Cardio Flashcards
red material. complete
what is the relationship between cardiac output, heart rate, and stroke volume?
cardiac output = heart rate x stroke volume
Name at least 3 general mechanisms of heart failure (there are 6 total)
pump failure, forward obstruction to blood flow, regurgitant blood flow, congenital shunts, rupture of heart or vessel, conduction disorders
What triggers sympathetic nervous system activation in early heart failure?
Decreased cardiac output
What are 3 acute changes to compensate for early heart failure? (Hint, these occur due to sympathetic activation)
increase HR, increased CO (cardiac output), increased TPR
Name at least 2 effects of chronic SNS activation as they relate to worsening heart failure
Chronic activation of SNS results in persistent tachycardia, adrenal receptor down regulation, increased myocardial oxygen demand, and myocyte necrosis. (These all result in myocardial injury and therefore worsen heart failure)
In response to decreased BP, is the conversion of angiotensinogen to angiotensin 1 increased or decreased? what enzyme is responsible for this conversion?
increased conversion of angiotensinogen to angiotensin 1. by renin from the kidney.
name 3 effects of angiotensin II
SNS activation, vasoconstriction, increased production of aldosterone
what is the effect of increased aldosterone on the kidney? how does this effect relate to blood volume?
aldosterone increases renal retention of Na and H2O. increases blood volume
most common type of heart disease in dogs?
chronic valvular heart disease (CVHD), also known as endocardiosis or myxomatous valve degeneration, accounts for 75% of these cases (left AV valve is most common)
how does CVHD/myxomatous valve degeneration/endocardiosis affect the ventricles of the heart?
changes in mitral valve collagen result in valve prolapse and mitral regurgitation. this leads to ventricular remodelling and dysfunction due to increased cardiac work
what are 6 basic pharmacological mechanisms to modify cardiac function
chronotropy, ionotrophy, peripheral resistance, blood volume, rate of conduction, neurohormonal input to heart
pharmacological modification aims to change one or more of these 5 cardiac parameters
preload, afterload, rate or rhythm, contractility, sympathetic or neurohormonal input
term for amount of ventricular stretch at end of diastole
preload
as preload increases, does strength of cardiac muscle contraction (ionotropy) increase or decrease? what is the name of this mechanism?
increase; Frank-Starling law
what determines preload
amount of blood returned to heart prior to contraction
term for resistance the heart must pump against to send blood out of the left ventricle and into the aorta
afterload
what determines afterload?
total peripheral resistance
if you increase vasoconstriction and decrease vasodilation, what is the effect on after load?
increased afterload (due to increased total peripheral resistance)
what drug class affects contractility of the heart
ionotropes
when skeletal muscle contracts, is the calcium released by the SR sufficient to interact with all of the troponin? what proportion of actin-myosin interactions will occur?
yes, sufficient. all potential actin-myosin interactions will occur
when cardiac muscle contracts, does all troponin interact with calcium? what proportion of actin-myosin interactions will occur?
not all troponin interacts with calcium in cardiac muscle contraction. number of actin-myosin cross-bridges will depend on intracellular calcium availability
name at least 2 positive ionotropes intended for chronic use
digoxin, pimobendan, dobutamine, dopamine, epinephrine
name at least 1 positive ionotropes intended for short-term use
ephedrine, isoproterenol
before pimobendan was discovered, this was the only positive ionotrope available for chronic use; now it is infrequently used. what is this drug? what is it still used for?
digoxin. useful in animals with atrial fibrillation
how does digoxin facilitate more interactions between actin and myosin to improve contractility?
digoxin inhibits Na-K pump in cardiac myocyte cell membrane, increasing Na concentration in cell, slowing or reversing action of Na-Ca exchanger, increasing Ca concentration in cell, increasing actin-myosin interactions
name at least 2 adverse effects of digoxin
arrhythmias, electrolyte interactions, drug interactions (eg. furosemide), GI effects (eg. vomiting, anorexia).
this high incidence of adverse effects is why digoxin in infrequently used in vet med
what is the positive ionotrope of choice in small animals
pimobendan
mechanism of action of pimobendan on heart
sensitizes troponin C complex to calcium leading to increased contraction. also inhibits PDE3 and 5 in blood vessels, resulting in arterial and venous vasodilation, reducing preload and afterload
what route of administration for the positive ionotrope beta 1 agonists, dopamine and dobutamine?
must be given IV
the Frank Starling law states that
the stroke volume of cardiac contraction increases as preload increases
dopamine1 (DA1) receptor activation causes vasodilation in which 4 organs
kidneys, mesentery, heart, brain
consider dobutamine vs dopamine. which has more positive ionotropic effects? more chronotropic effects? dilates the renal vascular bed?
dobutamine has more positive ionotropic effects and does not dilate the renal vascular bed. dopamine has more chronotropic effects and dilates the renal vascular bed
what two classes of drugs are used primarily as chronotropes
beta antagonists (beta blockers) and muscarinic antagonists (anticholinergics)
what is the effect of beta antagonists on heart rate
reduce heart rate
what is the therapeutic goal of the non-selective beta antagonists propranolol
negative chronotrope and negative ionotrope
this drug can be given orally or IV, has a large first pass effect, and has adverse effects of bradyarrhythmias, hypotension, bronchospasm, negative ionotropy (effects of beta blockade)
propanolol
you have concerns about pulmonary function. should you use atenolol or propranolol to treat Fluffington’s ventricular tachyarrythmia?
atenolol (because there are same beta 1 effects, but lacks the beta 2 effects)
do anticholinergics increase or decrease heart rate
increase heart rate
where are M2 receptors mainly located
in cells making up SA and AV nodes
does atropine affect only cardiac M2 receptors or all muscarinic receptors? how does its receptor activity relate to its adverse effects?
affects all muscarinic receptors, therefore non-specific effects which can be undesirable (eg. GI effects can cause colic in horses, also contraindicated in animals with glaucoma)
this drug is used for acute, short-term responses, increases cardiac output, used pre-anesthesia to decrease salivation and airway secretions, and is a positive chronotrope useful for treating bradycardia and asystole
atropine
when is a cardiac myocyte unable to initiate an action potential?
effective refractory period which lasts from phase 0 to early phase 4
what cells lack fast sodium channels
cardiac nodal cells
what are 4 effects of antiarrhythmic drugs on heart (not classes, think in terms of physiological effects)
alter automaticity, alter conduction velocity, change excitability of cardiac cells during ERF, alter membrane ion conductance to affect action potential
what are 5 classes of antiarrythmic drugs
class 1 sodium channel blockers, class 2 beta blockers, class 3 potassium channel blockers, class 4 calcium channel blockers, class 5 miscellaneous
class 1 sodium channel blocker antiarrhythmic drugs change which phase of the action potential? what is their effect on action potential duration?
phase 0 (reduce slope and amplitude); may increase, decrease, or not change AP
what class of antiarrhythmic drugs also has anticholinergic effects
class 1A
this class 1B antiarrythmic drug is used to treat tachyarrythmias, especially during anesthesia, has a large first pass effect, and has a rapid onset after IV administration
lidocaine
this class 1A antiarrythmic drug prolongs the ERP of atrial and ventricular muscle to allow atrial fibrillation conversion, is anticholinergic, and speeds AV conduction
quinidine
this class 1A antiarrythmic has a similar mechanism of action to quinidine but is used for controlling ventricular arrhythmias rather than atrial arrhythmias
procainamide
this class 3 antiarrhythmic prolongs the AP and slows depolarization, is also a beta blocker, and is used for control of ventricular arrhythmias
sotalol
this class 4 antiarrythmic blocks slow calcium channels in cardiac cells, is the calcium channel blocker of choice for arrhythmias, and is used for atrial fibrillation in dogs and hypertrophic cardiomyopathy in cats
diltiazem
name 3 ways vascular smooth muscle contraction can be triggered
passive stretching, electrical stimulation (AP), chemical stimulation (receptor binding triggering calcium release from SR)
this calcium channel blocker has potent vasodilatory effects, less direct effects on the heart, and is used to treat systemic hypertension as weak as severe mitral regurgitation in dogs
amlodipine
do alpha 1 antagonists have a greater dilation effect on arteries or on veins?
dilate both arteries and veins, but less of an effect on veins (therefore major effect is reduced preload)
what are the 2 goals of using a diuretic
reduce blood volume and mobilize edema
what is diuretic of choice for cardiovascular disease
furosemide
what is the effect of ACE inhibitors on blood vessels
vasodilation
what is the effect of ACE inhibitors on aldosterone
decrease aldosterone (so cause a diuretic effect)
what is the effect of ACE inhibitors on sympathetic input to the heart
decrease
ACE inhibitors are pro drugs, so they require a conversion to active metabolites. why does this matter clinically?
delayed onset of action, 1-2 weeks to see magnitude of response. they are for management rather than acute therapy.
what ion controls cardiac contractility
calcium
this drug is a positive ionotrope that does NOT increase heart rate at normal doses, can cause seizures in cats, and has a half-life of 2 minutes so is given as CRI
dobutamine
glycopyrrolate is similar to atropine but is a less polar molecule. what effect does this have on distribution compared to atropine?
less CNS penetration, so fewer adverse CNS effects
