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Cardiovascular - step > Physiology > Flashcards

Physiology Flashcards

1
Q

The Fick principle please

A

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

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2
Q

describe what happens in the early stages of exercise

A

Co is maintained by increased HR and increased SV

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3
Q

what maintaines CO in late stages of exercise?

A

CO is maintained by HR only because SV platueas

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4
Q

what increases pulse pressue

A

a) hyperthyroidism (decreased compliance = increased PP)
b) aortic regurgitation
c) aortic stiffening - isolated systolic hypertension in elferly (decreased compliance = increased PP)
d) obstructive sleep apnea - increased sympathetic tone (decreased compliance = increased PP)
e) exercise - transient

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5
Q

what decreases pulse pressure

A

aortic stenosis
cardiogenic shock (decrease SV)
cardiac tamponade
advanced heart failure (decreased SV)

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6
Q

relationship of PP with a) SV and b) arterial compliance

A

PP is proportional to SV

PP is inversely proportional to arterial complaince

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7
Q

describe effects of a) contractility b) preload and c) afterload on SV

A

Sv is increased by increased contractility
SV is decreased by increased afterload
SV is increased by increased preload

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8
Q

list what increases contractility

A

catecholamines
intraceullar Ca
decreased extracellular Na (less Na to move into the cell to kick Ca out)
digitalis (blocks Na K ATPase - less Na out of cell to move CA into the cell)

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9
Q

list what decreases contractility

A 
b1 blockade (decreased cAMP)
HF with systolic dysfunction (eccentric hypertrophy, in series; increased preload)
acidosis**
hypoxia/hypercapnia**
non-dihydropyridine CCBs
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10
Q

what increases myocardial oxygen demand

A

increased contractility
increased afterload (proportional to arterial pressure)
increased heart rate
increased diameter fo ventricle (increased wall tension)

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11
Q

Laplace’s law

A

wall tension = (pressure x radius)/(2x wall thickness)

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12
Q

what approximates EDV?

A

prolaod

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13
Q

what does preload depend on?

A

venous tone

circulating blood volume

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14
Q

effects of nitroglycerin on preload?

A

decrease - venodilation

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15
Q

what is used to approximate afterload?

A

MAP
increased afterload - increased pressure - increased wall tension via laplace - increased O2 use (contractility, afterload, heart rate too)

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16
Q

what do vasodilators do?

A

decreased afterload

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17
Q

what do ACEi and ARBs do/

A

decreased afterload and preload

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18
Q

what does the ejection fraction represent?

A

ventricular contractility

normal is > 55%

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19
Q

what type of heart failure has a normal EF?

A 
diastolic dysfunction  (heart cant relax but can pump out ) --> normal ejection fraction
systolic dysfunction (heart is relaxed, but cant pump) --> low ejection fraction
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20
Q

EJECTION FRACTION SI DECREASED IN SYSTOLIC HF (heart can relax, but cant pump ie dilated cardiomyopathy - decreased contractility)

A

EJECTION FRACTION IS NORMAL IN DIASTOLIC DYSFUNCTION (heart cant relax, but can pump)

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21
Q

frank starlign law

A

force of contraction is proportional to EDB of cardiac muscle fibre ie preload

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22
Q

formula: resistance =

A

(8 x viscosity x lenfth) / (pi resistance ^4)

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23
Q

what does viscosity depend most on?

A

hematocrit

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24
Q

when does viscosity increase?

A

hyperproteinemic states - multiple myeloma

poycythemia

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25
Q

when does viscosity decrease?

A

anaemia

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26
Q

describe the result on the vardiac and vascular function cruevs if inotropy

A

changes in contractility - altered CO for a ive RA pressure

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27
Q

describe the result on the cardiac and vascular function curves of venous rerun

A

changes in circulating colume or venous tone - altered RA for a given CO

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28
Q

describe the result on the cardiac and vascular function curves of TPR

A

changes in TPR - altered CO at a five RA pressure, however the mean systemic pressure is unchangesd

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29
Q

qhat causese the mean systemic pressure to change?

A

altered blood volume or venous tone

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30
Q

what is S3?

A

early diastolic
normal in chidren and pregnancy

abnormal when have increased filling pressures ie mitral regurgitation, HG, dilated ventricles (systolic dysfunction)

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31
Q

what is the a wave?

A

atrial contraction

absent in atrial fibrillation

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32
Q

when does the mitral valve close in relation to the jugular venous pulse wave?

A

low pressure point between a and c wave

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33
Q

what is the c wave?

A

rapid ejection of ventricular systole and tricuspid pushed up int othe atrium

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34
Q

what is the x descent

A

ventricle is platuea - occurs beore the t wave
blood still leaving ventricle, but its not squeezing at max
no tricuspid buldge

35
Q

what is the v wave?

A

atrila is filling and the ventricle is relaxed,

mitral valve is closed

36
Q

when does the mitral valve open in relation to the jugular venous pulse wave?

A

between the v and y wave

37
Q

what is the y descent?

A

when mitral valve opens and blood enters the ventricle from the atrium

38
Q

describe the phases of the myocardial action potential that occurs at the myocardium, bundle of HIs and purkinje fibres

A

phase 0 - rapid upstroke, depol, vg Na
phase 1 - initial repol 0 inactivation of vg Na, vg K start to open
phase 2 - platuea - vg Ca channels balance K efflux. Ca -induced calcium release from the sarcoplasmic reticulum
phase 3 - rapid repol - slow vg K open
phase 4 - resting potential - high K perm through leak channels

39
Q

describe the action potential phases in the pacemaker

A

phase 0 = upstroke - vg Ca channels. (fast vg Na are permanently inactivated bc resting membrane potential is about -70 too high to reactivate). results in a slow conduction veloscity that is used by the V node to prolong transmission from the a to the v for filling
phase 1 - absent
phase 2 - absent
phase 3 - inactivation fo CA channels and increased activation fo K channels - increased K efflux
phase 4 - slow spontaneous diastolic depol as na conductancec increased (If). accounts for automaticity of SA and AV nodes.

40
Q

what determines heart rate

A

the slow of phase 4.

41
Q

p wave?

A

atrial depol

42
Q

PR interval

A

3 small squares to 5 small squares
0.12-0.2 sec
atrial depol start to start of ventricular depol

43
Q

QRS complex

A

2 small squares to 2.5 small squares
0.8-0.1 sec
ventricular depolarization normally >120 msec

44
Q

QT interval

A

ventricular depolarization, mechanical contraction of the ventricles, nventricular repolarization
8 small squares to 11 small squares
0.32 sec to 0.40 seconds

45
Q

J point

A

junction between end of QRS complex, and start fo ST segment

46
Q

ST segment

A

isoelectic

ventricles depolarized

47
Q

U wave

A

caused by hypokalenima and bradycardia

48
Q

what effect does hypokalemia have on the ECG?

A

U wave appearance (also occurs in bradycardia)

49
Q

what predisposes to torsades de pointes?

A

increased QT interval

normal 8-12 small squares/0.32-0.4 sec

50
Q

list specific causes of increased QT interval and risk fo trades de pointes

A

antiatthythmics A (class IA and III, antibiotics B (macrolides), anticycholites C (haloperidol), antidepressnats D (TCAs), antiemetics E (ondansetron)
low potassium
low magnesium

51
Q

how to treat torsades de pointes

A

magnesium sulfate

52
Q

Romano-Ward SYndrome

A

AD
no deafness
inherited disorder of myocardial repolarization typically due to ion channel defects
increase risk of sudden cardiac death due to torsades de points

53
Q

Jervell and Lange-Nielsen syndrome

A

AR
sensineural deafness
inherited disorder of myocardial repolarization typically due to ion channel defects
increasd risk of sudden cardiac death due to torsades de pointes

54
Q

Brugada SYndrome

A

ECG changes: pseudo-RBBB and ST elevations in V123
AD
most common in Asian males
increasd risk of ventricular tachyarrhythmias and sudden cardiac deacl
prevent with implantable cardioverter-defibrillator

55
Q

Wolff-Parkinson-White Syndrome

A

MOST COMMON ventricular preexcitation syndrome
buncle of kent - bypass AV node delay to ventricles = DELTA wave and widened QRS complex with decreased PR interval

may result in re-entry circuit supraventricular tachycardia

56
Q

what is associated with atrial fibrillation

A 
hypertension
coronary artery disease
rheumatic heart disease
binge drinking
HF
valvular disease
hyperthyrodisin
atrial stasis -- cardioembolic events
57
Q

list the irregular ECG tracings

A

atrial fibrillation
ventricular fibrillation
second degree, Mobitz I aka Wenckebacj

58
Q

list the regular ECG tracings

A

atrial flutter
1st degree AV block
mobitz II 2nd degree AV block
3rd degree, complete

59
Q

lyme disease arrhtymia plase

A

3rd degree block

60
Q

regulary irregular

A

2nd degree block Mobitz I

61
Q

describe role of ANP

A

released from volume overloaded/increased pressure in atrial myocytes –> acts via cGMP to:

a) vasodilate
b) decrease absorption of Na in collecting ducts
c) dilates afferent arteriole, constricts efferents to promote diuresis
d) aldosterone escape

62
Q

describe role of BNP

A

released from ventricular myocytes in respone to increased tension. longer t1/2 than ANP
BNP blood test use to diagnose HF (good NPV)
can be used to treat HF (recombinant form - nesiritide)
a) vasodilates
b) decreased Na reabsorption in the collecting fucts
c) promotes diuresis - dilates afferent and constricts efferent arterioles
d) aldosterone escape

63
Q

aortic arch baroreceptors respond to?

A

increased BP only

64
Q

carotic body baroreceptors respond to?

A

increased and decreased BP

65
Q

how does cartodi massage work?

A

increased pressure on carotid body - mimics increased bp by stretching - increased afferent baroreceptor firing - increased AV node refractory period - decreased HR

66
Q

what is cushing reaction

A

increased intracranial pressure contricst arterioles - cerebral iscahemia - increased pCO2 and decreased pH - central reflex sympahteti increase perfusion pressine ie hypertension - causes strcht in barareceptors that increased para sympathetic output

a) hypertension
b) bradycardia
c) respiratory depression

67
Q

peripheral chemoreceptors are stimulated by?

A

<60 mmHg of PO2

increased PCO2 and decreased pH

68
Q

central chemoreceptors are stimulated by?

A

increasd PCO2 and decreased pH

69
Q

PCWP measures?

A

left atrial pressure

70
Q

pressure in RA?

A

< 5 mmHg

71
Q

pressue in RV?

A

25/5 mmHg

72
Q

pressure in pulmonary circulation

A

25/10 = mmHg

73
Q

PCWP should be what?

A

<12 mmHg

74
Q

Pressure in LA

A

<12 mmHg

75
Q

pressure in LV

A

130/10 mmHg

76
Q

pressure in aorta

A

130/90

77
Q

when will PCWP > LV diastolic pressure?

A

mitral stenosis

78
Q

autoregulatio in heart

A

adenosine, NO, CO2, decreased O2

79
Q

autoregulation in brain

A

CO2

80
Q

autoregulation in kidneys

A

myogenic and tubuloglomerular feedback

81
Q

autoregulation in lungs

A

hypoxia causes vasoconstriction **unique shunts blood to hyperox areas

82
Q

autoregulation in skeletal muscle

A

@ exercise - H, K, lactate, adenosine

@ rest - sympathetic tone

83
Q

autoregulation in skin

A

sympathetic control for temperature control is most importnat

84
Q

causes of oedema

A

increased capillary pressure @ HF
decreased plasma proteins @ nephrotic syndrome and liver failure
increased capillary permeability @ toxins, infection, burns
increased interstitial fluid colloid osmotic pressure @ lymphatic blocakge

Cardiovascular - step (8 decks)

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