CVS S11 - Heart Failure Flashcards
Define Heart Failure
A state in which the heart fails to maintain adequate circulation for the needs of the body despite adequate filling pressure
What are some of the causes of heart failure?
Most commonly ischaemic heart disease
Can also be:
- Hypertension
- Dilated cardiomyopathy (Bugs, alcohol, drugs, poison, pregnancy)
- Valvular disease (acquired or congenital)
- Hypertrophic cardiomyopathy
- Pericardial disease
- High output heart failure
- Arrhythmia
How does the relationship between end diastolic pressure and cardiac output change in heart failure?
As heart failure progresses the heart can no longer generate the same force of contraction (and hence cardiac output) at a given level of filling (end diastolic volume).
Make sure you recognise the graph of this relationship showing the difference between a healthy heart, mild failure and gross failure
How is heart failure classified?
Class I to IV depending on symptom severity
Describe class I heart failure
No symptomatic limitation of physical activity
Describe class II heart failure
Slight limitation of physical activity
Ordinary physical activity results in symptoms
No symptoms at rest
Describe class 3 heart failure
Marked limitation of physical activity
Less than ordinary physical activity results in symptoms
No symptoms at rest
Describe 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 proportion of hospital admissions is for heart failure annually?
What proportion of general medical care and care of the elderly hospital admissions are due to chronic heart failure?
In what subset of the population is heart failure the commonest cause of hospitalisation?
How common are heart failure consultations in primary care?
0.2%
5+%
> 65yrs
2nd most common after hypertension
What are the 4 main factors affecting cardiac output?
Preload (Venous capacity)
Afterload (peripheral impedance/TPR)
Myocardial contractility
Heart rate
On which side of the heart can heart failure occur?
Left, right or both
How can types of heart failure be classified?
Left sided HF
Right sided HF
Congestive HF (both)
Systolic HF
Diastolic HF
What are some of the features of systolic heart dysfunction?
Increased LV capacity (dilation) Reduced LV output Thinning of the myocardial wall (Fibrosis, necrosis, matrix proteinases) Mitral valve incompetence Neurohormonal activation Cardiac arrhythmias
What are some of the structural changes that occur during heart failure?
Loss of muscle
Uncoordinated or abnormal contraction (ECG changes)
Changes in ECM:
- Increased Collagen (mostly type 3) from 5% to 25%
- Slippage of myocardial fibre orientation
Changes in cellular structure and function:
- Myocytolysis and vacuolation of cells
- SR dysfunction
- Changes in Ca2+ availability and Ca2+ receptor regulation
- Diastolic failure = concentric hypertrophy
- Systolic failure = Eccentric hypertrophy
What factors are involved in neurohormonal activation in heart failure?
SNS RAAS Natriuretic hormones Anti-diuretic hormones Endothelin Prostaglandins/NO TNF-alpha
Describe how the SNS responds to HF
Early compensation:
- Increase in SNS output
- Improved CO, contractility, HR
- Vasoconstriction (arteries and veins)
Long term deleterious effects:
- Downregulation/uncoupling of b-adrenoceptors
- NA induces cardiac hypertrophy, myocyte apoptosis and necrosis via alpha receptors
- Upregulates RAAS
Also reduces heart rate variability (reduced PSNS and increased SNS)
Describe the RAAS and its effects on the CVS
Renin-angiotensin-aldosterone system
Reduced renal blood flow induces SNS output via macula densa (deleterious effects in HF)
Kidney releases renin in response to SNS
Renin is an enzyme that cleaves angiotensinogen to form angiotensin I
Angiotensin I is converted to angiotensin II by angiotensin cleaving enzymes (ACE)
Angiotensin II causes:
- Vasoconstriction
- Promote LV hypertrophy and myocyte dysfunction/apoptosis
Also promotes release of aldosterone causing:
- Na+/H2O retention
- Increased BP
Describe action of the natriuretic hormones
Atrial natriuretic peptide:
- Released in response to atrial stretch
- Predominant renal effect is to constrict afferent and dilated efferent arterioles
- Decreases Na+ absorption in collecting duct
- Inhibits secretion of renin and aldosterone
- Systemic arterial and venous dilation
Brain natriuretic peptide:
- Released in response to ventricular stretch
- Similar effects to Atrial version
These peptide balance the effects of the RAAS on vascular tone and Na+/H2O balance
Describe the action of anti-diuretic hormone (vasopressin) in HF
Increases H2O retention by the kidneys
Hypo-natraemia can result
Normally hypo-natraemia inhibits ADH release
But in HF it is increased:
- Increased H2O retention
- Tachycardia and vasoconstriction
Describe the actions of Endothelin and its role in HF
Secreted by vascular endothelial cells
Potent systemic and renal vasoconstrictor
Acts via autocrine activity
Activates RAAS in the kidney (reduced renal blood flow)
Evidence of increased levels in HF
Correlated with severity of HF
What are the actions of prostaglandins on the CVS?
Prostaglandin E2 and I2:
- Stimulated by NA and RAAS
- Act as vasodilators on afferent renal arterioles to attenuate effects of NA/RAAS
- NSAID Rx blocks de novo PG synthesis
What is the effect of nitric oxide on the CVS?
What is its role in HF?
Usually a potent vasodilator produced by endothelial cells via NO synthase
NO synthase may be blunted by HF
Loss of vasodilator balance
What is the effect of bradykinin on the CVS?
Promotes natriuresis and vasodilation
Stimulates Prostaglandin production
What is the role of TNF-alpha on the CVS?
Depresses myocardial function
May stimulate NO synthase
May have role in cachexia
Increased in HF
