CVS Session 11: Heart failure Flashcards
Define heart failure
Heart fails to maintain an adequate circulation for the needs of the body, despite an adequate filling pressure. Abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with requirements of the metabolising tissues.
Normally, by Starling’s law, the force developed in the myocardium depends on the degree to which the fibres are stretched (or heart is filled). In HF the heart can no longer produce the same amount of force (cardiac output) for a given level of filling
Clinically recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses
Heart failure aetiology?
Main cause= IHD
Other causes:
-hypertension
-dilated cardiomyopathy (viral/bacterial, alcohol/drugs/poisoning, pregnancy, idiopathic)
-valvular heart disease/congential (now less common as picked up before heart fails)
-restrictive cardiomyopathy e.g. amyloidosis
-hypertrophic cardiomyopathy
-pericardial disease
-high output heart failure
-arrhythmias
Describe the 4 stages of the NYHA functional classification of heart failure
Class I: no symptomatic limitations on physical activitiy
Class II: slight limitations, ordinary activity causes symptoms, none at rest
Class III: marked limitation, less than ordinary activity causes symptomes, none at rest
Class IV: can’t carry out physical activity without symptoms, may have symptoms at rest, discomfort increases with any degree of activity. 80% mortality at 3 years so palliative care role
Morbidity of heart failure
~0.2% of UK pop. hospitalised annually for HF
Chronic HF accounts for 5% of all adult general medical admissions and is commonest cause of admission in those >65years
State the factors that influence cardiac output
Heart rate
Myocardial contractility
LV preload (venous capacity)
Afterload (aortic and peripheral impedance)
Describe what happens in systolic dysfunction of the heart
Dilated heart
Increased LV capacity so decreased LV cardiac output
Thinning of the myocardial wall: fibrosis and necrosis of myocardium, activity of matrix proteinases
Mitral valve incompetence
Arrythmias
What structural changes does a failing heart undergo?
Loss of muscle
Uncoordinated or abnormal contraction
ECM changes: increase in collagen (more type III than I) and different fibre orientation
Change of cell structure/function: myocytolysis, myocyte hypertrophy (to compensate for those lost), SR dysfunction, Ca2+ availability changes
List the neuro-hormonal components that can be measured or altered in heart failure
Sympathetic nervous system Renin-angiotensin aldosterone system Natriuretic hormones (biomarker to identify severity) Anti-diuretic hormone Endothelin Prostaglandins/nitric oxide Kallkrien system Tissue necrosis factor alpha
i.e. a variety of systems work together!
What is the early compensatory mechanism to improve cardiac output that is regulated by the sympathetic nervous system?
Cardiac contractility increase
Arterial and venous vasoconstriction
Tachycardia
What are the long term pathological effects of higher sympathetic activity, which originally was helpful in increasing cardiac output?
Beta adrenoceptors are down-regulated: increases heart rate so increased O2 demand–>decreased contractility
Vasoconstriction increases wall stress, causing hypertrophy and increased O2 demand (so decreased contractility)
Noradrenaline:
-induces hypertrophy, myocyte apoptosis and necrosis via alpha receptors
-induces up-regulation of RAAS (so more fluid retention, more wall stress, so hypertrophy eventually)
Reduction in heart rate variability: reduced PNS and increased SNS
Describe the role of the renin-angiotensin-aldosterone system in heart failure
Commonly activated in heart failure: reduced renal blood flow + SNS induction of renin from macula densa Elevated angiotensin II: -potent vasoconstrictor -promotes LVH and myocyte dysfunction -promotes aldosterone release -promotes Na+ and H2O retention
What is the role of angiotensin II in organ damage?
Acts on the AT1 receptor:
- atherosclerosis
- vasoconstriction
- vascular hypertrophy
- endothelial dysfunction
- LV hypertrophy
- fibrosis, remodelling and apoptosis
- decreased glomerular filtration rate
- increased proteinuria and aldosterone release–>glomerular sclerosis
These events can lead to stroke, hypertension, MI, heart failure, renal failure, and death
What is the role of natriuretic hormones/peptide?
Induce the discharge of Na+ in urine: balance the effects of the RAAS on the vascular tone and Na+/H2O balance.
Stretch or increase in cardiac chamber volume leads to release: atrial NP, brain NP (ventricle stretch). Cause vasodilation and increased urinary Na+ excretion (decrease reabsorption in collecting duct). Also inhibits renin and aldosterone secretion
What is hypo-natraemia?
H2O in excess of Na+ retention, due to:
- increased water intake (thirst)
- action of ADH on V2 receptors in the collecting duct
Normally will inhibit ADH release
What are the effects of raised anti-diuretic hormone in heart failure?
- Increased H2O retention
2. Tachycardia and reduced systemic resistance –> increased cardiac output
What are the actions of endothelin?
- vasoconstriction, esp. renal. Autocrine activity so activates RAAS
- in patients with HF, more endothelin = poorer prognosis
- similar effects to angiotensin II, but more aggressive
Which prostaglandins are involved in HF and how?
E2 and I2
Stimulated by NA and RAAS
Vasodilation of afferent renal arterioles to attenuate the effects of NA/RAAS
