4-cardio Flashcards
what type of vessels is the main location of resistance in circulation
arterioles
what is afterload
the resistance that the heart has to pump against
what determines afterload
arteriolar pressure and peripheral resistance
what is preload
the stress on ventricular wall before systole
what happens to afterload when you increase peripheral resistance
it increases
what happens to afterload when you increase BP
it increases
what is another name of left ventricle end diastolic pressure
preload
weird question
how do you find cardiac output
stroke volume x heart rate
what is venous return
rate of return of blood to the heart
what does cardiac output equal in terms of veinous return
cardiac output=venous return
are veins or arteries more rigid
arteries
are veins or arteries more elastic
veins
what is capacitance
ability to store blood
is venous capacitance bigger or smaller than arterial capacitance
venous>arterial
what is another name for the intrinsic relationship in the heart
the Frank Starling relationship
what does the frank starling relationship tell us
that the force of contraction is proportional to initial fibre length (aka more blood in heart means more contraction)
what is the measure of initial fibre length
left ventricular end diastolic pressure
what happens during heart failure in the Frank Starling relationship
more blood in the heart doesnt cause more contraction
what is the extrinsic regulation of the heart contractility
baroreceptor reflex
what happens if BP increases in BR reflex
carotid sinus baroreceptors - CNS- enhances vagal flow- bradycardia
what happens if BP decreases in BR reflex
carotid sinus baroreceptors - CNS- decrease vagal flow- tachycardia +vasoconstriction
what are 4 causes of congestive heart failure
myocardial infarction
ischemia
increase presure
increase volume load (increased afterload - hypertension)
what is ischemia
inadequate blood supply to an organ or part of the body, dead tissue
what is infarction
obstruction of the blood supply to an organ or region of tissue, causing local death of the tissue.
what are 5 sings of congesttive heart failure
reflex tachycardia, enlarged heart, oedema, dyspnea (shortness of breath due to fluid build up), elevated venous pressure (swollen neck veins+ankles)
what is HF-ref
heart failure - reduced ejection fraction (decreased systolic volume)
what is HF-pef
heart failure - preserved ejection fraction
what is a main force that keeps circulation moving
the large pressure between arteries and veins (100-5mmHG)
why are veins more elastic than arteries?
they have the capacity to store blood
why do arteries more muscular than veins?
they need to withstand higher pressures
what causes venous distention
heart is too weak to pump, resulting in the veins storing blood
what happens to venous return in heart failure
decreases
what happens to cardiac output in heart failure
decreases
what happens to sympathetic outflow in heart failure
increases (caused by failure of heart to pump enough blood)
what happens to glomerular filtration in heart failure
decrease
what does the “congestive” in congestive heart failure mean +what does it come from
enhanced sympathetic outflow leads to the circulatory congestion
what does increased sympathetic outflow do to HR
increase
what does increased sympathetic outflow in heart failure do to venous pressure
increase
why is there edema in congestive heart failure
elevated venous pressure, fluid expelled from capillaries
what happens to heart size in congestive heart failure
becomes large (maladaptive hypertrophy)
why is renal blood flow decreased in congestive heart failure
because less cardiac output
what does low renal blood flow cause
increase in renin release
what happens to renin release in congestive heart failure and why
increase renin release because there is less renal blood flow
what does renin cause the conversion of
angiotensinogen to angiotensin 1
what happens to angiotensin 2 in congestive heart failure
increase
what does angiotension 2 do to preload in congestive heart failure
increase
what does angiotension 2 do to afterload in congestive heart failure
increase
what are 3 ways to treat heart failure (broad)
enhance contractility
diuretics to reduce fluid intake
reduce cardiac work load
what are 2 ways(drug types) to enhance contractility in congestive heart failure
cardiac glycosides and positive inotropic agents
how can you reduce fluid intake and increase fluid loss in congestive heart failure
diuretics
what are 3 ways (drug types) to reduce cardiac work load
vasodilators, ACE inhibitors and ARBs, beta-blockers
what is an example of a positive inotropic gent
cardiac digitalis glycosides / digoxin
what does digoxin do to inotropy
positive effect
what physiological benefits are there from digoxin’s positive inotropic effect
circulatory improvement
arterial BP preserved
what are 3 things that cardiac glycosides cause in terms of chronotropy
Overall: negative chronotopy
- reflex tachycardia & vasoconstriction eliminated
- venous return increased
- circulatory improvement lowers ventricular filling pressure
what are the 3 general effects of cardiac glycosides
positive inotropy
negative chronotropy
reduced oedema (due to improved glomerular circulation)
what happens to the heart size when you use cardiac glycosides
smaller
what are the 2 indirect effects of cardiac glycosides on supraventricular tissue
sensitization of baroreceptors, increased vagal tone (similar to ACh)
where are the 2 direct effects of cardiac glycosides on the heart (which parts of the heart)
purkinje fibres and ventricular myocardium
what do cardiac glycosides do to ventricular myocardium
increase force of contraction (positive inotropic effect)
ERP and APD reduced
what do cardiac glycosides do to SA node + net effect
indirectly increase vagal outflow, decease sinus rate, leading to bradycardia
which parts of the heart experience the indirect effects of cardiac glycosides
SA node and AV node
what do cardiac glycosides do to AV node + net effect
indirectly increase vagal outflow - promotes AV block!
what do cardiac glycosides do to purkinje fibres
directly increase automaticity and excitability
what do cardiac glycosides do to the ventricles
directly increase inotropy (contractility)
what is the therapeutic index of cardiac glycosides
low, 2-3x the therapeutic dose
what are some cardiotoxic effects of cardiac glycosides (5)
- arrhythmias
- enhancement of effects seen with therapeutic dose
- generation of after-depolarization
- AV block
- ectopic pacemakers in Purkinje fibres or ventricles
what ion triggers the contractile machinery of the heart
ca++ entry through ca channels
which ion exchange channel is occuring during phase 2 AP
Na+/Ca++ exchange (plateau)
which gradient provides evergy for the extrusion of Ca++
Na+ gradient
what is the mechanism of action of digoxin
inhibits the Na+/K+ ATPase pump, causing Na+ to accumulate in the cell after AP occurs, resulting in less Ca2+ to be removed by the NCX, and less Ca2+ to leave the cell during the plateau of an AP, thus increasing contractility
what happens to Na+ gradient with digoxin
it is decreased
what are 2 examples of catecholamines
dopamine and dobutamine
what are dopamine and dobutamine used for
acute heart failure
how do dopamine and dobutamine work
stimulate b1 adrenoceptors so they increase Ca++ influx through L-type Ca++ channel (increasing inotropy and chronotropy)
what are two examples of phosphodiesterase inhibitors
amrinone and milrinone
what are amrinone and milrinone used for
chronic heart failure
how are amrinone and milrinone administered
orally or via IV
what does phosphoodiesterase do
breaks down cAMP
what is the mechanism of action for amrinone and milrinone
inhibit PDE, increasing cAMP, activate PKA, increase phosphorylation of L tyoe channels, increased Ca++ through L-type channels, increased contractility
how do arteriolar vasodilators contribute to the therapeutic effects of amrinon and milrinone
vasodilation results in decreased afterload
why is the RAAS a problem in heart failure?
during heart failure, the kidney thinks BP is low due to reduced CO, and will activate RAAS. This increases BP further and results in increased afterload
name two ACE inhibitors
ramapril, captopril
what is the mechanism of action for ramapril and captopril
inhibit synthesis of AT-II, resulting in decreased BP and decreased afterload
name three angiotensin II receptor blockers (ARBs)
valsartan, losartan, candesartan
what is the mechanism of action of ARBs?
inhibit AT-II receptors, resulting in decreased BP and decreased afterload
