Life in the Fast Lane

AFTB lecture notes - Acute Pulmonary Oedema (APO)

DIAGNOSIS

Acute heart failure syndrome (AHFS) spectrum can be divided for therapeutic management into:

• Dyspnoea + /- congestion with elevated systolic blood pressure (SBP) >140 mmHg, usually with abrupt onset APO (most frequent type)
• Dyspnoea + /- congestion with normal SBP 100-140 mmHg, usually with gradual onset predominant systemic oedema and milder APO iii) dyspnoea + /- congestion with low SBP <100 mmHg, with predominant cardiogenic shock or end-stage cardiac failure (most fatal type)
• Dyspnoea + /- congestion with signs of ACS such as chest pain
• Isolated RV failure usually without APO.

Mebazza A, Gheoghiade M, Pina I et al. Practical recommendations for pre- hospital and early in-hospital management of patients presenting with acute heart failure. Crit Care Med 2008; 36: S129-39.

B-type natriuretic peptide (BNP)

• B-type natriuretic peptide (BNP) is elevated in left ventricular dysfunction and correlates with severity and prognosis. 
• May help differentiate acute heart failure (AHF) from pulmonary disease particularly in acutely dyspnoeic patients, although predictive cut-off levels, and exact role are unclear.

Chircop R, Jelinek G. B-type natriuretic peptide in the diagnosis of heart failure in the emergency department. Emerg Med Australas 2006; 18:170-7. [Reference]

Maisel AS. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Eng J Med  2002; 347:161-7. [Reference] 

TREATMENT - Aims

• Decrease left ventricular diastolic pressure, by decreasing systemic vascular resistance and improving systolic and diastolic functional reserve.
• Promote coronary blood flow.
• Correct acute respiratory failure.

MEDICATIONS - Options

• Nitroglycerin S/L, topical or IV titrated to avoid hypotension.  Most rapidly venodilates, reduces LV afterload and corrects myocardial ischaemia. Ideal for AHFS type 1. a) i) above. Consider in AHFS types 1. a) ii) and iv) if SBP > 110 mmHg. Avoid in AHFS type 1. a) iii) above.
• Frusemide IV.  Despite universal use, absolute efficacy is unclear. May cause decrease in cardiac output and increase PVR, plus increase PAOP in more chronic HF. Ideal for AHFS type 1. a) ii) above.
• ACE inhibitor IV, orally or SC also reduces pre- and afterload, but little data in acute situation. Precipitous hypotension is hard to reverse, so use best  established in longer term management of HF.
• Morphine has relatively ineffective venodilating and sympatholytic effects, and may result in poorer outcome, or respiratory depression in face of NIV. May have role in APO with diastolic dysfunction (ie. EF >40%) with elevated SBP.

Kumar R, Gandhi S, Little W. Acute heart failure with preserved systolic function. Crit Care Med 2008;36:S52-6. [Reference]

Kosowsky J, Kobayashi L. Acutely decompensated heart failure: Diagnostic and therapeutic strategies for the new millenium. Emergency Medicine Practice: An Evidence-based Approach to Emergency Medicine 2002; 4(2):1-28

Cotter G, Metzkor E, Kaluski E et al.  Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.  Lancet 1998; 351:389-93. [Reference]

Ventilatory assistance

• Non-invasive ventilation (NIV) with CPAP or bilevel non-invasive pressure support ventilation (NIPSV - note BiPAP is a tradename) reduces mortality by 40%, particularly with CPAP, and both reduce need to intubate.

Vital F, Saconato H, Ladeira M et al. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Syst Rev 2008;3. [Reference]

Peter JV et al. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet 2006;367:1155-63. [Reference]

Masip J et al. Noninvasive ventilation in acute cardiogenic pulmonary oedema: systematic review and meta-analysis. JAMA 2005;294:124-30. [Reference]

• Excess mortality not confirmed on meta-analysis, thought related to AMI onset with NIPPV, compared with using CPAP at 5-7.5 cm H2O for APO.

Ferrari G, Olliveri F, De Filippi G et al. Noninvasive positive airway pressure and risk of myocardial infarction in acute cardiogenic pulmonary edema: continuous positive airway pressure vs noninvasive positive pressure ventilation. Chest 2007;132:1804-9. [Reference]

Miscellaneous therapies

• Nesiritide (recombinant human brain natriuretic peptide BNP) longer acting vasodilator as effective as nitrates, but hypotension more persistent.

VMAC Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure. JAMA 2002; 287:1531-40. [Reference] (Editorial: Poole-Wilson P. Treatment of acute heart failure. Out with the old, in with the new. JAMA 2002; 287:1578-1580) [Reference]

• New drugs include levosimendan (calcium sensitiser), tezosentan (endothelin inhibitor) and pyruvate (alternate heart substrate).
• Traditional inotropic support is with dobutamine, dopamine, milrinone, enoximone or salbutamol for AHFS type 1. a) iii) above, but may disastrously increase myocardial oxygen demand, especially in ACS with AHFS type 1. a) iv). Rarely need to add vasoconstrictor noradrenaline.
• Surgery +/- intra-aortic balloon counterpulsation (IABC) for free wall rupture, acute VSD or mitral incompetence from papillary rupture etc.

Task Force on Acute Heart Failure of the European Society of Cardiology. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure. Eur Heart J 2005;26:384-416. [Reference] (Excellent overall summary).

Ware L, Matthew M. Acute pulmonary edema. NEJM 2005;353:2788-96. [Reference] (Differentiating acute cardiogenic and noncardiogenic pulmonary edema).

Tags: AFTB, aftb lecture notes, APO, pulmonary edema