Makindo Medical Notes

Related Subjects: Chronic Heart Failure | Acute Heart Failure and Pulmonary Oedema | Loop Diuretics | Entresto Sacubitril with Valsartan | Ivabradine | Furosemide | Angiotensin Converting Enzyme Inhibitors | Cardiac Resynchronisation Therapy (CRT) Pacemaker |

Even a simple bedside echo can help in the diagnosis and treatment. Get one as soon as possible. Causes of flash pulmonary oedema include severe left ventricular (LV) dysfunction, paroxysmal arrhythmias, three-vessel or left main stem coronary disease, in the context of hypertension, renal artery stenosis, and phaeochromocytoma. The initial assessment should include excluding/treating arrhythmia and/or acute mechanical problems and/or acute coronary syndrome.

About

• Presence of Cardiogenic pulmonary oedema due to cardiac dysfunction.
• Leads to progressive dyspnoea and respiratory failure.
• Acute heart failure has a 30-day mortality of 15% in those with NT-proBNP > 5000 ng/L.
• Prognosis for cardiac failure is often worse than many cancers.
• LV systolic function largely determines prognosis.
• Look for treatable, transient, and transplantable causes.
• Can worsen to become cardiogenic shock.

Aetiology

• There are forces at balance keeping fluid within the vessels:
• Plasma oncotic pressure (POP) (generally about 25 mmHg) holds water in the vessels.
• Pulmonary capillary pressure (PCP) (about 7-12 mmHg) pushes fluid out.
• A barrier formed by connective tissue and membranes.
• When POP > PCP, liquid accumulates in interstitial spaces.
• Raised LV end-diastolic pressure increases pulmonary vein pressures.
• Movement of interstitial fluid into alveolar spaces.
• Impaired gaseous exchange soon leads to hypoxia.
• Oedematous boggy lungs increase difficulty in breathing.

Terminologies

• Heart failure preserved Ejection Fraction (HFpEF) (diastolic heart failure).
• Heart failure with reduced Ejection Fraction (<35%).
• Left heart failure vs. right heart failure.
• Forward failure vs. backward failure.
• Systolic (emptying) failure vs. diastolic (filling) failure.
• High output (Paget's disease, anaemia) vs. low output.
• Congestive cardiac failure = LHF + RHF.
• Afterload - Blood pressure/peripheral resistance.
• Preload - Venous return.

Pathophysiological Causes

• Poor systolic function - problems emptying the LV.
• Poor diastolic function - problems filling the LV.
• Valve regurgitation - forward flow goes backwards.
• Valve stenosis - forward flow impeded.
• Tachycardias - can limit filling.
• Bradycardias - can limit emptying, especially if stroke volume is fixed.
• Severe anaemia.

Pathological Causes

• Ischaemic heart disease: ACS, STEMI, NSTEMI.
• Myocarditis: Viral, idiopathic, toxic.
• Hypertension.
• Cardiomyopathy: Dilated, restrictive, hypertrophic.
• Valve failure: Acute or chronic MR, AR, AS, endocarditis.
• Arrhythmia: VT, SVT, fast AF, bradycardia.
• Fluid overload: Blood transfusion, IV fluids.
• Altered medications: Beta-blockade, stopping diuretics, NSAIDs, steroids.
• Drug overdose: Negative inotropes with myocardial depression.
• Cardiac tamponade.

Why Now - Precipitating Causes

Epidemiology

• Heart failure is a chronic condition predominantly affecting people over the age of 50 years. The incidence of heart failure in the UK is 140 per 100,000 men and 120 per 100,000 women.
• Approximately 900,000 people in England and Wales have heart failure, of which at least half have left ventricular systolic dysfunction.
• The incidence and prevalence of heart failure increase with age, and the average age at first diagnosis is 76 years. Seen in 10% of those over age 80.
• People with heart failure are at risk of sudden cardiac death; this is the most common cause of death in people with mild to moderate heart failure.

Clinical: Right vs. Left Heart Failure

• Left Heart Failure
  • Breathless, distressed, cyanosed.
  • Orthopnea, paroxysmal nocturnal dyspnoea.
  • Tachycardia, pulsus alternans, gallop rhythm S3.
  • Bibasal fine inspiratory crepitations.
  • "Bat wings" pulmonary oedema on CXR.
• Right Heart Failure
  • Elevated JVP.
  • Hepatomegaly (pulsatile if TR), ascites, and even coagulopathy and deranged LFTs.
  • Peripheral oedema.
  • Parasternal heave.
  • Nocturia due to redistribution of fluid at night.
  • Pleural effusion (usually right-sided).
• Causes of Right Heart Failure
  • MI, Cor Pulmonale (lung disease).
  • PE, pulmonary hypertension.
  • Tricuspid/Pulmonary valve disease.
  • Left heart failure.
• Causes of Left Heart Failure
  • IHD/MI.
  • Systemic hypertension.
  • Aortic/Mitral valve disease.
  • Cardiomyopathy.
• Biventricular heart failure: Both sides of the heart are affected. Seen with IHD and cardiomyopathies. Left heart failure eventually causes right heart failure. Biventricular (both RHF + LHF), also called congestive cardiac failure, is the term for a combination.

A reduced EF < 35% is a poor prognostic indicator and needs expert assessment and management.

Clinical Assessment Using NYHA

Investigations: Bedside Echo Can Be Very Valuable

• FBC: Severe anaemia can cause or exacerbate failure.
• U&E: Assess renal function and monitor potassium and other electrolytes during treatment.
• TFT: Rarely, thyroid disease can be a precipitant of failure.
• Troponin: Exclude MI in all patients with acute LVF.
• NT proBNP: HF is likely if NT-proBNP is above:
  • 450 ng/L in those aged < 50.
  • 900 ng/L in those aged 50-75.
  • 1800 ng/L in those aged over 75.
  • If < 300 ng/L, then heart failure is unlikely.
• ABG: Hypoxia, but beware of hypercarbia, which may suggest Type 2 RF or exhaustion (DDx COPD, pneumonia).
• LFT: Often deranged with congestion.
• Chest X-ray: Findings include:
  • Cardiomegaly (CTR > 0.5).
  • Enlarged pulmonary arteries and increased vascular markings, possibly oedema.
  • Kerley B lines (engorged pulmonary lymphatics).
  • Pleural effusion.
  • Dilated upper lobe vessels.
• ECG: May be normal or show signs of IHD, old infarcts, hypertension, AF, bradycardia, CHB, or bundle branch blocks. May show arrhythmia, LV hypertrophy, or strain. A normal ECG makes heart failure unlikely.
• Echocardiography: Can demonstrate global or focal LV dysfunction and valve disease. The ejection fraction (EF) is key when assessing systolic heart failure:
  • EF 55% to 70%: Normal.
  • EF 40% to 54%: Below normal.
  • EF 35% to 39%: Moderately below normal.
  • EF less than 35%: Significant reduction.
• Nuclear cardiology: Using SPECT or PET can assess the viability of dysfunctional myocardium.
• Cardiac MRI: Can help identify myocardial issues combined with dobutamine.
• Myocardial biopsies: In a small fraction of cases with unexplained disease.
• Angiography: If IHD is suspected to be the underlying cause.

Other Causes of "Non-Cardiogenic" Pulmonary Oedema

• High altitude pulmonary oedema.
• Acute Respiratory Distress Syndrome (ARDS).
• Neurogenic pulmonary oedema.
• Heroin or other overdoses.
• Pulmonary embolism.
• Eclampsia, postcardioversion.

Ask: What Is the Cause?

• MI: 12-lead ECG; STEMI can be silent. May need reperfusion. LV infarct. Papillary muscle ischaemia leading to mitral regurgitation.
• Tachyarrhythmias: Fast AF, VT; consider Amiodarone or DC cardioversion.
• Bradycardia needing Atropine and/or pacemaker.
• Hypertension: Use IV GTN infusion.
• Valve damage or dysfunction:
  • Loud systolic murmur, acute MR or VSD.
  • Early diastolic murmur (EDM), acute AR from endocarditis or Type A dissection.
  • Pansystolic murmur (PSM): Functional MR from acute cardiomyopathy, myocarditis, endocarditis, or a VSD.
  • Assess for valve repair/replacement with cardiology.
• Infection: General sepsis; manage with antibiotics.
• Failure to take meds: Not taking diuretics, or taking NSAIDs or steroids.
• End-stage renal failure: Dialysis.
• Anaemia: Transfuse cautiously.
• Fluid overload: Commonly due to blood transfusion, excess IV fluid, or alcohol.

Batwing type pulmonary oedema

Complications

• Type 1 Respiratory failure with hypoxia. May become Type 2 if exhausted and hypoventilating or due to excess opiates.
• Atrial fibrillation: Assess CHADS-VASC and HAS-BLED score to reduce thromboembolic risk. Control rate with beta-blockade or Digoxin.
• Renal failure: Forward failure and use of diuretics and ACEI/ARB. Serum creatinine needs close monitoring.
• Liver congestion with abnormal LFTs and deranged coagulation.
• Cardiac cachexia: Sarcopenia, fatigue, and frailty.
• Hypokalaemia: Usually due to loop diuretics.
• Hyperkalaemia: As part of AKI or secondary to spironolactone/eplerenone or ACEI/ARB.
• Hyponatraemia: Due to failure medications or SIADH.
• VTE: Risk of DVT/PE; needs effective thromboprophylaxis when inpatient.
• Ventricular Tachycardia: Sustained and non-sustained VT. High risk may need ICD.
• Sudden cardiac death.

Management: Immediate Actions

• Position: Sit up with legs dependent and ensure patient comfort.
• Give high-flow O₂ targeting SaO₂ > 94-98% unless COPD, then 24-28%.
• Nitrates: GTN spray or GTN tablet sublingual if SBP > 110 mmHg. IV nitrates may help, e.g., GTN infusion, especially if BP is high.
• Opiates: For chest pain or acute pulmonary oedema:
  • Give slowly over several minutes: Morphine 5-10 mg IV or Diamorphine 2.5-5 mg IV.
  • Administer Metoclopramide 10 mg IV (avoid cyclizine).
• Furosemide 50-100 mg stat IV, which venodilates and causes diuresis.
• Salbutamol (Albuterol) 5 mg Neb if significant wheeze and bronchospasm. It may worsen tachycardia. IV formulation can worsen acidosis.
• Fast AF: Digoxin loading for fast AF can help. IV Amiodarone is an alternative when compromised.
• CPAP may help reduce oedema and improve oxygenation if respiratory failure and exhaustion are present; take senior advice. Mechanical ventilation and IPPV may be needed.
• Inotropes may be considered.
• Mechanical assist/Balloon pump where there is myocardial or valve failure to improve coronary and cerebral perfusion. Not if aortic regurgitation is present.
• Diastolic heart failure may be difficult to diagnose.

Ongoing Therapies

• Loop Diuretics: Furosemide 20-120 mg OD or IV in divided doses; Bumetanide 1-3 mg daily orally. Diuretics remain a key element in the treatment of heart failure.
• ACE Inhibitors: Ramipril 1.25 mg OD to 5 mg BD, Enalapril 2.5 mg OD to 10 mg BD. Measure renal function after each increase in dose.
• Angiotensin II Receptor Blockers: Used as second-line therapy when ACEI not tolerated. Monitor serum urea, electrolytes, creatinine, and eGFR.
• Beta-Blockers: Bisoprolol 1.25-10 mg OD or Carvedilol 3.125-50 mg OD. Start low and titrate up.
• Aldosterone Antagonists: Used in moderate to severe heart failure (NYHA class III-IV) or MI in the past month. Monitor potassium and creatinine levels and eGFR.
• Digoxin 125-250 mcg per day: In those not on it, start with normal renal function Digoxin 500 mcg PO stat and then 125 mcg daily after that.
• Potassium-Sparing Diuretics: Spironolactone or Eplerenone 12.5-25 mg OD.
• Amiodarone: Effective against most ventricular arrhythmias.
• Ivabradine: Useful in those with fast HR but cannot take beta-blockers. No use in atrial fibrillation.
• Levosimendan: Short-term treatment of acutely decompensated severe chronic heart failure.
• Hydralazine and Nitrates: Used in those who cannot tolerate ACE inhibitors or ARBs.
• Sacubitril: Often combined with Valsartan in the treatment of symptomatic heart failure.
• Anticoagulation: Warfarin or DOAC or LMWH may be indicated.
• End-stage disease: Consider opiates and patient-centered end-of-life care where appropriate.
• Cardiac Resynchronization Therapy (CRT): Recommended in patients with advanced HF.
• LV Assist Devices: Useful bridge to transplant or where there is an expected return of cardiac function.
• Heart Transplant: Considered in those with end-stage heart failure and under 60 but limited by donor heart shortage.

Further Management

• Is revascularization needed? Angiogram and assessment.
• Is valve repair or replacement needed? Angiogram and assessment.
• Salt restriction.
• Start ACE Inhibitor or ARB and uptitrate to max tolerated dose.
• Start Regular diuretic, e.g., Furosemide or Bumetanide.
• Start Beta-blocker (Bisoprolol or Carvedilol) and titrate up.
• Exercise rehabilitation program.
• Possible angiogram and revascularization by PCI or CABG.

Other Treatments

• Treat arrhythmias, e.g., defibrillate if VT or SVT.
• Treat severe hypertension if a hypertensive crisis.
• Defibrillate or rate control AF (Digoxin or Amiodarone).
• Consider pacemaker if heart block.
• If ECG shows acute MI, then revascularize, e.g., Aspirin + thrombolysis.
• Intra-aortic balloon pump can augment coronary and cerebral perfusion.
• Cardiac transplant if end-stage cardiac failure in a young patient.
• Progressive failure will ultimately need palliation.

Ongoing Care

• Daily weights. Check U&E, creatinine, watch I/O and NEWS score.
• Start regular diuretics. Watch renal function. Start ACEI/ARB if no contraindications and uptitrate dose.
• Spironolactone or Eplerenone can cause hyperkalaemia, so monitor K⁺ levels.
• Beta-blockade: Watch heart rate.
• Manage causes: PCI/CABG, valve replacement or repair, CRT pacing, transplant, ventricular assist devices.

References

• Acute and Chronic Heart Failure Guidelines, ESC Clinical Practice Guidelines 2016
• Full NICE Guidance on Heart Failure
• NICE Quickview