Acute HF

• Acute heart failure is often caused by decompensated chronic heart failure
• Causes of acute heart failure:

  • Overload with aggressive IVI
  • MI
  • Arrhythmias
  • Sepsis
  • Hypertensive emergency
• Symptoms of acute heart failure:

  • Chest pain - if ACS underlying cause
  • Acute dyspnoea
  • Confusion
  • Cough +/- frothy pink sputum
  • Fever - in sepsis
  • Palpitations - in arrhythmias
• Signs of acute heart failure on examination:

  • Tachypnoea
  • Hypoxia
  • Tachycardia
  • 3rd heart sound
  • Bilateral basal crackles- pulmonary oedema
  • Hypotension - cardiogenic shock
  • Raised JVP
  • Peripheral oedema
• BNP should tested in suspected acute heart failure. It is sensitive but not specific. When negative it can rule out heart failure as the cause of the patients symptoms.
• An ABG in acute heart failure will show type 1 respiratory failure- low oxygen without a raise in CO2
• Acute heart failure treatment = SODIUM

  S - Sit up

  O - oxygen

  D - diuretics

  I - IV fluids stopped

  U - underlying cause

  M - monitor fluid balance
• In severe cases of acute heart failure the following may be needed:

  • IV opiates - vasodilators (in severe hypertension or ACS)
  • IV nitrates - vasodilators (in severe hypertension or ACS)
  • Inotropes to increase cardiac output
  • Vasopressors such as noradrenaline to increase blood pressure
  • NIV or invasive ventilation
• AHF involves the acute failure of the heart to pump blood to meet the body’s demand.

  As a result, two courses of pathology develop:

  1. Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia. These patients are ‘WET’.
  2. Hypoperfusion of vital organs as the cardiac output is reduced. These patients are ‘COLD’.
• Patients may show signs of congestion, hypoperfusion, or both:

  • 50% of patients will show signs of congestion without signs of hypoperfusion (WET-WARM).
  • 45% of patients will show signs of congestion with signs of hypoperfusion (WET-COLD).
  • 5% of patients will show no signs of congestion (DRY-WARM or DRY-COLD).
• Signs of pulmonary or systemic congestion include:

  • Fine basal crackles (bilateral)
  • Peripheral oedema (bilateral)
  • Dull percussion at the lung bases
  • Raised jugular venous pressure (JVP)
  • Hepatomegaly
  • Gallop rhythm (S3 or S4 heart sounds)
  • Murmur
• Signs of hypoperfusion include:

  • Hypoxia
  • Tachypnoea and accessory muscle use
  • Tachycardia
  • Cyanosis
  • Cold, pale, and sweaty peripheries
  • Oliguria
  • Confusion/agitation
  • Syncope/pre-syncope
  • Narrow pulse pressure
• Imaging:

  • CXR
  • TTE
• Identify conditions early on which may have precipitated AHF and treat these urgently. Look out for CHAMP conditions:

  • Acute coronary syndrome (ACS)
  • Hypertensive crisis
  • Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
  • Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
  • Pulmonary embolism
• Oxygen:

  • If the patient is hypoxic, titrate oxygen to maintain saturations between 94-98% (or 88-92% in those with COPD). Patients often require 15L/minute with a reservoir mask.
  • Regularly reassess and down-titrate oxygen to avoid hyper-oxygenation which is associated with worsening myocardial ischaemia and other pathology.
• Loop diuretics:

  • Diuretics increase sodium excretion causing diuresis and decrease afterload. All ‘WET’ patients will require diuretics as the cornerstone of their management.
  • Administer 40 milligrams furosemide intravenously initially to improve symptoms of congestion fluid overload.
  • Patients with chronic kidney disease and those already on oral diuretics will need a greater dose. Monitor renal function and urine output to titrate dose according to clinical response.
• Nitrates:

  • Nitrates (sublingual glyceryl trinitrate or intravenous nitrates) are the second most used agents in AHF used for ‘WET’ patients. Do not use nitrates in those with SBP <90mmHg or aortic stenosis, who rely on sufficient preload to overcome their pressure gradient.
  • Nitrates cause venous and/or arterial dilation to reduce preload and/or afterload. They are given to patients with concomitant myocardial ischaemia or hypertension.
• Non-invasive ventilation (NIV)

  • CPAP or BiPAP are used for those with cardiogenic pulmonary oedema, dyspnoea
  • NIV improves ventilation to reduce respiratory distress and drives fluid out of alveoli and into vasculature in those whose respiratory failure is not controlled with oxygen therapy given via a face mask.