: STEP UP OXYGENTATION

2. Diagnose low-risk ventricular arrhythmia.

• For patients with bothersome palpitations, the first diagnostic test is an ECG.
• If the diagnosis is not established, 24- to 48-hour ambulatory monitoring is used to
diagnose and quantify the frequency of PVCs and determine if they are monomorphic or
polymorphic.
• Patients with frequent PVCs or polymorphic PVCs should undergo echocardiography,
stress test or other cardiovascular imaging (such as cardiac magnetic resonance [CMR]
imaging) to evaluate for the presence of structural heart disease.

3. Diagnose pericardial effusion.

• Initially asymptomatic
• Enlarged heart on chest radiographs
• Diminished (low-voltage) QRS complexes on EKG
• Progression of the effusion causes early symptoms and signs of cardiac tamponade:
dyspnea, orthopnea, chest pain, JVD, muffled heart sounds and hypotension.
• Echo is essential to establish the diagnosis before development of cardiac arrest.

4. Manage acute pericarditis.

• For analgesia and treatment of pericardial inflammation, NSAIDs provide effective relief
in 70% to 80% of patients.
• Relatively high doses of these medications are required (aspirin, 650-1000 mg every 6
to 8 hours; ibuprofen, 400-800 mg every 8 hours; indomethacin, 50 mg every 8 hours).
• Slow tapering over a period of 2 to 4 weeks is recommended to reduce the risk of
recurrent inflammation.
• In patients with pericarditis associated with myocardial infarction (Dressler syndrome),
treat with aspirin. These agents can impair myocardial healing and increase the risk of
mechanical complications in these patients.
5. Manage asymptomatic aortic stenosis.
• Mild: VMax 2-2.9 m/s and Mean Gradient <20mmHg => Echo every 3-5 years
• Moderate VMax 3-3.9 m/s, Mean Gradient 20-39mmHg => Echo every 1-2 years
• Severe: V Max>4m/s, Mean Gradient > 40mmHg and AVA <1.0cm=> Echo every
6-12 months

6. Manage cardiogenic shock.

• The initial therapy for cardiogenic shock includes vasoactive medications to increase
cardiac output and raise blood pressure through peripheral vasoconstriction.
• Patients with cardiogenic shock secondary to progressive heart failure are generally
given an inotropic agent, such as dobutamine or milrinone.
• For patients with symptomatic hypotension and end-organ dysfunction despite
vasopressor therapy, mechanical therapy should be considered.
o Mechanical support options include intra-aortic balloon pumps and
percutaneous or surgically implanted short-term mechanical ventricular assist
devices (VADs).

7. Manage ventricular fibrillation in a patient with acute myocardial infarction.

• Ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation) that occur in
the first 24 hours after STEMI diagnosis do not typically affect prognosis, require
antiarrhythmic medications, or require defibrillator implantation.
• The occurrence of recurrent ventricular arrhythmias later in hospitalization is associated
with a larger infarct and higher short- and long-term morbidity and mortality.

8. Preoperatively manage coronary artery disease.

• Patients with known CAD should not undergo elective noncardiac surgery within 30
days of bare metal stent implantation or 12 months of drug-eluting stent (DES)
placement, and dual antiplatelet therapy should not be interrupted during this time
frame.
• Optimally, surgery should be delayed for 12 months after DES placement. However, if
the risk of further surgical delay is thought to be greater than the expected risk of
ischemia and stent thrombosis, noncardiac surgery after DES implantation may be
considered after 180 days; in this case, aspirin should be continued and if the second
antiplatelet agent is withheld, the window of time off the agent should be as short as
possible.
• Antiplatelet therapy must also be managed carefully to balance the bleeding risks of
perioperative continuation and the thrombotic risks of cessation.
• Statins may also provide perioperative cardiac risk reduction, and limited data suggest
this benefit can be seen even when initiated shortly before surgery.
• Individuals who qualify for statin therapy according to the 2013 ACC/AHA cholesterol
treatment guidelines should begin this therapy preoperatively.
• Statins should also be continued perioperatively in patients already taking them.
• ACC/AHA guidelines do not recommend routine postoperative surveillance with ECG or
measurement of cardiac biomarkers unless symptoms of an acute coronary syndrome
are present.

9. Treat digoxin toxicity.

• Correct electrolytes, B-blockers, Lidocaine/Phenytoin.
• Digoxin immune Fab (Digibind) is an immunoglobulin fragment that binds with digoxin
that only will be administered on presence of significant dysrhythmias (eg, severe
bradyarrhythmia, second- or third-degree heart block, ventricular tachycardia or
fibrillation) from digitalis toxicity.

10. Treat stage III heart failure in a patient who is African American.
• Nitrate + Hydralazine to standard heart failure therapy is associated with
improvements in quality of life and a mortality benefit in African American.