LECTURE 14-17: CARDIOVASCULAR Flashcards
CO and equation
amount of blood pumped per min
CO = HR X SV
SV
Amount of blood pumped by a ventricle per beat
SV is affected by
Preload and Afterload
Preload
is the amount the ventricles stretch at the end of diastole (filling phase)
Afterload
pressure the ventricles must work against to pump blood out of the heart
Heart has an intrinsic rate set by
SA node
SNS is resposible for _____, innervates __ and __ nodes and also ___
tachycardia
SA
AV
muscle
PSNS is responsible for ____, via ____ nerve and __ and __ nodes, and has less of an effect on ___
bradycardia
SA
AV
Muscles
BP=
CO x peripheral vascular constriction
what would increase in 1) force contraction 2) preload and 3) afterload do to SV
inc
inc
dec
does vasoconstriction increase or decrease peripheral constriction
increase
a decrease in CO causes compensation in form of
SNS and RAAS activation
SNS mechanism to increase CO
and the side effects
1) ^HR and contrile force (B1)
2) Vasocontriction (^BP and ^ peripheral resitence)
- tachnyarrythmia an dO2 starvation
- ^ afterload, cyanosis
RAAS mechanism to increase CO
1) Vasocontriction (^BP and ^ peripheral resitence)
2) ^ blood volume
- ^ afterload, cyanosis
- oedema
Drugs we’re focussing on are
inotropes, vasodilators, antiarrythmias and diuretics
+inotrope
improve heart contractility
vasodilators
dilate BV
diuretics
remove accumulated fluid
antiarrhythmics
restore normal HR and rhythm
two +ve inotropes
digoxin and dobutamine
digoxin mechanism of action
inhibits Na-K-ATPase channel
Sodium cannot LEAVE
^ Na intracellular
Na cannot feed Na-Ca pump
Na-Ca pump inactivated
Ca builds up (calcium = contraction)
^ acxtivation of contractile proteins
decrease heart rate, more meaningful beats
dobutamine mechanism of action
improves myocardial contraction by B1 agonism
vasodilator examples (6)
AAABCN
- ACE inhibitors
- Angiotensin II receptor
- beta blockers
- calcium channel blockers
- A1 antagonists
- Nitrate
suffix of ACE inhibitors
opril
suffix of angiotensin II receptor blockers
sartan
How do ACE inhibitors and angiotensinogen II receptor blockers cause vasodilation
by inhibiting the formation of angiotensin II (which causes vasocinstriction)
how beta blockers cause vasodilation
B1 antagonism, decrease HR
kinda weak as alpha more involved with blood vessels
Calcium channel blockers and example for hypertension
improves blood flow and decreases afterload
amlodipine
Nitrates cause vasodilation by
being converted to nitric oxide
A1 antagonism will cause vasodilation by
A1 antagonism, such as prazosin
does vasoconstriction increase or decrease blood pressure?
increase, this is why vasodilators are used to decrease them
what is an arrythmia
asynchrony between electrical stimulation and mechanical contraction
antiarrythmic drugs
class I-IV
digoxin
Class I antiarrhythmic
sodium channel blocker
Class II antiarrythmic
Beta blocker
Class III antiarrythmic
potassium channel blocker
Class IV antiarrhythmic
Calcium channel blocker
example class I
lignocaine
example class II
atenolol
example class III
sotalol
example class IV
diltiazem, amlodipine
How do class III anti-arrhythmic drugs work? Give an example of this class of drug
During the normal heartbeat cycle, there is a rapid repolarisation with increasing K+ efflux (1 mark). When this process goes wrong, arrhythmia can result. Class III drugs are potassium channel blockers (1 mark) which prolong phase 3 repolarisation in the ventricular muscle fibres (1 mark). Examples include amiodarone, sotalol (1 mark).
Why use diuretic
remove fluid accumulation (heart failure patient)
Renal diuretics
1) loop diuretic
2) potassium sparring diuretic
loop diuretic
- fresumide
- loop of henle
- Na-K-Cl channel blocker
potassium-sparing diuretic
- spironolactone
- collecting duct
- aldosterone antagonist (aldosteron controls Na-K-ATPase pump)
- pump not induced = diuresis
osmotic diuretic
- mannitol
- increase osmolarity in plasma
osmotic diuretic indications
- cerebral oedema and glaucoma
Briefly describe the benefit that a positive inotrope can provide to a failing heart (3 marks)
The body’s compensatory mechanisms to heart failure often result in a heart that is beating stronger against a high level of resistance (afterload). This is unsustainable for a failing heart. Positive inotropes improve the efficiency of myocardial contractility and therefore reduce myocardial oxygen consumption, which helps to reduce ischemic injury to the heart and arrhythmias.
