Quartz 5

Cardiology (11%)

50 min read

CONDUCTION DISORDERS & ARRHYTHMIAS

Premature Beats (PACs & PVCs)

General:

  • Typically benign unless high burden or severe symptoms
  • Symptoms from low “effective” HR (not every beat perfuses effectively)

Presentation:

  • Asymptomatic, palpitations, dyspnea, chest discomfort, dizziness
  • Can be in patterns or irregular

Treatment (if symptomatic/high burden):

  • Beta-blockers, CCBs, Ablation

Supraventricular Arrhythmias (SVAs)

Atrial Fibrillation (AFib)

EKG findings:

  • NO p-waves
  • Atrial rate >400 bpm; ventricular rate 80-200 bpm
  • “Irregularly irregular” rhythm (R-R intervals completely chaotic)

Types:

  • Paroxysmal: self-terminates
  • Persistent: sustained, requires intervention
  • Permanent: continuous

Rate Control Goals: 110 bpm (lenient) or 80 bpm (strict); lenient strategy equally effective with fewer meds

Treatment Strategies:

Rate Control:

  • Beta-blockers (first-line)
  • CCBs (diltiazem, verapamil)
  • Digoxin

Rhythm Control:

  • Antiarrhythmic drugs (amiodarone, sotalol, flecainide, dofetilide)
  • Cardioversion
  • Ablation

Stroke Prevention (Anticoagulation):

  • CHA₂DS₂-VASc score determines need for anticoagulation
  • Score ≥1 in men, ≥2 in women → anticoagulation indicated
  • DOAC preferred over warfarin (except mechanical valve, MS)
  • If refusing anticoagulation → ASA (less effective)

Do’s & Don’ts:

  • Don’t cardiovert without anticoagulation (risk of thromboemboli)
  • Do check rate control, assess for HF exacerbation
  • Do address underlying causes (HTN, CAD, HF, hyperthyroidism)

Atrial Flutter

EKG findings:

  • Rapid atrial rate 250-350 bpm
  • “Sawtooth” pattern between QRS complexes (characteristic)
  • Regular or regular with variable block (often 2:1 conduction)
  • Can have pattern (1:2, 1:3, etc.) or atypical

Treatment:

  • Rate control: BB, CCB, digoxin
  • Rhythm control: antiarrhythmics, cardioversion, ablation
  • Anticoagulation: same as AFib (CHA₂DS₂-VASc score)

Atrial Tachycardia

Definition: Regular rapid atrial rhythm (150-250 bpm) originating above the AV node EGG: P-wave visible (abnormal morphology); PR interval varies Etiologies: Reentry, automaticity, triggered activity Treatment: Address underlying cause, rate control (BB/CCB), ablation if refractory

Sick Sinus Syndrome (SSS)

Definition: Collection of disorders with abnormal sinus node function

Components:

  • Sinus bradycardia
  • Sinus pauses/arrest
  • Atrial tachycardia/flutter/fib
  • Bradycardia-tachycardia syndrome

EKG patterns: Alternating episodes of rapid rates followed by very slow rates

Etiology:

  • Congenital heart disease surgery (most common in young)
  • Adults >50 yo (degenerative)
  • Medications: digoxin, CCB, BB, adenosine

Treatment:

  • Treat underlying cause
  • Rate-control medications for tachycardia
  • Pacemaker (PPM) for bradycardia (definitive treatment)

Junctional Rhythm

Definition: Rhythm originating at AV node (fallback pacemaker) Rate: 40-60 bpm (slower than normal sinus) EKG: No P-wave OR P-wave after QRS (retrograde) OR P-wave buried in QRS Etiologies: AV block, digitalis toxicity, ischemia, post-op Treatment: Address underlying cause; pacing if symptomatic

Idioventricular Rhythm (IVR)

Definition: Rhythm from ventricular myocardium (escape rhythm) Rate: 20-40 bpm (very slow, last resort pacemaker) EKG: Wide QRS complexes, no P-waves Etiologies: Severe bradycardia, complete AV block, post-MI Clinical significance: Marker of severe conduction disease Treatment: Pacing if symptomatic

Ventricular Arrhythmias

Ventricular Tachycardia (VT)

Rate: 160-240 bpm EKG: Wide QRS (>120 ms), regular or slightly irregular rhythm AV dissociation is diagnostic (P-waves marching through at different rate)

Etiologies:

  • Ischemic heart disease (MC)
  • Hypoxemia
  • Electrolyte abnormalities (K, Mg, Ca)
  • Acid-base disorders
  • Medications (Class IA/III antiarrhythmics)
  • Cardiomyopathy/LV dysfunction

Hemodynamically Stable VT:

  • Palpitations, mild CP, mild SOB
  • Treatment: Amiodarone, sotalol, lidocaine IV; ablation

Hemodynamically Unstable VT:

  • Dyspnea, CP, syncope, cardiac arrest
  • Treatment: Synchronized cardioversion; IV amiodarone, IV magnesium; ablation; ICD for secondary prevention

Torsades de Pointes (“Twisting of the Points”)

Definition: Polymorphic VT with beat-to-beat twisting appearance Mechanism: Long QT interval predisposes

QT Prolongation Causes:

  • Medications (Class IA/III antiarrhythmics, antipsychotics, macrolides, fluoroquinolones)
  • Electrolyte abnormalities (↓K, ↓Mg, ↓Ca)
  • Congenital long QT syndromes
  • Female, bradycardia, sudden cardiac events

Symptoms: Palpitations → syncope → arrest

Treatment:

  • IV magnesium (first-line, even if Mg normal)
  • Correct electrolytes (especially K, Mg)
  • Remove QT-prolonging drugs
  • Beta-blockers

Ventricular Fibrillation (VF)

Definition: Complete disorganized ventricular activity Clinical: Cardiac arrest, pulseless, apneic Mechanism: Often progression from VT

Etiologies:

  • Acute MI
  • Severe cardiomyopathy/LV dysfunction
  • Hypoxia, electrolyte severe abnormalities
  • Hypothermia, trauma

Treatment:

  • Unsynchronized defibrillation (NOT cardioversion)
  • IV amiodarone
  • IV magnesium
  • CPR
  • ICD placement after resuscitation

QT Prolongation

Definition: Duration of ventricular depolarization + repolarization >460 ms (men) or >470 ms (women) Clinical Significance: Increased risk of torsades de pointes → syncope/arrest Risk: High-risk meds + electrolyte abnormalities + female sex + bradycardia

AV Blocks

First-Degree AV Block

Definition: Prolonged (but consistent) delay from atrial to ventricular conduction

EKG findings:

  • PR interval >200 ms (>5 small boxes, or >0.2 seconds)
  • All P-waves followed by QRS
  • Regular rhythm

Clinical: Usually asymptomatic Treatment: Identify and treat underlying cause; discontinue AV nodal blocking agents if symptomatic

Second-Degree AV Block, Type I (Mobitz I, Wenckebach)

Definition: Progressive PR prolongation until one QRS is “dropped”

EKG findings:

  • PR intervals progressively lengthen → dropped QRS
  • “Regularly irregular” pattern (same pattern repeats)
  • Narrow QRS complexes
  • Site: AV node

Clinical: Usually asymptomatic, benign Treatment: Treat underlying cause; PPM only if symptomatic (rare)

Second-Degree AV Block, Type II (Mobitz II)

Definition: Intermittent QRS drops WITHOUT progressive PR prolongation

EKG findings:

  • PR intervals remain normal or prolonged but CONSTANT
  • Randomly dropped QRS (not progressive)
  • “Regularly irregular” or “irregularly irregular” depending on pattern (2:1, 3:1, etc.)
  • Often wide QRS (conduction delay at bundle of His/distal)
  • Site: Bundle of His or distal

Clinical Significance: SERIOUS—risk of progression to complete block Treatment:

  • Pacemaker (required)
  • Discontinue AV nodal blocking agents
  • Treat underlying cause

Third-Degree AV Block (Complete Heart Block)

Definition: Complete dissociation between atrial and ventricular activity; no conduction A→V

EKG findings:

  • P-waves and QRS complexes march independently (no relationship)
  • Regular atrial rate, regular ventricular rate (different rates)
  • Regular R-R intervals
  • Rate: 30-60 bpm (junctional escape) or 20-40 bpm (ventricular escape)
  • QRS wide (if ventricular escape) or narrow (if junctional escape)

Clinical: Symptomatic bradycardia, syncope, arrest risk Treatment:

  • Pacemaker (required) — urgent if symptomatic
  • Discontinue AV nodal blocking agents
  • Temp pacing if unstable pending PPM placement

Bundle Branch Block (BBB)

Right BBB (RBBB):

  • EKG: RsR’ pattern in V1-V2 (“M-shaped” or “rabbit ears”)
  • QRS >120 ms
  • Clinical: May indicate right-sided pathology; monitor

Left BBB (LBBB):

  • EKG: Broad, notched R-waves in I, aVL, V5-V6
  • QRS >120 ms
  • Clinical: Implies structural heart disease (CAD, cardiomyopathy); LBBB = ASCVD risk

Clinical Significance:

  • Blocks themselves don’t require treatment
  • Identify underlying cause (MI, cardiomyopathy, congenital)
  • Monitor for progression to heart block
  • Note LBBB impairs stress test interpretation

PHARMACOLOGICAL MANAGEMENT OF ARRHYTHMIAS

Adenosine:

  • AV nodal blockade with very short half-life
  • Useful for paroxysmal SVT termination
  • Brief asystole expected (< 1-2 seconds)

Atropine:

  • Blocks vagal nerve
  • Increases HR (positive chronotrope)
  • Used in symptomatic bradycardia/AV block

Summary Table: Antiarrhythmic Drug Selection

RhythmClass II (BB)Class IaClass IbClass IcClass IIIClass IV (CCB)Other
Sinus Tachycardia✓✓
AFib/AFlutter✓✓✓✓✓
Paroxysmal SVT✓✓✓Adenosine
AV BlockAtropine
VT/VF✓✓✓✓Defibrillation
BradycardiaAtropine

Pearl: Not all drugs work in every class! Specific contraindications exist in HF and other disease states.

CONGENITAL HEART DISEASE

”Pink Babies” (Acyanotic—adequate oxygenation)

Patent Ductus Arteriosus (PDA)

Anatomy: Failure of ductus arteriosus (fetal shunt between pulmonary artery and aorta) to close after birth

Presentation:

  • Often asymptomatic or mild symptoms
  • If large: volume overload → HF (especially premature infants)

Physical Exam:

  • “Machinery” murmur (continuous throughout systole and diastole at left infraclavicular area)
  • Wide pulse pressure (hyperdynamic pulses)
  • Bounding pulses, hyperactive precordium

Diagnosis: TTE/TEE, cardiac cath Treatment:

  • NSAIDs (indomethacin, ibuprofen) to promote closure
  • Acetaminophen (emerging option)
  • Surgical/catheter closure if medical therapy fails

Coarctation of the Aorta

Anatomy: Narrowing of descending thoracic aorta, usually distal to left subclavian artery

Presentation:

  • Hypertension in upper extremities, hypotension in lower extremities (pathognomonic)
  • Weak/delayed femoral pulses (key finding)
  • May have associated Turner syndrome (or other syndromes)

Physical Exam:

  • “3 on 3” pulse pattern: Brachial pulses 3 beats strong, femoral pulses 3 beats delayed
  • Systolic ejection murmur (from stenosis and collateral vessels)
  • Upper extremity HTN, lower extremity hypotension

Diagnosis: CXR (rib notching from collaterals), TTE, MRI, cardiac cath Complications: LV hypertrophy, HF, aortic dissection, aneurysm Treatment: Surgical or catheter-based repair

Atrial Septal Defect (ASD)

Definition: Defect in atrial septum allowing L→R shunt

Types:

  • Ostium secundum (most common, 70%)
  • Ostium primum
  • Sinus venosus
  • Unroofed coronary sinus (rare)

Presentation:

  • Often asymptomatic in childhood
  • May develop signs later (exercise intolerance, AFib)
  • Risk of paradoxical embolism (if PFO-type)

Physical Exam:

  • Fixed, widely split S2 (key finding—doesn’t vary with respiration)
  • Systolic flow murmur (pulmonary) at left upper sternal border
  • May have RV heave (from RV volume overload)

Diagnosis: TTE (gold standard), cardiac cath Treatment:

  • Closure indicated if Qp:Qs >1.5 or symptoms
  • Surgical or catheter closure
  • Consider closure even if asymptomatic to prevent arrhythmias

Patent Foramen Ovale (PFO)

Definition: Probe-patent opening in atrial septum (normal variant during fetal life that persists) Clinical significance: Risk of paradoxical embolism (DVT clot crosses to systemic circulation via PFO) Diagnosis: TTE with bubble study (agitated saline) Treatment: Closure if paradoxical embolism documented

Ventricular Septal Defect (VSD)

Definition: Defect in ventricular septum allowing L→R shunt MC congenital heart defect (20-30% of all CHD)

Presentation:

  • Small defects: asymptomatic, incidental murmur
  • Large defects: HF symptoms (dyspnea, poor feeding, failure to thrive), cyanosis if Eisenmenger develops

Physical Exam:

  • Holosystolic (pansystolic) murmur at left lower sternal border (best heard with diaphragm)
  • Thrill may be palpable
  • Signs of HF if large defect

Diagnosis: TTE (gold standard) Natural history: Many small VSDs close spontaneously Treatment:

  • Closure indicated if: Qp:Qs >1.5, symptoms of HF, or large shunt
  • Surgical or catheter closure

”Blue Babies” (Cyanotic—inadequate oxygenation)

Tetralogy of Fallot (TOF)

Definition: Most common cyanotic congenital heart defect Embryology: Anterior deviation of infundibular septum causes 4 defects

The “Tet” (4 Defects):

  1. Ventricular septal defect (VSD)
  2. Right ventricular outflow tract obstruction (infundibular/valvular pulmonary stenosis)
  3. Overriding aorta (receives blood from RV and LV)
  4. Right ventricular hypertrophy (RVH) (compensatory, from increased workload)

Presentation:

  • “Blue baby” (degree of cyanosis depends on severity of RV outflow obstruction)
  • Cyanosis usually appears in first weeks/months of life
  • “Tet spells” — sudden episodes of severe cyanosis, SOB, syncope (from dynamic RVOT obstruction)
    • Triggered by crying, defecation, exertion
    • Mechanism: RV contracts harder → pulmonary stenosis worsens → R→L shunt increases → cyanosis
    • Infant squatting position increases SVR → decreases R→L shunt (self-protective)

Symptoms:

  • Cyanosis
  • Poor feeding, failure to thrive
  • Exercise intolerance (dyspnea, “word dyspnea”)
  • Clubbing (chronic cyanosis)

Physical Exam:

  • Cyanosis, clubbing
  • Single S2 (from pulmonary stenosis)
  • Systolic ejection murmur at left sternal border (from pulmonary stenosis, NOT VSD murmur)
  • Boot-shaped heart on CXR (due to RVH and small pulmonary artery)

Diagnosis: Clinical + CXR + TTE (confirms anatomy)

Management:

  • Tet spells: Knee-chest position, oxygen, morphine, beta-blockers, IV fluids
  • Surgical repair: Definitive; usually in infancy

Transposition of the Great Arteries (TGA)

Definition: Aorta arises from RV, pulmonary artery arises from LV (embryologic discordance) Frequency: 3% of all CHD, 20% of cyanotic CHD

Physiology: Incompatible with life unless there’s a way for oxygenated and deoxygenated blood to mix (PDA, ASD, or PFO)

Presentation:

  • Often NOT apparent in utero (fetal circulation accommodates)
  • Presents in first hours/days of life with severe cyanosis
  • Respiratory distress, tachypnea
  • Mild/no murmur

Classic findings:

  • “Egg on string” appearance on CXR (narrow mediastinum, right aorta)
  • Single, loud S2 (no physiologic splitting; aorta anterior)
  • Cyanosis NOT responsive to high-flow O₂ (shunt is right-to-left; mixing problem, not oxygenation)

Diagnosis: TTE, cardiac catheterization

Emergency management:

  • Prostaglandin E₁ (PGE₁) infusion to keep ductus arteriosus open (allows mixing)
  • Balloon atrial septostomy (Rashkind procedure) to enlarge PFO and improve mixing
  • Definitive: Arterial switch operation (Jatene procedure)

CARDIOMYOPATHIES

Dilated Cardiomyopathy (DCM)

Definition: Enlarged ventricle with systolic dysfunction (LVEF <35-40%)

Etiologies:

  • Alcohol (most common reversible cause)
  • Myocarditis (viral, autoimmune)
  • Peripartum (pregnancy-related; can be reversible)
  • Chemotherapy (doxorubicin, trastuzumab)
  • Hypothyroidism
  • Genetic/familial
  • Idiopathic

Pathophysiology: Loss of contractility → ↓ CO → compensatory mechanisms (SNS, RAAS activation) → further remodeling → HF

Presentation:

  • Dyspnea, fatigue, orthopnea, PND
  • Edema, ascites (volume overload)
  • Low cardiac output (cool extremities, AMS)
  • Arrhythmias (AFib, VT from reentry)

Physical Exam:

  • Displaced, diffuse PMI
  • S3 gallop
  • Murmur of MR (from papillary muscle dysfunction/annular dilation)
  • Rales, JVD, hepatomegaly

Diagnosis: TTE (enlarged LV, LVEF <35-40%), EKG (nonspecific), cardiac biomarkers (BNP/NT-proBNP elevated)

Treatment:

  • Guideline-directed medical therapy (GDMT) for HFrEF:
    • ACE-I/ARB/ARNI
    • Beta-blockers
    • Aldosterone antagonist
    • SGLT2i
  • Diuretics for congestion
  • ICD if LVEF ≤35% after optimal medical therapy
  • CRT if LBBB + LVEF ≤35%
  • Treat underlying cause (alcohol cessation, hypothyroidism)

Hypertrophic Cardiomyopathy (HCM)

Definition: Abnormal left ventricular hypertrophy (usually septum) with PRESERVED or improved systolic function

Genetics:

  • Autosomal dominant (most common inherited cardiomyopathy)
  • Mutations in sarcomeric proteins
  • NOT always obstructive

Pathophysiology:

  • Diastolic dysfunction (stiff ventricle impairs filling) → ↑ diastolic pressures
  • May have left ventricular outflow tract (LVOT) obstruction (dynamic, worsens with ↓ afterload)
  • Arrhythmia substrate from disorganized fibers

Presentation:

  • Often asymptomatic (discovered incidentally on echo)
  • Syncope (exertional; from LVOT obstruction or arrhythmia)
  • Dyspnea (from diastolic dysfunction)
  • Common cause of sudden cardiac death in young athletes

Physical Exam:

Murmur (if obstructive):

  • Systolic crescendo-decrescendo (midsystolic ejection murmur)
  • Increases with ↓ venous return (Valsalva, standing) — distinguishes from AS
  • Decreases with ↑ venous return (squatting, handgrip, leg raise)

Other findings:

  • S4 (atrial kick into stiff LV)
  • Sustained LV impulse (from hypertrophy)
  • Pulsus bisferiens (double-peaked pulse from LVOT obstruction)
  • Jerky carotid pulse

Diagnosis:

  • EKG: LVH + repolarization changes (deep T-wave inversions, especially lateral/inferior leads)
  • TTE (gold standard):
    • Septal wall thickening (usually ≥15 mm)
    • Small LV cavity
    • LVEF >70% (hyperdynamic)
    • Systolic anterior motion (SAM) of mitral valve (if obstructive)
    • Diastolic dysfunction
  • Cardiac MRI: Better characterization, late gadolinium enhancement (scar)

Treatment:

  • Lifestyle:
    • Avoid strenuous exercise/competitive sports
    • Avoid dehydration, excessive diuretics (↓ preload → worsens obstruction)
    • Avoid stimulants, alcohol
  • Medications:
    • Beta-blockers or non-dihydropyridine CCBs (first-line; reduce contractility, slow HR, improve filling)
    • Avoid vasodilators (ACE-I, ARB, dihydropyridine CCBs, diuretics) — worsen LVOT obstruction
    • Disopyramide (negative inotrope; if BB/CCB inadequate)
  • Interventional:
    • Septal myectomy (surgical) if LVOT obstruction refractory to meds
    • Alcohol septal ablation (percutaneous)
    • ICD if high-risk features (family hx SCD, massive LVH, syncope, abnormal BP response to exercise)

Restrictive Cardiomyopathy (RCM)

Definition: Normal or small ventricular size with diastolic dysfunction (impaired relaxation/filling)

Etiologies:

  • Cardiac amyloidosis (AL or ATTR—most common)
  • Sarcoidosis (cardiac involvement)
  • Hemochromatosis
  • Fabry disease
  • Prior chemotherapy (anthracyclines)
  • Radiation to chest
  • Hydroxychloroquine (chronic use)

Risk Factors:

  • Prior mantle/chest radiation
  • Anthracycline or hydroxychloroquine use
  • Family history

Pathophysiology:

  • Infiltrative or fibrotic process → stiff ventricle
  • ↓ filling → ↑ diastolic pressures → HF symptoms (despite preserved EF initially)
  • Risk of conduction abnormalities, arrhythmias

Presentation:

  • Dyspnea, fatigue, orthopnea
  • Lower extremity edema, ascites
  • Symptoms of HFpEF
  • Arrhythmias, syncope

Diagnosis:

  • TTE:
    • Normal or reduced LVEF
    • Dilated atria (from ↑ diastolic pressures)
    • Restrictive filling pattern on doppler
    • Findings vary by etiology
  • Cardiac MRI: Excellent for amyloidosis (late gadolinium enhancement pattern)
  • Cardiac biopsy: May be needed for definitive diagnosis (Congo red staining for amyloid)
  • Lab testing: Tissue typing for amyloid (AL vs ATTR), BNP/NT-proBNP

Treatment:

  • Treat underlying cause (amyloid-specific therapy, iron chelation, etc.)
  • BB/ACE-I/ARB for symptom management (but limited benefit; diuretics main therapy)
  • Monitor for arrhythmias (pacemaker/ICD as needed)
  • Fluid restriction, salt restriction
  • Diuretics for congestion

Stress Cardiomyopathy (Takotsubo)

Definition: Transient cardiac dysfunction triggered by acute physical or emotional stress

Synonyms: Stress-induced cardiomyopathy, apical ballooning syndrome

Pathophysiology: Likely catecholamine surge → transient LV dysfunction with characteristic apical wall motion abnormality

Presentation:

  • Acute onset chest pain/dyspnea following stressor (loss of loved one, accident, surgery, sudden surprise)
  • Mimics ACS (chest pain, ST elevation, troponin elevation)
  • More common in postmenopausal women

Mayo Clinic Diagnostic Criteria:

  1. Transient regional wall motion abnormalities (with or without apical involvement)
  2. Single epicardial coronary vascular distribution preceded by stressful trigger
  3. Absence of obstructive CAD or acute plaque rupture (normal coronaries on angiography)
  4. New EKG abnormalities (ST elevation/depression, T-wave inversions) + modest troponin elevation
  5. Absence of pheochromocytoma or myocarditis

Diagnosis:

  • Troponin (elevated but modest)
  • EKG (ST elevation, T-wave changes)
  • TTE: Regional wall motion abnormality (usually apical ballooning), reduced LVEF acutely
  • Coronary angiography: Normal coronaries (rules out ACS)

Treatment:

  • GDMT for HFrEF (ACE-I/ARB, BB, aldosterone antagonist, SGLT2i)
  • ASA, statin (secondary prevention)
  • LVEF typically recovers over 2-4 weeks
  • Continue BB, ACE-I/ARB/ARNI × 6 months even if LVEF normalizes
  • Most patients have complete recovery

HEART FAILURE

Classification by LVEF (2021 ACC/AHA/HFSA Guideline)

HFrEF (Heart Failure with reduced EF): LVEF ≤40%

  • HFimpEF: LVEF 41-49%
  • HFpEF: LVEF ≥50%

Clinical Stages:

  • Stage A: At high risk but no HF yet
  • Stage B: Structural disease but no symptoms
  • Stage C: Structural disease + symptoms
  • Stage D: Refractory/end-stage HF

Presentation & Physical Exam

History:

  • Dyspnea (exertional, orthopnea, PND)
  • Fatigue/exercise intolerance
  • Edema (peripheral, weight gain)
  • Weight loss/cardiac cachexia (advanced disease, low output)
  • Altered mental status (low output, renal dysfunction)

Physical Exam:

  • Vital signs: Pulse (brady/tachy), BP (hypo/hypertensive), weight trends
  • Cardiovascular:
    • JVD (elevated venous pressure)
    • S3 gallop (ventricular filling sound; indicates systolic HF)
    • S4 gallop (atrial contraction into stiff ventricle; diastolic HF)
    • Displaced PMI (LV enlargement)
    • RV heave (RV enlargement from pulmonary HTN)
  • Congestion:
    • Rales/crackles (pulmonary edema)
    • Peripheral edema (LE)
    • Hepatomegaly, ascites (RV dysfunction/elevated CVP)
  • Perfusion:
    • Cool extremities (low cardiac output)
    • Warm extremities (adequate perfusion)

Ischemic vs Nonischemic HF

Ischemic HF (HFrEF):

  • CAD/prior MI causes regional wall motion abnormality → global dysfunction
  • Regional wall thinning, aneurysm, MR

Nonischemic HF:

  • Cardiomyopathy (dilated, myocarditis, peripartum, toxic)
  • Valvular disease
  • Uncontrolled HTN
  • Arrhythmia-induced (VT, frequent PVCs, AFib)

Treatment of HFrEF (Reduced EF, LVEF ≤40%)

Guideline-Directed Medical Therapy (GDMT):

Cornerstone medications:

  1. ACE-Inhibitor/ARB/ARNI (reduces mortality)

    • ACE-I: lisinopril, enalapril, ramipril
    • ARB: losartan, valsartan
    • ARNI (Angiotensin-neprilysin inhibitor): Sacubitril/valsartan (Entresto) — preferred over ACE-I/ARB

  2. Beta-blockers (improves EF, reduces mortality)

    • Metoprolol succinate (extended-release)
    • Carvedilol
    • Bisoprolol
    • Target: Maximum tolerated dose

  3. Aldosterone antagonist (spironolactone, eplerenone)

    • Monitor K+ and renal function

  4. SGLT2 Inhibitors (newer class; proven benefit in HFrEF)

    • Empagliflozin, dapagliflozin
    • Reduces mortality, HF hospitalizations, improves symptoms

  5. Diuretics (for congestion, NOT mortality benefit)

    • Loop diuretics (furosemide, torsemide): first-line for congestion
    • Dose to euvolemic state, avoid excessive diuresis (worsens renal function)

Additional medications PRN:

  • Ivabradine (if HR >70 and EF ≤35% in SR)
  • Hydralazine + nitrate (especially in African American patients)
  • Digoxin (rarely; weak inotrope, improves symptoms but no mortality benefit; monitor levels)

Device therapy:

  • ICD (implantable cardioverter-defibrillator) if LVEF ≤35% after ≥3 months optimal GDMT
    • Reduces sudden cardiac death
  • CRT (cardiac resynchronization therapy/biventricular pacing) if LBBB + LVEF ≤35%
    • Improves EF, reduces HF hospitalizations

Lifestyle modifications:

  • Salt restriction (<2 g/day)
  • Fluid restriction (1.5-2 L/day if moderate-severe)
  • Daily weights (report if >2-3 lbs in 1 day)
  • Exercise program/cardiac rehab
  • Avoid NSAIDs (worsen HF, renal function)
  • Avoid excessive alcohol, illicit drugs
  • Vaccinations (influenza, pneumococcal)

HFrEF Do’s & Don’ts:

  • ✅ DO start ACE-I/ARB/ARNI, BB, aldosterone antagonist, SGLT2i
  • ✅ DO use diuretics for congestion
  • ✅ DO place ICD for EF ≤35%
  • ❌ DON’T use vasodilators without BB first (can worsen)
  • ❌ DON’T use calcium channel blockers (negative inotrope, except diltiazem if HR control needed)
  • ❌ DON’T use NSAIDs

Treatment of HFpEF (Preserved EF, LVEF ≥50%)

Pathophysiology: Diastolic dysfunction (impaired relaxation/filling) Common causes: HTN (most common), obesity, DM, CAD, AFib, restrictive physiology

Treatment:

  • Treat underlying comorbidities:

    • Aggressive BP control
    • Iron deficiency anemia screening/treatment
    • AFib rate control and anticoagulation
    • Diabetes management
    • Weight loss
    • CAD management

  • Cardiac rehab/exercise program (proven benefit)

  • Diuretics for congestion (main symptomatic therapy)

  • Limited GDMT benefit (BB, ACE-I/ARB for HTN control)

  • SGLT2i (emerging evidence of benefit)

  • Sodium-glucose cotransporter 2 inhibitor (SGLT2i): Empagliflozin, dapagliflozin (newer evidence for HFpEF)

  • Research studies (many ongoing; no single proven therapy yet)

VALVULAR HEART DISEASE

Aortic Stenosis (AS)

Definition: Narrowed aortic valve → ↑ LV pressure + hypertrophy → eventual ↓ LVEF

Etiologies:

TypeEtiologyValve ChangesAge of Symptom Onset
CongenitalUnicuspid, bicuspidProgressive calcification30-50s
Calcific (Degenerative)Age-relatedTrileaflet valve calcification60-80s
RheumaticPost-rheumatic feverFusion of commissures, thick fibrous leafletsVariable

Pathophysiology:

  • Stenotic valve increases afterload → LV hypertrophy (compensatory initially)
  • Concentric LVH maintains EF initially
  • Eventually → systolic dysfunction (LVEF ↓)

Presentation:

Classic triad (when severe):

  • Syncope (exertional; from fixed CO and cerebral hypoperfusion)
  • Dyspnea (exertional; from pulmonary edema)
  • Angina (chest pain; may have normal coronaries; from LVH and ↑ demand)

Other symptoms:

  • Palpitations, fatigue, orthopnea

Physical Exam:

Murmur:

  • Systolic ejection murmur (midsystolic)
  • Best heard at right upper sternal border
  • Radiates to carotids (distinguish from MR)
  • Increases with ↓ afterload (standing) and decreases with ↑ afterload (squat)

Other findings:

  • Weak, delayed carotid pulses (“pulsus parvus et tardus”)
  • Narrow pulse pressure (from fixed CO)
  • S4 (stiff LV)
  • Sustained LV impulse

Diagnosis:

  • EKG: LVH + repolarization changes (ST depression, T-wave inversion, left axis deviation)
  • CXR: Normal in early disease; later → cardiomegaly, pulmonary edema
  • TTE (gold standard):
    • Valve area, gradient (mean/peak)
    • Severity staging:
      • Mild: AVA 1.5-2 cm², mean gradient <25 mmHg
      • Moderate: AVA 1.0-1.5 cm², mean gradient 25-40 mmHg
      • Severe: AVA <1.0 cm², mean gradient >40 mmHg
    • LVEF (preserved until late)

Severity Assessment:

  • Mild: Asymptomatic, normal activity tolerance
  • Moderate: Asymptomatic or mild exertional symptoms
  • Severe symptomatic: Surgery indicated
  • Severe asymptomatic: Consider surgery if LVEF <50% or other markers of LV dysfunction

Medical Management:

  • No medical therapy slows progression
  • Avoid volume depletion (maintain preload)
  • Avoid vasodilators if severe (can worsen)
  • Manage HTN, coronary disease
  • Monitor closely; repeat echo every 1-2 years

Surgical Treatment (Definitive):

  • Surgical aortic valve replacement (SAVR)
  • Transcatheter aortic valve replacement (TAVR) — for high-risk/elderly patients
  • Indications: Symptomatic severe AS (Class I); asymptomatic severe with LV dysfunction, abnormal stress test, or need for other surgery

Mitral Stenosis (MS)

Definition: Narrowed mitral valve → ↑ LA pressure → pulmonary congestion

Etiologies:

  • Rheumatic heart disease (most common worldwide; post-rheumatic fever)
  • Congenital
  • RA tumor
  • Carcinoid syndrome
  • Endomyocardial fibrosis

Pathophysiology:

  • Stenotic MV impairs LV filling → ↑ LA pressure → pulmonary edema
  • AFib from LA enlargement/stretch

Presentation:

  • Dyspnea (exertional, orthopnea, PND)
  • Hemoptysis (from ruptured pulmonary vessels)
  • Palpitations (from AFib)
  • Syncope (from ↓ CO or arrhythmia)
  • Thromboembolism (AFib + LA thrombus)

Physical Exam:

  • Diastolic rumble at apex (best heard in left lateral decubitus position, with diaphragm)
  • Opening snap (early diastole; from abrupt opening of stenotic MV)
  • Loud S1 (forceful MV closure)
  • Atrial fibrillation (irregular rate)
  • Prominent a-wave on JVD (from forceful RA contraction against stenotic MV)
  • Signs of RV dysfunction (RV heave, hepatomegaly, RV S3)

Diagnosis:

  • EKG: AFib (usually present), LA enlargement (broad P-wave in lead II, bifid P-wave)
  • CXR: LA enlargement (double density), pulmonary edema (Kerley B lines), RV enlargement
  • TTE:
    • MVA <2.0 cm² = severe
    • Mean gradient >10 mmHg = significant stenosis
    • LA size, LVEF

Medical Treatment:

  • Rate control: Beta-blockers or CCBs (slow HR to allow LV filling)
  • Diuretics (for congestion)
  • Anticoagulation: Warfarin only (NOT DOACs) if AFib or prior LAA thrombus
  • Rhythm control: Aim to restore SR if possible (improves prognosis)

Surgical Treatment:

  • Percutaneous balloon mitral valvotomy (minimally invasive, good for stenosis without calcification)
  • Open commissurotomy (surgical)
  • Mitral valve replacement (MVR) (if heavily calcified or regurgitant)
  • Indications: Symptomatic MS with significant stenosis

Aortic Regurgitation (AI/AR)

Definition: Aortic valve leak → LV volume overload → LV dilation/dysfunction

Etiologies:

Valve-related:

  • Rheumatic heart disease
  • Endocarditis
  • Bicuspid aortic valve
  • Trauma

Aortic root/vessel-related:

  • Marfan syndrome (cystic medial necrosis → aortic root dilation)
  • Aortic dissection
  • Hypertension
  • Aortic aneurysm
  • Syphilis (luetic aortitis)
  • Ankylosing spondylitis
  • Takayasu arteritis
  • Giant cell arteritis

Pathophysiology:

  • Aortic leak → LV volume overload (from aortic diastole + mitral filling)
  • Eccentric LVH (volume overload type)
  • Progressive LV dilation and systolic dysfunction

Presentation:

  • Acute AI: Sudden hemodynamic compromise (anginal CP, pulmonary edema, shock)
  • Chronic AI: Often asymptomatic until advanced
    • Dyspnea, orthopnea (late finding)
    • Fatigue, exercise intolerance
    • Palpitations (forceful beats from large SV)
    • Chest pain (angina-like, from tachycardia and ↑ O₂ demand)

Physical Exam Signs of Chronic AR (Wide pulse pressure manifestations):

  • “Water hammer” pulses (bounding, rapid, collapsing) — palpate radial artery
  • Widened pulse pressure (↑ systolic, ↓ diastolic)
  • Hyperdynamic apical impulse (displaced lateral, hyperdynamic, hyperpulsatile)
  • “Pistol shot” pulses (Quincke sign — visible capillary pulsation in nailbed)
  • “Cannon” a-waves (prominent systolic waves from vigorous atrial contraction)
  • Bounding carotid pulses (“bisferiens” appearance)

Murmur:

  • Early diastolic blowing murmur at left upper sternal border (high-pitched, decrescendo)
  • Best heard with patient sitting forward, in full expiration
  • Austin Flint murmur (optional): Mid-diastolic rumble at apex (from AI jet hitting anterior mitral leaflet)

Diagnosis:

  • EKG: LVH + repolarization changes (ST depression, T-wave inversion)
  • CXR: Cardiomegaly, aortic root dilation, pulmonary edema (if advanced)
  • TTE (initial test):
    • Aortic root size (important for Marfan syndrome monitoring)
    • LV size/function (LVEF, LV dimensions)
    • AI severity (jet width, regurgitant volume)
    • Coexistent AS, MS
  • TEE: If TTE nondiagnostic or endocarditis suspected
  • Cardiac MRI: Better assessment of aortic root, LV function

Medical Management:

  • Vasodilators reduce regurgitant volume and symptoms
    • ACE-I/ARB (especially if aortic root dilation)
    • Calcium channel blocker (nifedipine)
    • Hydralazine
  • Beta-blockers: Slow HR (allows more diastole for filling; reduces regurgitation effect)
  • Avoid diuretics if possible (maintain preload for adequate LV filling)
  • Serial imaging: Monitor aortic root size, LVEF

Surgical Indications:

  • Symptomatic severe AR
  • Asymptomatic severe AR with:
    • LVEF <50%
    • LV end-systolic dimension >55 mm
    • LV end-diastolic dimension >80 mm
    • Aortic root >6 cm (Marfan syndrome: >5 cm)

Surgical options:

  • Aortic valve replacement (AVR)
  • Aortic root replacement (if aorta dilated; Bentall procedure or valve-sparing)

Mitral Valve Prolapse (MVP)

Definition: Systolic bulging of mitral leaflet into LA (prolapse)

Epidemiology:

  • Most common form of valvular heart disease (affects 2-3% of population)
  • Most benign valvular lesion (excellent prognosis)
  • More common in women, younger patients
  • Associated with Marfan syndrome, EDS, POTS

Classification:

  • Primary MVP: Myxomatous degeneration (congenital)
  • Secondary MVP: From rheumatic disease, HCM, etc.

Clinical Syndrome (MVP Syndrome):

  • Palpitations
  • Chest pain at rest (atypical, often musculoskeletal)
  • Fatigue, dyspnea on exertion (may be anxiety-related)
  • Syncope/lightheadedness
  • Anxiety (high association)

Physical Exam:

  • Mid-systolic click (acoustic phenomenon; from sudden tensioning of chordae tendinae)
  • ± Late systolic murmur (if MR present)
  • Clicks/murmurs vary with position (increase with standing/Valsalva, decrease with squatting/handgrip)

Diagnosis:

  • TTE (gold standard):

    • 2 mm superior displacement of mitral leaflets into LA in long axis

    • Myxomatous leaflet thickening (>5 mm)

    • MR assessment

Management:

  • Reassurance (excellent prognosis; most need no treatment)
  • Surveillance: TTE every 3-5 years
  • Beta-blockers: PRN for symptoms (palpitations, chest pain)
  • Avoid triggers: Caffeine, stimulants
  • Antibiotics: NOT routinely indicated (changed 2007); consider only in endocarditis risk (recent IE, complex cyanotic heart disease)
  • Restriction: Usually no activity restriction
  • Pregnancy: Generally safe

Complications (rare):

  • Infective endocarditis
  • Sudden death (very rare)
  • Progressive MR (usually degenerative in elderly)

Mitral Regurgitation (MR)

Definition: Mitral valve leak → LA volume overload → LA dilation, pulmonary congestion; LV volume overload

Etiologies (Causes):

Primary MR (valve pathology):

  • Rheumatic heart disease
  • Endocarditis
  • MVP (myxomatous degeneration)
  • Trauma (papillary muscle rupture)
  • Congenital

Secondary/Functional MR (LV/LA dysfunction):

  • Ischemic: Post-MI papillary muscle dysfunction or rupture, global LV dilation
  • Non-ischemic dilated cardiomyopathy: Global LV dilation from any cause
  • HypertensiveDisease: LV hypertrophy from HTN

Pathophysiology:

  • MR → backflow into LA → LA volume overload → LA dilation/AFib
  • Hyperdynamic LV from increased regurgitant flow
  • Progressive LV dilation if chronic

Presentation:

Acute severe MR:

  • Sudden pulmonary edema, shock, hemoptysis
  • Emergency (usually post-MI papillary muscle rupture, endocarditis)

Chronic MR:

  • Often asymptomatic (normal function)
  • Late: dyspnea, orthopnea, fatigue, palpitations (AFib)
  • Systolic murmur heard incidentally

Physical Exam:

Murmur:

  • Holosystolic (pansystolic) murmur at apex
  • Radiates to axilla (distinguish from AS which radiates to carotids)
  • Increases with ↑ afterload (handgrip, squatting)
  • Decreases with ↓ afterload (Valsalva, standing)

Other findings:

  • Hyperdynamic, displaced apical impulse (LV volume overload)
  • S3 gallop (from rapid LV filling)
  • Prominent CVP (if RV dysfunction)
  • Hepatomegaly, ascites (advanced)

Diagnosis:

  • EKG: LAD or LA enlargement, AFib (if chronic), LVH (if severe)
  • CXR: LA enlargement, pulmonary edema (if advanced)
  • TTE (initial diagnostic test of choice):
    • MR severity: Mild, moderate, severe (based on jet area, regurgitant volume, vena contracta)
    • LA size, LV size/EF
    • Mechanism (primary vs secondary)
    • Coexistent lesions

Management:

Medical (Limited benefit for asymptomatic MR):

  • Vasodilators (ACE-I/ARB): Reduce afterload, decrease regurgitant flow
  • Diuretics: For congestion
  • Beta-blockers: Control rate if AFib
  • Anticoagulation: If AFib or thrombus

Surgical Indications:

  • Symptomatic severe MR (dyspnea, HF)
  • Asymptomatic severe MR with:
    • LVEF <60%
    • LV end-systolic dimension >45 mm
    • AFib
    • Pulmonary HTN

Surgical options:

  • Mitral valve repair (preferred if possible; preserves function, better long-term outcomes)
  • Mitral valve replacement (if repair not possible)

Tricuspid Regurgitation (TR)

Definition: Tricuspid valve leak → RA/RV volume overload

Etiologies:

  • Functional/secondary (MC): From RV dilation (pulmonary HTN, LV failure, RV infarction)
  • Primary: Endocarditis, rheumatic, carcinoid, trauma, Ebstein anomaly

Clinical presentation:

  • RV dysfunction symptoms (fatigue, dyspnea)
  • Right-sided HF symptoms (hepatomegaly, ascites, peripheral edema)
  • Pulsatile hepatomegaly (“hepatic pulsations” with systolic impulse from RV pressure rise)

Physical Exam:

  • Pansystolic murmur at left lower sternal border (LLSB)
  • Prominent “cv wave” on JVD (large systolic waves)
  • JVD, peripheral edema, hepatomegaly

Diagnosis:

  • TTE: RV size, RVSP (from TR jet if present), RV function, underlying cause
  • EKG: Right axis deviation, RVH

Management:

  • Treat underlying cause (pulmonary HTN, LV failure, AFib)
  • Diuretics for volume overload
  • Management of pulmonary HTN (if present)
  • Surgical repair/replacement: Only if severe and fails medical therapy; less common than left-sided surgery

Pearl: TR in absence of PH usually doesn’t require surgery; improves with treatment of underlying RV dysfunction

Pulmonic Valve Disease

Pulmonic Stenosis (PS):

  • Etiologies: Congenital (MC), rheumatic, carcinoid
  • Systolic ejection murmur at left upper sternal border (LUSB), radiates to left shoulder
  • Treatment: Valvotomy if symptomatic or severe (RV pressure >50 mmHg)

Pulmonic Regurgitation (PR):

  • Etiologies: Pulmonary HTN (MC), idiopathic PA dilation, connective tissue disorders (Marfan), endocarditis
  • Early diastolic murmur at LUSB
  • Usually from RV dysfunction rather than valve pathology
  • Treat underlying cause

SHOCK

Types of Shock

TypeDefinitionEtiologyKey Finding
Cardiogenic↓ CO from cardiac dysfunctionMI, cardiomyopathy, VT, rupture, tamponade↓ CO, ↑ CVP, ↑ PCWP, cool skin
Hypovolemic↓ circulating volumeHemorrhage, dehydration, third-spacing↓ CO, ↓ CVP, ↓ PCWP, cool skin
Distributive↓ SVR, maldistribution of flowSepsis, anaphylaxis, sympathomimetic toxin↑ CO, ↓ SVR, warm skin, bounding pulses
ObstructivePhysical obstruction to flowPE, tamponade, tension pneumothorax, dissectionVariable (depends on cause)

Diagnostic Clues

SignHypovolemicCardiogenicDistributive
ExtremitiesCool, clammyCool, clammyWarm, bounding
Pulse pressure↓↓↔ or ↑
Cardiac output↓↓↔ or ↑
Venous O₂ sat↓↓↔ or ↑
Lactate↑↑↑
Echo findingsSmall IVC, empty ventriclesDistended IVC, RV/LV/valve dysfunctionNormal or hyperdynamic LV
CVP↓↑Variable

Initial Management

  1. Identify shock type (history, exam, imaging)
  2. Restore perfusion (fluids for hypovolemic; medications for others)
  3. Support oxygenation/ventilation
  4. Treat underlying cause

INFECTIOUS & INFLAMMATORY HEART CONDITIONS

Acute Pericarditis

Definition: Inflammation of pericardium

Etiologies:

  • Viral (MC, often enterovirus)
  • Bacterial (rare, often TB)
  • Autoimmune (SLE, RA, sarcoid)
  • Post-MI (Dressler syndrome)
  • Post-cardiac surgery
  • Neoplastic (lung, breast, lymphoma)

Classic Triad:

  1. Chest pain (pleuritic, positional; worse supine, better sitting forward)
  2. Pericardial friction rub (audible triphasic sound)
  3. Diffuse ST elevation on EKG

Presentation:

  • Acute chest pain (sharp, positional)
  • Dyspnea
  • Palpitations

Physical Exam:

  • Pericardial friction rub (best heard at LLSB, patient leaning forward)
  • Tachycardia
  • Low-grade fever (if viral)

Diagnosis:

  • EKG: Diffuse ST elevation (stage 1 acute; concave upward) → PR depression → ST normalization → T-wave inversion (stage 2-3)
  • Troponin: May be mildly elevated (myocardial inflammation)
  • TTE: Pericardial effusion (if present)
  • CRP/ESR: Elevated
  • Lab/imaging: Tailor to suspected cause (TB, autoimmune, neoplasm)

Treatment:

  • NSAIDs (high-dose, e.g., ibuprofen 800 mg TID)
  • Colchicine (reduces recurrence)
  • Corticosteroids (if autoimmune or post-cardiac surgery)
  • Treat underlying cause
  • Restrict activity until inflammation resolves

Complications:

  • Pericardial effusion (→ tamponade)
  • Constrictive pericarditis (chronic)

Pericardial Effusion

Definition: Fluid accumulation in pericardial space

Etiologies:

  • Pericarditis (viral, bacterial, autoimmune)
  • Malignancy (lung, breast, lymphoma)
  • Heart failure (transudative)
  • Renal failure (uremic)
  • Post-cardiac surgery
  • Hemorrhagic (trauma, anticoagulation)

Presentation:

  • Often asymptomatic
  • Dyspnea, orthopnea (if large or tamponade)
  • Chest pain (if pericarditis)

Diagnosis:

  • TTE: Size (small <1 cm, moderate 1-2 cm, large >2 cm), location
  • EKG: Low voltage (if large effusion)
  • CXR: Enlarged cardiac silhouette

Management:

  • Treat underlying cause
  • Serial echos to monitor size
  • Pericardiocentesis if symptoms or signs of tamponade
  • Diuretics if HF-related
  • NSAIDs if pericarditis

Cardiac Tamponade

Definition: Pericardial fluid accumulation → ↑ intrapericardial pressure → impaired diastolic filling → ↓ SV/CO → hypotension/shock

Pathophysiology:

  • Fluid restricts ventricular filling during diastole
  • ↑ intracardiac pressures equalize
  • Pulsus paradoxus (excessive BP drop during inspiration)

Etiologies:

  • Acute pericarditis with hemorrhagic effusion
  • Malignancy
  • Post-cardiac surgery/trauma
  • Hemopericardium (rupture, anticoagulation)

Presentation:

  • Dyspnea, chest pain
  • Tachycardia, hypotension
  • Beck triad:
    1. Hypotension
    2. JVD
    3. Muffled heart sounds

Physical Exam:

  • Pulsus paradoxus (SBP drops >10 mmHg with inspiration) — place on cuff, inflate above SBP, slowly deflate; note SBP at which Korotkoff sounds first heard intermittently (inspiration only) vs consistently (all phases)
  • JVD (elevated venous pressure)
  • Muffled heart sounds
  • Tachycardia
  • Hypotension (late, ominous finding)
  • Anxiety, restlessness

Diagnosis:

  • EKG: Low voltage (from damping effect of fluid)
  • CXR: Enlarged cardiac silhouette (“water bottle” silhouette)
  • TTE (gold standard):
    • Pericardial effusion
    • Diastolic RA/RV collapse (indicates hemodynamic significance)
    • Septal bounce (from pressure equalization)
    • IVC distension

Emergency Management:

  1. Pericardiocentesis (needle aspiration) — DEFINITIVE TREATMENT
    • Can be done blindly or with ultrasound/echo guidance
    • Even small amount of fluid (100 mL) can relieve symptoms
  2. Fluid resuscitation (temporary measure only; don’t delay pericardiocentesis)
  3. Supplemental oxygen
  4. Prepared for emergency surgery (if hemorrhagic or post-op)

Infective Endocarditis (IE)

Definition: Infection of heart valve(s) endocardium

Epidemiology:

  • Incidence: ~10-30 per million annually
  • Mortality: 18-23% at discharge, 22-27% at 6 months (HIGH)

Risk factors:

  • Prosthetic valve (especially early post-op)
  • Congenital heart disease (especially cyanotic, uncorrected)
  • IV drug use (IVDU)
  • Previous endocarditis
  • Rheumatic/degenerative valve disease
  • Immunosuppression

Causative organisms:

Native valve (most common):

  • Streptococcus species (50-60%): viridans strep (dental), pneumococcus, bovis
  • Staphylococcus aureus (20-30%): poor prognosis
  • Enterococcus
  • HACEK organisms (gram-negative fastidious)

Prosthetic valve:

  • Staph aureus, Staph epidermidis, Streptococcus, Enterococcus

IVDU (endocarditis):

  • Staph aureus (MC, 60%), often tricuspid valve
  • Pseudomonas, Candida
  • Right-sided more common in IVDU

Presentation:

  • Subacute: Low-grade fever, fatigue, malaise, arthralgias (can be indolent over weeks)
  • Acute: High fever, sepsis picture (especially Staph aureus)
  • Cardiac: New/worsening murmur, HF, arrhythmias, conduction delays

Classic clinical findings (Duke criteria — use for diagnosis):

Major criteria (2 needed):

  1. Blood cultures: Positive for typical IE organisms OR persistently positive
  2. Echocardiography: Vegetation, new regurgitation, prosthetic valve dehiscence

Minor criteria (cumulative):

  • Fever >38°C
  • Vascular phenomena: Janeway lesions (painless red macules on palms/soles), Osler nodes (painful nodules on fingertips/toe pads), Roth spots (retinal hemorrhages with white center), splinter hemorrhages (linear streaks under nails)
  • Immunologic phenomena: Roth spots, Osler nodes, rheumatoid factor, glomerulonephritis
  • Echocardiography findings consistent but not diagnostic
  • Predisposing condition (valvular disease, IVDU, PDA, VSD, coarctation)

Diagnosis:

  • Blood cultures (obtain 3 sets before antibiotics; must be sterile technique)

    • Hold for 5 days (fastidious organisms)

    • 90% positive if untreated

    • Negative in IVDU, prior abx, culture-negative IE

  • EKG: Look for conduction delays, AV block (abscess involvement)
  • TTE (first-line imaging):
    • Vegetations (typically on valve closure side)
    • Prosthetic valve dehiscence
    • New regurgitation
    • Abscess, fistula
    • Sensitivity ~60% (limited by acoustic windows)
  • TEE (better sensitivity ~95%): Especially for prosthetic valves, posterior lesions, complications
  • Labs: CBC (anemia), ESR/CRP (elevated), complement (low), rheumatoid factor (positive), UA (hematuria, casts)

Modified Duke Criteria diagnosis:

  • Definite: 2 major OR 1 major + 3 minor OR 5 minor
  • Possible: 1 major + 1 minor OR 3 minor

Treatment:

  • Empiric antibiotics (BEFORE identifying organism):
    • Vancomycin (covers staph including MRSA)
    • Typically add gentamicin (synergy against gram-negatives and streptococci)
  • Narrow based on cultures once organism/sensitivities known
  • Duration: ≥6 weeks (longer if prosthetic valve)
  • Infectious disease consultation (strongly recommended)

Poor prognostic indicators (associated with worse outcomes):

  • Staph aureus (most virulent)
  • Persistently positive blood cultures despite antibiotics (suggests vegetation, abscess, or immune suppression)
  • Heart failure (from severe regurgitation or abscess)
  • AV involvement (abscess)
  • Prosthetic valve endocarditis
  • Increased age
  • Paravalvular or myocardial abscess
  • Septic emboli

Complications:

  • Cardiac:
    • Acute regurgitation (vegetation on closure side of valve)
    • Abscess formation (myocardial, perivalvular)
    • Heart failure
    • Conduction abnormalities/AV block (from abscess)
    • Rupture (catastrophic)
  • Septic emboli: Stroke, septic embolization to organs, septic arthritis
  • Immune complex disease: GN, vasculitis
  • Relapse/recurrence: Despite adequate therapy

Surgical indications (Urgent/emergent):

  • Prosthetic valve endocarditis with dehiscence
  • Large vegetation (>10 mm, especially with emboli)
  • Heart failure from regurgitation unresponsive to medical therapy
  • Myocardial abscess (especially with conduction delay)
  • Fungal endocarditis
  • Culture-negative IE with large vegetations
  • Persistent sepsis despite antibiotics

Antibiotic Prophylaxis for Infective Endocarditis

Indicated for REASONABLE risk patients (at highest risk of adverse outcomes):

  • Prosthetic cardiac valves or material
  • Previous or recurrent infective endocarditis
  • Unrepaired cyanotic congenital heart disease (uncorrected)
  • Repaired congenital heart disease with residual shunts or regurgitation
  • Repaired congenital heart disease with catheter-based intervention involving occlusion device/stent (first 6 months)
  • Cardiac transplant with valve regurgitation (structurally abnormal valve)
  • LVAD patients

NOT indicated for:

  • MVP without regurgitation
  • Rheumatic/degenerative valve disease without above risk factors
  • Isolated PDA, ASD, VSD (most cases)

Procedures requiring prophylaxis:

  • Dental: Extractions, periodontal, implants, endodontic (if involves apex outside root canal)
  • Respiratory: Procedures involving manipulation of respiratory mucosa
  • GI/GU: For high-risk patients, avoid if possible; if needed, give prophylaxis

Regimens:

  • Dental/respiratory: Amoxicillin 2 g PO 30-60 min before (or ampicillin/cephalosporin/clindamycin if PCN-allergy)
  • GI/GU (high-risk only): Ampicillin + gentamicin

Myocarditis

Definition: Inflammation of myocardium

Etiologies:

  • Viral (MC: enterovirus, especially coxsackievirus B; also influenza, parvovirus B19, EBV, CMV)
  • Bacterial: Rare (TB, strep, meningococcus, Corynebacterium diphtheriae)
  • Autoimmune: Giant cell myocarditis, sarcoidosis, SLE, Behçet
  • Drugs/toxins: Alcohol, chemotherapy (doxorubicin), cocaine, catecholamines
  • Other: Chagas (T. cruzi), giant cell myocarditis

Pathophysiology:

  • Viral invasion + immune-mediated myocyte damage
  • Range from subclinical to fulminant cardiogenic shock

Presentation:

  • Often preceded by viral prodrome (fever, URI, GI symptoms 1-2 weeks prior)
  • Chest pain (can mimic ACS; pleuritic, positional)
  • Dyspnea, orthopnea (from HF)
  • Palpitations, syncope (from arrhythmias)
  • Fulminant: Cardiogenic shock, hemodynamic collapse

Physical Exam:

  • Low-grade fever, tachycardia
  • Signs of HF (S3, rales, JVD, edema)
  • Murmur if regurgitation

Diagnosis:

  • EKG:
    • Diffuse ST elevation (may mimic ACS but usually not in coronary distribution)
    • ST depression, T-wave inversions
    • AV block, arrhythmias
    • Nonspecific changes
  • Troponin: Elevated (myocyte injury)
  • BNP/NT-proBNP: Elevated (HF marker)
  • TTE:
    • Global or regional wall motion abnormality
    • Reduced LVEF (ranges from mildly reduced to severe)
    • Dilated LV (if myocarditis leads to cardiomyopathy)
    • Pericardial effusion (if concurrent pericarditis)
  • Cardiac MRI (gold standard for diagnosis):
    • Late gadolinium enhancement (LGE) pattern typical for myocarditis (subepicardial or mid-myocardial)
    • High sensitivity/specificity
  • Endomyocardial biopsy: If diagnosis unclear, giant cell myocarditis suspected, or fulminant course

Management:

  • Supportive care:

    • Bed rest (limit activity)
    • GDMT for HFrEF if EF reduced
    • Arrhythmia management

  • Medications:

    • ACE-I/ARB, beta-blockers, aldosterone antagonist (if HF develops)
    • NSAIDs (controversial; may worsen in some cases, but often used for symptom relief)
    • Immunosuppression (consider for giant cell myocarditis, fulminant myocarditis)
    • Antivirals (limited evidence)

  • Device support:

    • Mechanical circulatory support (ECMO, VAD) if cardiogenic shock/fulminant course
    • ICD if refractory arrhythmias

Prognosis:

  • Fulminant myocarditis: Better response to aggressive support (paradoxically) but high risk of death if untreated
  • Acute myocarditis: Majority recover fully with supportive care over weeks-months
  • Some progress to dilated cardiomyopathy (chronic myocarditis)

CORONARY ARTERY DISEASE (CAD) & ACUTE CORONARY SYNDROMES (ACS)

Stable Angina

Definition: Predictable chest pain from fixed coronary stenosis causing transient ischemia during stress

Characteristics:

  • Reproducible: Same triggers (exertion, emotion, cold)
  • Rapid onset: Builds quickly over seconds-minutes
  • Predictable duration: 5-15 minutes
  • Relieved by: Rest, nitroglycerin (within minutes)
  • Quality: Dull, squeezing, substernal; may radiate to neck, jaw, left arm, left shoulder

Associated symptoms:

  • Diaphoresis, dyspnea, nausea
  • NOT present at rest (distinguishes from unstable)

Risk factors (ASCVD):

  • Age, male, smoking, HTN, HLD, diabetes, family hx, obesity, physical inactivity

Physical Exam:

  • Often normal at rest
  • May have S3, S4 if prior MI or HF
  • Aortic stenosis murmur (if valvular cause)

Diagnosis:

  • Troponin: Negative (no myocyte necrosis)
  • EKG:
    • Often normal at rest
    • May show old infarct, LVH
    • ST depression or T-wave inversion during symptoms (ischemia)
  • Stress testing:
    • Positive = reversible ischemia (diagnostic)
    • Stress EKG, stress echo, nuclear imaging depending on baseline EKG/ability to exercise
    • Options: Treadmill, bicycle, pharmacologic (dobutamine, adenosine, dipyridamole)

Canadian Cardiovascular Society Classification:

  • Class I: Angina only with strenuous activity
  • Class II: Slight limitation of activity
  • Class III: Marked limitation
  • Class IV: Angina at rest

Treatment (GDMT):

Anti-ischemic:

  • Beta-blockers (reduce HR, contractility, BP) — first-line
  • Calcium channel blockers (non-dihydropyridines: diltiazem, verapamil) — alternative if BB C/I
  • Dihydropyridine CCBs (nifedipine, amlodipine) — combined with BB if needed
  • Long-acting nitrates (isosorbide dinitrate, isosorbide mononitrate) — tolerance with continuous use; need 10-14 hour nitrate-free interval
  • Ranolazine (partial oxidase inhibitor) — reduces late inward current, improves myocardial energetics

Antiplatelet:

  • ASA (75-325 mg daily) — reduces MI/stroke/death
  • P2Y12 inhibitor (clopidogrel, ticagrelor) — consider if ASA intolerant

Lipid-lowering:

  • High-intensity statin (atorvastatin 80 mg or rosuvastatin 40 mg)
  • Ezetimibe if LDL not at goal
  • PCSK9 inhibitor if still not at goal

Other:

  • ACE-I/ARB (especially if HTN, DM, LV dysfunction)
  • Diabetes management (target A1c <7%)
  • Blood pressure control
  • Exercise, smoking cessation, diet

Revascularization:

  • Percutaneous coronary intervention (PCI/stenting)
  • Coronary artery bypass graft (CABG)
  • Indication: When medical therapy inadequate, severe ischemia, suitable anatomy

Unstable Angina

Definition: Angina at rest or angina that changes in character (crescendo pattern)

Characteristics:

  • At rest OR during minimal exertion
  • New onset (weeks) OR previously stable angina worsens (different threshold, longer duration)
  • Crescendo angina (pattern of worsening exertional angina)
  • Duration: Often >20-30 minutes (unlike stable angina)

Pathophysiology:

  • Partial coronary occlusion from plaque rupture/erosion ± thrombosis ± vasospasm
  • May progress to complete occlusion → MI

Presentation:

  • Chest pain characteristics:
    • Retrosternal or epigastric location
    • Radiation to neck, jaw, left arm
    • Dull, squeezing, pressure sensation
    • Atypical presentations: Epigastric pain, dyspnea, weakness, nausea (especially women, elderly, diabetics)

Physical Exam:

  • Often normal
  • May have S4 (from LV dysfunction)
  • Systolic murmur (if MR, VSD from papillary muscle involvement)

Diagnosis:

  • Troponin: Negative (KEY DIFFERENCE from NSTEMI) — distinguishes unstable angina from AMI
  • EKG:
    • Variable changes; may be normal
    • ST depression/T-wave changes during symptoms
    • May revert to normal at rest
  • CXR: Normal or signs of HF

Risk Stratification:

  • HEART score, TIMI score — assess risk of recurrent ischemia/MI

Treatment (Reduce risk for MI progression):

Acute phase:

  • Antiplatelet:

    • ASA (300-325 mg loading, then 75-100 mg daily)
    • P2Y12 inhibitor loading: Clopidogrel 600 mg, ticagrelor 180 mg, prasugrel 60 mg

  • Anticoagulation:

    • Unfractionated heparin (UFH) or enoxaparin (LMWH)
    • Fondaparinux (if heparin C/I)

  • Beta-blockers: Target HR 50-60 bpm

  • Nitroglycerin: SL for acute symptoms, IV if persistent

  • ACE-I/ARB: Start if HTN, DM, or LV dysfunction

  • Statin: High-dose (loadingdose improves outcomes)

  • Calcium channel blocker: If BB C/I

Revascularization:

  • Coronary angiography: Usually recommended (±PCI/stenting)
  • Timing depends on risk stratification and ischemia

Acute Myocardial Infarction (AMI)

Definition: Myocardial necrosis from acute coronary insufficiency

Pathophysiology:

  • Coronary stenosis (atherosclerotic plaque rupture/erosion → thrombosis) reduces flow below critical threshold
  • Myocardial ischemia → necrosis if sustained

Presentation:

Symptoms:

  • Severe, intolerable chest pain (worse than stable angina)
  • Duration: 30 minutes to hours
  • Quality: “Crushing,” “constricting,” “compressing,” “squeezing”
  • Location: Substernal, may radiate
  • Associated symptoms (50%):
    • Nausea/vomiting
    • Dyspnea
    • Weakness, dizziness
    • Diaphoresis (cold sweat)
    • Sense of impending doom
    • Palpitations

Atypical presentations (women, elderly, diabetics):

  • Epigastric pain
  • Dyspnea without chest pain
  • Fatigue, weakness
  • Syncope

Physical Exam:

  • May be normal
  • Diaphoresis, pallor
  • Hypertension or hypotension
  • Tachycardia or bradycardia
  • S4 (anterior or inferior MI)
  • Systolic murmur (papillary muscle dysfunction/rupture, VSD)
  • Crackles/rales (pulmonary edema from LV dysfunction)
  • Signs of RV infarction (inferior MI — JVD, hypotension, RV heave)

Types (EKG differentiation):

STEMI (ST-Elevation MI)

Definition: Complete coronary occlusion → full-thickness transmural infarction

EKG findings:

  • ST elevation >1 mm in 2 contiguous leads (or >2 mm in V1-V3)
  • New LBBB (or RBBB with anterior STE)
  • Reciprocal ST depression in non-infarcted territory
  • Evolution:
    • Stage 1 (acute, hours): STE, peaked T-waves
    • Stage 2 (hours-days): T-wave inversion, Q-wave development
    • Stage 3 (days-weeks): Persistent Q-wave, T-wave normalization

Coronary territory & EKG changes:

TerritoryLeadsArteryRV involvement
AnteriorV1-V4LADNo
AnterolateralV5-V6, I, aVLLAD/LCxNo
InferiorII, III, aVFRCA (90%) or LCxYes (30%)
PosteriorV7-V9, or reciprocal ST depression in V1-V3RCA or LCxVariable
Right ventricular (RV)V4R, V5RRCA (usually)—

Q-waves (late manifestation):

  • Appear within hours to days
  • Indicate transmural infarction
  • Not in all STEMI (depends on collaterals)

Management (STEMI):

Primary goal: Restore coronary perfusion ASAP

Pre-hospital:

  • Aspirin 300 mg
  • Nitroglycerin (if SBP >90 mmHg, HR <60, RV infarction)
  • Oxygen (if SpO₂ <90%)
  • Pain control
  • Activate cardiac cath lab

In hospital (Acute phase):

  1. Primary PCI (PPCI) — PREFERRED (door-to-balloon <90 min)

    • Emergency coronary angiography
    • Percutaneous coronary intervention (stent ± thrombus aspiration)
    • Success rates >95%

  2. OR Fibrinolytic therapy (if PCI not available, door-to-drug <30 min)

    • tPA, reteplase, tenecteplase
    • Caution: Contraindications (active bleeding, recent surgery, severe HTN, stroke)

STEMI protocol (Acute medications):

  • Atorvastatin 80 mg (loading) ± 40 mg daily
  • Metoprolol (IV then PO; HR goal 50-60 bpm)
  • Dual antiplatelet therapy (DAPT):
    • ASA 300-325 mg loading, then 81 mg daily
    • P2Y12 inhibitor: Clopidogrel 600 mg, ticagrelor 180 mg, or prasugrel 60 mg
  • Anticoagulation: UFH 70-100 U/kg bolus (less in DAPT + bleeding risk)
  • Nitroglycerin: IV then switch to PO/topical (if tolerating)
  • ACE-I: Start (if EF reduced, anterior MI)

Special considerations:

Right Ventricular Infarction (RV MI):

  • Occurs in 30% of inferior MIs (RCA occlusion)
  • Key finding: ST elevation in V4R (obtain RIGHT-sided EKG)
  • Pathophysiology: RV loses preload-dependent function
  • Treatment: Aggressive IV fluids (unlike inferior MI where fluids may worsen symptoms)
  • AVOID: Nitroglycerin (worsens by reducing preload), diuretics
  • Monitor: JVD, hypotension

Mechanical complications:

  • Papillary muscle rupture → acute severe MR → cardiogenic shock
  • Ventricular free wall rupture → hemopericardium → tamponade
  • Ventricular septal defect (VSD) → L→R shunt

NSTEMI (Non-ST-Elevation MI)

Definition: Partial coronary occlusion → subendocardial infarction (nontransmural)

EKG findings:

  • NO ST elevation (this is the key difference)
  • ST depression (especially in territory of occluded artery) OR T-wave inversions
  • Normal EKG possible even with positive troponin

Troponin:

  • POSITIVE/ELEVATED (myocyte necrosis) — KEY DIFFERENCE from unstable angina
  • Rise and fall pattern (serial troponins)
  • Highly sensitive (modern assays)

Diagnosis:

  • Troponin elevation + compatible symptoms/EKG
  • Troponin becomes positive within 3-6 hours
  • May need serial troponins (repeat at 3 hours if initially negative)

Risk stratification:

  • TIMI score, GRACE score — assess risk of adverse events
  • Guide intensity of treatment

Management (NSTEMI):

Similar to unstable angina but with more intensive anticoagulation:

  • DAPT: ASA + P2Y12 inhibitor (load)
  • Anticoagulation:
    • UFH, LMWH, fondaparinux, or bivalirudin
    • Dose/choice based on renal function, bleeding risk
  • Beta-blocker
  • ACE-I/ARB
  • Statin (high-dose)
  • Nitroglycerin PRN

Coronary angiography:

  • Timing: Varies by risk
    • High-risk (shock, arrhythmias, hemodynamic instability): Urgent angiography (within hours)
    • Moderate-high risk: Angiography within 24 hours
    • Lower risk: Angiography within 72 hours or after stress testing

PCI/stenting: If suitable anatomy and ongoing ischemia

Diagnostic Testing in ACS

Troponin (cardiac troponin I or T):

  • Gold standard for myocardial necrosis
  • Highly sensitive/specific (modern assays)
  • Rises 3-6 hours after symptoms
  • Peaks at 24-48 hours
  • Remains elevated 10-14 days
  • Serial troponins improve diagnostic accuracy

EKG:

  • First diagnostic test
  • Obtain within 10 minutes of arrival
  • Interpret in context of symptoms
  • Arrhythmias, conduction blocks common

Echocardiography (TTE):

  • LVEF assessment (prognosis, guides therapy)
  • Wall motion abnormalities (helps localize infarct)
  • Complications: MR, VSD, free wall rupture, LV aneurysm
  • Thrombus: LV thrombus risk if anterior apical MI + reduced EF

Chest X-ray:

  • Pulmonary edema, cardiomegaly
  • Exclude other diagnoses (pneumonia, pneumothorax)

Coronary angiography:

  • Gold standard for diagnosis of CAD
  • Identifies culprit vessel, other lesions
  • Allows therapeutic intervention (PCI/stenting)
  • Timing depends on STEMI vs NSTEMI, risk stratification

BNP/NT-proBNP:

  • Prognostic marker
  • Elevated with reduced EF, HF

HYPERTENSION

Blood Pressure Categories (2017 ACC/AHA)

  • Normal: <120 and <80 mmHg
  • Elevated: 120-129 and <80 mmHg
  • Stage 1 HTN: 130-139 or 80-89 mmHg
  • Stage 2 HTN: ≥140 or ≥90 mmHg
  • Hypertensive crisis: >180 and/or >120 mmHg

Primary (Essential) Hypertension

Definition: Elevated BP without identifiable secondary cause (90-95% of cases)

Risk factors:

  • Age, obesity, physical inactivity, excess salt/alcohol
  • Family history, race (African American higher risk)
  • Sleep apnea, stress

Management:

  • Lifestyle modifications (weight loss, exercise, DASH diet, salt restriction)
  • Pharmacotherapy if:
    • Elevated BP x 3+ visits OR
    • CVD risk factors present
  • First-line antihypertensives:
    • Thiazide/thiazide-like diuretics (HCTZ, chlorthalidone)
    • ACE-I
    • ARB
    • Calcium channel blocker (CCB)
  • Combination therapy if monotherapy inadequate
  • Goal BP: <130/80 mmHg (especially if ASCVD, DM)

Secondary Hypertension

Definition: HTN from identifiable underlying cause (5-10% of cases)

When to suspect secondary HTN:

  • Age <30 with stage 2 HTN
  • Sudden worsening of previously controlled HTN
  • Failure to achieve BP control on 3+ medications
  • Hypokalemia WITHOUT diuretics → consider aldosteronism
  • Labile HTN (wide BP swings)
  • Headaches, palpitations, diaphoresis → pheochromocytoma
  • Renal failure after ACE-I → renal artery stenosis

Causes:

  • OSA (MC; prevalence rising)
  • CKD (from any cause)
  • Primary aldosteronism (hypokalemia, metabolic alkalosis)
  • Renal artery stenosis (atherosclerotic or fibromuscular dysplasia)
  • Cushing syndrome (MST, hirsutism, purple striae, weight gain despite HTN)
  • Pheochromocytoma (rare but important; episodic HTN, headache, diaphoresis, anxiety)
  • Coarctation of aorta (young, hypertension in upper extremities, weak femoral pulses)
  • Thyroid disease (hyperthyroidism → HTN; hypothyroidism → HTN)
  • Drug-induced: OCPs, NSAIDs, sympathomimetics, stimulants
  • Pregnancy: Gestational HTN, preeclampsia

Management: Treat underlying cause

Hypertensive Urgency

Definition: Markedly elevated BP (>180/120 mmHg) WITHOUT end-organ damage

Presentation: Often asymptomatic or mild headache

Management:

  • Can initiate or intensify oral medication
  • No need for IV medications
  • Close follow-up (24-48 hours)
  • Reassurance, address medication adherence

Hypertensive Emergency

Definition: Markedly elevated BP (>180/120 mmHg) WITH end-organ damage (acute organ dysfunction)

Signs of end-organ damage:

  • Hypertensive encephalopathy (severe HA, confusion, seizures, coma)
  • Acute MI, unstable angina
  • Acute pulmonary edema/HFpEF
  • Acute ischemic or hemorrhagic stroke
  • Aortic dissection
  • Acute renal failure
  • Microangiopathic hemolytic anemia

Goals:

  • Initial goal: Reduce MAP by 10-20% within 1st hour (avoid sudden drops → stroke risk)
  • Further reduction to <160/100 over next 2-6 hours

Treatment — Specific agents by scenario:

ScenarioFirst-lineAvoid
Ischemic/hemorrhagic strokeLabetalol, nicardipine—
Head traumaLabetalol, nicardipine (goal ↓ ICP)Hydralazine (unpredictable, can increase ICP)
Acute decompensated HFpEFLoop diuretics + vasodilators (NTG, hydralazine)BB (may precipitate acute decompensation)
ACS (MI/angina)IV NTG, IV BBHydralazine (reflex tachycardia increases demand)
Aortic dissectionIV BB first (reduce dP/dt), then vasodilator (NTG)Vasodilator alone (causes reflex tachycardia, worsens dissection)
Renal dysfunctionCautiously reduce BP; preserve renal perfusionAggressive reduction (worsens renal failure)
Sympathomimetic OD (cocaine, amphetamine)Phentolamine (direct alpha-blockade)BB monotherapy (unopposed alpha activity worsens HTN)
Iatrigenic (clonidine withdrawal)Vasodilators (NTG, CCB, hydralazine)Re-dosing clonidine can cause severe HTN

Common IV agents:

  • Labetalol: 20 mg IV q 10 min, titrate
  • Nicardipine: Infusion 5-15 mg/hr, titrate
  • Nitroglycerin: 5-100 mcg/min infusion
  • Hydralazine: 5-20 mg IV, less predictable
  • Esmolol: Short-acting BB for tachycardia

HYPOTENSION

Orthostatic Hypotension

Definition: Decrease in SBP >20 mmHg or DBP >10 mmHg OR pulse rise >15 bpm when transitioning from supine to standing

Symptoms:

  • Dizziness, lightheadedness
  • Blurred vision
  • Syncope, pre-syncope
  • Weakness

Etiologies:

  • Iatrogenic: Antihypertensive meds (especially diuretics, vasodilators), antipsychotics
  • Autonomic: Diabetes (neuropathy), Parkinson, multiple system atrophy
  • Hypovolemia: Dehydration, GI bleed, diuretics
  • Cardiac: Arrhythmia, valvular disease, cardiomyopathy
  • Spinal cord injury
  • Prolonged bed rest

Diagnosis:

  • Orthostatic vital signs: BP/HR supine × 5 min, then immediately standing (repeat if asymptomatic)
  • Tilt table test: More formal testing

Management:

  • Treat underlying cause
  • Increase fluid/salt intake
  • Compression stockings
  • Slow position changes (sit up, dangle legs, then stand)
  • Sleep with head elevated
  • Medication adjustment (reduce doses, change timing)
  • Consider fludrocortisone (mineralocorticoid) or midodrine (sympathomimetic)

Vasovagal Hypotension (Neurocardiogenic Syncope)

Definition: Sudden loss of consciousness from sudden BP drop and/or bradycardia

Triggers:

  • Emotional stress (fear, pain, blood drawing)
  • Prolonged standing
  • Micturition (post-void syncope)
  • Coughing, defecation
  • Swallowing

Prodrome:

  • Lightheadedness, nausea, diaphoresis, visual changes
  • Brief confusion/altered mental status

Recovery:

  • Quick regaining of consciousness (unlike seizure)
  • Postictal confusion unusual (unless prolonged ischemia)

Management:

  • Educate on triggers
  • Avoid prolonged standing
  • Increased salt/fluid
  • Leg crossing, muscle tensing at first sign
  • Medications (rarely needed): Beta-blockers, fludrocortisone, SSRIs

VASCULAR DISEASE

Superficial Thrombophlebitis

Definition: Thrombosis + inflammation of superficial vein

Presentation:

  • Pain, erythema, induration along vein
  • Palpable cord
  • Usually lower extremity (saphenous vein)

Etiologies:

  • Varicose veins (MC)
  • IV lines, catheters
  • Malignancy (Trousseau syndrome; migratory thrombophlebitis)
  • Thrombophilia (rare)

Diagnosis:

  • Clinical
  • Ultrasound to confirm

Management:

  • NSAIDs, leg elevation, compression
  • Antibiotics only if cellulitis/infection signs
  • Anticoagulation NOT routinely needed unless near SFJ (saphenofemoral junction) — then screen for DVT

Septic Thrombophlebitis

Definition: Infection of thrombosed vein; medical emergency

Etiologies:

  • Superficial thrombophlebitis that becomes infected
  • Contaminated IV line
  • Injection drug use

At risk:

  • Hospitalized patients, IVDU

Pathogens:

  • Staph aureus (MC)
  • Strep, gram-negatives

Presentation:

  • Persistent fever >3 days DESPITE antibiotics (key sign)
  • Bacteremia (despite appropriate AB)
  • Sepsis, shock
  • Localized vein tenderness, erythema, induration

Diagnosis:

  • Blood cultures (often positive)
  • Imaging: Ultrasound, CT with contrast
  • Elevated WBC, CRP, lactate

Treatment:

  • Broad-spectrum IV antibiotics: Vancomycin + piperacillin/tazobactam (Zosyn)
  • Explore, debride, or excise infected vein (NOT just antibiotics)
  • Anticoagulation (controversial; may be considered if major vessel)

Virchow’s Triad (DVT/PE Risk Factors)

  1. Venous stasis: Immobility, atrial fibrillation, cardiomyopathy, pregnancy
  2. Endothelial injury: Trauma, surgery, central lines, malignancy
  3. Hypercoagulability: Malignancy, thrombophilia, OCP, pregnancy, postpartum, surgery, sepsis

Deep Venous Thrombosis (DVT)

Definition: Blood clot in deep veins (usually legs)

Risk factors: Virchow’s triad components, malignancy, surgery, immobility, OCP/HRT, genetic thrombophilia

Presentation:

  • Unilateral leg swelling, pain, warmth
  • Pitting edema
  • Positive Homan sign (pain with dorsiflexion) — sensitive but not specific

Diagnosis:

  • Compression ultrasound (gold standard)
  • D-dimer (rule out if low pretest probability)
  • CT/MR if ultrasound nondiagnostic

Management:

  • Anticoagulation: DOAC (apixaban, rivaroxaban) vs LMWH/warfarin
  • IVC filter if absolute contraindication to anticoagulation
  • Thrombectomy/thrombolysis if massive DVT (phlegmasia cerulea dolens, limb threat)
  • Duration: 3 months (provoked), longer if unprovoked

Peripheral Arterial Disease (PAD)

Definition: Atherosclerotic narrowing of peripheral arteries (usually lower extremities)

Risk factors: Smoking (MC modifiable), age, HTN, HLD, diabetes, CKD

Symptoms:

  • Intermittent claudication: Pain, cramping in leg muscles with walking, relieved by rest
  • Critical limb ischemia: Rest pain (ischemic rest pain), tissue loss/ulceration, gangrene (limb-threatening)

Physical Exam:

  • Absent pulses (femoral, popliteal, dorsalis pedis, posterior tibial)
  • Decreased/delayed capillary refill
  • Pale or cyanotic skin, coolness
  • Muscle atrophy, hair loss
  • Ulcers (ischemic, non-healing)
  • Bruits (over stenotic arteries)

Diagnosis:

  • Ankle-brachial index (ABI): <0.9 diagnostic of PAD
    • Normal: 1.0-1.4
    • Borderline: 0.91-0.99
    • Mild-moderate: 0.71-0.90
    • Moderate-severe: 0.51-0.70
    • Severe: ≤0.50
  • Duplex ultrasound
  • CTA, MRA for surgical planning

Management:

  • Lifestyle: Smoking cessation (most important), exercise (supervised walking program), weight loss
  • Medications:
    • Antiplatelet (ASA, clopidogrel)
    • Statin (high-dose)
    • ACE-I (improves claudication)
    • Cilostazol (phosphodiesterase inhibitor, improves walking distance)
  • Revascularization:
    • Percutaneous intervention: Angioplasty, stenting
    • Surgery: Bypass grafting
    • Indication: Claudication limiting lifestyle, critical limb ischemia

Giant Cell Arteritis (Temporal Arteritis)

Definition: Large-vessel vasculitis with granulomatous inflammation

Epidemiology:

  • Age >50 (MC temporal artery involvement)
  • Higher in women, Scandinavian/Northern European ancestry
  • Associated with polymyalgia rheumatica (PMR) in 15-20%

Locations affected:

  • Temporal artery (MC, classic location)
  • Thoracic aorta (aortic arch syndrome → arm claudication, pulseless disease)
  • Internal/external carotids
  • Branches of aorta

Symptoms (Temporal artery involvement):

  • Unilateral headache (throbbing, temporal region; severe)
  • Jaw claudication (pain with chewing, talking, yawning) — highly specific
  • Visual symptoms: Diplopia, blurred vision, amaurosis fugax (transient monocular blindness) → permanent vision loss if untreated
  • Scalp tenderness
  • Fever, malaise, weight loss
  • Polymyalgia rheumatica: Morning stiffness in shoulders/hips, pain with movement

Physical Exam:

  • Tender, pulseless temporal artery
  • Decreased visual acuity, visual field defect
  • Jaw pain with palpation
  • Signs of large-vessel involvement (arm/leg claudication if aortic)

Diagnosis:

  • ESR, CRP (elevated, often markedly)
  • Temporal artery biopsy (gold standard; shows granulomatous inflammation with giant cells, fragmented internal elastic lamina)
    • Best within 1-2 weeks of symptom onset
    • Contralateral biopsy if first negative but high suspicion
  • Imaging: Ultrasound, PET scan (can assess for aortic involvement)

Management:

  • High-dose corticosteroids: Prednisone 1 mg/kg/day initially
    • Start BEFORE biopsy if high suspicion (prevents blindness; biopsy can be done within 1 week)
    • Taper slowly based on ESR/CRP and clinical response
  • Vision-threatening complications: IV methylprednisolone
  • Steroid-sparing agents: Methotrexate, azathioprine for long-term management
  • Monitor for steroid side effects; prophylaxis (PPI, calcium/vitamin D)

Prognosis:

  • Without treatment: Risk of permanent blindness (15-30%)
  • With treatment: Good response to corticosteroids; vision loss rare

Aortic Aneurysm

Definition: Permanent localized dilation of aorta >50% of normal diameter

Location:

  • AAA (abdominal aorta): MC location, MC type of aneurysm
  • TAA (thoracic aorta): Less common

Risk factors:

  • Smoking (MC modifiable risk factor)
  • Age (>60 years)
  • Male gender
  • Hypertension
  • Atherosclerosis/ASCVD
  • Family history
  • Connective tissue disorders: Marfan, Ehlers-Danlos, Loeys-Dietz

Presentation:

  • Often ASYMPTOMATIC (incidental finding on imaging)
  • AAA: Asymptomatic or steady gnawing pain in lower abdomen, back, flank
  • TAA: Chest, back pain

Rupture:

  • Hemodynamic instability, shock
  • Severe pain (abdominal, back, flank; constant)
  • Medical emergency

Physical Exam (AAA):

  • Pulsatile abdominal mass (may not be felt if obese or tight abdomen)
  • Femoral bruits
  • Absent femoral pulses (if aneurysm extends to iliac vessels)

Diagnosis:

  • Abdominal ultrasound:
    • Screening test
    • Measures aortic diameter
    • <3 cm normal; 3-4 cm borderline; >4 cm aneurysmal
    • AAA screening: Men >65 with smoking history (or known ASCVD); cost-effective
  • CT angiography (CTA):
    • Gold standard for diagnosis, measurement, operative planning
    • Shows size, location, involvement of branches

Management:

Asymptomatic, stable AAA:

  • Surveillance imaging:

    • <5 cm: Ultrasound every 2-3 years
    • 5-5.5 cm: Ultrasound every 6-12 months

    • 5.5 cm: Surgical repair usually recommended

  • Medical therapy:

    • Smoking cessation (critical to slow growth)
    • Blood pressure control with beta-blockers (reduce dP/dt, slow aortic expansion)
    • Statin (may slow progression)
    • Exercise program

Surgical repair:

  • Indication: Aneurysm >5.5 cm (standard); 5.0-5.5 cm if symptomatic, rapidly expanding, or connective tissue disorder
  • Options:
    • Open surgical repair (AAA/TAA): Definitive; invasive
    • Endovascular repair (EVAR): Less invasive; good for AAA if suitable anatomy

Ruptured AAA:

  • Medical emergency
  • Immediate surgical consultation
  • High mortality (50% pre-hospital, higher if reach OR)

Aortic Dissection

Definition: Tear in aortic intima → blood dissects into media → separates aortic layers

Classification:

  • Type A: Involves ascending aorta ± descending (requires surgery)
  • Type B: Descending aorta only, below left subclavian (usually medical management)

Risk factors:

  • Hypertension (MC)
  • Atherosclerosis
  • Connective tissue disease: Marfan, Ehlers-Danlos, Turner
  • Aortic aneurysm
  • Cocaine use (acute HTN)
  • Pregnancy (rare but increased risk)
  • Aortic coarctation

Presentation:

  • Severe, sudden, “tearing” or “ripping” chest pain (excruciating)
  • Radiation to back, interscapular region (classic)
  • Onset: Sudden (unlike ACS which is gradual)
  • May present as ACS: Mimics STEMI if involves coronary ostium
  • Syncope (rupture risk, severe shock)

Physical Exam:

  • HTN (early) or hypotension (if rupture)
  • Tachycardia
  • Pulse differential: Different BP/pulses between arms (Type A) or between upper/lower extremities
  • Focal neurologic deficit (if carotid/spinal artery involved)
  • Aortic regurgitation murmur (if dissection extends to aortic valve)

Key findings distinguishing from ACS:

  • Sudden onset (vs gradual ACS)
  • Severe, excruciating pain (vs ischemic pain)
  • Radiation to back (specific to dissection)
  • Normal or equivocal EKG (vs ST elevation in ACS)
  • Pulse differential (may be present)

Diagnosis:

  • CT angiography (CTA chest): Gold standard
    • Shows dissection flap, entry tear, extent, complications
    • High sensitivity (>95%) and specificity
  • TEE (transesophageal echo): Alternative if CTA unavailable; high sensitivity
  • MRI: Good for chronic dissection; too time-consuming for acute
  • Aortography: Invasive; rarely needed now

Management:

Type A (ascending — EMERGENCY):

  • Immediate CT to confirm
  • Emergent surgical repair (definitive)
  • Pre-operative medical management:
    • GOAL: Reduce BP and dP/dt (rate of change of pressure)
    • Start IV beta-blocker FIRST: Esmolol, labetalol (reduce dP/dt, prevent propagation)
    • Then add vasodilator: IV NTG, nicardipine (reduce BP)
    • Target: SBP 100-120 mmHg, HR 60 bpm, reduced pain
    • Avoid vasodilators alone (reflex tachycardia worsens dissection)

Type B (descending — usually medical):

  • Medical therapy: Beta-blockers + vasodilators
  • Target: SBP <120 mmHg, HR 60 bpm
  • Serial imaging: CTA to assess progression
  • Surgery/intervention: If expanding, rupture risk, symptoms, or malperfusion

Complications:

  • Aortic regurgitation, rupture, tamponade, malperfusion (limb, organ), false aneurysm

KEY CARDIOLOGY PANCE EXAM PEARLS

Arrhythmias:

  • AFib = irregularly irregular rhythm, no p-waves, treat with rate control ± anticoagulation
  • Flutter = sawtooth pattern, regular rhythm (if constant block)
  • VT vs SVT: AV dissociation diagnostic for VT; concordance suggests VT
  • Adenosine for PSVT (short-lived AV block)
  • Torsades = long QT + low K/Mg → IV Mg + correct electrolytes
  • BBB: RBBB = rsR’ V1 (rabbit ears); LBBB = broad R waves I, V6

Cardiomyopathy:

  • HCM murmur: Crescendo-decrescendo, ↑ with standing/Valsalva (↓ preload), ↓ with squat/handgrip (↑ preload) — treat with BB/CCB, avoid vasodilators
  • Dilated: Enlarged ventricle, ↓ EF, GDMT (ACE-I, BB, aldo antagonist, SGLT2i)
  • Restrictive: Stiff ventricle, diastolic dysfunction, often from infiltrative process (amyloid)
  • Stress (Takotsubo): Transient wall motion abnormality, normal coronaries, acute stressor, troponin mildly elevated

Congenital:

  • PDA: Machinery murmur, treat with NSAIDs (or PGE1 to keep open acutely)
  • Coarctation: Upper extremity HTN, weak femoral pulses, “3 on 3” sign
  • ASD: Fixed split S2 (doesn’t vary with respiration), volume overload from L→R shunt
  • VSD: MC congenital lesion, pansystolic murmur at LLSB
  • TOF: Blue baby, tet spells, “boot-shaped” heart, 4 defects (VSD, RVOT obstruction, overriding aorta, RVH)
  • TGA: Cyanotic newborn, “egg on string” CXR, single S2, cyanosis unresponsive to O₂ → PGE1 to keep ductus open → balloon septostomy

Valvular:

  • AS: “Syncope, dyspnea, angina” triad, systolic ejection murmur radiating to carotids, weak delayed pulses → surgery if symptomatic or EF ↓
  • AI: Wide pulse pressure, “water hammer” pulses, early diastolic murmur at LUSB → surgery if severe + EF <50% or dilated LV
  • MS: Diastolic rumble (apex), opening snap, loud S1, AFib risk → PBMV or surgery
  • MR: Pansystolic murmur radiating to axilla, hyperdynamic apical impulse → repair if possible
  • MVP: MC valvular lesion, mid-systolic click, benign → reassurance

CAD/ACS:

  • Stable angina: Predictable, exertional, relieved by rest/NTG (5-15 min), normal troponin, treat with BB, NTG, statin
  • Unstable angina: At rest or crescendo pattern, prolonged (>20 min), troponin NEGATIVE (differentiates from NSTEMI), treat with antiplatelet, anticoagulation, revascularization
  • NSTEMI: Troponin POSITIVE, ST depression or T-wave changes, DAPT + anticoagulation + β-blocker + statin
  • STEMI: ST elevation >1 mm in 2 contiguous leads, troponin ↑, PPCI <90 min or fibrinolytic <30 min
    • Anterior (LAD): V1-V4; inferior (RCA/LCx): II,III,aVF
    • RV MI (inferior MI + V4R ST elevation): Give fluids (not nitrates/diuretics)
  • Q-waves = transmural MI (late finding)

HF:

  • HFrEF: GDMT = ACE-I/ARB/ARNI, β-blocker, aldosterone antagonist, SGLT2i; avoid diltiazem (negative inotrope)
  • HFpEF: Treat comorbidities (HTN, DM, AFib), diuretics, cardiac rehab; limited pharmacotherapy
  • S3 = systolic HF (ventricular filling sound)
  • S4 = diastolic HF (atrial kick into stiff ventricle)

Shock:

  • Cardiogenic: ↓ CO, ↑ CVP, cool skin → echo, support LV; avoid fluids unless RV infarct
  • Hypovolemic: ↓ CO, ↓ CVP, cool skin → fluid resuscitation
  • Distributive (septic): ↑ CO initially, warm skin, bounding pulses, ↓ SVR → antibiotics, vasopressors

Pericardium:

  • Pericarditis: Pleuritic CP, friction rub, diffuse STE, NSAIDs + colchicine
  • Tamponade: Hypotension + JVD + muffled sounds = Beck triad, pulsus paradoxus → pericardiocentesis

Endocarditis:

  • Blood cultures first (before abx)
  • Duke criteria: 2 major OR 1 major + 3 minor
  • Vegetations on TTE/TEE
  • Vancomycin empiric (then narrow)
  • 6 weeks IV antibiotics minimum
  • S. aureus has worst prognosis

Aortic disease:

  • Aortic aneurysm: Smoker + HTN + >5.5 cm → surgery; surveillance <5.5 cm
  • Aortic dissection: Sudden excruciating chest pain radiating to back, pulse differential → BB first (reduce dP/dt), then vasodilator → Type A = surgery (urgent), Type B = medical

Graph View