What is the pathophysiology, development, and management of congestive heart failure (CHF), including common prescriptions, prehospital treatments, and recognition of emergencies?

Congestive Heart Failure: Comprehensive Breakdown

Pathophysiology

CHF develops from the heart's inability to maintain adequate cardiac output, triggering a cascade of neurohormonal compensatory mechanisms that ultimately worsen the condition. 1

Core Mechanisms

• Neurohormonal activation drives the pathophysiology through sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) upregulation, leading to sodium and water retention (sodium avidity) 1

• Impaired kidney function and neurohormonal drive create inability to control water-ion homeostasis, resulting in volume shifts and clinically overt congestion 1

• Non-osmotic vasopressin release and peripheral resistance to natriuretic peptides further increase sodium avidity and facilitate congestion development 1

• Proinflammatory pathways contribute to disease progression and symptom development 1

Symptom Generation

• Fatigue results from changes in peripheral muscle metabolism secondary to decreased vasodilative capacity and physical inactivity 2

• Dyspnea occurs from acute pulmonary congestion (backward failure) and increased physiological dead space ventilation caused by pulmonary ventilation/perfusion mismatch 2

• Congestion is not a direct cause of HF but its consequence, occurring from complex underlying pathophysiology 1

Disease Development and Progression

HF progresses through defined stages, with most hospitalizations and deaths occurring in apparently stable NYHA class II-III patients who have subclinical progression. 3

Progressive Nature

• Pre-HF state encompasses asymptomatic patients with structural/functional cardiac abnormalities or elevated natriuretic peptides/cardiac troponin 4

• Silent progression occurs without clinical symptoms due to underlying deleterious effects of neurohormonal imbalance and endothelial dysfunction 3

• Decompensation triggers include medication non-compliance (listed as top precipitating factor), dietary indiscretion, infection, arrhythmias (especially atrial fibrillation), and myocardial ischemia 1

Common Prescriptions for Chronic Management

Guideline-directed medical therapy (GDMT) for HF with reduced ejection fraction includes four foundational drug classes that must be initiated and optimized. 4

First-Line Therapies (HFrEF)

• Angiotensin receptor-neprilysin inhibitors (ARNi) such as sacubitril/valsartan are superior to ACE inhibitors in reducing cardiovascular death and HF hospitalization 3

• ACE inhibitors or angiotensin receptor blockers (ARBs) if ARNi not tolerated, shown to slow HF progression and substantially decrease morbidity and mortality 2, 5

• Beta-blockers are life-saving drugs that improve prognosis and should not be withheld based on age alone 6, 5

• Mineralocorticoid receptor antagonists (MRA) like spironolactone reduce mortality by 30% in NYHA class III-IV patients with EF ≤35% 7

• SGLT2 inhibitors are now foundational therapy across the HF spectrum (HFrEF, HFmrEF, HFpEF) 4

Symptomatic Therapies

• Loop diuretics (furosemide) are first-line for congestion relief and symptom improvement, though they don't modify disease progression 1, 2

• Digoxin improves hemodynamics and symptoms by increasing inotropy and slowing heart rate in atrial fibrillation, though prognostic effects remain unproven 2, 8

Medication Dosing Principles

• Start low, titrate aggressively with reassessment every 1-2 weeks until target or maximum tolerated doses achieved 6, 3

• Spironolactone dosing: Start 25 mg daily, may increase to 50 mg daily if tolerated at 8 weeks; reduce to 25 mg every other day if intolerant 7

Prehospital and Emergency Recognition

Acute decompensated HF presents with respiratory distress requiring immediate assessment and intervention, with severity determining transport destination. 1

Critical Recognition Parameters

• Respiratory distress indicators: Respiratory rate >25/min, SpO₂ <90%, use of accessory breathing muscles, orthopnea 1, 9, 6

• Hemodynamic instability: Systolic BP <90 mmHg, altered mental status, signs of hypoperfusion (cold peripheries, oliguria, elevated lactate >2 mmol/L) 1, 9

• Congestion signs: Peripheral edema, pulmonary rales, jugular venous distension, hepatojugular reflux, ascites 9

Prehospital Treatment Algorithm

Position patient upright immediately to reduce work of breathing and improve ventilation. 9

Respiratory Support

• Oxygen therapy when SpO₂ <90%, but avoid hyperoxia 1, 9

• CPAP should be initiated in prehospital setting for respiratory distress—it's simpler than PS-PEEP, requires minimal training, and reduces intubation rates 1, 6

• Non-invasive ventilation (NIV) started as soon as possible in acute pulmonary edema reduces respiratory distress and may decrease mortality 1

Pharmacological Interventions

For systolic BP >110 mmHg: Administer IV vasodilators (nitroglycerin) plus IV loop diuretics (furosemide). 1, 6

For systolic BP <110 mmHg: Administer IV loop diuretics only; vasodilators are contraindicated. 1, 6

• Furosemide dosing: 40 mg IV if diuretic-naïve; at least equivalent to (or double) chronic oral dose if already on diuretics 1, 6

• Vasodilators (nitrates, nitroprusside) are associated with lower mortality when given early, but only if SBP >110 mmHg 1

Medications to AVOID

• Morphine is NOT recommended routinely—associated with higher rates of mechanical ventilation, ICU admission, and death in ADHERE registry 1, 6

• Vasopressors/inotropes have no role if SBP >110 mmHg or when signs of low cardiac output are absent 1

• Dobutamine should not be given when pulmonary edema occurs with normal or high systolic blood pressure 1

Transport Decisions

• High-risk patients (any of: RR >25, SpO₂ <90%, SBP <90 mmHg, altered mental status, signs of hypoperfusion) require immediate transport to facility with ICU/CCU capability 10, 6

• Cardiogenic shock patients must be rapidly transferred to tertiary care center with 24/7 cardiac catheterization and dedicated ICU with mechanical circulatory support availability 1

Emergency Department Management

Continue NIV if respiratory distress persists; switch to PS-PEEP if acidosis and hypercapnia present, especially with COPD history. 1, 9

Monitoring Requirements

• Continuous monitoring: Pulse oximetry, blood pressure, ECG, respiratory rate, mental status, fluid balance 1, 9

• Reassess response within 2-6 hours: urine output, respiratory rate, blood pressure 6

• Laboratory assessment within 24-48 hours: renal function (creatinine, BUN), electrolytes (potassium, sodium, bicarbonate) 6

Chronic Medication Management During Acute Episode

Continue ACE inhibitors/ARBs and beta-blockers in absence of hemodynamic instability (SBP >85 mmHg, HR >50 bpm). 1, 10, 9

Medication Adjustment Algorithm 1

Stop if:

• SBP <85 mmHg: ACE-I/ARB, beta-blocker, MRA, other vasodilators
• Heart rate <50 bpm: Beta-blocker, rate-slowing drugs
• Potassium >5.5 mEq/L: ACE-I/ARB, MRA
• Creatinine >2.5 mg/dL or eGFR <30: ACE-I/ARB, MRA

Reduce dose if:

• SBP 85-100 mmHg: ACE-I/ARB, beta-blocker, diuretics, other vasodilators
• Heart rate <60 bpm: Beta-blocker, rate-slowing drugs

Beta-blockers can be safely continued during AHF presentations except in cardiogenic shock 1

Rate Control in Atrial Fibrillation

• Beta-blockers are preferred first-line for ventricular rate control in stable patients 1, 9

• IV cardiac glycosides should be considered for rapid ventricular rate control in HF with atrial fibrillation 1, 9

Cardiogenic Shock Recognition and Management

Cardiogenic shock is defined as SBP <90 mmHg for >30 minutes despite adequate volume status, with signs of hypoperfusion. 1

Diagnostic Criteria

• Hypoperfusion signs: Oliguria (<0.5 mL/kg/h for ≥6 hours), altered mentation, cool extremities with livedo reticularis, lactate >2-4 mmol/L, metabolic acidosis, SvO₂ <65% 1

Immediate Management

• Fluid challenge first: Saline or Ringer's lactate >200 mL over 15-30 minutes if no overt fluid overload 1

• Invasive monitoring with arterial line is required 1

• ECG and echocardiography immediately in all suspected CS patients 1

Pharmacological Support

• Dobutamine may be used to increase cardiac output; levosimendan may be considered, especially in CHF patients on oral beta-blockade 1

• Norepinephrine is recommended over dopamine if vasopressors needed for persistent hypoperfusion 1

• IABP is NOT routinely recommended in cardiogenic shock 1

Critical Decision Point

• Short-term mechanical circulatory support may be considered in refractory CS depending on patient age, comorbidities, and neurological function 1

Common Pitfalls and Caveats

Fluid Management Paradox

• Excessive diuresis can paradoxically reduce stroke volume and cardiac output, especially in diastolic dysfunction 6

• Conservative fluid approach required when HF coexists with conditions requiring fluid resuscitation (e.g., dengue fever)—use smaller boluses with frequent reassessment 10

Medication Interactions

• NSAIDs and COX-2 inhibitors are common precipitants of CHF exacerbations and increase hyperkalemia risk when combined with aldosterone antagonists and ACE inhibitors 6

• Thiazide diuretics are often ineffective in elderly due to reduced GFR; loop diuretics should be used instead 6

• Hyperkalemia monitoring is crucial when combining ACE inhibitors/ARBs with aldosterone antagonists, especially with renal dysfunction 6

Discharge Criteria

Patients should only be discharged when hemodynamically stable, euvolemic, established on evidence-based oral medication, and with stable renal function for at least 24 hours. 10, 9

Follow-up Requirements

• Primary care follow-up within 1 week of discharge 1, 9

• Cardiology follow-up within 2 weeks of discharge 1, 9

• Multidisciplinary HF program enrollment for continuation and uptitration of disease-modifying therapies 1, 9