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Cardiology Flashcards

1
Q

What is the potential energy?

A

Additional work that could be accomplished by contraction if ventricle would empty completely

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2
Q

What is preload?

A

Degree if tension on muscle when it begins to contract

Usually considered end diastolic pressure

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3
Q

What is afterload?

A

Load the muscle has to work against

Pressure in the aorta for Lv

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4
Q

Tension time index

A

Oxygen consumption = tension in heart muscle with contraction by duration of time

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5
Q

Heart efficiency

A

Ration of work output to total chemical energy expenditure

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6
Q

Frank Starling mechanism

A

The greater the stretching of heart muscle during filling, the great the force of contraction

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7
Q

Calculate stroke volume

A

End diastolic volume - end systolic volume

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8
Q

Calculate cardiac output

A

Stroke volume X HR

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9
Q

What are possible causes of long QT syndromes

A

Congenital (mutations if Na or K channel genes)

Hypomagnesemia
Hypokalemia
Hypocalcemia
Drugs: quinidine, fluorquinolones, erythromycin

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10
Q

Lidocaine

A

Depresses increase in Na permeability during AP, Blocks rhythmical discharge of focal point of abnormal rhythm

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11
Q

What are reasons for impulse re-entry(circus movement)

A

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)
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12
Q

Digitalis

A

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 )

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13
Q

Atrial natiuretic peptide

A

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

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14
Q

Tetralogy of fallot

A

VSD
Overriding aorta
Right ventricular outflow obstruction
Right ventricular hypertrophy

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15
Q

Eisenmenger‘s Syndrome

A

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

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16
Q

Which breeds are predisposed for VSD?

A

Bovine: Hereford, Limousine
Equine: Arabians, SB, QH

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17
Q

NT - proBNP
From, stimulated by, functions

A

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

18
Q

Urotensin II

A

Endogenous cardiostimulatory peptide
Potent vasoconstriction
Potent positive inotropy
May pay role in cardiac hypertrophy

Not yet used in vetmed

19
Q

Neuropeptide Y

A

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

20
Q

Endothelin

A

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

21
Q

Epinephrine and norepinephrine
- Function and receptors

A

Epinephrine:
- b1 - myocytes, increased contractility
- b2- vasculature, vasodilation

Norepinephrine
b1 - myocytes, increased contractility
a1 - vasculature, vasoconstriction

22
Q

Effects of angiotensin

A
  • 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
23
Q

ADH

A

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

24
Q

ANP
Mechanism, Stimulated by, effects

A

atrial natriuretic peptide

from atrium, reacts to stretching of myocytes = increased preload

  • stimulates vasodilation (via cGMP)
  • stimulates diuresis by kidneys
  • inhibits aldosteron secretion
25
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
26
Ivabradine
direct If channel inhibitor
27
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
28
Class II antiarrythmic drugs
mechanism: acting on beta receptors, beta BLOCKERS, decrease HR and contractility drugs: atenolol, propanolol, metoprolol
29
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
30
Class VI antiarrythmic drugs
mechanism: blockage of voltage sensitive Ca channels slower conduction, reduced contractility drugs: diltiazem, verapamil (both supra ventricular and afib)
31
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
32
Mg Sulfate
33
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)
34
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.
35
Angiotensin receptor blockers
block the actual effect of angiotensin - less vasoconstriction, decreased ADH and aldosterone Drugs: Telmisartan, Candesartan, Losartan, Valsartan
36
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
37
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
38
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
39
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
40
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
41
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
42
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

General Exam (12 decks)

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