Lecture 10: Heart Failure Flashcards
Define heart failure
- Failure of the heart to pump enough blood to satisfy the body’s requirements.
- Acute or chronic
- Characterized by a clinical syndrome involving a characteristic pattern of hemodynamic, renal, neural, and hormonal responses. Heart failure is considered a multisystem disorder.
Causes of heart failure
- Diminished coronary blood flow (ischemic heart disease)
- Damaged heart valves
- thyrotoxicosis
- Vitamin B deficiency
- Cardiac muscle disease
What are the acute effects of moderate heart failure?
- Sudden damage (MI)
- Reduced cardiac output → fatigue
- Fall in arterial pressure
- Damming of blood in veins → congestion
- RESULT: compensation
What is the role of sympathetic reflexes in heart failure compensation?
- Baroreceptor that measure arterial pressure
- Detect fall in BP
- NET EFFECT
- Sympathetic nervous system activated
- Parasympathetic nervous system inhibited
- TLDR: fall in CO, body compensates by increase CO n BP
- Direct effect on the heart
- SNS speeds up the heart n contractility of the heart (positive ionotropic effect)
- Positive ionotropic n chronotropic
- Increases venous return [causes blood vessel constriction] → more blood cmng to the heart → increases cardiac output → raises filling pressure
What is the effect of heart failure on the Starling curve?
- Increase filling pressure → bigger CO
- Stretching the muscles fibers of the myocardium
- When they contract, they push out more blood
- More preload (blood cmng back to the heart in the vein) → shift along the curve
- Sudden fall in BP [lack of CO] → curve shift to the right [more filling pressure bc constricting the vein]
- Sympathetic nervous system increases contractility → efficiency of pumping increased
- For given pressure, more CO
- Direct effect of sympathetic nervous system by beta receptors
- Pushes the curve upwards
- Fall in CO → body compensates in short term by shifting along the curve n shifting curve up
- Result net increase in CO for increase filling pressure
How does the baroreceptor reflex compensate for a decrease in BP?
- Decrease in BP [fall in CO] detected by baroreceptors in carotid sinus n aortic arch
- Reduces number of nerve impulses in vasomotor centers in medulla
- Inhibits parasympathetic nervous system
- Activates SNS
- Increase heart rate n contractility
- Increase vasomotor tone (constricts blood vessels) -> increases TPR n venous return
- More pressure for the heart to push against can help compensate in short term but may be damaging in the long term
- When the heart fails, makes the heart work harder -> can be damaging
What is the role of fluid retention in heart failure compensation?
- Long term try n increase fluid retention
- Retention of fluid by kidneys -> reduced urine output via release of aldosterone n ADH
- Effects of aldosterone n ADH
- Increased blood volume -> increased venous return ->
increased systemic filling pressure
- Reduces venous resistance which eases flow of blood to the heart
- Moderate fluid retention is beneficial
- Large amt of fluid retention is not beneficial
What are the causes of reduced renal urine output?
- Decreased glomerular filtration
- Caused by a fall in arterial pressure
- Renin-angiotensin system
- Aldosterone secretion
What are the aims of treating CHF?
- Relieve symptoms
- Improvise exercise tolerance
- Reduce acute exacerbations
- Reduce mortality
What are some first line treatments of chronic CHF?
- ACE inhibitors
- Angiotensin II receptor antagonists
- β-adrenoreceptor blockers
What are some second line treatments of chronic CHF?
- Aldosterone antagonist (spironolactone)
- Cardiac glycosides (digoxin)
- Increase heart contractility
What do ACE inhibitors and angiotensin II receptor antagonists do and what are some examples?
- ACE inhibitor: enalapril
- Angiotensin II receptor antagonists: candersarta
- FUNCTION
- Reduce peripheral resistance (afterload)
- Stop angiotensin II vasoconstriction
- Reduce blood volume (preload) via reducing aldosterone release
- Increase K+ concentration counteracting loss via diuretics
- Helps to prevent cardiac remodeling
- Increase in size
- Strong evidence that they increase survival
- Reduce peripheral resistance (afterload)
What do β-adrenoreceptor blockers do and what are some examples?
- EXAMPLES: bisoprolol n carvedilol
- Reduce the work of the heart n slow disease progression
- Reduce renin-angiotension-aldosterone
- Some also block α receptors on blood vessels leading to vasodilation
- Start at low dose n slowly titrate
- Only use in stable heart failure
- Can shift along the curve w/o changing CO
- Reducing work of the heart
What do cardiac glycosides do?
- Block Na+/K+ exchange → greater Ca2+ influx via Na+/Ca2+ exchanger → increases myocardium contractility
- Suitable for patients w CHF n atrial fibrillation
- Worsening or severe heart failure due to left ventricular systolic dysfunction despite ACE inhibitor, β-blocker n diuretic therapy
What is ivabradine?
- Used to treat angina
- Slows heart by direct action on SA node
- Probably blocks pacemaker current (If)
- Increases filling time n CO