Week 11 - Heart Failure Flashcards
What is heart failure?
A state in which the heart fails to maintain an adequate circulation for the needs of the body’s despite an adequate filling pressure
What are some causes of systolic heart failure?
- Main cause = Ischaemic heart disease
- Hypertension
- Dilated cardiomyopathy (bugs, alcohol/drugs/poisoning, pregnancy, idiopathic)
- Valvular heart disease/congenital
- Restrictive cardiomyopathy
- Hypertrophic cardiomyopathy
- Pericardial disease
- High-output heart failure
- Arrhythmias
What are the different classes 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 IV:
- Inability to carry out any physical activity without symptoms
- May have symptoms at rest
- Discomfort increases with any degree of physical activity
What is congestive heart failure?
When both ventricles are affected
What are the different types of heart failure?
- Left-sided
- Right-sided
- Biventricular
- Systolic
- Diastolic
What are some causes of right-sided heart failure?
- Secondary to left HF
- Pulmonary embolism/hypertension
- Pulmonary/tricuspid valvular disease
- Left –> right shunts
- Isolated right ventricular cardiomyopathy
What are the signs of right-sided HF?
- Relate to distension and fluid accumulation in areas drained by the systemic veins
- Fatigue, dyspnoea, anorexia, nausea
- Raised JVP
- Tender, smooth hepatic enlargement
- Dependent putting oedema
- Ascites
- Pleural effusion
What are some signs of left sided heart failure?
- Fatigue, shortness of breath upon exertion or when lying flat, waking from sleep with shortness of breath
- Tachycardia
- Cardiomegaly
- 3rd or 4th heart sound
- Functional murmur of mitral regurgitation
- Basal pulmonary crackles
- Peripheral oedema
What is the Renin-Angiotensin-Aldosterone system?
A system that is activated in heart failure in an attempt to maintain cardiac output
- Makes an already struggling heart work harder
- A drop in blood pressure stimulates renin release from the kidneys
- Angiotensinogen is converted to angiotensin I by renin, which is then converted to angiotensin II by angiotensin converting enzyme
- Angiotensin II can act on ATiR to cause vasoconstriction
- Or it can act on ATiiR to cause aldosterone release, which causes salt and H2O retention which hence increases blood volume
- ATiiR stimulation can also release nitric oxide (as does bradykinin) which causes vasoconstriction
What does the sympathetic nervous system do in heart failure?
- Causes vasoconstriction of blood vessels via the α1-receptor
- – This increases blood pressure, which increases the workload of the heart
- Innervation of the heart’s β1-receptor will cause an increase in both chronotropy and inotropy
- It can stimulate the renin-angiotensin system
- Can cause direct cardiotoxicity (myocyte damage)
How can oedema form in heart failure?
- In left HF: pulmonary oedema can form
- In right HF: HF causes distension and fluid accumulation in areas drained by the systemic veins, which leads to systemic oedema
- – Can cause hepatomegaly and ascites
Which drugs can be used to manipulate cardiac output?
- ACE inhibitors: prevent the conversion of angiotensin I to angiotensin II
- – These have an indirect vasodilatory and diuretic effect, so reduce the workload of the heart
- Diuretics: reduce blood volume and thus oedema
- β-blockers: prevent the sympathetic innervation of the myocardium, hence reducing the wokload
What are the principles of management of heart failure?
- Correct underlying cause
- Non-pharmacological measures
- Pharmacological therapy
- Treat complications/associated conditions/cardiovascular risk factors
Which drugs can be used to treat heart failure?
- ACE-inhibitors
- β-blockers
- Ca2+ channel blockers
- Organic nitrates
- Cardiac glycosides (increase CO and heart contractility by inhibiting the Na/K pump. raising the intracellular Na inhibits NCX so intracellular Ca2+ increases, leading to an increase in contractility)
