Acute Heart Failure & Cardiogenic Shock

• Acute Heart Failure and Cardiogenic Shock, presentation by Dave Harnett, MD, MSc, FRCPC, Cardiologist, Eastern Health, and Clinical Assistant Professor, Faculty of Medicine, Memorial University on February 16, 2023.

Objectives

• Discuss the differences between interstitial and alveolar edema and their mechanisms.
• Discuss the importance of lung lymphatics in prevention of pulmonary edema.
• Define cardiogenic shock and differentiate it from other shock states.
• Discuss the causes, clinical features, and natural history of cardiogenic shock.
• Discuss the treatment principles in the management of cardiogenic shock.

Cardiac Output Mediators

• Determinants of stroke volume: contractility, preload, and afterload. Cardiac output = Heart rate × Stroke volume.

Definitions of Heart Failure

• Heart failure (HF) is a complex clinical syndrome where abnormal heart function results in clinical indicators like decreased cardiac output and/or pulmonary or systemic congestion. It represents the heart's inability to maintain organ perfusion without raising filling pressures.
• Acute heart failure (AHF) is the new occurrence or increase in heart failure symptoms and signs, usually tied to systemic congestion. The possibility of cardiogenic shock should be considered to any signs of low cardiac output.

Heart Failure Classifications

• Left-Sided HF: Dysfunction from the left ventricle to increased pulmonary pressures +/- decrease in cardiac output/forward flow. Acute heart failure (AHF) is the focus in acute left-sided HF.
• Right-Sided HF: RV dysfunction to more systemic venous pressures and edema. Isolated acute right heart failure is less common, and usually due to right ventricle myocardial infarction or pulmonary embolism.
• Biventricular HF: Over time chronic left-sided HF transmits increased pulmonary pressures to the right ventricle causing compensation failure.

Heart Failure Classifications by Left Ventricular Ejection Fraction (LVEF)

• Heart failure with reduced ejection fraction (HFrEF) is when LVEF is ≤ 40% and is know as 'systolic HF'
• Heart failure with mid-range ejection fraction (HFmEF) is when LVEF is 41-49%.
• Heart failure with preserved ejection fraction (HFpEF) is when LVEF is ≥ 50%, or 'diastolic HF'.

Heart Failure Pathophysiology

• Left-sided heart failure conditions can stem from impaired ventricular systolic or diastolic function. It may result in heart failure with preserved EF due to ventricular hypertrophy and increased diastolic stiffness with a compensatory effect.
• Left heart disease starts with LV systolic and/or diastolic dysfunction leading to increased left atrial pressure.
• Lung lymphatics maintain fluid balance allowing return of extravascular fluid from pulmonary interstitial back to the central vasculature.
• Lymphatic flow can increase by 3-10x if there is hydrostatic pulmonary edema like in left heart failure.
• Thoracic duct drains the L lung, emptying into venous system near left subclavian and L internal jugular vein.
• The right lung is drained by the right lymphatic duct which empties into venous system near right subclavian and right internal jugular vein.

Edema

• Tissue edema occurs when fluid moving from capillaries into the interstitium is faster than the lymphatic system's ability to drain it.
• Increased venous pressures can impair lymphatic drainage.

Physiological Determinants of Edema

• Hydrostatic pressure is pressure within the capillaries that drives fluid out of the vessel.
• Oncotic pressure is when pressure and macromolecules in the blood retain fluid.
• Membrane permeability is how fluid easily moves by way of the capillary or alveolar walls.
• Lymphatic drainage allows return of extravascular fluid back to the central vasculature.

Pulmonary Edema Types

• Interstitial Edema: increased hydrostatic pressure within the capillaries (left heart failure, volume overload) OR increased capillary endothelium permeability without alveolar injury (high altitude pulmonary edema). Linear/reticular structure with too many line. Cephalization occurs with increased blood flow to upper lobes.
• Alveolar Edema: Increased membrane permeability due to direct injury to alveolar epithelium +/- capillary endothelium. It can be attributed to respiratory distress syndrome ‘ARDS’ or MRSA bacteremia. Fluffy ill-defined margins can segment the lobes like in pneumonia or widespread for diffusing spread.
• Mixed Edema: a combination of hydrostatic pressure and membrane permeability.

Clinical Signs and Symptoms

• Acute Heart Failure:
  • Symptoms: include shortness of breath at rest, orthopnea, paroxysmal nocturnal dyspnea (PND), abdominal swelling, lower extremity edema, and weight gain.
  • Examination findings: may show abnormal vital signs (elevated BP), low cardiac output, tachycardia, tachypnea, hypoxemia, elevated JVP, +S3 heart sound, murmurs, lung crackles, and lower extremity edema.
  • Emergency Room Investigations: include routine labs (CBC/LBC), LFTs, blood gas analysis(if perfusion deficits are suspected), cardiac troponin testing, ECG, chest X ray, point-of-care ultrasound or echocardiography.

Management of Acute Heart Failure

• Phase 1 includes:
  • Positioning the patient upright
  • Providing supplemental oxygen if SpO2 is less than 92%
  • Considering NIPPV for significant respiratory distress
  • Administering IV loop diuretics like furosemide
  • Considering nitroglycerin if hypertensive
  • Identifying triggers/precipitants
  • Assessing perfusion status
  • Making a decision to admit.
• Common AHF triggers: arrhythmia, dietary indiscretion, medication non-adherence or side effect, concurrent infection, valvular heart disease, ischemia, toxin use.
• Loop diuretics (like Furosemide) block the Na-Cl-K cotransporter in the thick ascending limb of the loop of Henle which results in increased excretion of Na, K, and Cl, or sodium, potassium and chloride. Route: IV in AHF and then transition to PO once improved. Watch out for hypokalemia, hypomagnesemia, volume depletion/worsening renal dysfunction
• Spironolactone works as an aldosterone antagonist blocking this secretion in the collecting duct of the distal tubule resulting in increased sodium excretion and potassium retention.

Treatment for AHF

• Metolazone, a thiazide diuretic, is used only if not responding despite a spironolactone or furosemide resistance. Blocks the the Na-Cl transporter in the distal convoluted tubule to push Na and Cl excretion. Administer 30-60 minutes before furosemide due to absorption.
• SGLT2 inhibitors block the Na-glucose co-transporter 2 (SGLT2) protein in proximal convoluted tubule to push natriuresis and osmotic diuresis. Provides mortality benefit with AHF and chronic heart failure independent of ejection fraction (HFrEF and HFpEF). Expect treatment with an upward trend to care.
• Diuretics lower preload and LV filling pressures. And reduces renal venous pressure.
• Intravascular Refill is how fluid moves from the overhydrated interstitium to the intravascular after fluid removal. It depends on fluid moving along capillary walls due to hydrostatic/oncotic pressure grades.
• Non-pharmacologic management: dietary sodium restriction (2-3 grams/day) and reducing fluid to less than 2L/day, daily weight monitoring, and regular exercise.
• Phase 2 management of AHF: improves symptoms, hemodynamics (BP, HR), volume status and monitors renal function (electrolytes and creatinine). Also initiate/optimize chronic heart failure therapies.

Cardiogenic Shock

• Oxygen target saturation should be greater than 92%. Use oxygen, CPAP, and eventually mechanical intubation. Then review SBP/MAP.
• Characterized by ineffective cardiac output due to a primary cardiac disorder, inadequate issue perfusion and ~30-50% mortality. Most common phenotype: 'Cold and wet' has lowered cardiac output, increased Pulmonary Capillary Wedge Pressure, and increased systemic vascular resistance. SBP is less than 90 for more than 30 minutes or elevated pressures (PCWP greater than 15) and poor organ perfusion.
• Hemodynamic parameters for cardiogenic shock include increased Preload, decreased Contractility, and increased Afterload. Pulmonary Capillary Wedge Pressure and Cardiac Output can be used for measurements.
• Distributive shock classically has cardiac output that increases, but can lower due to myocardial stunning. Measurement depends on etiology of variable cause.

Pulmonary Artery Catheter

• Pulmonary artery catheter ('Swan Ganz' catheter) has a balloon tip inserted through sheath ('Cordis') in vein. Goes into artery until flow is occluded. Provides measurement of pulmonary capillary wedge pressure to surrogate left atrial pressure and LVEDP with some variables.

Clinical Clues for Cardiogenic Shock:

• Consider pre-existing/newly severe LV systolic dysfunction presentations, watch for hypotension, narrow pulse pressure, tachycardia, nausea, cold/pale extremities, end-organ dysfunction and altered consciousness.
• Main Causes: 70% stems from acute myocardial infarction/acute severe LV dysfunction or 30% due to mechanical complication, RV infarction, or decompensation.
• Cardiogenic Shock ('cold and wet') goals with medical therapy: increase cardiac output/ improve end organ perfusion and decrease filling, therefore, cardiacOutput=strokeVolume x heartRate; the volume is determined by preload, afterload and contractility. The treatments therefore involve diuretics, inotropes and afterload reducing medications, but must be done carefully.

Medical Therapy

• Treats inotropes' (contractions, afterload, rates)
• Vasopressors can use norepinephrine agonism to maintain pressure. However, pure pure a1 agonism causes pure cardiogenic shock.
• Resuscitation requires medical interventions via inotropes and vasopressors, volume removal, pulmonary artery catheter, PCI/CABG, or IABP/LVAD/ECMO.