HEART FAILURE
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Presentation
→ typically manifests with dyspnoea and fatigue which may limit exercise tolerance. Usually also with features of fluid
retention.
▪ Shortness of breath (SOB)
▪ Paroxysmal nocturnal dyspnoea
▪ Orthopnoea
▪ Ankle swelling
▪ Wheeze
▪ Fatigue
▪ Weight loss
▪ Tiredness
▪ Falling exercise tolerance
▪ Palpitations
▪ Depression
▪ Gout
▪ Raised JVP
▪ Displaced apex
▪ Crackles and pulmonary crepitations
▪ Heart sounds S3/4
▪ Pulsus alternans
▪ Hepatomegaly
▪ Ascites.
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Pathophysiology
→ inability of the heart to maintain adequate cardiac output (CO)
▪ Many sources of cause:
o Vascular (most common) → IHD, HT
o Muscular → dilated cardiomyopathy, hypertrophic cardiomyopathy (HCM), congenital heart disease
o Valvular → stenotic or regurgitant valves
o Electrical → arrhythmias may cause acute HF through decompensation
o High-output → low systemic vascular resistance with high CO due to anaemia, septicaemia, thyrotoxicosis,
liver failure.
▪ HF pathophysiology is based on the Frank-Starling law
o This is the relationship between ventricular stretching and contractility
o Stretching cardiac muscle → increase force of contraction
o The ability of the heart to respond to increased venous return by increasing the stroke volume (SV) is essential
to normal cardiac function
o ↑ venous pressure → ↑ venous return and ↑ end diastolic volume (EDV) → ↑ preload
o ↑ EDV → ↑ cardiomyocyte stretch and ↑ length of sarcomere → ↑ force of contraction → ↑ SV
o Failure to do this would → input-output mismatch ad pooling of the blood in systemic or pulmonary
circulation
▪ Primary determinants of SV → preload, myocardial contractility, afterload
▪ At a point, increase in preload leads to a depression of contractility and SV
▪ As the heart fails, the amount of blood left after each contraction increases (the ejection fraction decreases)
▪ This increased end-systolic volume (ESV) → myocardium experiences greater stretch
▪ In a failing heart, this causes a reduction in SV and → reduction in cardiac output (CO)
▪ The body may compensate for this reduced CO in many ways:
o Increasing preload (increasing venous pressures)
▪ This increases EDV compensating for the reduced ejection fraction
▪ This will aim to maintain CO
▪ In severe cases this causes → pulmonary oedema, ascites, peripheral oedema
o Increasing heart rate (sinus tachycardia)
▪ CO = SV x HR.
▪ RAS is also triggered by reduced CO
o Reduced CO → renal hypoperfusion and activation of RAS
o This contributes to increased venous pressures
o Also causes sodium and water retention → oedema.
▪ The sympathetic NS is also triggered by reduced CO
o This activates the SNS via baroreceptors → increases myocardial contractility and HR
o Chronic activation is detrimental
, o This triggers myocyte cell death and further RAS activation.
▪ To maintain CO → hypertrophy of myocardium
o Patients tend to be asymptomatic at rest initially
o Physical activity may lead to → decompensation and symptoms.
Types
HF is a complex condition that can be split into many classifications: acute or chronic, right or left, systolic or diastolic and
high or low output.
Systolic vs diastolic
▪ Systolic
o Reduced left ventricular ejection fraction (LVEF)
▪ The heart is pumping out a reduced proportion of the blood that fills the ventricles during diastole
o = ventricular dilation and eccentric remodelling.
▪ Diastolic
o Impaired ventricular relaxation or filling
o Contraction is unaffected so → LVEF preserved
o May be called “heart failure with preserved LVEF”
o = ventricular hypertrophy and concentric remodelling may occur
o Echo shows: LV hypertrophy, LA dilation, abnormal relaxation
o Stiffness of the ventricular wall with impaired filling and reduced CO
Acute vs chronic
§ Acute
o Rapid onset of worsening symptoms and/or signs of HF
o Life-threatening
o May occur acutely (cardiogenic shock) or as a consequence of acute decompensation of chronic HF (CHF)
o Most common causes: acute myocardial dysfunction (ischaemic, inflammatory), acute valvular disease,
pericardial tamponade
o Can be dramatic with flash pulmonary oedema
▪ Present in extremis, requires precipitant (ischemia, arrhythmia, intercurrent infection)
o Can also be due to gradual deterioration → fluid accumulation, falling exercise tolerance, orthopnoea and
paroxysmal nocturnal dyspnoea
§ Chronic
o Progressive cardiac dysfunction due to structural and/or functional cardiac abnormalities
o Results in reduced CO and/or elevated intracardiac pressures at rest or on stress
o Precipitated by conditions that affect muscles (cardiomyopathy), vessels (ischaemic heart disease), valves (AS)
or conduction (AF)
o Slowly progressive, punctuated by periods of acute decompensation
o Px develop chronic, progressive symptoms but may present with acute decompensation.
Right vs left
▪ Left
o May be caused by many conditions affecting the heart
o Advanced LSHF commonly causes → right sided HF due to increased intrathoracic pressure and pulmonary
HT
▪ Right
o Commonly result of advanced LSHF
▪ Biventricular failure often called = congestive heart failure
o Primary RSHF is uncommon
o Causes broadly divided into 3 categories:
▪ Secondary to pulmonary HT
▪ May occur secondary to LSHF, primary pulmonary HT or significant pulmonary disease (e.g. COPD)
▪ Secondary to pulmonary/tricuspid valve pathology
▪ Pericardial disease.
Classification
Class I: no symptoms
Class II: symptoms on exertion
Class III: symptoms on minimal exertion
Class IV: symptoms at rest.
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Presentation
→ typically manifests with dyspnoea and fatigue which may limit exercise tolerance. Usually also with features of fluid
retention.
▪ Shortness of breath (SOB)
▪ Paroxysmal nocturnal dyspnoea
▪ Orthopnoea
▪ Ankle swelling
▪ Wheeze
▪ Fatigue
▪ Weight loss
▪ Tiredness
▪ Falling exercise tolerance
▪ Palpitations
▪ Depression
▪ Gout
▪ Raised JVP
▪ Displaced apex
▪ Crackles and pulmonary crepitations
▪ Heart sounds S3/4
▪ Pulsus alternans
▪ Hepatomegaly
▪ Ascites.
-----------------------------------------------------------------------------------------------------------------------------------------------------
Pathophysiology
→ inability of the heart to maintain adequate cardiac output (CO)
▪ Many sources of cause:
o Vascular (most common) → IHD, HT
o Muscular → dilated cardiomyopathy, hypertrophic cardiomyopathy (HCM), congenital heart disease
o Valvular → stenotic or regurgitant valves
o Electrical → arrhythmias may cause acute HF through decompensation
o High-output → low systemic vascular resistance with high CO due to anaemia, septicaemia, thyrotoxicosis,
liver failure.
▪ HF pathophysiology is based on the Frank-Starling law
o This is the relationship between ventricular stretching and contractility
o Stretching cardiac muscle → increase force of contraction
o The ability of the heart to respond to increased venous return by increasing the stroke volume (SV) is essential
to normal cardiac function
o ↑ venous pressure → ↑ venous return and ↑ end diastolic volume (EDV) → ↑ preload
o ↑ EDV → ↑ cardiomyocyte stretch and ↑ length of sarcomere → ↑ force of contraction → ↑ SV
o Failure to do this would → input-output mismatch ad pooling of the blood in systemic or pulmonary
circulation
▪ Primary determinants of SV → preload, myocardial contractility, afterload
▪ At a point, increase in preload leads to a depression of contractility and SV
▪ As the heart fails, the amount of blood left after each contraction increases (the ejection fraction decreases)
▪ This increased end-systolic volume (ESV) → myocardium experiences greater stretch
▪ In a failing heart, this causes a reduction in SV and → reduction in cardiac output (CO)
▪ The body may compensate for this reduced CO in many ways:
o Increasing preload (increasing venous pressures)
▪ This increases EDV compensating for the reduced ejection fraction
▪ This will aim to maintain CO
▪ In severe cases this causes → pulmonary oedema, ascites, peripheral oedema
o Increasing heart rate (sinus tachycardia)
▪ CO = SV x HR.
▪ RAS is also triggered by reduced CO
o Reduced CO → renal hypoperfusion and activation of RAS
o This contributes to increased venous pressures
o Also causes sodium and water retention → oedema.
▪ The sympathetic NS is also triggered by reduced CO
o This activates the SNS via baroreceptors → increases myocardial contractility and HR
o Chronic activation is detrimental
, o This triggers myocyte cell death and further RAS activation.
▪ To maintain CO → hypertrophy of myocardium
o Patients tend to be asymptomatic at rest initially
o Physical activity may lead to → decompensation and symptoms.
Types
HF is a complex condition that can be split into many classifications: acute or chronic, right or left, systolic or diastolic and
high or low output.
Systolic vs diastolic
▪ Systolic
o Reduced left ventricular ejection fraction (LVEF)
▪ The heart is pumping out a reduced proportion of the blood that fills the ventricles during diastole
o = ventricular dilation and eccentric remodelling.
▪ Diastolic
o Impaired ventricular relaxation or filling
o Contraction is unaffected so → LVEF preserved
o May be called “heart failure with preserved LVEF”
o = ventricular hypertrophy and concentric remodelling may occur
o Echo shows: LV hypertrophy, LA dilation, abnormal relaxation
o Stiffness of the ventricular wall with impaired filling and reduced CO
Acute vs chronic
§ Acute
o Rapid onset of worsening symptoms and/or signs of HF
o Life-threatening
o May occur acutely (cardiogenic shock) or as a consequence of acute decompensation of chronic HF (CHF)
o Most common causes: acute myocardial dysfunction (ischaemic, inflammatory), acute valvular disease,
pericardial tamponade
o Can be dramatic with flash pulmonary oedema
▪ Present in extremis, requires precipitant (ischemia, arrhythmia, intercurrent infection)
o Can also be due to gradual deterioration → fluid accumulation, falling exercise tolerance, orthopnoea and
paroxysmal nocturnal dyspnoea
§ Chronic
o Progressive cardiac dysfunction due to structural and/or functional cardiac abnormalities
o Results in reduced CO and/or elevated intracardiac pressures at rest or on stress
o Precipitated by conditions that affect muscles (cardiomyopathy), vessels (ischaemic heart disease), valves (AS)
or conduction (AF)
o Slowly progressive, punctuated by periods of acute decompensation
o Px develop chronic, progressive symptoms but may present with acute decompensation.
Right vs left
▪ Left
o May be caused by many conditions affecting the heart
o Advanced LSHF commonly causes → right sided HF due to increased intrathoracic pressure and pulmonary
HT
▪ Right
o Commonly result of advanced LSHF
▪ Biventricular failure often called = congestive heart failure
o Primary RSHF is uncommon
o Causes broadly divided into 3 categories:
▪ Secondary to pulmonary HT
▪ May occur secondary to LSHF, primary pulmonary HT or significant pulmonary disease (e.g. COPD)
▪ Secondary to pulmonary/tricuspid valve pathology
▪ Pericardial disease.
Classification
Class I: no symptoms
Class II: symptoms on exertion
Class III: symptoms on minimal exertion
Class IV: symptoms at rest.
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