Introduction

Heart failure (also CCF – congestive cardiac failure) is a clinical syndrome which refers to a state of reduced cardiac output. Typically it is defined as:

  • The inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands

Heat failure is the end stage of many cardiac diseases. It is a serious condition with a high rate of mortality and morbidity. 50% of patients will die within 5 years of diagnosis. The annual mortality rate is 10%, and 50% for those with severe heart failure.

Studies show that heart failure is chronically under treated. It accounts for 5 in 1000 hospital admission each year in the UK

The classical presentation includes shortness of breath, fatigue and ankle oedema. Signs may include peripheral oedema, hepatomegaly, tachycardia, tachypnoea and raised JVP.
Historically diagnosed clinically (without the need for investigations) with the Framingham Criteria, although more recent guidelines from the European Society of Cardiology require the presence of signs and symptoms of heart failure, with “objective evidence” (usually an echocardiogram).
  • Sometimes heart failure is divided into two broad groups – those with a normal ejection fraction, and those with a reduced ejection fraction, however, the management is essentially the same
  • There is a correlation between ejection fraction and prognosis – the lower the ejection fraction, the worse the prognosis

ACE-inhibitors are the mainstay of treatment and have been shown to increase survival. In the acute presentation with fluid overload, diuretics (particularly frusemide) and GTN are used. B-blockers can improve systolic function in cases where it is impaired. Other drugs that may be considered include digoxin, where atrial fibrillation is a contributory factor, and spironolactone may be added additional to frusemide for symptomatic patients.

The exact drug choices will be influenced by the specific features of the individual case.

Controlling other risk factors and co-morbidities can also prolong survival, for example;

  • Smoking cessation
  • Reducing alcohol consumption
  • Controlling lipids
  • Managing diabetes
  • Encourage exercise
    • May involvedspecific cardiac rehabilitation. Has been shown to improve function and reduce symptoms
  • Diet control
    • Fluid restriction in severe heart failure
    • Minimising salt intake

Terms

There are many terms used in the description of heart failure. In the specialist setting, defining the specific type of heart failure may have an impact on the management (e.g. certain drugs will be more effect in different types of heart failure).

  • Systolic HF – inability of the heart to contract efficiently to eject adequate volumes of blood to meet the body metabolic demand [most common].
  • Diastolic HF – reduction in the heart compliance resulting in compromised ventricular filling and therefore ejection [pericardial disease, restrictive cardiomyopathy, tamponade]. Increasingly recognised as an important cause of heart failure – it is often present in elderly patients with a normal CXR and otherwise unexplained SOBOE (shortness of breath on exertion)
  • Left HF –  inability of the left ventricle to pump adequate amount of blood leading to pulmonary circulation congestions and pulmonary edema. Usually results in RHF due to pulmonary hypertension. Defined as an ejection fraction of <40%. 
  • Right HF –  inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion, therefore peripheral edema and hepatic congestion and tenderness.
  • Congestive HF –  failure of both right and left ventricles, which is more common.
  • Low-output HF –  heart failure resulting from reduced cardiac output [Most common]
  • High-output HF –  heart failure that occurs in normal or high cardiac output due to metabolic demand and supply mismatch, either due to reduced blood oxygen carrying capacity [Anemia] or increase body metabolic demand [thyrotoxicosis]
  • Acute HF –  acute onset of symptom presentation often, but not always due to an acute event [MI, persistent arrhythmia, Mechanical event (ruptured valve, ventricular aneurysm)]
    • Often an acute presentation to hospital
    • May be the first presentation, or may be “acute on chronic”
  • Chronic HF – slow symptoms presentation usually due to slow progressive underlying disease [CAD, HTN]
    • Typically a GP based diagnosis
  • Acute-on-chronic –  acute deterioration of a chronic condition, usually following an acute event [anaemia, infections, arrhythmias, MI]

Epidemiology

  • Affects about 920,000 people in the UK – about 1 in 70 people
  • In the developed world it typically affects 1-2% of the population
    • 10% of the over 70s
    • 50% of over 85s
  • Incidence increases with age – average age of diagnosis is 77
  • Regular Physical activity has been shown to reduce the risk of developing heart failure

Causes of Heart Failure

  • Ischaemic heart disease
    • Myocardial Ischemia
    • Myocardial Infarction
    • In IHD infarction causes impaired ventricular function, therefore reduced contractility function and HF. IHD are the most common cause of HF along with HTN
  • Hypertension
    • Increases strain on the heart, since the heart has to pump blood against a high afterload, leading to hypertrophy which increase the chances of arrhythmias. The heart eventually gets too big for the coronary system to perfuse leading to IHD and compromised ventricular function
  • Valvular disease
    • Mitral Regurgitation [volume overload]
    • Aortic stenosis [Pressure overload] – particularly chronic excessive afterload
    • Tricuspid Regurgitation [volume overload]
    • VSD/ASD [volume overload] – excessive preload
  • Pericardial disease
    • Pericarditis
    • Pericardial effusion
  • Drugs
    • Chemotherapeutic drugs –  Beta-blockers are the most common cause, but calcium channel blockers and ant-arrhythmics are also implicated
    • Alcohol – acute heart failure, arrhythmias such as AF and dilated cardiomyopathy are more common in alcoholics. Alcohol also increases the risk of infection – infection can worsen chronic heart failure due to toxic effects of infection on heart itself along with vasodilation and tachycardia increase myocardial oxygen demand
    • Cocaine
  • Myocarditis
  • Thyrotoxicosis/Myxedema – can cause HF due to direct effects on myocardium, bradycardia and pericardial disease
  • Arrhythmias
    • Bradycardia – CO = HR X SV. Therefore reduced HR reduces CO
    • Tachycardia –Reduced ventricular filling duration, increased heart oxygen demand and ventricular dilatation
    • Abnormal atrial and ventricular contractions  – AF removes active ventricular filling leading to reduced EDV and CO. VT also causes reduced EDV due to reduced ventricular filling period.
  • Cardiomyopathies
    • These are disease of the heart muscle that is not secondary to IHD, HTN, valvular, congenital or pericardial disease. Several types;
      • Congestive; weakening and dilation of ventricular walls leading to overstretching, therefore reduced contractile efficiency. Most common cause of HF in the absence of IHD, valvular disease and HTN. Might have a familial link
      • Hypertrophic; thickening of the heart muscle wall leading to reduced compliance and therefore reduced CO. The thickening involves an increase in fibrous tissue of the heart, which increases the chances of arrhythmias such as ventricular fibrillation, which is a common cause of death in young adults. This disease has a strong familial link.
      • Restrictive; reduced heart compliance without significant increase in muscle wall thickness leading to reduced EDV and CO. This can be caused by infiltrative disease such as sarcoidosis, amyloidosis, hemachromatosis and endocardial fibrosis.
  • Severe Anemia
  • Pulmonary hypertension- Pulmonary pathologies – e.g. COPD

Pathophysiology

  • MAP = CO x TPR
  • CO = SV x Heart Rate
  • SV = EDV – ESV
MAP – Mean Arterial Pressure
CO – Cardiac Output
TPR – Total Peripheral Resistance
SV – Stroke Volume
EDV – End Diastolic Volume
ESV – End Systolic Volume
HF causes a drop in MAP that initially stimulates baroreceptors that feed back into the medullary cardiovascular center [MCVC]. MCVC tries to increase and maintain the MAP by reducing vagal tone and increase sympathetic tone leading to increase heart contractility and rate therefore output. The sympathetic system also stimulates the contraction of arteries [increasing TPR] and veins [increasing venous return] and the release of adrenaline from adrenal medulla, which stimulate all of the above actions. The renin-angiotensis-system [RAS] is also stimulated in heart failure due to reduced kidney perfusion caused by reduced MAP and vasoconstriction and direct sympathetic stimulations. The end product, Angiotensin II, causes vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys. These mechanisms are beneficial initially as they increase blood volume, therefore venous return and SV, TPR and HR, therefore maintaining a high CO, however, chronically these compensatory mechanisms act to worsen the situation;

Increase TPR

  • Increase afterload therefore increasing workload and strain on the heart
  • Tissue underperfusion leading to ischemia
  • RAS system stimulation

Increase HR

  • Increase workload and therefore oxygen demand of the heart

Fluid retention

  • Increase stretching of the heart eventually leading to dilatation of ventricles which possess reduced contractility
  • Fluid build up causes fluid transudation into interstitial tissue causing peripheral and pulmonary oedema
  • Hyponatremia and hypokalemia

Clinical presentations

Symptoms
  • Dyspnea
    • Especially on exertion
    • Due to pulmonary edema and respiratory muscle weakness
  • Orthopnoea – breathlessness on lying flat
  • Paroxysmal nocturnal dyspnoea
    • Dyspnea that occurs during lying down/sleeping forcing sudden awakening of the patient. This occurs due to blood redistribution during lying down causing increase venous blood in the lungs causing transudation of plasma into the alveolar spaces [Pulmonary edema]
    • Ask patients how many pillows they use to sleep at night
  • Fatigue, lethargy and exercise intolerance
    • Exercise intolerance occurs due to inability of the heart to raise the CO during exercise – it is already at the limit of its cardiac output. Fatigue and lethargy occur due to compromised CO leading to tissue hypoperfusion. Muscle tissues are one of the tissues that undergo atrophy and altered metabolism due to hypoperfusion, causing lethargy and fatigue, as well as exercise intolerance when it involves respiratory muscles
  • Peripheral Swelling [oedema]
  • Weight loss
  • Wheeze
  • Cough
    • Often worse at night
    • The ‘classical’ pink frothy sputum is rarely seen
Symptoms of Heart Failure

Symptoms of Heart Failure

Signs
  • Fluid overload
    • Peripheral oedema – ankles +/- sacrum
    • Ascites
    • Elevated JVP [venous congestion]
    • Occurs predominantly due to right heart failure causing blood congestion in systemic circulation, causing increased venous pressure, therefore fluid transudation into the interstitial spaces. These spaces can be the lungs, ankles/sacrum and liver
Elevated JVP

Elevated JVP

Pitting Oedema

Pitting Oedema

  • Pulsus alternans
  • Hypotension
  • Tachycardia
  • Cardiac heave
  • Displaced Apex Beat [sign of cardiomegaly]
    • Normal apex beat is felt around the 5th intercostal space at the mid-clavicular line
    • In cardiomegaly it may be displaced lateral and / or distally (down and out)
  • Gallop [S3]
  • Bilateral Crepitations +/- wheeze
  • Cardiomegaly on CXR
  • Cachexia [deccreased appetite, weight loss, lethargy, muscle atrophy]
  • Hepatic Tenderness / hepatomegaly

Diagnosis

Guidelines about the diagnosis of heart failure vary. Traditionally it was a clinical diagnosis (see Framingham Criteria below), but in recent years, this has been superseded by the use of echocardiography. Most guidelines now recommend a combination of clinical suspicion and echocardiography to confirm the diagnosis.

  • In the UK, the use of a blood test for BNP (brain natriuretic peptide) – particularly N-terminal pro-B-type natriuretic peptide (NT-proBNP) is used to stratify patients in primary care:
    • >2,000 – require urgent referral to cardiology for an echocardiogram (<2 weeks)
    • 400 – 2,000 – require referral to cardiology for an echocardiogram (<6 weeks)
    • <400 – heart failure is unlikely and consider an alternative diagnosis
  • In Australia, the use of BNP testing is reserved for specialists, and patients should be referred for an echo when heart failure is suspected clinically. (There is no medicare rebate for BNP testing by GPs)

The Framingham Criteria

A formal set of diagnostic criteria for congestive heart failure (CHF) resulted from the well-known Framingham Heart Study (an excellent example of a prospective study, to be mentioned in any public health examinations!). As with other diagnostic criteria systems this one makes use of Major and Minor criteria which, apart from being study aids in themselves, are sure to impress finals examiners if you can remember them (mnemonics provided for this purpose!).

Diagnosis of congestive heart failure using the Framingham criteria requires simultaneous presence of 2 Major or 1 Major and 2 Minor criteria, which provide for a 100% sensitivity (but 78% specificity) value when diagnosing the symptoms and signs of CHF.

  • Major
    • S3 heart sound present (‘gallop’ sound)
    • Acute pulmonary oedema (left side of heart is unable to clear fluid from lungs)
    • Weight loss of more than 4.5kg in 5 days when treated (patients lose their retained fluids)
    • Paroxysmal nocturnal dyspnoea
    • Abdominojugular reflux (JVP waveform rises when pressure applied over liver area)
    • Neck vein distended (i.e. JVP elevated at rest)
    • Increased cardiac shadow on X-ray (cardiomegaly: heart occupies more than ≈50% of chest diameter)
    • Crackles heard in lungs
  • Minor
    • Hepatomegaly
    • Effusion, pleural
    • Ankle oedema bilaterally
    • exeRtional dyspnoea
    • Tachycardia
    • Vital capacity decreased by a third of maximum value
    • Nocturnal cough

Small print is that the Minor criteria can only be used if they are not attributable to other medical conditions (eg. pleural effusions cannot be due to infection, malignancy, etc).

One set of mnemonics for the criteria is the following: SAW PANIC for the Major, and HEART ViNo for the Minor. Although, there are probably infinite other (less tame) personalized mnemonics out there!

Investigations

The single most useful investigation is echocardiogram. However, this is not always practicable or timely to access. Initially all patients should have an ECG and CXR, and in the UK, BNP.

ECG

  • Should be performed on all suspected heart failure patients
  • May indicate the underlying cause of the heart failure such as;
    1. Myocardial infarction/ischemia
    2. Bundle Branch Block
    3. Ventricular hypertrophy
    4. Pericardial disease
    5. Arrhythmias
  • A normal ECG makes heart failure unlikely (sensitivity 89%)

CXR

  • Recommended for all suspected HF patients
  • Look for signs of pulmonary congestion, and rule out an alternative cause
    • Cardiomegaly [CTR (cardiothoracic ratio)>50% on PA]
      • L or RVH
      • Pericardial effusion if cardiac silhouette has a global appearance
    • Kerley B lines
    • Upper lobe diversion (prominent upper lobe veins)
    • Pleural effusions
    • Fluid in fissures
  • A normal CXR does not exclude the possibility of Heart Failure
CXR Signs in Heart Failure

CXR Signs in Heart Failure

BNP (Brian natriuretic peptide)

  • BNPs are peptides that cause natriuresis, diuresis and vasodilation. They are the body’s “natural defence” against hypervolaemia
  • BNP levels have been proven to be correlated with cardiac filling pressures
  • Recommended in all patients with suspected HF (UK guidelines) to stratify how urgently they need to see a specialist
  • Also recommended in Australian Heart Foundation guidelines (2018) – but due to lack of medicare rebate for GPs is usually only performed by cardiologist

Other Blood Tests

  1. FEB – for anaemia
  2. U+E for Hyponatremia [in severe disease due to dilution] and Hypokalemia / Hyperkalemia
  3. LFT’s to detect extent of liver congestion/damage
  4. TFT’s to rule out thyrotoxicosis or myxedema
  5. HbA1c to check for co-existing T2DM

Echocardiogram

  • Recommended in all patients with suspected heart failure
  • Can confirm the diagnosis
  • Can calculate the ejection fraction, ventricular wall thickness and other cardiac kinetics
  • Can confirm any underlying structural abnormalities – such as valve disease
  • Helps to stratify the type of HF present and therefore guides management

Angiography – can be used to assess the extent of IHD
Pulmonary function tests – to exclude lung disease causing breathlessness

Classification of Heart Failure

New York Heart Association [NYHA] Classification of Heart Failure. One year mortality in brackets
  • Grade I –(5%)
    • No limitation of function
  • Grade II – (10%)
    • Slight limitation. Moderate exertion causes symptoms, but no symptoms at rest
  • Grade III – (20%)
    • Marked limitation – mild exertion causes symptoms, but no symptoms at rest
  • Grave IV – (50%)
    • Severe limitation. Any exertion causes symptoms. May also have symptoms at rest – but not always the case

Prognosis

  • Depends on the Age, sex and severity of the disease
  • Overall 8 years survival rate of all NYHA classes is 30%
  • One year mortality rate of NYHA class 4 is over 60%
Survival Rates (%) for comparison with heart failure
Time from Dx
1 Year
2 Years
5 Years
Heart Failure
67
41
24
88
80
72
75
64
55
56
48
42

Complications of HF

  1. Muscle underperfusion causing muscle weakness and atrophy causing fatigue, exercise intolerance and dyspnea
  2. Increase risk of thromboembolism and stroke development. This is due to blood stasis, arrhythmias and existing atheromas.
  3. Arrhythmias – arrhythmias are tightly associated with HF and are responsible for a large proportion of death in patients with HF. Arrhythmias usually results from increase in fibrous tissue deposition during tissue remodeling post-insults. Arrhythmias themselves lead to HF therefore they worsen the situation when they exist. AF is the most common atrial arrhythmia that co-exists with HF and is associated with increased risk of thromboembolism and stroke development. Ventricular Tachycardia [VT] is common in advanced HF, which may evolve into ventricular arrhythmias and cardiac arrest. Beta-blockers treatments are used to minimize these VT, hence sudden death
  4. Increased risks of infections that can initiate an acute-on-chronic event

Management

All those suspected of heart failure should be referred to a cardiologist for specialist management. In the meantime, treatment can be initiated in the community (or in the emergency department if an acute presentation). Below, we first discuss chronic, and then emergency management.

Non-pharmacological interventions
  • Exercise
    • Involve in supervised physical activity as this increase general wellbeing
  • Diet
    • Avoid processed foods, plant based whole-food diet
    • Reduce salt intake
    • Monitor weight
    • Fluid restriction (e.g. <1.5L / day) if severe
      • Be wary of dehydration
      • Monitor weight daily
      • If >2kgs weight increase in a day – should seek medical assesment
    • If obese, aim to lose weight
  • Reduce alcohol intake
    • Alcohol increases the risk of arrhythmia
    • It is also a negative ionotrope
    • Advise the recommended safe limits of alcohol intake
  • Smoking cessation
  • Flu vaccination
    • Should be given every year
  • Travel
    • There are no specific travel restrictions for patients with NHYA class I and II
    • For those in III oxygen may be required and is recommended for class IV
  • Sex
    • There are no specific limitations on sexual activity
    • Sublingual GTN may help relieve dyspnoea and chest pain associated with sexual activity but should NEVER be used in conjunction with phosphodiesterase inhibitors (e.g. sildenafil [viagra])
    • Many HF patients also suffer from sexual dysfunction – due to underlying cardiovascular disease, diabetes or another co-morbidity
  • Depression
    • Is common – up to 20% of patients

Pharmacological intervention

Most patients with class I and I disease will be treated with an ACE-i and a diuretic. More severe cases may require additional medications. The choice of beta-blocker and calcium channel blocker is particularly important, as some can worsen prognosis and clinical features.

A(ACEi), B(b-blocker), C(Ca blockers and vasodilators), D(diuretics, digoxin)

ACE inhibitors [enalapril, lisinopril, captopril]

  • Should be used in all patients with an LVEF (left ventricular ejection fraction) <40%
  • Strong vasodilators
  • Reduce afterload and fluid retention therefore slowing down left ventricular disease progression
  • Also improve neuroendocrine abnormalities in CHF
  • Improve prognosis, regardless of the grade of heart failure
  • Recommended for ALL patients, unless renal artery stenosis or previous angioedema
  • Start with a low dose and titrate upwards to control symptoms
  • Can cause dry cough, if intolerable use Angiotensin II inhibitors [e.g. candesartan, valsartan, losartan]
  • Potassium sparing diuretics (e.g. spironolactone) in combination with an ACE can cause hyperkalaemia and should be used with caution

Other vasodilators

  • Hydralazine + Nitrates may be considered in patients intolerant to ACEI and ARB’s

Beta-blockers [e.g. atenolol, bisoprolol, carvedilol]

  • Reduce afterload and heart rate to prevent arrhythmias
  • Shown to improve survival in patients with mild to moderate CHF in combination with an ACE-i
  • Should be used in all patients with an LVEF <40% unless contraindicated
  • Start with low doses and titrate upwards every 2-3 weeks
  • Monitor BP and heart rate with each increase in dose. Maintain normotensive BP and HR >60bpm
  • Use a cardioselective beta-blocker, e.g.
    • Bisoprolol – 1.25mg – 10mg daily
    • Carvediolol – 3mg – 25mg daily
    • Mertoprolol (extended release) – 25mg – 190mg daily
    • Nebivolol 1.25mg – 10mg daily
  • Contraindications
    • Asthma
    • 2nd or 3rd degree heart block
    • Sick sinus syndrome
    • Sinus bradycardia (<50bpm)

Diuretics

  • Useful for helping with fluid overload
  • Avoid using as a monotherapy – particularly in patients with LV systolic dysfunction
  • Require close monitoring of weight and electrolytes
  • Smaller dose of multiple agents rather than large dose of a single agent is preferred
  • Loop diuretics [frusemide] – commonly used first line
    • SE; Electrolyte imbalance, gout
  • Thiazide diuretics
    • Cause a more gentle and slower onset diuresis. Often used first line in milder forms of heart failure. Examples include bendroflumethiazide, hydrochlorothiazide, chlorthalidone or Indapamide
    • SE; Electrolyte imbalances K/Na/Mg, acute gout, hyperglycemia
  • Potassium sparing diuretics [Amiloride, spironolactone] [SE: gynecomastia]
  • Once fluid overload has been controlled, diuretics can be ceased, and patients fluid and salt restricted to maintain euvolaemia.
    • Diuretics are very good at acutely controlling fluid overload, but unlike ACE-inhibitors do not improve long-term outcomes

Digoxin; considered in;

  • Sinus rhythm patients that remain symptomatic even after other pharmacological interventions (third line after ACE-i and diuretics)
  • Patients with severely impaired left ventricular function
  • Recurrent hospital admissions
  • Treating AF in CHF
  • 5 – 250mcg daily
  • Previously was used much more widely before the advent of ACE inhibitors

Amiodarone in arrhythmic patients

Calcium channel blockers

  • Diltiazem and verapamil should be avoided
  • Amlodipine is the recommended agent
  • Other calcium channel blockers may be appropriate but usually initiated with specialist supervision

A stepwise approach

  • ACE inhibitors or ARB
    • ADD diuretic
    • ADD beta-blocker
    • ADD aldosterone antagonist
    • ADD digoxin
    • Consider another vasodilator, e.g. isosorbide dinitrate or hydralazine

Drugs to avoid

  • Felcanide
  • Verapamil, diltiazem and other calcium channel blockers (other than amlodipine)
  • Tricyclic antidepressants
  • Lithium
  • NSAIDs
  • Corticosteroids
  • Drugs known to prolong QT interval (e.g. erythromycin)
Improve Prognosis
Improve Symptoms (but not prognosis)
ACEi
Cardioselective β- blockers (β1)
E.g.  atenolol, bisoprolol, carvedilol
Angiotensin-II receptor antagonists
Spironolactone
  • Loop diuretics
  • Digoxin
  • Vasodilators – e.g. nitrates

Surgical intervention

  • Revascularization in IHD [CABG or Angioplasty (PTA)]
  • Valvular replacement
  • Implanted Automatic cardiodefibrillator or pacemaker
  • Heart transplant may be considered in the end stages

Implantable devices

  • Pacemaker
    • Biventricular pacemakers are useful in patients with heart failure and bundle branch block
  • ICD – implantable cardiac defibrillator
  • Left ventricular assist device (e.g. VentrAssist)

Diastolic heart failure

  • Has a different treatment – aim for ionotropic effect
  • Use calcium channel blockers early – often in combination with beta-blockers
  • Avoid use of diuretics and strong vasodilators as these can worsen the condition – sometimes catastrophically due to decreased cardiac output
  • ACE inhibitors are only sometimes used – and with caution

Common pitfalls in management

  • Overuse of diuretics
  • Use of diuretics as a monotherapy – without use of an ACE-inhibitor
  • Failure to treat underlying causes
  • Failure to monitor electrolytes and renal function

Emergency management

HF can present acutely as acute HF or acute-on-chronic HF

Acute HF
Usual clinical presentations are dyspnea, anxiety and tachycardia. Acute HF can evolve into cardiogenic shock, which is an acute circulatory failure due to improper/inappropriate fluid distribution. Pallor and Hypotension [systolic <90], reduced CO and oliguria characterize cardiogenic shock. SHOCK CAC
Acute HF usually results from an acute event such as MI, arrhythmias, mechanical disease [valve rupture], pericardial disease etc…
Management involves;

  • Sit up and 100% oxygen flow
  • Do an ECG, FBC, U/E, Cardiac enzymes, ABG, CXR
  • Sublingual 2 puffs nitrates or oral to enhance myocardial perfusion
  • IV opiates [diamorphine 2.5-5mg] to reduce anxiety and preload
  • IV frusemide 40-80mg i.v. to reduce fluid retention, hence pulmonary edema
  • If Systolic>90 then give IV infusion isosorbide dinitrate 2-10mg/h, if Sys<90 then treat as cardiogenic shock

In advanced situation can consider;

  • IV inotropic drug [dobutamine] to increase contractility and CO
  • IV Dopamine to enhance renal perfusion to prevent renal failure
  • IV aminophylline to enhance contractility and bronchodilate [slow]
  • Assisted ventilation

Acute-on-Chronic HF

  • Chronic HF is characterized by a slow progressive onset of symptom development. Patients in a stable chronic HF have a compensated heart, which undergo decompensation by acute events such as myocardial ischemia/infarction, infections, persistent arrhythmias, anemia, electrolyte imbalance etc…
  • Patient can either present as acute pulmonary edema i.e. like acute HF with acute dyspnea, tachycardia, anxiety and frothy productive cough, or can present as worsening of chronic HF symptoms i.e. increase breathlessness, fatigue and malaise. In either case, the management stays the same, along with identification and treatment of decompensation cause.

References

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