Left ventricular failure

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Clinical presentation

  1. Breathlessness
  2. Tachycardia
  3. Pulsus alternans
  4. Gallop rhythm
  5. Basal fine inspiratory crepitations


Acute cardiogenic pulmonary oedema

Acute cardiogenic pulmonary oedema is acute pulmonary venous hypertension due to a cardiac cause. Not always easy to diagnose but often satisfying to treat with what turn out to be treatments with evidence base deficiencies.


It is known that preserved left ventricular ejection fraction, which is more common with the more elderly presentation, has the lowest in hospital mortality. However half of elderly patients will have have moderately to severely reduced left ventricular systolic function[1]. Elderly patients with impaired left ventricular function, coronary artery disease, low systolic blood pressure, tachycardia, hyponatraemia and/or renal failure have the worse outcomes[2].

  • The evidence base for all acute drug therapies directed specifically at acute cardiogenic pulmonary oedema is very poor in terms of long term outcomes such as mortality benefit and reduced hospitalisation
  • Intravenous diuretics are claimed by some to be illogical but in volume overloaded patients do improve outcome[3]
  • Opiates rapidly relieve distress but do not improve other outcomes
  • The use of iv nitrates is not so robust as some believe. However inhospital mortality is reduced by early treatment[4].
  • There is no evidence for inotropes[5]
  • The universal use of high flow oxygen is anecdotal
  • Treat a precipitating MI with thrombolysis or primary PCI
  • Treat a precipitating arrhythmia

Emergency treatment

Apart from upright posture there are deficiencies in the evidence base for all treatments that do not address an underlying physiological or pathological issue. The clinical evidence base is confused because patients with subacute heart failure, biventricular heart failure, pulmonary hypertension, low cardiac output and fluid overload due to renal dysfunction are often not regarded as separate problems. The order of the correct interventions vary according to guidelines[6][7][8][9], and this might reflect say different patient casemix seen in the emergency room, in coronary care units and inpatient wards. It might also reflect the outcome that is to be averted; so you can reduce ITU admissions by using less morphine and more acute ace inhibitor [10] (not a universal accepted treatment due to evidence base issues[11] and known worse outcome if cause of the pulmonary oedema is myocardial ischaemia[12]). In conditions such as pulmonary oedema caused by myocardial infarction without cardiogenic shock there may be an evidence base for a particular order[13], but applying such an order as a generalisation can lead to patient harm[14]. Some authorities might remove opiates which would not be appropriate if palliation of symptoms was a priority.

  • Upright posture
  • Oxygen 60-100% with caution in chronic respiratory disease
    • Indicated in hypoxia
    • Proceeding to NIV (CPAP[15]) although this does not improve long term survival[16]
    • Consider invasive ventilation if hypercapnia. A score predicting the need for intubation has been proposed[17].
  • Furosemide[18]
    • Absolute indication in volume overload[3]
    • Usually 40mg in diuretic naive, double oral dose IV in non-naive
    • Consider that non-naive patient on an alternative to furosemide such as bumetanide may have true allergy to frusemide
  • Morphine/diamorphine
    • Give with metoclopramide and morphine IV in range 2.5-5mg most used dose in adults
    • There is poor evidence that improve outcome[19]
  • GTN (sublingual and infusion (eg in adults start at 2mg/hour) if sBP >100. Other vasodilators have a weaker or negative evidence base or are less quickly reversible[20].
    • Deprecated as first line treatment as of 2014[21]
    • Indicated if myocardial ischaemia
    • Place of combined preload and afterload reducing agents unclear
    • As of 2010 nitroprusside and nesiritide can not be generally recommended as the first does run the risk of cyanide toxicity, particularly in the poor perfusion subgroup, without clear benefit over GTN except in the delay of tachyphylaxis and the second requires further study as long term mortality data was worrying, as was outcome if given with poor renal function[3].
    • Note that nitrate induced hypotension worsens prognosis and intensive haemodynamic monitoring is advised if initial BP <120mmHg
    • They are only a clear choice in hypertensive presentations
  • Treat arrhythmias
    • Digitalisation/amiodarone can be overlooked if you do not react to the ECG after initial measures make patient better in terms of rate control
  • Treat BP if systolic <90 or >180
    • If in acute cardiogenic shock the proven treatments are those directed at underlying cause, circulatory support is only a bridge !
  • Ultrafiltration if gross fluid overload. There is no evidence of benefit in unselected patients compared to fursomide alone[3].
  • Heparin - either thromboprophylactic dose or treatment dose if new atrial fibrillation or myocardial infarction
  • Unproven but possible treatment options as of 2010 are[1]:
    • Tolvaptan (note that conivaptan does not work.
    • Relaxin
    • Adenosine antagonists seem less promising after development was stopped on rolofylline due to poor long term outcomes.
    • Ularitide is a small natriuretic peptide under development
    • Levosimendan and other calcium sensitisers. However levosimendan is no better than dobutamine and preliminary safety signals appear to be arising from more long term follow up.

Chronic left ventricular failure

Suggest refer to guidelines freely available until Ganfyd can do justice to this important topic:

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  1. a b Joseph SM, Cedars AM, Ewald GA, Geltman EM, Mann DL. Acute decompensated heart failure: contemporary medical management. Texas Heart Institute journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital. 2009; 36(6):510-20.
  2. Tribouilloy C, Rusinaru D, Leborgne L, Mahjoub H, Szymanski C, Houpe D, Béguin M, Peltier M. In-hospital mortality and prognostic factors in patients admitted for new-onset heart failure with preserved or reduced ejection fraction: a prospective observational study. Archives of cardiovascular diseases. 2008 Apr; 101(4):226-34.
  3. a b c d Peacock WF, Fonarow GC, Emerman CL, Mills RM, Wynne J. Impact of early initiation of intravenous therapy for acute decompensated heart failure on outcomes in ADHERE. Cardiology. 2007; 107(1):44-51.(Link to article – subscription may be required.)
  4. Abraham WT, Adams KF, Fonarow GC, Costanzo MR, Berkowitz RL, LeJemtel TH, Cheng ML, Wynne J. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). Journal of the American College of Cardiology. 2005 Jul 5; 46(1):57-64.(Link to article – subscription may be required.)
  5. Cuffe MS, Califf RM, Adams KF, Benza R, Bourge R, Colucci WS, Massie BM, O'Connor CM, Pina I, Quigg R, Silver MA, Gheorghiade M. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA : the journal of the American Medical Association. 2002 Mar 27; 287(12):1541-7.
  6. a b Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA, Strömberg A, van Veldhuisen DJ, Atar D, Hoes AW, Keren A, Mebazaa A, Nieminen M, Priori SG, Swedberg K, Vahanian A, Camm J, De Caterina R, Dean V, Dickstein K, Filippatos G, Funck-Brentano C, Hellemans I, Kristensen SD, McGregor K, Sechtem U, Silber S, Tendera M, Widimsky P, Zamorano JL, Tendera M, Auricchio A, Bax J, Böhm M, Corrà U, Della Bella P, Elliott PM, Follath F, Gheorghiade M, Hasin Y, Hernborg A, Jaarsma T, Komajda M, Kornowski R, Piepoli M, Prendergast B, Tavazzi L, Vachiery JL, Verheugt FW, Zamorano JL, Zannad F. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). European heart journal. 2008 Oct; 29(19):2388-442.(Link to article – subscription may be required.)
  7. Bosomworth J. Rural treatment of acute cardiogenic pulmonary edema: applying the evidence to achieve success with failure. Canadian journal of rural medicine : the official journal of the Society of Rural Physicians of Canada = Journal canadien de la médecine rurale : le journal officiel de la Société de médecine rurale du Canada. 2008; 13(3):121-8.
  8. Sacchetti AD, Harris RH. Acute cardiogenic pulmonary edema. What's the latest in emergency treatment? Postgraduate medicine. 1998 Feb; 103(2):145-7, 153-4, 160-2 passim.
  9. Elkayam U, Janmohamed M, Habib M, Hatamizadeh P. Vasodilators in the management of acute heart failure. Critical care medicine. 2008 Jan; 36(1 Suppl):S95-105.(Link to article – subscription may be required.)
  10. Sacchetti A, Ramoska E, Moakes ME, McDermott P, Moyer V. Effect of ED management on ICU use in acute pulmonary edema. The American journal of emergency medicine. 1999 Oct; 17(6):571-4.
  11. Tang WH. Pharmacologic therapy for acute heart failure. Cardiology clinics. 2007 Nov; 25(4):539-51; vi.(Link to article – subscription may be required.)
  12. Lamond NW, Howlett JG. Should we inhibit angiotensin-converting enzymes in acute heart failure? Heart failure monitor. 2007; 5(3):70-6.
  13. Verma SP, Silke B, Hussain M, Nelson GI, Reynolds GW, Richmond A, Taylor SH. First-line treatment of left ventricular failure complicating acute myocardial infarction: a randomised evaluation of immediate effects of diuretic, venodilator, arteriodilator, and positive inotropic drugs on left ventricular function. Journal of cardiovascular pharmacology. 1987 Jul; 10(1):38-46.
  14. Kirk JD, Parissis JT, Filippatos G. Pharmacologic stabilization and management of acute heart failure syndromes in the emergency department. Heart failure clinics. 2009 Jan; 5(1):43-54, vi.(Link to article – subscription may be required.)
  15. Ferrari G, Milan A, Groff P, Pagnozzi F, Mazzone M, Molino P, Aprà F. Continuous Positive Airway Pressure vs. Pressure Support Ventilation in Acute Cardiogenic Pulmonary Edema: A Randomized Trial. The Journal of emergency medicine. 2009 Oct 7.(Epub ahead of print) (Link to article – subscription may be required.)
  16. Gray AJ, Goodacre S, Newby DE, Masson MA, Sampson F, Dixon S, Crane S, Elliott M, Nicholl J. A multicentre randomised controlled trial of the use of continuous positive airway pressure and non-invasive positive pressure ventilation in the early treatment of patients presenting to the emergency department with severe acute cardiogenic pulmonary oedema: the 3CPO trial. Health technology assessment (Winchester, England). 2009 Jul; 13(33):1-106.(Link to article – subscription may be required.)
  17. Di Marco F, Tresoldi S, Maggiolini S, Bozzano A, Bellani G, Pesenti A, Fumagalli R. Risk factors for treatment failure in patients with severe acute cardiogenic pulmonary oedema. Anaesthesia and intensive care. 2008 May; 36(3):351-9.
  18. Biddle TL, Yu PN. Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction. The American journal of cardiology. 1979 Jan; 43(1):86-90.
  19. Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema. Emergency medicine Australasia : EMA. 2008 Oct; 20(5):384-90.(Link to article – subscription may be required.)
  20. Hollenberg SM. Vasodilators in acute heart failure. Heart failure reviews. 2007 Jun; 12(2):143-7.(Link to article – subscription may be required.)
  21. Acute heart failure: diagnosing and managing acute heart failure in adults NICE CG187 2014