Heart failure

Question 1

What is heart failure?

Answer 1

clinical syndrome - when heart cannot maintain adequate output or can only do so at expense of elevated ventricular filling pressure

Question 2

What is congestive heart failure?

Answer 2

patient with breathlessness

AND abnormal Na/H20 retention resulting in edema

Question 3

What would be considered mild/moderate HF?

Answer 3

Cardiac output normal at rest - only impaired when metabolic demand increases during exercise/stress

Question 4

What symptoms may someone present with?

Answer 4

• low cardiac output

- pulmonary congestions or systemic venous congestion

Question 5

What are the most common causes of heart failure?

Answer 5

• coronary artery disease

- myocardial infarction

Question 6

What are the classifications of HF based on left ventricular ejection fraction?

Answer 6

Based on left ventricular ejection fraction:

Heart failure with reduced ejection fraction (symptoms and signs with LVEF <40%)

Heart failure with midrange ejection fraction (symptoms and signs with LVEF 40-49%)

• Elevated BNP
• Relevant structural heart disease (LVH) or diastolic dysfunction

Heart failure with preserved ejection fraction (symptoms and signs >50%)
• As above

Question 7

What are the different types of heart failure and their causes?

Answer 7

Systolic failure; causes: IHD, MI, cardiomyopathy

Diastolic failure (preserved ejection fraction); causes: hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy,

LVF; symptoms: poor ET, fatigue, orthopnoea, PND, pink sputum

RVF; causes: LVF, pulmonary stenosis, cor pulmonale; symptoms: oedema

Question 8

What does diastolic HF have?

Answer 8

preserved ejection fraction

Poor ventricular filling and high filling pressures stemming from abnormal ventricular relaxation (diastolic dysfunction).

Stiff, non-compliant ventricle

Commonly found in patients with left ventricular hypertrophy.

Question 9

What is the pathophysiology in left-sided HF?

Answer 9

• Reduction in left ventricular output
• Increase in left atrial and pulmonary venous pressure.
• Acute increase in left atrial pressure → pulmonary congestion or pulmonary oedema
• Gradual increase in left atrial pressure (e.g. mitral stenosis) → reflex pulmonary vasoconstriction (protects patient from pulmonary oedema) → Increases pulmonary vascular resistance → causes pulmonary hypertension (CAN impair right ventricular function)

Question 10

What is the pathophysiology in right sided HF?

- causes of isolated right HF

Answer 10

•	Reduction in right ventricular output 
•	Increase in right atrial and systemic venous pressure. 
•	Causes of isolated right HF:
o	Chronic lung disease (cor pulmonale)
o	Pulmonary embolism 
o	Pulmonary valvular stenosis

Question 11

What is the pathophysiology of biventricular HF?

- what may cause it?

Answer 11

• Disease process may affect both ventricles
o Dilated cardiomyopathy
o Ischaemic heart disease
• Disease of left heart leads to chronic elevation of left atrial pressure, pulmonary hypertension and right heart failure

Question 12

High-output failure 


Answer 12

Due to excessively high cardiac output

Large arteriovenous shunt
Beri-beri
Severe anaemia
Thyrotoxicosis

Question 13

What might be a cause of sudden heart failure?

Answer 13

MI

Question 14

What are some causes of gradual HF?

Answer 14

Valvular heart disease

Question 15

What event may precipitate overt or acute HF?

Answer 15

o Myocardial ischaemia or infarction
o Intercurrent illness – infection
o Arrhythmia – atrial fibrillation
o Innapropriate reduction of therapy
o Administration of drug with negative inotropic (beta-blocker) or fluid-retaining properties (NSAIDs, corticosteroids)
o Pulmonary embolism
o Conditions associated with increased metabolic demand – pregnancy, thyrotoxicosis, anaemia
o IV fluid overload – post-operative IV infusion

Question 16

Left vs Right heart failure

• JVP
• signs
• oedema

Answer 16

Left heart failure	
Raised JVP +/++
Pulmonary oedema
Pleural effusion
Cardiomegaly	
Pitting oedema +/++

Right heart failure
Raised JVP +++
Hepatomegaly
Ascites
Peripheral pitting oedema +++

Question 17

Framingham’s criteria for CHF

• what criteria must be met - how many major/minor?
• what are major criteria?
• what are minor criteria?

Answer 17

2 major or 1 major/2 minor

Major criteria: neck vein distension, rales, pulmonary oedema, S3 gallop, raised JVP, hepatojugular reflux, cardiomegaly, PND

Minor criteria: ankle oedema, night cough, SOBOE, hepatomegaly, pleural effusion, tachycardia

Question 18

Acute left heart failure

What would you expect in - acute de novo L ventricular failure
- Acute-on-chronic HF

Answer 18

Acute de novo left ventricular failure
o Sudden onset dyspnoea at rest → rapidly progresses to acute respiratory distress
o Orthopnoea
o Prostration
o Precipitant – e.g. acute MI - often apparent from history
o Agitated, pale and clammy.
o Cool peripheries
o Rapid pulse
o Inappropriate bradycardia / excessive tachycardia should be identified – as may be precipitant
o BP usually high - SNS activation. May be normal or low if patient is in cardiogenic shock.
o JVP - usually elevated esp. if have fluid overload or right heart failure.
o There has been no time for ventricular dilatation → apex not displaced.
o ‘Gallop’ rhythm, with third heart sound (S3/4)
• Heard quite early
o New systolic murmur may signify acute mitral regurgitation or ventricular septal rupture.
o Pulmonary oedema → crepitations at lung bases, or throughout the lungs if pulmonary oedema is severe.
• May also have expiratory wheeze.

Acute-on-chronic heart failure
o Additional features of long-standing heart failure
o Precipitating factors leading to decompensation of chronic heart failure:
• Cor pulmonale (raised hydrostatic pressure, ventricle dilatation)
• Changes in medication (beta-blockers, inappropriate cessation of water tablets, ibuprofen)
• Infection (esp. viral myocarditis in young patients or endocarditis, upper resp tract infection)
• Sepsis (high output disease)

Question 19

Chronic heart failure

• how does it progress?
• what are the symptoms of low cardiac output?
• what finding would suggest left heart failure?
• what findings would suggest right heart failure?
• what unusual findings may be seen?

Answer 19

• Commonly relapsing & remitting course - periods of stability and episodes of decompensation → worsening symptoms that may need hospitalisation.
• Features seen depend on underlying heart disease, type of heart failure, and neurohumoral changes that have developed.
• Low cardiac output → fatigue, listlessness and poor effort tolerance
o Cold peripheries
o Low BP
o To maintain perfusion of vital organs, blood flow is diverted away from skeletal muscle → may contribute to fatigue and weakness.
o Poor renal perfusion → oliguria and uraemia. 

• Left heart failure - pulmonary oedema presents as above and with inspiratory crepitations over lung bases.
• Right heart failure → high JVP with hepatic congestion and dependent peripheral oedema.
• Oedema
o Ambulant – ankles
o Bed-bound – thighs and sacrum
o May get ascites or pleural effusion.
• May be associated with marked weight loss (cardiac cachexia)
o Caused by combination:
• Anorexia
• Impaired absorption due to GI congestion
• Poor tissue perfusion due to low cardiac output
• Skeletal muscle atrophy due to immobility. 


Question 20

What is the ddx of peripheral edema?

Answer 20

Cardiac failure: right or combined left and right heart failure, pericardial constriction, cardiomyopathy 


Chronic venous insufficiency: varicose veins 


Hypoalbuminaemia: nephrotic syndrome, liver disease, 
protein-losing enteropathy; often widespread, can affect 
arms and face 


Drugs: 
Sodium retention: fludrocortisone, NSAIDs 
Increasing capillary permeability: nifedipine, amlodipine 


Idiopathic: women > men 


Chronic lymphatic obstruction 


Question 21

What complications may occur in advanced heart failure?

Answer 21

Renal failure
o Due to poor renal perfusion because of low cardiac output
o May be exacerbated by diuretic therapy, ACE inhibitors & angiotensin receptor blockers 


Hypokalaemia
o Due to:
• Treatment with potassium-losing diuretics
• Hyperaldosteronism caused by activation of RAAS
• Impaired aldosterone metabolism due to hepatic congestion.
• Most of body’s potassium is intracellular → may be depletion of potassium stores, even when plasma concentration is in reference range. 


Hyperkalaemia
o May be due to drugs which promote renal resorption of potassium
o E.g.
combination of ACE inhibitors
(or angiotensin receptor blockers) and mineralocorticoid receptor antagonists.
o Effects amplified if there is renal dysfunction due to low cardiac output or atherosclerotic renal vascular disease. 


Hyponatraemia
o Feature of severe heart failure - poor prognostic sign.
o Causes:
• Diuretic therapy
• Inappropriate water retention due to high ADH secretion
• Failure of cell membrane ion pump. 


Impaired liver function
o Caused by hepatic venous congestion and poor arterial perfusion
o Mild jaundice and abnormal liver function tests
o Reduced synthesis of clotting factors - anticoagulant control may be difficult. 


Thromboembolism.
o Deep vein thrombosis and pulmonary embolism
o May occur due to effects of low cardiac output and enforced immobility.
o Systemic emboli:
• Patients with atrial fibrillation or flutter
• Intracardiac thrombus complicating conditions (e.g mitral stenosis, MI or left ventricular aneurysm)

Atrial and ventricular arrhythmias
o Very common
o May be related to:
• Electrolyte changes (e.g. hypokalaemia, hypomagnesaemia)
• Underlying cardiac disease
• Pro-arrhythmic effects of sympathetic activation.
o Atrial fibrillation
• 20% of patients with heart failure
• Causes further impairment of cardiac function.
o Sudden death
• 50% of patients with heart failure
• Often due to a ventricular arrhythmia.
o Frequent ventricular ectopic beats and runs of non-sustained ventricular tachycardia common findings
• Associated with adverse prognosis. 


Question 22

Heart failure investigations?

Answer 22

Investigations
• Serum urea, creatinine and electrolytes, haemoglobin, thyroid function, ECG and chest X-ray may help establish nature and severity of underlying heart disease and detect complications.
• Electrolytes→ calcium, magnesium, potassium
• Ferritin - Transferrin saturation→ for evaluation of cardiomyopathy due to iron overload cardiomyopathy (elevated)
• Brain natriuretic peptide (BNP)
o Elevated in heart failure
o Marker of risk
o Useful in patients with breathlessness or peripheral oedema. 

• ECHO – consider in all patients
o Determine aetiology
o Detect hitherto unsuspected valvular heart disease, such as occult mitral stenosis, and other conditions that may be amenable to specific remedies 

o Identify patients who will benefit from long-term drug therapy – e.g. ACE inhibitors
o Systolic HF: depressed/dilated LV and RV; Diastolic HF: LVH
• Chest x-ray
o High pulmonary venous pressure in left-sided heart failure
• 1st shows as abnormal distension of upper lobe pulmonary veins (with patient in the erect position).
• Vascularity of lung fields becomes more prominent - Right and left pulmonary arteries dilate.
• Subsequently, interstitial oedema causes thickened interlobular septa and dilated lymphatics – horizontal lines in costophrenic angles (septal or ‘Kerley B’ lines).
• More advanced changes due to alveolar oedema → hazy opacification spreading from the hilar regions, and pleural effusions.

Question 23

HF - what would be found on CXR?

Answer 23

High pulmonary venous pressure in left-sided heart failure

1st shows as abnormal distension of upper lobe pulmonary veins (with patient in the erect position).

Vascularity of lung fields becomes more prominent - Right and left pulmonary arteries dilate.

Subsequently, interstitial oedema causes thickened interlobular septa and dilated lymphatics – horizontal lines in costophrenic angles (septal or ‘Kerley B’ lines).

More advanced changes due to alveolar oedema → hazy opacification spreading from the hilar regions, and pleural effusions.

Question 24

Management of chronic HF

Answer 24

o Beta-blocker: improves symptomatic and prognosis by reducing contractility e.g. carvedilol
o ACEi: improves prognosis by prevent cardiac remodelling from RAAS
o Diuretic: improves symptoms (loop e.g. furosemide 40mg or bumetanide 1-2mg), improves prognosis (spironolactone) by prevent mineralocorticoid effects
o Digoxin: reduces admissions
o Pace-makers for chronic management to manage arrhythmias
o If decompensation: withhold beta-blocker and ACEi due to possible AKI

Question 25

Management of acute HF

Answer 25

o No beta-blockers, only given in chronic HF when tachycardic
o Oxygen reservoir
o GBT: dilates vessels to reduce pulmonary oedema
o Diuretics
o Morphine
o Dobutamine: positive inotropes to increase heart function
o CPAP
o Dobutamine/CPAP fixes low BP without using IV bolus and maintains oxygen

Question 26

Management of acute pulmonary edema

Answer 26

Acute medical emergency

Sit patient up to reduce pulmonary congestion

Give oxygen (high-flow, high-concentration)
 - Non-invasive positive pressure ventilation (continuous positive airways pressure (CPAP) of 5–10 mmHg) by a tight-fitting facemask 

Administer nitrates

• IV glyceryl trinitrate (10–200 μg/min or buccal glyceryl trinitrate 2–5 mg, titrated upwards every 10 minutes)
• Until clinical improvement occurs or systolic BP falls to less than 110 mmHg. 


Administer loop diuretic, such as furosemide (50–100 mg IV). 


Patient should initially be kept rested, with continuous monitoring of cardiac rhythm, BP and pulse oximetry.

IV opiates must be used sparingly in distressed patients

• May cause respiratory depression and exacerbation of hypoxaemia and hypercapnia.
• If ineffective → inotropic agents may be required to augment cardiac output, particularly in hypotensive patients.

Insertion of an intra-aortic balloon pump may be beneficial in patients with acute cardiogenic pulmonary oedema and shock. 


Question 27

In what patients might you want to reduce preload?

Answer 27

patients with high end-diastolic filling pressures and evidence of pulmonary of systemic venous congestion

Question 28

In what patients might you want to reduce after load or increase myocardial contractility?

Answer 28

Signs/symptoms of low cardiac output

Question 29

What is the main aim of diuretic therapy?

Answer 29

• Increase in urinary Na & water excretion → reduce blood and plasma volume
• Reduces preload
• Improves pulmonary and systemic venous congestion.
• May also reduce afterload and ventricular volume → fall in ventricular wall tension & increased cardiac efficiency.
• Fall in preload (ventricular filling pressure) tends to reduce cardiac output, BUT ‘Starling curve’ in heart failure is flat
o So there may be substantial and beneficial fall in filling pressure with little change in cardiac output
o Excessive diuretic therapy may cause undesirable fall in cardiac output, especially in patients with marked diastolic component to their heart failure. This leads to hypotension, lethargy and renal failure.
• In some patients with severe chronic heart failure, particularly if there is associated renal impairment, oedema may persist, despite oral loop diuretic therapy.
o IV infusion of furosemide (5–10 mg/hr) may initiate diuresis.
o Combining loop diuretic with thiazide diuretic (e.g. bendroflumethia- zide 5 mg daily) may be effective, but can cause excessive diuresis.
• Mineralocorticoid receptor antagonists
o Spironolactone and eplerenone → potassium-sparing diuretics that
o Good in patients with heart failure with severe left ventricular systolic dysfunction.
o May cause hyperkalaemia, especially if used with ACE inhibitor.
o Improve longterm clinical outcome in patients with severe heart failure or heart failure following acute MI.

Question 30

What is the main aim of ACEinhibitor treatment?

Answer 30

• Preventing the conversion of angiotensin I to angiotensin II → prevent peripheral vasoconstriction, activation of SNS, and salt and water retention due to aldosterone release.
• Also prevent undesirable activation of RAAS caused by diuretic therapy.
• Moderate/severe heart failure
o ACE inhibitors - improvement in effort tolerance and in mortality, outcome and prevent onset of overt heart failure in patients with poor residual left ventricular function following MI
• Can cause symptomatic hypotension and impairment of renal function, especially in patients with bilateral renal artery stenosis or those with pre- existing renal disease.
• An increase in serum K concentration may occur that can offset hypokalaemia associated with loop diuretic therapy.
• Short-acting ACE inhibitors can cause marked falls in BP, particularly in elderly or when started in the presence of hypotension, hypovolaemia or hyponatraemia.
• Stable patients without hypotension (systolic BP > 100 mmHg), ACE inhibitors can usually be safely started in community.
• Inother patients, usually withhold diuretics for 24 hours before starting treatment with a small dose of a long-acting agent, preferably given at night
• Renal function and serum potassium must be monitored and should be checked 1–2 weeks after starting therapy.

Question 31

Angiotensin receptor blocker therapy

Answer 31

• Block action of angiotensin II on heart, peripheral vasculature and kidney.
• Heart failure - produce beneficial haemodynamic changes similar to effects of ACE inhibitors but generally better tolerated.
• Comparable effects on mortality and useful alternative for patients who cannot tolerate ACE inhibitors
• Have serious SE like ACEi - renal dysfunction and hyperkalaemia.
• Normally used as alternative to ACE inhibitors, but can be combined in patients with resistant or recurrent heart failure.

Question 32

Vasodilator therapy

Answer 32

• Use: chronic heart failure, when ACE inhibitor or ARB drugs are contraindicated (e.g. in severe renal failure).
• Venodilators – e.g. nitrates- reduce preload
• Arterial dilators – e.g. hydralazine - reduce afterload
• Use limited by pharmacological tolerance and hypotension

Question 33

Beta-adrenoceptor blocker therapy

Answer 33

• Counteract deleterious effects of enhanced sympathetic stimulation and reduces risk of arrhythmias and sudden death.
• When initiated in standard doses, may precipitate acute-on-chronic heart failure
• When given in small incremental doses (e.g. bisoprolol started at a dose of 1.25 mg daily, and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily), can increase ejection fraction, improve symptoms, reduce frequency of hospitalisation and reduce mortality in patients with chronic heart failure
• More effective at reducing mortality than ACEi: relative risk reduction of 33% versus 20%, respectively.

Question 34

Ivabardine

Answer 34

• Acts on If inward current in SA node → reduce HR
• Reduces hospital admission and mortality rates in patients with HF due to moderate or severe left ventricular systolic impairment.
• Best results in those with high HR (>77/min) →best suited to patients who cannot take β-blockers or in whom HR remains high despite β-blockade.
• Ineffective in patients in atrial fibrillation.

Question 35

Digoxin

Answer 35

• Provide rate control in patients with HR and atrial fibrillation
• In severe heart failure (NYHA class III–IV) - reduces likelihood of hospitalisation for HF, although has no effect on long-term survival.

Question 36

Amiodarone

Answer 36

• Potent anti-arrhythmic drug - little negative inotropic effect
• Use: patients with poor left ventricular function.
• Only effective in treatment of symptomatic arrhythmias,
• Should not be used as preventative agent in asymptomatic patients.