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Cardio Drugs > Physiology > Flashcards

Physiology Flashcards

0
Q

CO =

Ficks Principle

A

CO= rate of O2 consumption / arterial O2 content - venous O2 content

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1
Q

CO=

A

CO= SV X HR

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2
Q

MAP=

A

MAP= CO X TPR

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3
Q

MAP =

A

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

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4
Q

Pulse Pressure=

A

PP= systolic pressure - diastolic pressure

widened PP seen in aortic regurgitation

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5
Q

SV=

A

CO / HR = EDV - ESV

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6
Q

Stroke volume affected by

A

Contractility
Preload
Afterload (resistance in aorta to prevent blood from leaving the ventricle)

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7
Q

Stroke volume increased when

A

Increased preload
Decreased afterload
Increased contractility

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8
Q

Contractility increases with

A

Catecholamines (increase Ca from SR)
Increased intracellular Ca
Decreased extracellular Na (decreased Na/Ca exchanger)
Digitalis (blocks Na/K pump, increase intracellular Na, decrease Na/Ca exchanger, increase intracellular Ca)

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9
Q

Contractility decreases with

A 
B1 blockade (decrease cAMP)
Heart failure (systolic dysfunction)
Acidosis 
Hypoxia/ hypercapnea
Non dihydropyridine Ca channel blockers
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10
Q

Myocardial oxygen demand is increased by

A

Increased afterload
Increased contractility
Increased HR
Increased heart size (increased wall tension)

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11
Q

Nitroprusside

A

Decreases preload (venodilator) and decreases afterload (vasodilator)

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12
Q

EF=

A

EF= SV / EDV = EDV -ESV / EDV

Normal is > 55%

EF decreases in systolic heart failure but is normal in diastolic heart failure

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13
Q

Resistance

A

Directly related to viscosity

Inversely related to radius ^ 4

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14
Q

Viscosity increases in …….. Thus causing more resistance and High Cardiac Output Failure

A

Polycythemia
Hyperproteinemic states
Hereditary spherocytosis

Viscosity depends mostly on hematocrit

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15
Q

Viscosity decreases in

A

Anemia

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16
Q

Total resistance in series

A

R1 + R2 + R3….

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17
Q

Total resistance in parallel

A

1/R = 1/R1 + 1/R2 + 1/R3….

Remember to flip the answer to get R total

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18
Q

Operating point of heart

A

CO and venous return are equal

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19
Q

Decrease TPR

A

Curve shift up and right

Exercise, AV shunt/fistula

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20
Q

Increase TPR

A

Curve shift down and left

Hemorrhage before compensation can occur

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21
Q

Decrease contractility

A

Curve shifts down and right

Heart failure, narcotic overdose, B blockers

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22
Q

X intercept of venous return curve=

A

Mean systemic filling pressures

23
Q

AV shunts

A

Increase preload, decrease afterload

24
Q

Pressure volume loop

A

“CAP”

Shift left= increased Contactility
Shift up= increased Afterload
Shift right= increased Preload

25
Q

A wave

A

Atrial contraction

26
Q

C wave

A

RV contraction (closed tricuspid valve bulging into atrium)

27
Q

X descent

A

Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

28
Q

V wave

A

Increased right atrial P due to filling against closed tricuspid valve

29
Q

Y descent

A

Blood flow from RA to RV

30
Q

S1

A

Mitral and tricuspid close, loudest at mitral area

31
Q

S2

A

Aortic and pulmonary valve close, loudest at left sternal border

32
Q

Normal splitting

A

Delayed closure of pulmonic valve during inspiration

33
Q

Wide splitting

A

Occurs in both I and E; seen in pulmonic stenosis, RBB block

34
Q

Fixed splitting

A

ASD; left to right shunt causes extra blood to exit thru pulmonic valve so closure is greatly increased in both I and E

35
Q

Paradoxical splitting

A

P closes before A, on I there is no split at all; due to aortic stenosis, LBB block

36
Q

What determines HR

A

The slope of phase 4 (funny Na channels) which controls the SA node

37
Q

PR interval

A

Conduction delay thru AV node (<200msec)

38
Q

QRS

A

Normally <120 msec

39
Q

QT

A

Mechanical contraction of ventricles (systole)

40
Q

T wave

A

Inversion may indicate recent MI

41
Q

ST segment

A

Isoelectric, ventricles depolarized

can be depressed or elevated with MI

42
Q

U wave

A

Hypokalemia, bradycardia

43
Q

Speed of conduction

A

PavA

Purkinke> atria> ventricles> AV node

44
Q

Pacemakers

A

SA> AV> bundle of His/purkinke/ ventricles

45
Q

Conduction pathway

A

SA node- atria- AV node- common bundle- bundle branches- purkinje fibers- ventricles

46
Q

AV nodal delay

A

100 msec- Allows time for ventricular filling

47
Q

Atrial fibrillation

A

Irregularly irregular with no discrete P waves

48
Q

Atrial flutter

A

Sawtooth appearance

Rapid succession of identical back to back atrial depolarization

49
Q

1st degree AV block

A

PR interval prolonged >200msec

Bigger than 1 large square

50
Q

2nd degree Mobitz type 1 (wenckebach)

A

Progressive lengthening of PR until a P wave is dropped

51
Q

2nd degree Mobitz type 2

A

Normal PR intervals

No QRS following P wave

52
Q

3rd degree heart block

A

P waves and QRS waves are independent of each other

Can be caused by Lyme disease

53
Q

PCWP = pulmonary capillary wedge pressure

A

Approximation of LA pressure

In mitral stenosis, PCWP> LV diastolic pressure

Measured with pulmonary artery catheter= swan-ganz catheter

54
Q

Coronary arteries need more oxygen……what’s the response

A

Increased blood flow…..they already extract 80% of oxygen……so only way to get more oxygen is to increase blood flow

55
Q

Edema causes:

A

Increased capillary pressure (heart failure)
Decreased plasma proteins (nephrotic syndrome, liver failure)
Increased capillary permeability (toxins, infections, burns)
Increased interstitial fluid colloid osmotic pressure (lymphatic blockage)

56
Q

Net filtration pressure =

A

Pnet= ((Pc-Pi)- (colloid c- colloid i))

Cardio Drugs (7 decks)

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