Dressler syndrome is a delayed, immune-mediated pericarditis that occurs after myocardial infarction, usually weeks after the initial cardiac injury.

In this episode, Chris and Mars review:

• Dressler syndrome versus early post-MI pericarditis
• Why timing is the key shelf clue
• Positional pleuritic chest pain, friction rub, fever, and pericardial effusion
• How to distinguish pericarditis from recurrent myocardial ischemia
• Why aspirin is preferred after myocardial infarction
• The role of colchicine
• Pericardial effusion, tamponade, recurrence, and constrictive pericarditis

Episode pearl: Pericarditis within days of an MI is usually local inflammation. Pericarditis several weeks later suggests the immune-mediated process of Dressler syndrome.

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Acute pericarditis is inflammation of the pericardium classically presenting with sharp, pleuritic chest pain that improves when sitting forward.

In this episode, Chris and Mars review:

• Classic positional chest pain and the pericardial friction rub
• Diffuse ST elevation and P R depression
• The four diagnostic criteria for acute pericarditis
• How to distinguish pericarditis from STEMI and myocarditis
• First-line treatment with aspirin or an NSAID plus colchicine
• Uremic and post-MI pericarditis
• High-risk features that warrant hospitalization
• Pericardial effusion, cardiac tamponade, and recurrent pericarditis

Episode pearl: Diffuse ST elevation plus positional pleuritic chest pain should make you think acute pericarditis—then look for an effusion and signs of tamponade.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Myocarditis is inflammation of the heart muscle that can present with chest pain, heart failure, arrhythmias, or cardiogenic shock.

In this episode, Chris and Mars review:

• The classic post-viral presentation
• Why myocarditis can mimic myocardial infarction
• Troponin, E C G, echocardiography, and cardiac M R I findings
• Myocarditis versus pericarditis
• When endomyocardial biopsy is indicated
• Fulminant and giant-cell myocarditis
• Heart-failure and arrhythmia management
• Exercise restriction and return to activity
• Dilated cardiomyopathy and sudden cardiac death as important complications

Episode pearl: Elevated troponin means myocardial injury—not necessarily myocardial infarction. In the right clinical setting, think myocarditis.

Medicine Shelf Prep is sponsored by Scrub Battle.

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Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Restrictive cardiomyopathy is a diastolic heart failure syndrome caused by stiff, noncompliant ventricles that cannot fill normally.

In this episode, Chris and Mars review:

The classic *big atria, small ventricles** pattern

* Amyloidosis, sarcoidosis, hemochromatosis, and other major causes

* Kussmaul sign and right-sided heart failure findings

* How to distinguish restrictive cardiomyopathy from constrictive pericarditis

* Echocardiography and cardiac M R I

* Why diuresis must be used cautiously

* Cause-specific treatment including tafamidis, plasma-cell therapy, immunosuppression, and iron reduction

Episode pearl: Restrictive cardiomyopathy is a myocardial filling problem. When you see biatrial enlargement with nondilated ventricles and preserved systolic function, think restriction—and then determine the cause.

Medicine Shelf Prep is sponsored by Scrub Battle.

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Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Hypertrophic cardiomyopathy is an inherited myocardial disease characterized by unexplained left ventricular hypertrophy, impaired diastolic filling, and sometimes dynamic left ventricular outflow tract obstruction.

In this episode, Chris and Mars review:

* The classic genetics and asymmetric septal hypertrophy of HCM

* Systolic anterior motion of the mitral valve

* Why the murmur gets louder with standing and Valsalva

* Exertional dyspnea, angina, syncope, and sudden cardiac death

* Echocardiography and cardiac M R I findings

* Beta blockers as first-line treatment for symptomatic obstructive HCM

* Medications and volume changes that can worsen outflow obstruction

* Sudden-death risk assessment and implantable cardioverter-defibrillator indications

* Atrial fibrillation, anticoagulation, exercise, genetics, and family screening

Episode pearl: In obstructive HCM, a smaller left ventricular cavity means more obstruction—which explains both the murmur maneuvers and many of the treatment decisions.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Dilated cardiomyopathy is a major cause of heart failure with reduced ejection fraction characterized by ventricular dilation and impaired contractility.

In this episode, Chris and Mars review:

* The “big ventricle, weak squeeze” physiology of dilated cardiomyopathy

* Classic causes including alcohol, myocarditis, anthracyclines, genetic disease, peripartum cardiomyopathy, and tachycardia-mediated cardiomyopathy

* Key examination and echocardiographic findings

* How to distinguish dilated cardiomyopathy from ischemic, valvular, hypertrophic, and restrictive disease

* The role of cardiac M R I and genetic evaluation

* The four foundational medications for HFrEF

* Why reversible causes must be identified early

* Ventricular arrhythmias, sudden cardiac death, and left ventricular mural thrombus

* Why first-degree relatives may need cardiac and genetic screening

Episode pearl: A dilated, poorly contracting ventricle gives you the diagnosis pattern—but the next question should always be: why did it become dilated?

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Cardiogenic shock is a life-threatening state of inadequate tissue perfusion caused by severe cardiac dysfunction. The key is to recognize low-output physiology, support perfusion, and rapidly identify the underlying cause.

In this episode, Chris and Mars review:

• The classic hemodynamic pattern of cardiogenic shock
• How to distinguish cardiogenic shock from septic, hypovolemic, and obstructive shock
• Why cool extremities, elevated jugular venous pressure, pulmonary edema, oliguria, and rising lactate matter
• Norepinephrine as the preferred first-line vasopressor for hypotensive cardiogenic shock
• When to add an inotrope such as dobutamine or milrinone
• Why large fluid boluses can worsen left-sided cardiogenic shock
• Myocardial infarction as a major cause and the importance of emergency reperfusion
• Post-MI mechanical complications including papillary muscle rupture, ventricular septal rupture, and free wall rupture
• When persistent shock should prompt invasive hemodynamic assessment and consideration of temporary mechanical circulatory support

Episode pearl: Support the pressure with norepinephrine, support cardiac output with an inotrope when needed, and always treat the cause of the shock.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Heart failure with preserved ejection fraction, or HFpEF, is a form of heart failure caused primarily by impaired ventricular relaxation and reduced left ventricular compliance despite a preserved ejection fraction.

In this episode, Chris and Mars review:

• Why a normal ejection fraction does not mean normal cardiac function
• The classic HFpEF patient: older adults with hypertension, obesity, diabetes, chronic kidney disease, or atrial fibrillation
• The role of concentric left ventricular hypertrophy and diastolic dysfunction
• Classic symptoms and physical exam findings, including the S four
• How HFpEF is diagnosed using clinical heart failure plus evidence of elevated filling pressures or diastolic dysfunction
• Why obesity can lower B N P levels
• S G L T two inhibitors as foundational therapy
• Loop diuretics for congestion and the importance of blood pressure control
• Why HFpEF treatment should not simply copy the HFrEF medication regimen
• Management of associated conditions including atrial fibrillation, obesity, kidney disease, coronary disease, and sleep apnea

Episode pearl: Preserved ejection fraction does not mean preserved cardiac function. HFpEF is a filling-pressure problem caused by a stiff, poorly relaxing ventricle.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

Acute decompensated heart failure is a high-yield medicine shelf emergency where management depends on two key questions: Is the patient congested, and is the patient adequately perfusing?

In this episode, Chris and Mars review:

• Classic signs of pulmonary and systemic congestion
• Intravenous loop diuretics for volume overload
• Nitrates and noninvasive positive pressure ventilation in hypertensive pulmonary edema
• How to recognize cardiogenic shock
• Why norepinephrine is the preferred first-line vasopressor in hypotensive cardiogenic shock
• When to add an inotrope such as dobutamine or milrinone
• Cardiorenal syndrome and why a rising creatinine does not always mean diuresis should stop
• Common triggers for acute heart failure decompensation

Episode pearl: Congested but perfusing? Decongest. Hypotensive with end-organ hypoperfusion? Think cardiogenic shock.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.

ST-elevation myocardial infarction, or STEMI, is an acute coronary emergency caused by coronary plaque rupture and thrombotic occlusion leading to transmural myocardial ischemia. The key is rapid recognition and immediate reperfusion.

In this episode, Chris and Mars review:

• Classic STEMI presentation and important atypical symptoms
• How to localize infarction using the E C G
• Why treatment should not wait for troponin or echocardiography
• Emergency reperfusion with percutaneous coronary intervention
• When fibrinolytic therapy may be considered
• Antiplatelet therapy, anticoagulation, statins, and nitroglycerin
• Recognition and management of right ventricular infarction
• Why nitrates can be dangerous in preload-dependent right ventricular infarction
• Major post-MI complications, including ventricular arrhythmias, papillary muscle rupture, interventricular septal rupture, and left ventricular free wall rupture

Episode pearl: In a clear STEMI, do not let additional testing delay reperfusion. Opening the occluded coronary artery is the priority.

Medicine Shelf Prep is sponsored by Scrub Battle.

Download Scrub Battle: CK in the iOS App Store for five new high-yield clinical questions every day, immediate answers and explanations, and daily individual and medical school leaderboards.

Use promo code MEDICINE1 for your first month free. Introductory offer limited to the first 500 users.