S9) Heart Failure Flashcards
What is heart failure?
Heart failure is a state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure
either due to an inibility of the heart muscle to contract properly or due to heart not being able to fill properly
Outline the aetiology (causes) of heart failure
- Ischaemic Heart Disease - heart becomes stiff and doesnt contract properly
- Hypertension
- Dilated/hypertrophic Cardiomyopathy
- Valvular/Congenital Heart Disease
- Pericardial disease
- Arrhythmias
= remodelling of cardiac muscles = changes ventricular size and shape = impair ventricular filling and ventricular ejection
What are the clinical signs of chronic heart failure?
- Pulmonary congestion
- Venous congestion
- Dependent oedema
What are the symptoms of chronic heart disease?
- Dyspnoea (waking up suddenly gasping for breath)
- Lethargy
- Orthopnoea (breathlessness worse when they are lying flat)
Describe the clinical features of Class I heart failure
No symptomatic limitation of physical activity
Describe the clinical features of Class II heart failure
- Slight limitation of physical activity
- Ordinary physical activity results in symptoms
- No symptoms at rest
Describe the clinical features of Class III heart failure
- Marked limitation of physical activity
- Less than ordinary physical activity results in symptoms
- No symptoms at rest
Describe the clinical features of Class IV heart failure
- Inability to carry out any physical activity without symptoms
- May have symptoms at rest
- Discomfort increases with any degree of physical activity
What are the factors affecting cardiac output?
- Heart rate
- Venous capacity (preload - how much the ventricles can expand)
- Myocardial contractility
- Arterial and peripheral impedance (afterload - how much ventricles contract)
What is Starling’s Law of the Heart?
“The force developed in a muscle fibre depends on the degree to which the fibre is stretched.”
Describe the pathophysiology of Left Ventricular Systolic Dysfunction
- Increased LV capacity
- Reduced LV cardiac output
- Thinning of the myocardial wall
I. Fibrosis and necrosis of myocardium
II. Activity of matrix proteinases
What are the causes of Left Ventricular Systolic Dysfunction?
- Mitral valve incompetence or tricupid valve stenosis
- Neuro-hormonal activation
- Cardiac Arrhythmias
Which structural heart changes occur after Left Ventricular Systolic Dysfunction?
- Loss of muscle
- Uncoordinated myocardial contraction
- Changes to the ECM (increase in collagen)
- Change of cellular structure and function (myocyte hypertrophy)
Describe ventricular remodeling after acute infarction
Describe ventricular remodeling in diastolic and systolic heart failure
Label the following images:
concentric hypertrophy - to do with dialation of the left ventricle wall
eccentric hypertrophy - dialtion of the lumen
Identify the 5 different pathways for neuro-hormonal activation
- Sympathetic Nervous System
- Renin-Angiotensin-Aldosterone System
- Natriuretic Hormones
- Anti-Diuretic Hormone
- Endothelin
Why is SNS stimulated in heart failure?
Early compensatory mechanism to improve cardiac output:
- Cardiac contractility
- Arterial and venous vasoconstriction
- Tachycardia
Outline the long-term deleterious effects of the SNS in heart failure
When is RAAS commonly activated in heart failure?
- Reduced renal blood flow
- SNS induction of renin from macula densa
Outline the action of RAAS in heart failure
In terms of the brain, blood vessels, heart and kidney, explain how Angiotensin II plays a key role in organ damage
When are natriuretic peptides released in heart failure?
- Atrial distension (atria remains in diastole and the valves wont open so their is a build up of blood)
- Increased blood volume and pressure
Outline the action of natriuretic peptides in heart failure
Outline the effect of ADH (vasopressin) in heart failure
ADH is increased in heart failure:
- Increased H2O retention
- Tachycardia and increased TPR → increased CO
Outline the action of endothelin in heart failure
- Endothelin is secreted by vascular endothelial cells resulting in renal vasoconstriction via autocrine activity
- Activates RAAS (increased levels in some patients with heart failure)
Outline the effect of other chemicals in heart failure:
- Prostaglandin E2 and I2
- Nitric oxide
- Bradykinin
- Prostaglandins: vasodilators stimulated by NA and RAAS to counter their effects
- Nitric oxide: potent vasodilator produced by endothelial cells via NO synthase (NO synthase may be blunted in HF)
- Bradykinin: promotes natriuresis, vasodilatation and stimulates production of PGs
What is oedema?
- Oedema is the excessive volume of fluid within the tissues (interstitial / intracellular) which can occur due to changes in capillary dynamics
- It is often seen in heart failure as there is increased capillary hydrostatic pressure
Vascular endothelium increases in peripheral arterial resistance.
Why is this?
- SNS
- RAAS
- Reduced NO
- Increased endothelin
Changes in vascular endothelium leads to skeletal muscle changes.
Identify some
- Reduced skeletal muscle blood flow
- Reduction in skeletal muscle mass (cachexia)
- Abnormalities of structure and function
Describe the renal effects associated with changes in the vascular endothelium
- GFR (glomerular filtration rate) is maintained in early HF by haemodynamic changes at the glomerulus – increased Na+ /H2O retention due to neurohormonal activation
- GFR falls in severe HF due to reduced renal blood flow leading to a subsequent rise in serum urea and creatinine
Describe the multi-factorial aetiology of anaemia associated with vascular endothelium changes
- Chronic inflammatory disease
- Expanded plasma volume
- Drug therapy (ACEi / Aspirin)
- Iron malabsorption
- Chronic renal failure
Heart Failure with Preserved Ejection Fraction (HFpEF) occurs in almost 50% of heart failure patients.
Describe the clinical features of this condition
- Frequently elderly and female
- Often history of hypertension / diabetes / obesity
- Normal LV function with concentric remodelling
In four steps, describe the pathophysiology of HFpEF
⇒ Reduced LV compliance and impaired myocardial relaxation
⇒ Impaired diastolic LV filling (dependent on high LA pressure)
⇒ RV dysfunction results from high LA and PA pressure
⇒ Triggers neuro-hormonal activation as per systolic heart failure
Identify the 5 clinical syndromes of heart failure
- Left Sided Heart Failure
- Right Sided Heart Failure
- Congestive cardiac failure
- LVSD (left ventricular systolic dysfunction - pump failure)
- HFpEF (failure of LV relaxation)
Identify the symptoms of Left Sided Heart Failure
- Fatigue
- Exertional dyspnoea (difficulty breathing)
- Orthopnoea (breathlessness while lying down but relieved when standing or sitting)
- Paroxysmal nocturnal dyspnoea (PND)
What are the clinical signs of Left Sided Heart Failure?
- Tachycardia
- Cardiomegaly (displaced apex beat)
- 3rd or 4th heart sound (‘Gallop rhythm’)
- Functional murmur of mitral regurgitation
- Basal pulmonary crackles (fluid in the lungs)
- Peripheral oedema
Describe the aetiology of Right Sided Heart Failure
- Chronic lung disease
- Pulmonary embolism / pulmonary hypertension
- Pulmonary/tricuspid valvular disease
- Left-to-right shunts (ASD/VSD)
- Secondary to left heart failure (most frequent)
What are the signs and symptoms of Right Heart Failure?
- Fatigue
- ↑ JVP
- Pitting oedema (when the are is pressed and relieved the skin stays pitted for a while)
- Ascites (build up of fluid in abdomen)
- Pleural effusion (when there is a build up of fluid in abdomen)
- Dyspnoea
What is congestive (biventricular) heart failure?
- Congestive heart failure is a chronic progressive condition in which the heart’s function as a pump is inadequate to meet the body’s needs
- Both the right and left sides of the heart fail to pump adequately, hence, the signs and symptoms of both right and left heart failure develop
timeline of an organ system failure
dips because they catch infections or something bad happens
heart failure classification
1) no symptomatic limitation of physical activity
2) slight limitation of ordinary physical activity and symptoms
3) marked limitation of physical activity, less than ordinary physical activity - symptoms
4) cant carry out any physical activity without symptoms and have symptoms at rest, any movement = discomfort
Investigations
does patient have heart failure?
history (breathlessness, ankle odema, sleeping upright in bed), clinical examination (elevation of JVP, 3rd heart sound, crepatations in the chest), investigation (mt probe vmp) differential diagnosis
What sort of heart failure do they have?
- HFrEF
- HFpEF
- valvular/ structural heart failure
- right ventricular failure
- high output cardiac failure
whats causing the heart failure?
ischaemic heart disease
hypertension
viral
alochol
managment
symptomatic treatment - Furosemide (makes you urinate more and is a venodialator, lower prelaod and heart doesnt struggle to push it out)
prognostic treatment - HFrEF only
- cardiac rehabilitation
- ACE/ARB
- mineral corticoid receptor antagonist
- sacubitril valsarta
- ICD +/- biventricular pacemaker
what do crepitations suggest
fluid in lungs
blood tests to help classify heart failure
- NTpro-BNP (natriuretic peptide) ANP and BNP - oppose neurohormonal effects, promote vasodialation and renin secretion
- FBC - full blood count tells you if they are anemic
- U+Es - urea and electrolytes so tests kidney function
- LFTs - liver function test (may be elevated)
- clotting - anticoagulation
- thyroid function, vit D level, CRP
light and dark side of heart failure
left = dark (the body doesnt understand that the heart is weak so it makes it work harder to try and get more blood arounf the body)
right = light (but only occurs when the heart is severely weak) damps down sympathetic nervous system and drains out some fluid
common prognostic treatments to learn for OSCE
- ACE inhibitor and ARB (angiotensin 2 receptor blockers)
- Beta blockers - reduce contractility
- mineralcorticoid receptor antagonist - aldosterone antagonist so reduces sympathetic system
- biventricular ICD - pacemaker in right ventricle
what is ejection fraction
stroke vol
end diastolic volume (amount of blood just before systole)
normally between 50-70%
a normal value still might mean thet have heart failure because ventricle may be fine at contracting there is just reduced filling as the ventricle is stiff, so diastolic vol is reduced
compare HFrEF and HFpEF → classification
- HFrEF - heart failure with reduced ejection fraction
- HFpEF - heart failure with preserved ejection fraction
problems with both
- HFrEF - contractility problem (not enough force) but there is enough space
- HFpEF - not a contractility problem but less filling due to stiff ventricle walls (preload is reduced slightly as there is less space)
value on echocardiogram for ejection fraction
- HFrEF - <40%
- HFpEF - >50%
symptoms
- dyspnoea
- fatigue
- oedema (pulmonary or peripheral)
which side of the ventricle is commonly effected
left = pulmonary odema
but sometimes it can be so bad that
rough pathophysiology of heart failure
B1 → tachycardia
A1 → renin
what are some lifestyle factors to reduce heart failure
reduce salt intake and liquid intake
how do ACEi and ARBS treat hypertension and heart failure?
what are some adverse effects
- it inhibits vasoconstriction and aldosterone, so there is reduced resistance on blood vessels and a lower volume
- dry cough, angioedema (bradykinin increases vascular permeability, if it can’t be broken down then permeability increases), hypotension, renal impairment
- people to avoid: people who already have angioedema
what are sacubitril/valsartan
- neprilysin inhibitor
- neprilysin breaks down natriuretic peptides
- natriuretic peptides → cause natriuresis (Na out into urine)
- so if we inhibit the breakdown then the peptides have a longer lasting effect and then more Na out and more urination and so helps reduce heart workload
