Cardiology Flashcards
What is the potential energy?
Additional work that could be accomplished by contraction if ventricle would empty completely
What is preload?
Degree if tension on muscle when it begins to contract
Usually considered end diastolic pressure
What is afterload?
Load the muscle has to work against
Pressure in the aorta for Lv
Tension time index
Oxygen consumption = tension in heart muscle with contraction by duration of time
Heart efficiency
Ration of work output to total chemical energy expenditure
Frank Starling mechanism
The greater the stretching of heart muscle during filling, the great the force of contraction
Calculate stroke volume
End diastolic volume - end systolic volume
Calculate cardiac output
Stroke volume X HR
What are possible causes of long QT syndromes
Congenital (mutations if Na or K channel genes)
Hypomagnesemia
Hypokalemia
Hypocalcemia
Drugs: quinidine, fluorquinolones, erythromycin
Lidocaine
Depresses increase in Na permeability during AP, Blocks rhythmical discharge of focal point of abnormal rhythm
What are reasons for impulse re-entry(circus movement)
Can cause ventricular fibrillation
Overall happens when impulse come to already stimulated muscle that is not refractory any more
- pathway around circle is longer (dilated heart)
- velocity of conduction is decreased (purkinje system blockage, ischemia, hyperkalemia)
- shortened refractory period (drugs- epi)
Digitalis
Cardiotonic drug
Increases Ca in cardiac muscle cells by inhibition of Na/K ATPase
—> increase of intracellular Na and slowing of Na/Ca exchange pump = more Ca in cardiomyocytes
also has some parasympathetic effects, especially on atria - can decrease HR and be used for atrial arrhythmia ( afib and flutter )
Atrial natiuretic peptide
Released by atrial walls when stretched
- heart failure increases right and left atrial pressures
Direct effect on kidney to excrete water and Na - prevent extreme congestive symptoms
Tetralogy of fallot
VSD
Overriding aorta
Right ventricular outflow obstruction
Right ventricular hypertrophy
Eisenmenger‘s Syndrome
When initial left-right shunt reversed to right- left due to progressive increase in pulmonary hypertension - pulmonary vascular resistance increases and if pulmonary vascular pressure is high enough reversal happens
More common in cattle
Which breeds are predisposed for VSD?
Bovine: Hereford, Limousine
Equine: Arabians, SB, QH
NT - proBNP
From, stimulated by, functions
From ventricular and atrial myocytes
Due to volume overload / stretching
Functions:
Decrease vagal tone
Decrease renin and aldosterone
Decrease venous and arterial tone
Decrease vascular proliferation
Decrease cardiac fibrosis and proliferation
Increase GFR and decrease Na absorption
Non cardiac reasons: hyperthyroidism, systemic hypertension, pulmonary hypertension, renal insufficiency
Urotensin II
Endogenous cardiostimulatory peptide
Potent vasoconstriction
Potent positive inotropy
May pay role in cardiac hypertrophy
Not yet used in vetmed
Neuropeptide Y
Released with NE from sympathetic endings
Influence in coronary vasoconstriction
Myocardial contraction
Mitogenic and hypertrophic effects on vascular smooth muscle and cardiomyocytes
Increase in heart failure
Not yet used in vetmed
Endothelin
Potent vasoconstrictor
ET-1 produced in heart failure
- increase contractility, vasoconstriction, cardiac fibroblast activation, worsening of hypertrophy
High in pre clinical and overt heart failure
Epinephrine and norepinephrine
- Function and receptors
Epinephrine:
- b1 - myocytes, increased contractility
- b2- vasculature, vasodilation
Norepinephrine
b1 - myocytes, increased contractility
a1 - vasculature, vasoconstriction
Effects of angiotensin
- vasoconstriction
- increased sympathetic tone (central, ganglionic and presynaptic NE release and decrease of presynaptic NE uptake)
- aldosterone secretion
- fluid and Na retention
- increased cardiac hypertrophy and fibrosis
ADH
produced in supraotpic nuclei in hypothalamus
saved and secreted by neurohypophysis
secretion stimulated by:
osmoreceptors in hypothalamus and ATII
AV1 receptors - vasconstriction
AV2 receptors - distal collecting ducts
ANP
Mechanism, Stimulated by, effects
atrial natriuretic peptide
from atrium, reacts to stretching of myocytes = increased preload
- stimulates vasodilation (via cGMP)
- stimulates diuresis by kidneys
- inhibits aldosteron secretion
Nitric oxide
Effect, Mechanism, stimulated by
vasodilation
caused by: via cGMP –> inhibits myosin light chain kinase (MLCK activates MLC which causes contraction)
stimulated by: Ash and sheer stress
Ivabradine
direct If channel inhibitor
Class I antiarrythmic drugs
Sodium channel blockers
Ia = act mostly on fast Na channels - phase 0
mechanism: prolonged AP and prolonged refractory period
drugs: procainamide, quinidine
use: V tach, Afib
Ib = late phase 2 Na channel blockers
mechanism: shortened AP, shortened RP, act on open or inactivated state of channel, lidocaine will go into prematurely activated cell and stabilize its inactivated state - works preferentially on diseased cells
drugs: lidocaine, mexiletine
use: Ventricular arrhythmias
Ic= powerful phase 0 blockers, fast Na channel blockers
drugs= flecainide, propanefol
Class II antiarrythmic drugs
mechanism: acting on beta receptors, beta BLOCKERS, decrease HR and contractility
drugs: atenolol, propanolol, metoprolol
Class III antiarrythmic drugs
mechanism: potassium channel blockers, phase 3
drugs: amiodarone, sotalol (has beta blocker activity also!!) , ibutilide
use: supra ventricular and ventricular arrhythmias, afib and flutter
Class VI antiarrythmic drugs
mechanism: blockage of voltage sensitive Ca channels
slower conduction, reduced contractility
drugs: diltiazem, verapamil (both supra ventricular and afib)
Adenosine
antiarrythmic
does not fit into I-IV classes
acts on A1- adenosine receptor (atria, AV and SA node)
decerased automaticity, decreased conduction velocity, prolonged refractory period
short duration of action- has to be given IV
Mg Sulfate
Beta blockers
Block beta 1 receptors on heart
some also act on beta 1 on kidney - decreased renin release
Metoprolol
Carvedilol - also alpha 1 on vessels = vasodilation, decreased vascular resistance
Bisoprolol
effects: decrease HR, decrease CO, but normal to increased stroke volume (by better filling during diastole)
ACE inhibitors
inhibit angiotensin converting enzyme
decrease ADH, aldosterone and generally inhibit effects of RAAS
also increase effect of bradykinin = vasodilation (ACE usually breaks down bradykinin)
Drugs: Enalapril, Forsinopril, Lisinpril etc.
Angiotensin receptor blockers
block the actual effect of angiotensin
- less vasoconstriction, decreased ADH and aldosterone
Drugs: Telmisartan, Candesartan, Losartan, Valsartan
Angiotensin receptor- neprilysin inhibitor
Neprilysin inactivates natriuretic peptides (ANP, BNP, CNP)
inhibitors of neprilysin and angiotensin receptor inhibit AT1 receptor and also keep longevity of ANP,BNP and CNP and therefore increase Na and HO2 secretion, vasodilation, and cardiac relaxation and decrease cardiac fibrosis and hypertrophy, sympathetic outflow
Aldosterone antagonists
potassium sparing diuretic
competitively blocking the binding of aldosterone to mineralocorticoid receptor
decreases water and Na resorption and decreases potassium wasting
drugs: Spironolactone; Epleronone
Loop diuretics
inihibit Na/K/2Cl transporter in thick ascending loop of Henle
reduce absorption of much greater portion of Na in comparison to others
Drugs: Furosemide, Torsemide, Bumetanide
Vasodilators in heart failure
Hydralazine, Isosorbide dinitrate
both cause release of NO – cGMP release and decreased Ca = decreased muscle contraction = vascular smooth muscle relaxation = vasodilation
Dobutamine
beta agonist
highly selective for beta 1
increase in adenylate cyclase – stimulates ATP to cAMP– cAMP accumulation to more PKA – PKA leads to phosphorylation of calcium channels and more calcium inside the cells
also some beta 2 effects:
vasodilation on vessels - decreased peripheral resistance
effects: increase in HR and contractility, but also increase O2 and energy demands of heart
Phosphodiesterase inhibitors
inhibits PDE – decreased break down of cAMP – increase PKA activity - phosphorylation of Ca channel - more calcium influx = increased cardiac contraction, vasodilation
drugs:
Milrinone (cardiac selective)
Sildenafil, caffeine, theophylline, pentoxyphylline
Omega-3-fatty acids
EPA, DHA (both fish), ALA (veggie)
decrease TG – bind to enzymes that put 3 free fatty acids together and therefore decrease TG in blood
prevent prostaglandin H synthase
anti-thrombotic: decrease platelet aggregation, inhibits thromboxane synthesis, reduction of fibrinogen, increase in TPA
antiarrythmic: decrease ion-channel action on sarcolemma = prolonged refractory period
NO enhancement - vasodilation
