cardiovascular (not finished yet!) Flashcards
what is the equation for cardiac output?
heart rate x stroke volume
what is a simple deifnition of heart failure?
the inability of the heart to meet the metabolic needs of the peripheral tissues
what are the 6 different ways in which the heart can fail?
pump failure, forward obstruction, reguritant blood flow, congenital shunts, rupture of heart or vessel, conduction disorders
when cardiac output is decreased due to heart failure, _____ drops. this causes _____ activation and subsequent ______ as well as ______.
blood pressure, sympathetic, vasoconstriction, increase in HR and total peripheral resistance,
how does a failing heart affect the kidneys?
if the heart is failing there is decreased perfusion of the kidneys, so the renin-angiotensin-aldosterone system will be activated: renin causes the release of angiotensin II (eventually), and angiotensin II causes vasocontrcition which will increase blood pressure and peripheral resistance. Angiotensin II also stimulates the adrenal cortex to secrete aldosterone, which causes the kidney to retain sodium and water which increases blood volume. This leads to an increase in hydrostatic pressure and a decrease in colloid osmotic pressure, which can cause edema. increase in blood pressure increases preload which can cause the heart to dilate. The heart can only handle this for so long.
what are the two ways in which angiotensin II can make heart failure worse?
it causes vasoconctriction and increases peripheral resistance, making it more difficult for the heart to pump blood through the system. it also causes the release of aldosterone, which ultimately causes an increase in blood volume, giving the heart more blood to actually pump
one of the first responses to early heart failure is _____, which is triggered by_____
sympathetic nervous system activation, decreased cardiac output
what are the normal ACUTE responses to heart failure, and what are the abnormal CHRONIC responses?
ACUTE: increase in heart rate, cardiac output, and total peripheral resistance
CHRONIC: persistent tachycardia, adrenergic receptor downregulation, increased myocardial oxygen demand, myocyte necrosis
describe the process of the RAAS system
decrease in BP is senses by the JG apparatus in the kidney, causing release of renin. Renin converts angiotensin (from the liver) into angiotensin I, and angiotensin converting anzyme (in the lungs), converts it into angiotensin II. Angiotensin II causes vasocontriction, activation of the sympathetic system, and production of aldosterone. aldosterone causes kidneys to retain sodium and water. NOTE: ACE can also convert bradykinin (a vasodilator) into it’s inactive form leading to vasodilation
edema indicates that there is a ____ problem with the heart
preload–>heart can’t pump enough blood from the returning systemic circulation
list the 5 things we can adjust with drugs to help with heart disease
preload, afterload, rate/rhythm, contracility, neurohormonal/sympathetic input
what is Frank-Starling’s Law? How does it relate to heart failure?
it is essentially the increase in cardiac output in response to an increasing preload, the more the heart stretches, the more blood it can pump. If your heart is diseased, the preload can increase but the CO does not increase as much as it should, aka, changes in preload have less of an effect on CO of a diseased heart than on the output of a healthy heart.
explain in regards to Frank-Starling’s law, what happens when you treat with diuretics?
diuretics decrease the symptoms of congestive heart failure because they reduce preload which move preformance left on the curve to a place below the threshold for congestion. Diuretics have little effect on cardiac output however.
explain in regards to frank starling’s law what happens when you treat CHF with positive inotropes?
positive inotropesincrease cardiac output at any preload, but do not directly affect preload itself (so it will not help to avoid congestion)
in regards to frank starling’s law, what happens when you treat with both a positive inotrope AND a diuretic?
you can avoid congestion with diuretics AND you can increase CO, so it shifts the curve UP and to the LEFT.
when are positive inotropes useful?
when there is decreased cardiac output due to decreased myocardial contractility (like dilated cardiomyopathy)
when are negative inotropes useful?
when you want to allow cardiac relaxation and filling in hypertrophic cardiomyopathy or if you want to decrease cardiac oxygen consumption
briefly deschibe how a regular cardiac muscle contraction works
calcium binds to troponin, which pulls trypomyosin out of the way to allow actin to bind. the only actin heads that can bind are the ones that have been “spring loaded” by ATP. So, both ATP and calcium are required for contraction!
why is cardiac muscle so dependent on calcium?
in skeletal muscle, the calcium released by the sarcoplasmic reticulum is enough calcium to interact with all of the troponin causing ALL actin-myosin interactions to ocurr, whereas with cardiac muscle, non all the troponin interacts with the calcium, so more or fewer (depending on the calcium levels) actin-myosin interaction can form. therefore, inotropy or the strength of contraction is directly proportional to the calcium concentration
what kind of drug is Digoxin? what are its effects on HR? what is it’s mechanism of action? Is this drug commonly used?
a positive inotrope, increasing contractility and cardiac output
decreases heart rate
MOA: restores baroreceptor reflex sensitivity in heart failure patients decreasing sympathetic tone. it blocks the Na-K pump which causes sodium to build up in the cell. more sodium slows down the Na-Ca exchanger which leads to a build up of calcium which improves contractility by allowing more actin myosin interactions.
this drug is not commonly used because of its adverse effects and there are better options
what are the adverse effects of digoxin?
long half life, arrhythmias, electrolyte interactions, interactions with other drugs like furosemide, GI effects like vomiting and anorexia
what kind of drug is pimobendan? what is it used for? what is the common trade name?
inodilator (positive inotrope and vasodilator)
used to treat DCM or MVI
vetmedin, very common in small animals
what are the two mechanisms of action of pimobendan?
-sensitizes troponin to calcium allowing for a stronger contraction and inhibits phosphodiesterase (cAMP isn’t broken down, allowing for stronger contractions)
-inhibits PDE3 and 5 in blood vessels resulting in arterial and venous vasodilation which reduces preload and afterload
what are some adverse effects of pimobendan?
very protein bound, maybe some GI signs, tachycardia, PU/PD, CNS toxicity
what kind of drugs are dopamine and dobutamine? how are they administered?
they are beta 1 agonists, they both have low bioavailability so must be given IV in a hospital setting
beta 1 receptors mostly act on ____ and beta 2 receptors act mostly on ____
the heart (increase in cAMP which leads to more calcium)
blood vessels (increase in cAMP causing vasodilation)
what kind of drug is dobutamine? does it affect HR? how is it given?
beta 1 agonist, positive inotrope
does not affect HR
given as CRI
should you give dobutamine to cats?
most of the time no, it causes seizures in cats!
what kind of a drug is dopamine? what are the four places it affects? how is it given?
it acts on many receptors: beta 1, alpha 1, and alpha 2, and DA1
causes vasodilation in kidneys, mesentery, heart, and brain
given as CRI, short half life
what are some adverse effects of dopamine?
arrhythmias, renal vasoconstriction
comparing dobutamine and dopamine, which has:
-more inotropic effects
-more chronotropic effects
-shorter half life
- dilates renal vascular beds
dobutamine
dopamine
dopamine
dopamine
how does epinepherine act on all the receptors?
a positive inotrope and chronotrope due to beta 1 effects, increase TPR due to alpha 1 effects, bronchodilator due to beta 2 effects
what is an adverse effect of epinepherine?
increases myocardial oxygen demand and energy consumption
what are the two main kinds of chronotropes?
beta antagonists (beta blockers)
muscarinic antagonists (anticholinergics)
how do beta antagonists (blockers) work?
they competitively bind to beta receptors. they can be selective or nonselective. they are negative chronotropes so they decrease heart rate
what kind of drug is propranolol? what are it’s effects? what is it used for?
non selective beta antagonist, a negative chronotrppe and inotrope
can also vasoconstrict and bronchoconstrict
used to treat CHF and tachycardia, to decrease sympathetic input to the heart
what are the adverse effects of propranolol?
has a large first pass effect (high oral dose), bradyarrhythmias, hypotension, bronchospasm
what kind of drug is atenolol? what is it used for?
a beta 1 selective antagonist
used to treat ventricular tachyarrhythmias or treating HCM in cats or to help chronic kidney disease
what do anticholinergics do to HR?
increase it because they are blocking the parasympathetic nervous system
M2 (muscarinic) receptors are mainly located where? what does this mean for anticholinergic drugs?
in the cells that make up the SA and AV nodes
this means anticholinergics drugs will have large effects on the nodes of the heart
how does atropine effect heart function?
it is a competitive muscarinic antagonist, preventing Ach from interacting with the receptor. Ach normally has a negative chronotropic and dromotropic effect, so this becomes blocked
what is atropine used for? what are it’s effects? should it be used after anesthesia?
used to treat bradycardia and asystole, for acute short term responses
positive chronotropy, increased cardiac output
NO it is used pre anestehsia to decrease salivation and airway secretions
what are the adverse effects of atropine?
they are all due to it’s non selective nature, has GI effects which can cause colic in horses (GI stasis), red as a beat, dry as a bone, blind as a bat, hot as a firestone, mad as a hatter, the heart runs alone
how is glycopyrrolate different from atropine?
it is more polar so there is less CNS penetration and therefore less CNS adverse effects, doesn’t cross the placenta
what is different about cells within the SA and AV nodes?
they do not have fast sodium channels, they do not have a truse resting potential and instead spontaneously depolarize becuae of a slow influx of sodium
all anti-arrhythmic drugs alter _____
membrane ion conductiance to affect the action potential
what are the 4 classes of antiarrhythmic drugs
na channel blockers
beta blockers
k channel blockers
ca channel blockers
list 3 Na channel blockers
lidocaine, quinidine, procainamide
how do Na channel blockers work?
they bind to the fast sodium channels responsible for rapid depolarization of fast response cardiac action potentials
