L 54 Flashcards
What are the 3 components of the cardiovascular function
The pump
The blood volume
The blood pressure
Heart failure because of ?
abnormality of the heart muscles
What is heart failure?
Inability of the heart to pump enough blood to meet the needs of the body, resulting in low cardiac output.
What changes may occur during HF ? (immediate)
Structural and functional changes
that impair the ability of the ventricle to fill and eject blood.
What are the Primary causes of HF
Long standing HTN, MI
Determinants of cardiac output
CO = HR x SV
How is HR controlled?
By SNS and simulation of B adrenergic receptors
How is SV regulated?
It is a function of preload, afterload and contractility
There are many compensatory mechanisms that try to maintain cardiac output in a failing heart such as: x3 + examples
- SNS (tachycardia and inc contractility, vasoconstriction)
- Neurohormonal (ventricular hypertrophy/remodelling)
- RAA system (inc preload via H2O and Na+ retention, vasoconstriction)
What are the consequences of these compensatory mechanisms?
They paradoxically lead to cardiac damage, and pathological remodelling, therefore producing symptoms experienced by patients.
What are the consequences of the following mechanisms?
- Tachycardia: increased oxygen demand - worsens ischaemia
- Ventricular hypertrophy/remodelling: structural changes increases oxygen demand, causing myocyte cell death.
- Increased preload: oedema and congestion
- Increased contractility: increased oxygen demand
- Vasoconstriction: decreased CO, activation of further compensatory mechanisms
What drug classes target the following?
- Tachycardia: B-blockers
- Ventricular hypertrophy/remodelling: ARB, ACEI, spironolactone
- Increased preload: Sacubitril, spironolactone, diuretics, ARB, ACEI
- Increased contractility: B blocker, digoxin
- Vasoconstriction: ARB, ACEI, sacubitril
Examples of 3x B blockers used in HF
Metoprolol, bisoprolol, carvedilol
… diuretics have no role in HF but a role in HTN, and … diuretics have no role in … but a role in HF.
Thiazide diuretics have no role in HF but a role in HTN
Loop diuretics have no role in HTN but have a role in HF.
In a heart attack, we use …/… to stop the heart from thickening and remodelling.
In a heart attack, we use ACEI/ARBs to stop the heart from thickening and remodelling.
Giving small doses of … is also pertinent so you don’t shut down the heart.
The purpose of this drug is to slow down the heart and protect it from itself.
Giving small doses of B blockers is also pertinent so you don’t shut down the heart. The purpose of this drug is to slow down the heart and protect it from itself.
What 2 B blockers have a greater affinity for B1?
What 2 B blockers are “non-selective”?
What is the importance of this?
Metoprolol and bisoprolol have a greater affinity for B1
Propanolol and carvedilol are non-selective for alpha receptors.
Want a selective B blocker, so that it helps to vasodilate and nothing else. Can have a non-selective alpha inhibitor.
Rank the following in terms of highest to lowest lipophilicity (and therefore CNS penetration): metoprolol, bisoprolol, propranolol
What is a notable side effect of propranolol?
Which drug doesn’t affect diabetic/lipid control? (may not be from this list)
Propranolol > metoprolol > bisoprolol (low)
Propranolol = sleep disturbances
Carvedilol = limited impact on diabeties/lipid control.