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Cardiology Review: Heart Failure, Vascular Diseases, and Related Conditions

Cardiac preload, afterload, and basic hemodynamics

  • Preload: the amount/volume of blood returning to the heart. Factors increasing preload include: excessive fluids intake, high sodium intake, and valvular regurgitation.
  • Afterload: the resistance the heart must pump against; increased by high blood pressure and peripheral vasoconstriction.
  • Stroke volume (SV): the volume of blood ejected in a single contraction. Unit: mL.
  • Cardiac output (CO): the amount of blood the heart pumps per minute. Relationship: CO = SV imes HR where HR is heart rate.
  • Tachycardia in cardiogenic states: compensatory mechanism to raise CO when stroke volume is reduced.
  • Ejection fraction (EF): fraction of blood pumped out of the ventricle per contraction. Normal range: EF \,=\,\frac{SV}{EDV} \times 100\% \approx 50\%-70\%. A practical picture: the ventricle ejects about 50–70% of the end-diastolic volume.
  • Echocardiography and EF: Echo provides EF and helps categorize cardiomyopathy and filling status; software in ultrasound aids EF calculation.
  • Cardiorenal interactions: reduced cardiac output → reduced renal perfusion → hormonal responses that worsen heart failure (e.g., angiotensin release → vasoconstriction; aldosterone release → sodium and water retention → increased preload).
  • Cardiorenal syndrome: heart–kidney communication leading to fluid retention and worsened cardiac function.

Heart failure overview and classifications

  • Left-sided vs right-sided heart failure signs
    • Left-sided failure (left ventricle not pumping well or filling with problems): dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), basilar rales/crackles, exertional dyspnea, nocturnal cough, hemoptysis; S3 gallop.
    • Right-sided failure: signs of systemic venous congestion (jugular venous distension, hepatojugular reflux, ascites, peripheral edema, weight gain).
  • NYHA functional classes (clinical measure of symptoms)
    • Class I: at risk for symptoms but none with ordinary activity.
    • Class II: symptoms with ordinary activity.
    • Class III: symptoms with minimal activity (comfortable at rest; symptoms with ordinary activity).
    • Class IV: symptoms at rest; orthopnea and PND typical in advanced disease.
  • Common etiologies and phenotypes of heart failure
    • High-output heart failure: due to conditions with increased metabolic demand (hyperthyroidism, severe anemia, beriberi, sepsis, pregnancy, AV fistula). These are often reversible with treatment of the underlying cause.
    • Low-output heart failure: due to systolic dysfunction (reduced EF) or diastolic dysfunction (preserved EF with impaired filling).
  • Types of cardiomyopathy and filling states
    • Dilated cardiomyopathy: chamber dilation, systolic dysfunction (EF < 40%). Causes include viral myocarditis, alcohol, postpartum cardiomyopathy, chemotherapy-induced cardiomyopathy (e.g., doxorubicin).
    • Hypertrophic cardiomyopathy (HCM): thickened ventricular walls; can be obstructive or non-obstructive. Symptoms can include exertional chest pain and syncope; risk of ventricular arrhythmias.
    • Restrictive cardiomyopathy: stiff ventricular walls due to infiltration (e.g., amyloidosis, sarcoidosis, hemochromatosis) leading to diastolic dysfunction with relatively preserved EF.
    • Heart failure with preserved ejection fraction (HFpEF): diastolic dysfunction with EF typically ≥ 50%; filling is impaired due to stiff ventricle.
  • Examples of diastolic dysfunction and HFpEF contributors
    • Hypertension, hypertrophic cardiomyopathy, restrictive cardiomyopathy.
  • Pharmacologic and non-pharmacologic goals in HF management
    • Reduce preload and afterload to decrease cardiac workload.
    • Lifestyle: weight reduction, exercise, limit alcohol, smoking cessation, sodium restriction, fluid management.
    • Diuretics to relieve congestion; careful monitoring to avoid over-diuresis.

Workup and diagnostic approach to heart failure

  • Baseline labs and tests
    • CBC and TSH to evaluate causes of high-output failure (anemia, thyrotoxicosis).
    • BNP or N-terminal proBNP (NT-proBNP): markers of volume overload; elevated in CHF; BNP rises with ventricular stretch to coordinate diuresis.
    • Electrolytes and renal function (potassium, creatinine, BUN) due to diuretic/renally cleared therapies.
  • Imaging and functional assessment
    • Chest X-ray: Kerley B lines indicate interstitial edema; pulmonary edema; pleural effusions may require thoracentesis if persistent.
    • Echocardiography: critical for EF, type of HF (HFrEF vs HFpEF), valve disease, wall motion abnormalities, and chamber sizes; used serially to monitor therapy response (every 3–6 months in many cases).
    • Abdominal and vascular imaging as indicated for comorbid vascular disease.
  • Bedside and exam clues
    • Pulmonary edema signs (crackles), S3 gallop in systolic HF, JVD, ascites, edema.
    • Kerley B lines on chest imaging as a hallmark of interstitial edema.
  • Diagnostic thresholds and indicators
    • ABI in peripheral arterial disease (PAD): abnormal if ABI < 0.9; indicates moderate to severe disease.
    • D-dimer (coagulation marker) used in suspected DVT/PE; correlate with imaging for diagnosis.
  • Common workup topics for exam questions
    • Distinguish HFpEF vs HFrEF via EF.
    • Interpret NYHA class from symptom description.
    • Role of Echo in planning therapy and monitoring progression.

High-output vs low-output heart failure specifics

  • High-output HF (HOCF) details
    • EF may be normal or high; underlying causes elevate metabolic demand.
    • Reversible causes include hyperthyroidism, severe anemia, beriberi, sepsis, pregnancy, AV fistula.
    • Treatment focuses on correcting the underlying cause to reduce cardiac demand.
  • Low-output HF (LOHF) details
    • Systolic dysfunction (HFrEF): EF < 40% (HFrEF).
    • Diastolic dysfunction (HFpEF): EF can be normal or near normal; filling is impaired.
  • Explicit EF thresholds mentioned
    • HFrEF = EF < 40% (left ventricular systolic dysfunction).
    • HFpEF = preserved EF with diastolic dysfunction.

Guideline-directed medical therapy for HFrEF (the four pillars)

  • Absolute medications every HFrEF patient should be on 1) ARNIs (angiotensin receptor neprilysin inhibitors): sacubitril/valsartan
    • Mechanism: sacubitril inhibits neprilysin, increasing natriuretic peptides (BNP); valsartan blocks angiotensin II receptor, reducing afterload.
    • Benefit: reduces hospitalizations and improves survival.
    • Practical notes: if patient is on an ACE inhibitor or ARB, switch to ARNI by stopping ACE/ARB for at least 36 hours before starting ARNI to reduce angioedema/renal risk.
      2) Beta blockers (select from three first-line options): carvedilol, metoprolol succinate, bisoprolol
    • Benefits: reduce arrhythmic risk, slow heart rate, improve EF with time; up-titrate to max tolerated dose.
    • Considerations: start low, monitor for hypotension and bradycardia.
      3) Mineralocorticoid receptor antagonists (MRAs): spironolactone or eplerenone
    • Benefits: block aldosterone, mitigate salt/water retention and fibrosis.
    • Monitoring: check potassium and renal function due to hyperkalemia risk; spironolactone can cause gynecomastia; may switch to eplerenone if needed.
      4) SGLT2 inhibitors: dapagliflozin or empagliflozin (gliflozins)
    • Benefits: osmotic diuresis and natriuresis; reduce HF hospitalization and mortality in HFrEF even with non-diabetics.
    • Special cautions: avoid in type 1 diabetes due to risk of diabetic ketoacidosis (DKA); monitor for urinary tract infections and genital infections.
  • Additional medications and considerations
    • Loop diuretics (e.g., furosemide): common in HF to manage congestion; monitor electrolytes and volume status; risk of over-diuresis leading to hypotension and metabolic alkalosis; potential ototoxicity with rapid high-dose use.
    • ACE inhibitors or ARBs: traditional first-line for many patients; may be replaced with ARNI for additional benefits.
    • Isosorbide dinitrate/hydralazine: alternative in patients who cannot tolerate ARNI/ACE/ARB.
    • Afterload and preload reduction is a core aim to reduce myocardial workload.
    • Advanced therapies (for selected patients): implantable cardioverter-defibrillator (ICD) for sudden death risk; left ventricular assist device (LVAD); heart transplant.

Diastolic dysfunction and HFpEF management

  • Diastolic HF (HFpEF) management principles
    • Focus on symptom relief and blood pressure/volume status management.
    • Diuretics for volume overload; consider mineralocorticoid receptor antagonists and ARNI as parts of a comprehensive approach.
    • Recent shifts support using some of the same medications beneficial in HFrEF (e.g., MRAs, ARNIs) in certain HFpEF patients.

Restrictive cardiomyopathy and related infiltrative diseases

  • Restrictive cardiomyopathy (infiltrative and stiff ventricle)
    • Common infiltrative etiologies: amyloidosis, sarcoidosis, hemochromatosis.
    • Presentation: signs of heart failure with preserved EF; reduced filling due to stiff ventricular walls.
    • Amyloidosis (example): endomyocardial biopsy showing amyloid deposition; associated with restrictive physiology.
    • Management: similar initial HF therapies; treat underlying disease (e.g., chelation for hemochromatosis); prognosis often poor; transplant candidacy limited by systemic disease.

Hypertrophic cardiomyopathy (HOCM) and related phenotypes

  • Hypertrophic cardiomyopathy (HCM/HOCM)
    • Can be obstructive or non-obstructive; risk of ventricular arrhythmias and sudden cardiac death, especially in young athletes.
    • Physical findings: loud S4; sometimes a double apical impulse; murmur that increases with standing or Valsalva.
    • Treatments and interventions
    • Beta blockers are first-line to reduce heart rate and myocardial contractility.
    • Open-heart surgery (myectomy) to relieve LV outflow tract obstruction.
    • Alcohol septal ablation as a catheter-based alternative to reduce septal thickness.
    • Consideration of an implantable cardioverter-defibrillator (AICD/ICD) for high-risk patients (unexplained syncope, documented arrhythmias, family history of sudden death).

Stress-induced cardiomyopathy (Takotsubo)

  • Takotsubo cardiomyopathy (apical ballooning syndrome, broken heart syndrome)
    • Often triggered by severe emotional or physical stress (e.g., bereavement, cancer diagnosis, stroke, severe illness).
    • Characteristic transient LV dysfunction; mural thrombus may develop at the apex.
    • Management includes addressing LV dysfunction and potential anticoagulation if mural thrombus is present; typically recovers with time.

Thrombus and anticoagulation in heart disease

  • LV thrombus risk with reduced EF (especially in apical segments during Takotsubo or post-MI)
    • Anticoagulation may be indicated to prevent embolization until LV function recovers.

Peripheral vascular disease (PAD) and arterial supply disease

  • PAD overview and claudication
    • Symptoms depend on where the arterial blockage is (iliac, femoral, popliteal, tibial arteries).
    • Claudication: pain with exertion relieved by rest; location of claudication reflects level of arterial disease.
    • Signs: rubor on dependency, elevation pallor; hair loss, skin changes, necrotic ulcers at the ankles/toes in advanced disease.
    • Chronic limb-threatening ischemia: cyanosis, non-pitting edema, ulcers, potential gangrene; urgent intervention.
  • Diagnostic approach to PAD
    • Ankle-brachial index (ABI): diagnostic test of choice for initial PAD evaluation. Threshold: ABI < 0.9 indicates PAD.
    • Arterial Doppler ultrasound to localize stenosis; CT angiography for detailed anatomy and planning.
    • Vascular surgery input for revascularization (stent, bypass) if indicated.
  • Management and risk factors
    • Risk factor modification: diabetes control, smoking cessation, lipid control, blood pressure optimization, weight management, exercise for collateral formation.
    • Pharmacotherapy in PAD include antiplatelets (aspirin, clopidogrel), statins, and occasionally rivaroxaban (direct oral anticoagulant) for guideline-supported PAD management.
    • Cilostazol (PDE-3 inhibitor) can improve claudication symptoms by vasodilation and antiplatelet effect.
    • After an intervention (stent/bypass), antithrombotic therapy considerations include dual antiplatelet therapy or single-agent therapy depending on the intervention and comorbidities.
  • Acute limb ischemia and DVT considerations
    • Acute arterial occlusion presents with sudden pain, pulseless limb, cyanosis; immediate anticoagulation (heparin or enoxaparin) followed by surgical evaluation.
    • DVT risk factors: stasis (hospitalization, long car rides), hypercoagulable states (smoking, pregnancy, malignancy, renal failure, estrogen therapy), vascular damage.
    • DVT management: anticoagulation for 3–6 months depending on provoking vs unprovoked; consider hematology referral for thrombophilia workup; INR goal for warfarin therapy: 2.0-3.0.
    • IVC filters reserved for contraindication to anticoagulation or specific clinical scenarios with ongoing bleeding.
  • Other venous problems
    • Venous insufficiency and varicosities: primary (superficial) vs secondary (deep) venous reflux; leg edema and venous stasis ulcers managed with compression, leg elevation, and venous Doppler assessment.
  • Raynaud's phenomenon and Buerger disease
    • Raynaud's: vasospasm of digital arteries; treat with calcium channel blockers (amlodipine, nifedipine) and avoid cold exposure.
    • Buerger disease (thromboangiitis obliterans): vasculitis strongly associated with smoking; cessation of tobacco is essential; can cause distal ischemia and, in severe cases, gangrene.

Mesenteric and abdominal vascular disease

  • Ischemic bowel disease presentations
    • Acute mesenteric ischemia: pain out of proportion to exam; metabolic acidosis; CT scan aids diagnosis; requires urgent surgical resection of necrotic bowel.
    • Chronic mesenteric ischemia: postprandial abdominal pain; fear of eating leading to weight loss; often involves celiac or superior mesenteric arteries with high-grade stenosis; diagnosed with CT angiography or mesenteric Doppler; treated with angioplasty or surgical revascularization.

Aortic disease: aneurysm and dissection

  • Abdominal aortic aneurysm (AAA)
    • Most AAAs are infrarenal; aneurysmal if >3\,\text{cm}.
    • Screening: USPSTF recommends abdominal ultrasound for men who have smoked at least 100 cigarettes in their lifetime, aged 65–75.
    • Symptom pattern: many AAAs are asymptomatic until rupture; rupture causes hypotension and severe back/flank pain.
    • Repair thresholds: generally repair if diameter > 5.5\,\text{cm}; earlier repair at 5.0–5.5 cm for certain populations (e.g., Marfan's).
    • Repair methods: open surgical graft or endovascular stent graft; post-repair BP management is important; beta blockers help slow aneurysm growth in general.
  • Thoracic aortic aneurysm (TAA)
    • Size assessment via CT with contrast.
    • Beta-blockers to slow growth apply to aneurysms anywhere in the aorta.
    • Marfan’s/Ehlers-Danlos: earlier repair thresholds due to higher risk of complications.
  • Aortic dissection
    • Two main types: Type A (ascending aorta and arch) vs Type B (descending aorta beyond the left subclavian).
    • Type A: requires immediate surgical repair.
    • Type B: initial medical management with IV beta-blockers to control BP; possible later stent grafting if needed.
    • BP control is central to dissection management; avoid high blood pressure as a driving factor.

Venous and inflammatory vascular disorders

  • Temporal arteritis (giant cell arteritis)
    • Presentation: unilateral scalp tenderness, jaw claudication, severe scalp pain.
    • Diagnostic and treatment steps: ESR elevated; temporal artery biopsy by vascular surgery; start high-dose prednisone (often with aspirin and sometimes methotrexate) while evaluating and treating.
    • Age group: typically around 70 years old; 50% also have polymyalgia rheumatica. Risk of vision loss if ophthalmic involvement occurs.

Syncope and presyncope: evaluation and causes

  • General approach to syncope/presyncope
    • Requires thorough physical exam (murmurs, neuro symptoms), orthostatic BP measurement, ECG, and baseline labs (CBC, electrolytes, renal function, troponin).
    • Consider non-ST elevation MI or PE as causes that may present with syncope; troponin elevation can occur in various etiologies.
    • Tilt-table testing can be considered in outpatient evaluation for certain syncope patterns.
  • Reflex syncope (vasovagal, situational)
    • Vasovagal syncope: most common; triggered by pain, emotional distress, or prolonged standing; symptoms precede fainting (lightheadedness, diaphoresis, vasodilation).
    • Situational syncope: triggered by coughing, defecation, urination, swallowing; example of a patient with coughing-induced syncope.
  • Orthostatic (neurally mediated) syncope
    • Common in older adults; dehydration and medications (nitrates, beta blockers, antidepressants) contribute.
    • Orthostatic hypotension: a drop in BP > 20\,\text{mmHg}$
    • Management: elevate head of bed, encourage fluids, leg elevation and compression stockings; pharmacologic option includes Midodrine (vasopressor) and, if needed, fludrocortisone to retain fluids.
  • Cardiogenic syncope
    • Due to arrhythmias (VT/VF, torsades), SVT, aortic stenosis, or HOCM-related obstruction.

Practical exam-style questions (key takeaways)

  • Restrictive cardiomyopathy with amyloidosis: presentation with amyloid deposition on biopsy and pulmonary hypertension suggests restrictive physiology.
  • Systolic HF (EF ≈ 25%) on lisinopril and furosemide: add carvedilol (beta-blocker) to improve EF and mortality.
  • Right-heart failure signs (hepatomegaly, JVP elevation, edema) point to predominantly right ventricular dysfunction or failure.

Quick reference: recurring therapeutic themes and cautions

  • Always assess EF to classify HF type (HFrEF vs HFpEF).
  • Afterload reduction strategies include ARNI/ACE inhibitors, ARBs, beta-blockers, and, if needed, isosorbide/hydralazine.
  • Preload reduction primarily via diuretics and, in some cases, salt/fluid restriction.
  • SGLT2 inhibitors offer mortality and hospitalization benefits in HFrEF and can be used irrespective of diabetes status, except in type 1 diabetes due to DKA risk.
  • Monitor electrolytes, renal function, and potassium with MRAs and diuretics.
  • Consider device therapy (ICD, LVAD) and transplant for eligible patients with advanced HFrEF not adequately managed by meds.
  • PAD management hinges on lifestyle modification, ABI-guided diagnosis, revascularization when needed, and antithrombotic therapy.
  • Aorta pathology requires aggressive BP control with beta-blockers and timely surgical/interventional repair based on size thresholds and etiologies (Marfan’s, etc.).
  • Vasculitis (temporal arteritis) requires prompt corticosteroids to prevent vision loss; coordinate with vascular surgery for biopsy.
  • Syncope workup should distinguish reflex, orthostatic, and cardiogenic causes; treat accordingly with a stepwise approach.
  • Regular follow-up imaging (echo, Doppler) is essential to monitor HF therapy effectiveness and structural changes over time.

Summary of key numerical/expressions

  • Normal EF range: EF \in [50\%, 70\%]
  • HFrEF definition: EF < 40\%
  • PAD diagnostic threshold: ABI < 0.9
  • DVT treatment duration: 3-6 months (provoked vs unprovoked)
  • Anticoagulation INR target: 2.0 \text{ to } 3.0
  • Revascularization thresholds for AAA: \text{repair if } \text{diameter} > 5.5\,\text{cm}$$ (Marfan's at 5.0 cm)