Chronic Heart Failure |
Acute Heart Failure and Pulmonary Oedema |
Loop Diuretics |
Entresto Sacubitril with Valsartan |
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.
|Initial Cardiogenic Pulmonary Oedema Management Summary|
- Sit patient up legs dependent, ensure comfort. O2 target > 92%
- IV Furosemide 40-80 mg IV. Repeated doses may be needed
- Morphine 2.5-5 mg slow IV or Diamorphine 2.5-5 mg slow IV + Ondansentron or Metoclopramide 10 mg IV
- Consider GTN spray and IV Nitrate if BP > 110 mmHg
- Consider Continuous positive airways pressure 5-10 mmHg
- Control rate with Digoxin if AF. Amiodarone or DC countershock
- Look for cause: STEMI, Arrhythmias, Aortic stenosis.
- A Bedside Echo can be invaluable
- Treat hypertension with IV Nitrates.
- Dialysis/Ultrafiltration if oliguric and renal failure
- 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 > 5000ng/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
- 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 (about 7-12 mmHg) pushes fluid
- A barrier formed by connective tissue and membranes
- When POP > PCP then 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
- Heart failure preserved Ejection fraction (HFpeEF) (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
- 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 fixed
- Severe Anaemia
- Ischaemic heart disease: ACS, STEMI, NSTEMI
- Myocarditis: Viral, Idiopathic, Toxic
- 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 of diuretics, NSAIDs, Steroids.
- Drug overdose: negative inotropes with myocardial depression
- Cardiac tamponade
- 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 aged 80.
- People with heart failure are at risk from 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 noctural dyspnoea
- Tachycardia, Pulsus alternans, Gallop rhythm S3
- Bibasal fine inspiratory crepitations
- Bat wings pumonary oedema on CXR
- Right heart failure
- Elevated JVP
- Hepatomegaly (pulsatile if TR) ascites and even a coagulopathy
and deranged LFTs
- Peripheral oedema
- Parasternal heave
- Nocturia due to redistribution of fluid at night
- Pleural effusion (Right sided usually)
- 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
- Systemic hypertension
- Aortic/Mitral valve disease
- 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
|New York Heart Association (NYHA) Heart Failure Class Patient Symptoms|
| I|| No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).
|II ||Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).
|III|| Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnoea.
|IV|| Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.
Investigations: bedside echo can be very valuable
- FBC: severe anaemia can cause or exacerbate failure
- U&E: renal function and keep a close watch of 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 in those aged < 50
- 900 in those aged 50-75
- 1800 in those aged over 75
- If < 300 ng/L then probably not heart failure.
- 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 and possibly oedema.
- Kerley B lines (engorged pulmonary lymphatics).
- Pleural effusion
- Dilated upper lobe vessels
- ECG: may be normal or signs of IHD, old infarcts, hypertension, AF or bradycardia or CHB or bundle branch blocks, May show arrhythmia, LV hypertrophy or strain. Normal ECG makes heart failure unlikely.
- Echocardiography: can demonstrate global or focal LV dysfunction and valve disease. If the NT proBNP is significantly elevated (see above) acute heart failure is likely and should be confirmed by echocardiography if not already documented. The exception would be the frail elderly for whom an echocardiogram is very unlikely to alter management. The ejection fraction is key when assessing systolic heart failure. It may be expressed as a ratio or percentage
- Ejection Fraction (EF) %: 55% to 70% is normal
- Ejection Fraction (EF) %: 40% to 54% below normal
- Ejection Fraction (EF) %: 35% to 39% Moderately below normal
- Ejection Fraction (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 tiny fraction of cases with unexplained disease
- Angiography - if IHD is suspected to be the underlying
Other causes of "non cardiogenic" Pulmonary Oedema
- High altitude pulmonary oedema
- Acute Respiratory distress syndrome
- 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 + Mitral regurgitation
- Tachyarrhythmias: fast AF, VT, Amiodarone. DC cardioversion
- Bradycardia needing Atropine and/or Pacemaker
- Hypertension: Use IV GTN infusion
- Valve damage or dysfunction:
- Loud Systolic murmur, acute MR or VSD
- EDM, Acute AR from endocarditis or Type A dissection
- PSM: Functional MR from acute cardiomyopathy or myocarditis or endocarditis or a VSD.
- Assess valve repair/replacement with cardiology
- Infection: General sepsis. Manage with antibiotics.
- Failure to take meds: Not taking diuretics, is taking NSAIDS or steroids.
- End stage renal failure: Dialysis.
- Anaemia: Transfuse cautiously
- Fluid overload: seen commonly as a risk of blood transfusion or excess IV fluid or alcohol
Batwing type pulmonary oedema
- Type 1 Respiratory failure with hypoxia. May become Type 2 if exhausted and hypoventilating or 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 closely monitored
- 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/eplenerone or ACEI/ARB
- Hyponatraemia: due to failure medications or SIADH
- VTE: risk of DVT/PE and VTE so 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 get patient comfortable.
- Give High flow O2 target SaO2 > 94-98 % unless COPD then 24-28%
- Nitrates: GTN spray or GTN tablet S/L if SBP > 110 mmHg. IV nitrates may help e.g. GTN Infusion may be considered especially if the BP is actually high.
- Opiates: Chest pain or APO: Give slowly over several minutes Morphine 5-10 mg IV or Diamorphine 2.5-5 mg IV Metoclopramide 10 mg IV (Avoid cyclizine)
- Furosemide 50-100 mg stat IV which venodilates and causes diuresis
- Salbutamol (Albuterol) 5mg 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 to reduce oedema and improve oxygenation if respiratory failure and exhausted : take senior advice and 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.
- Diastolic Heart failure may be difficult to diagnose
- A proportion of elderly patients are on diuretics but have no objective evidence of heart failure (systolic or diastolic).
- Echo should be performed in all patients to identify an aetiology.
- ACEIs should be given to all patients unless contraindicated (i.e. renal impairment, aortic stenosis, renal artery stenosis)
- 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. Diuretics preceded the advent of randomised control trials, and there are no large or long-term placebo-controlled trials of their use. A systematic review of a number of small randomised trials indicated a possible benefit from diuretics in terms of mortality, compared to placebo. However, evidence is very light mainly due to the inability to do an ethical trial. Infusions of Furosemide are used with intractable oedema and a maximum dose of 120 mg over 30 minutes may be administered via a syringe driver.
- ACE inhibitors: Ramipril 1.25 mg od to 5 mg bd, Enalapril 2.5 mg od to 10 mg bd: Systematic reviews of randomised controlled trials comparing ACE inhibitor to placebo have found that ACE inhibitor therapy in patients with heart failure due to left ventricular systolic dysfunction increases life expectancy compared to placebo. The effect is more marked in patients with more severe LV systolic impairment, or more severe symptoms, although there is a benefit for all NYHA classes. Compared with placebo, ACE inhibitor therapy also reduces the risk of hospitalisation for heart failure in such patients, and also for patients with asymptomatic left ventricular systolic dysfunction. 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 for signs of renal impairment and hyperkalaemia
- Beta-Blockers : Bisoprolol 1.25-10 mg od or Carvedilol 3.125-50 mg od : Many large clinical trials reviewed in four meta-analyses, and one subsequent RCT have shown that several Beta-blockers increase life expectancy in patients with heart failure due to LV systolic dysfunction, compared with placebo. This effect has been seen
- Aldosterone antagonists: are licensed for heart failure (option for second-line treatment) usually under specialist advice. Used in moderate to severe heart failure (NYHA class III-IV) or MI in the past month. Monitor potassium and creatinine levels and eGFR. Seek specialist advice if hyperkalaemia develops or renal function deteriorates.
- 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: Despite a small systematic review that suggests that fewer patients withdraw from randomised trials of therapy when on Digoxin than on placebo, there are no published data from randomised control trials on the effect of Digoxin on the signs and symptoms (except for exercise performance) and quality of life of patients with heart failure. Digoxin reduces the risk of admission to hospital with worsening heart failure in patients with heart failure due to LV systolic dysfunction in sinus rhythm and may reduce heart failure-specific mortality. However, a large systematic review and two additional RCT's with medium-term follow up, suggest that it does not increase overall life expectancy. Advised to maintain potassium level > 4.5 mmol/l when on Digoxin.
- Potassium Sparing diuretics:Spironolactone or Eplenerone: 12.5-25 mg od with moderate to severe heart failure (NYHA Class III and IV) due to LV systolic dysfunction, the addition of low-dose spironolactone to therapy with a loop diuretic and ACE inhibitor has been shown in a large randomised controlled trial to increase life expectancy when compared to placebo. In addition, hospitalisation for cardiac causes is greatly reduced.
- Metolazone: potent thiazide diuretic sometimes used under close supervision
- Amiodarone: A small number of RCT and meta-analyses have demonstrated that Amiodarone is effective against most ventricular arrhythmias. Evidence from one-meta analysis with long-term outcome assessment suggests a neutral effect on mortality in patients with heart failure
- Ivabradine: acts on the If inward current in the SAN. Reduction in hospital admission and mortality rates in patients with heart failure due to
moderate or severe left ventricular systolic impairment. 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. Often used where conventional therapy is not considered adequate
- Hydralazine and Nitrates: were one of the earliest combined treatments for heart failure before ACE inhibitors and are still used in whom ACE/AT2 blockers cannot be used. Especially in people of African or Caribbean origin with moderate to severe heart failure (NYHA class III-IV).
- Sacubitril: Inhibitor of neprilysin which breaks down ANP and BNP thus enhancing their effects. Sacubitril is often combined with Valsartan in the treatment of symptomatic heart failure
- Anticoagulation: Warfarin or DOAC or LMWH: may be indicated if there is a failure as CCF gains a point in CHADS scoring. May also be indicated for PE or for LV thrombus or severely impaired LV function and a worry over cardioembolic emboli.
- End stage disease: Consider opiates and patient centred end of life care where appropriate
- Cardiac resynchronization therapy: CRT is recommended in patients with advanced HF (usually NYHA class III or IV), severe systolic dysfunction (eg, left ventricular ejection fraction <35 percent) or intraventricular conduction delay (eg, QRS >120 msec).
- LV assist devices useful bridge to transplant or where there is an expected return of cardiac function e.g. myocarditis.
- Heart Transplant: Contemplated in those with end stage heart failure and under 60 but limited by donor heart shortage
- Is revascularisation needed - angiogram and assessment
- Is valve repair or replacement needed - angiogram and assessment
- Salt restriction
- Start ACE Inhibitor or ARBI and uptitrate to max tolerated dose
- Start Regular diuretic e.g.Furosemide or Bumetanide
- Start Beta blocker (Bisoprolol or Carvedilol) and titrate up
- Exercise rehab program
- Possible angiogram and revascularization by PCI or CABG
- 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
- ECG shows acute MI then Revascularise e.g. Aspirin + thrombolysis (May be too unstable to attempt PCI)
- Intra arterial balloon pump can augment coronary and cerebral perfusion
- Cardiac transplant if end-stage cardiac failure in the young patient
- Progressive failure will ultimately need palliation
- Daily weights. Check U&E, Creatinine, Watch I/O and NEWS score.
- Start Regular diuretics. Watch renal function. Start ACEI/ARB if no C/I and up-titrate dose
- Spironolactone or Eplenerone cause hyperkalaemia so watch K
- Beta blockade watch heart rate.
- Manage causes: PCI/CABG, Valve replacement or repair. CRT pacing. Transplant/Ventricular assist devices