Session 11 Flashcards
Explain the pathophysiology of heart failure
Ischaemic heart disease is the primary cause of systolic heart failure. Other causes include: hypertension, dilated cardiomyopathy (drugs, alcohol, pregnancy), valvular heart disease, pericardial disease, arrhythmias etc.
Define heart failure
Heart failure - a state in which the heart fails to maintain an adequate circulation for the needs of the body, despite an adequate filling pressure
Be able to draw and explain the normal relationship between central venous pressure (or end diastolic pressure) and cardiac output, and how that relationship alters with increasing severity of heart failure
Starling’s law of the heart.
The force developed in the myocardium depends on the degree to which the fibres are stretched (how much the heart is filled). In heart failure the heart can no longer produce the same amount of force (cardiac output) for a given level of filling.
Describe the different types of heart failure
Class I - no symptomatic limitation of physical activity
Class II - slight limitation of physical activity, ordinary physical activity results in symptoms, no symptoms at rest
Class III - marked limitation of physical activity, less than ordinary physical activity results in symptoms, no symptoms at rest
Class VI - inability to carry out any physical activity without symptoms, discomfort increases with any degree of physical activity, may have symptoms at rest
Describe the clinical signs of right and left sided heart failure
Left sided heart failure:
Fatigue, shortness of breath upon exertion or when lying flat, tachycardia, cardiomegaly, 3rd or 4th heart sound, murmur of mitral regurgitation, basal pulmonary crackles, peripheral oedema
Right sided heart failure:
Chronic lung disease, pulmonary embolism, hypertension, left–> right shunts, isolated right ventricular cardiomyopathy, ascites, pleural effusion
Describe the involvement of the renin-angiotensin-aldosterone system and the sympathetic nervous system in heart failure
A drop in blood pressure (as in heart failure) stimulates renin release from the kidneys. Renin is an enzyme that catalyses the conversion of angiotensin to angiotensin I. Angiotensin I is converted to angiotensin II by ACE.
Angiotensin II is a powerful vasoconstrictor and promotes the release of aldosterone from the kidneys.
Aldosterone causes salt and water retention in the kidneys, increasing blood volume.
The sympathetic nervous system causes vasoconstriction of blood vessels via a1 receptors. This increases blood pressure, increasing the workload of the heart. Sympathetic innervation of b1 receptors also causes an increase in chronotrophy and inotrophy.
Identify targets for drug action to manipulate cardiac output
ACE inhibitors prevent the conversion of angiotensin I –> angiotensin II. They have an indirect vasodilatory and diuretic effect, reducing workload of the heart.
Diuretics reduce blood volume and thus oedema.
B-blockers prevent sympathetic innervation of the myocardium, reducing workload of the heart.
Describe the principles involved in the general management of heart failure, and the categories of drugs used in its therapy
Correct underlying cause, non-pharmacological measures, pharmacological therapy (symptomatic improvement, delay progression of heart failure, reduce mortality)
Treat complications/associated conditions (e.g. arrhythmias)
Drugs used include:
B-blockers - block b1 receptors on myocardium
ACE inhibitors - prevent conversion of angiotensin I –> angiotensin II
Ca2+ channel blockers - reduce contractibility of myocardium
Organic nitrates - veno/vasodilator –> reduce bp
Cardiac glycosides - increase cardiac output and heart contractibility by inhibiting Na+ pump –> inhibiting NCX –> increases intracellular Ca2+
