Clinical management of heart failure Flashcards
To maintain normal cardiac function it is required to have adequate:
- Myocardial contractility
- Effective blood supply
- Effective conduction system
- Effective valve function
What is heart failure
- Clinical syndrome characterised by typical symptoms (e.g., breathlessness and fatigue)
- May be accompanied by signs (e.g., elevated Jugular Venous Pressure, pulmonary crackles and peripheral oedema)
- Caused by a structural and/ or functional cardiac abnormality
- Resulting in reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.
Pathophysiology of heart failure involves changes in:
- cardiac function
- neurohormonal status
- systemic vascular function
- blood volume
- integration of cardiac and vascular changes
These can be seen as compensatory changes to help maintain CO (by the Starling mechanism of the heart) and arterial B pressure (by systemic vasoconstriction).
Over a long time these changes can worsen cardiac function. Therefore some of the best treatments for HF control these changes e.g., diuretics, vasodilators
Compensatory mechanisms during heart failure
Cardiac
- Frank-stalring mechanism
- chronic ventricular dilation or hypertrophy
- tachycardia
Autonomic nerves
- Increased sympathetic adrenergic activity (ßR’s activated by NE elevate cAMP- decrease contractility in sm muscle but increases it in cardiac)
- Reduced vagal activity of the heart (parasympathetic action on heart)
Hormones
- RAAs system
- ADH
- Circulating catecholamines (e.g,. adrenaline)
- Natriuretic peptides
What is the change in cardiac function seen in HF?
decreased CO duie to decreased SV.
how can the neurohormonal changes result in pathology
can aggravate heart failure by:
- increasing ventricular afterload (which depresses stroke volume)
- increasing preload to the point where pulmonary or systemic congestion and edema occur
therefore attenuating these changes can help in heart failure e.g.,
- beta blockers decrease excessive symp activity in the heart
- ACE inhibitors, AngR blockers and aldosterone R antagonists
What are the 2 reasons that stroke volume may change in HF?
1) systolic dysfunction results from:
a) loss of intrinsic inotropy (contractility) - caused by alterations in signal transduction mechanisms responsible for regulating inotropy
b) loss of viable contracting muscle following acute myocardial infarction
2) Diastolic dysfunction (vent less compliant so doesn’t fill as it should– less ejection – starling’s law)
Both dysfunctions result in a greater EDV– Starling’s law of the heart (stretches walls, more cross bridges, stroke volume???)
Therapeutic interventions to improve cardiac function include
use of cardiostimulatory drugs (B2 agonists and digitalis) that stimulate HR and contractility
and
use of vasodilators to reduce ventricular afterload (average arterial pressure- pressure vents must overcome to eject blood)
What are the neurohormonal responses to HF (patho)
- Activation of sympathetic nerves and the renin-angiotensin-aldosterone system and
- increased release of ADH and ANP
What are the net changes casued by the neurohormonal changes?
They all have the target of keeping organs perfused in face of decreased CO
- arterial vasoconstriction (maintain arterial pressure)
- venous constriction (maintain venous pressure)
- increased blood volume (increase ventricular filling- EDV- starling’s- increase SV)
How does blood volume change in heart failure
compensatory increase in BV to increase ventricular preload and thereby increase SV by Starlings law of the heart:
Reduced renal perfusion (symp constriction of afferent renal a) results in decreased urine output and retention of fluid
combination of reduced renal perfusion and sympathetic activation of the kidneys stimulates the release of renin, thereby activating the renin-angiotensin system
increase in circulating ADH
why can the blood volume change become pathological
raises venous pressures leading to pulmonary and systemic oedema
When edema occurs in the lungs, this can result in exertional dyspnea (shortness of breath during exertion). Therefore, most patients in heart failure are treated with diuretic drugs to reduce blood volume and venous pressures in order to reduce edema.
Which sided heart failure results in congetsion of the pulmonary vascualr system and pleural effusions
left
causes of heart failure
- Arrythmias
- Cardiotoxins (e.g., chemotherapy, alcohol, illicit drugs)
- Congenital heart disease
- Genetic cardiomyopathies (e.g. dilated or hypertrophic cardiomyopathies)
- Hypertensive heart disease
- Infection (e.g. myocarditis, infective endocarditis)
- Ischaemic heart disease
- Lung disease
- Pregnancy
- Thyroid disease/ anaemia
- Valvular heart disease
3 most common causes of heart failure
- Ischaemic heart disease
- MI
- Angina
