4-cardio Flashcards
what type of vessels is the main location of resistance in circulation
arterioles
where is renin released
kidneys
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
in the shovel snow example, what is preload and afterload
preload=how much snow on shovel
afterload=how high lift snow
what happens to afterload when you increase peripheral resistance
it increases
what happens to afterload when you increase BP
it increases
how do you find left ventricle end diastolic pressure / what is another name for it
pulmonary wedge pressure, it is the preload
weird question
how do you find cardiac output
stroke volume x heart rate
is left or right ventricular pressure bigger
left because it has to pump to the whole system
what is venous return
rate of return of blood to the heart
what does cardiac output equal in terms of vein
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 does left ventricular end diastolic pressure =
=preload
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 make 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
infarction
ischemia
increase presure
increase volume load
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), elevated venous pressure (swollen neck veins+ankles)
what is dyspnea
shortness of breath
what is a main force that keeps circulation moving
the large pressure between arteries and veins
what causes venous distention
heart is too weak to pump
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
increase (accumulate fluid)
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 congestive heart failure do to arterial pressure
maintain!
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
what happens to sympathetic outflow in congestive heart failure
increase
what happens to renal blood flow in congestive heart failure
decrease
what happens to cardiac output in congestive heart failure
decrease
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
diuretic+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 2 ways(drug types) to reduce cardiac work load
vasodilators and beta-blockers
what is an example of a positive inotropic gent
cardiac/digitalis glycosides / digoxin
what do positive inotropic agents do
increase force of contraction
what do negative inotropic agents do
decrease force of contraction
what are 2 things that positive inotropic agents cause via the increased force of contraction
circulatory improvement and preserved arterial blood pressure
what are 3 things that negative chronotropics agents cause
- reflex tachycardia & vasoconstriction eliminated
- venous return increased
- circulatory improvement lowers ventricular filling pressure
what happens to the heart size when you use cardiac glycosides
smaller
what happens to edema with cardiac glycosides
it becomes reduced
what do cardiac glycosides do to baroreceptors
sensitize (indirect)
what do cardiac glycosides do to vagal tone
increase (indirect)
what are the indirect effects of cardiac glycosides like
ACh
what are the 2 indirect effects of cardiac glycosides on supraventricular tissue
sensitization of baroreceptors, increased vagal tone
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
increase vagal outflow, decease sinus rate (indirect) -bradycardia
where are the 2 indirect effects of cardiac glycosides on heart tissue
SA node and AV node
what do cardiac glycosides do to SA node + net effect
increase vagal outflow (indirect) - promotes AV block!
what is the net effect of cardiac glycosides on the SA node
bradycardia
what is the net effect of cardiac glycosides on the AV node
promotes AV block
what do cardiac glycosides do to purkinje fibres
increase automaticity and excitability
what do cardiac glycosides do to ERP
reduce
what do cardiac glycosides do to APD
reduce
what is the TI of cardiac glycosides
low, 2-3 of TI
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 causes the contractile machinery during AP
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 digitalis
inhibits the Na+/K+ ATPase pump
what happens to intracellular Na+ with digitalis
accumulation due to the AP
what happens to Na+ gradient with digitalis
it is decreased
what happens to Na+/Ca+ exchange with digitalis
it is reduced
what happens to the amount of Ca++ that leaves the cell during plateau phase of AP with digitalis
less leaves
what kind of dysrhythmia are cardiac glycosides good for
atrial and supraventricular
what is the role for cardiac glycosides in atrial dysrhythmias + How!?
control ventricular rate by impeding transmission through AV node
are cardiac glycosides good for ventricular dysrhythmias
bad
are cardiac glycosides good for do supraventricular dysrhythmias
good
are cardiac glycosides good for atrial dysrhythmias
good
how do cardiac glycosides help atrial dysrhythmias
impede transmission through AV node
what do cardiac glycosides do to AV node
impede transmission
are catecholamines positive or inotropic agents
positive
are phosphodiesterase inhibitors positive or inotropic agents
positive
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 (increase force) so they increase Ca++ influx through L-type Ca++ channel (increase force more so than rate)
is the inotropic or chronotropic effect bigger in dopamine and dobutamine
inotropic (more force rather than rate)
what are two examples of phosphodiesterase inhibitors
amrinone and milrinone
what are amrinone and milrinone used for
chronic heart failure
what does phosphoodiesterase do
breaks down cAMP
what would a phosphodiesterase inhibitor do to cAMP level
increase
what does amrinone and milrinone do to contractility and how
increases because it increases Ca++ through L-type channels
what does amrinone and milrinone do to arteries
vasodilates
what does amrinone and milrinone do to force
increase
what does amrinone and milrinone do to afterload
lower
