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step 1 - physiology > cardio > Flashcards

cardio Flashcards

1
Q

fick principle?

A

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

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2
Q

formulae for MAP?

A

MAP = CO x TPR

MAP = 1/3 SysBP + 2/3 DiaBP

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3
Q

what is pulse pressure proportional to?

A

proportional to SV

inversely proportional to arterial compliance

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4
Q

how is CO maintained in exercise?

A

early stages: increase in HR and SV

late stages: increase in HR only (SV plateaus)

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5
Q

when HR increases, what phase of cycle is shortened?

A

diastole leads to less filling time –> decreased CO

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6
Q

causes of increased pulse pressure?

A

hyperthyroidism

aortic regurg

being old (aortic stiffening)

OSA (increased sympathetic tone)

exercise

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7
Q

causes of decreased pulse pressure?

A

aortic stenosis

cardiogenic shock

tamponade

advanced HF

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8
Q

factors that affect stroke volume?

A

contractility

afterload

preload

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9
Q

factors that increase contractility?

A

catecholamines

increased intracellular Ca

decreased extracellular Na

digitalis

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10
Q

mechanism of catecholamines –> increased contractility?

A

increased activity of Ca pump in SR

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11
Q

factors that decrease contractility?

A

B-blockade

HF with systolic dysfn

acidosis

hypoxia/hypercapnia

non-DHP CCBs

narcotic overdose

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12
Q

mechanism of BBs decreasing contractility?

A

decreased cAMP

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13
Q

Laplace’s law?

A

wall tension = ( P x radius) / (2 * wall thickness)

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14
Q

which mx decrease both preload and afterload?

A

ACEs and ARBs

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15
Q

formula for resistance (based on viscosity length and radius)?

A

resistance = driving P / flow

= (8 * viscosity * length) / (pi * radius^4)

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16
Q

resistance of vessels in series vs in parallel?

A

series: TR = R1 + R2 + …
parallel: 1/TR = 1/R1 + 1/R2 + …

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17
Q

how does organ removal affect TPR and CO?

A

increases TPR

decreases CO

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18
Q

which vessels account for majority of TPR?

A

arterioles

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19
Q

how does spinal anesthesia affect venous return?

A

decreases it

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20
Q

identify marked components of jvp tracing?

A

a wave = atrial contraction

c wave = RV contraction

x descent = atrial relaxation during ventricular contraction

v wave = atrial filling

y descent = RA emptying into RV

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21
Q

factors that contribute to normal splitting?

A

inspiration –> decreased thoracic pressure

decreased pulmonary impedance –> increased pulmonary capacitance

** both cause delayed closure of pulmonic valve –> delayed P2

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22
Q

what causes wide splitting?

A

conditions that delay RV emptying

** pulmonic stenosis, RBBB

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23
Q

what causes fixed splitting?

A

ASD –> increased RA and RV volumes –> increased pulmonic flow

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24
Q

what causes paradoxical splitting?

A

conditions that delay aortic valve closure

** aortic stenosis, LBBB

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25
Q

sustained hand grip affects murmurs in what way?

A

increases afterload –>

increases MR, AR, VSD murmurs

decreases HOCM murmurs

later onset of MVP click

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26
Q

valsalva affects murmurs in what way?

A

decreases preload –>

decreases intensity of most murmurs

** increases HOCM and MVP (earlier click/murmur)

27
Q

squatting affects murmurs in what way?

A

increases preload –>

decreases HOCM and MVP

** increases intensity of AS murmur

28
Q

causes of MR?

A

ischemic heart disease (post MI)

MVP

LV dilation

rheum fever/endocarditis

29
Q

what causes systolic click in MVP?

A

tensing of chordae tendineae

30
Q

which channels contribute fo phase 0 of myocardial AP?

A

voltage-gated Na channels

31
Q

what channels in phase 1 of myocardial AP?

A

inactivation of Na channels

opening of K channels

32
Q

what channels in phase 2 of myocardial AP?

A

= plateau

Ca influx balances K efflux

** Ca influx triggers Ca release from SR –> contraction

33
Q

what channels in phase 3 of myocardial AP?

A

Ca channels closed

voltage gated slow K channels open –> massive K efflux

34
Q

what channels in phase 4 of myocardial AP?

A

= resting potential

high K permeability through K channels

35
Q

myocardial vs skeletal mm contraction?

A

1) cardiac AP has plateau
2) cardiac contraction due to Ca-induced Ca release
3) myocytes coupled by gap jcts
4) nodal cells spontaneously depolarize

36
Q

myocardial vs pacemaker AP?

A

1) phase 0 in nodal: mediated by Ca channels (Na channels permanently inactivated bc resting voltage less negative)
2) phase 1 and 2 absent
3) phase 4: If - Na conductance –> slow spontaneous diastolic depol

37
Q

what do ACh and adenosine do to the rate of nodal depol?

A

decrease it

–> decrease HR

38
Q

what do catecholamines do to the rate of nodal depol?

A

increase it –> increase HR

39
Q

how does sympathetic stimulation affect nodal cells?

A

increases chance that If channels are open –> increases HR

40
Q

speed of conduction of heart tissues?

A

Purkinje > atria > ventricles > AV node

41
Q

conduction pathway in heart?

A

SA –> atria –> AV –> common bundle –> bundle branches –> fascicles –> Purkinje –> ventricles

42
Q

where is the AV node?

A

in posteroinferior interatrial septum

** blood supply from RCA

** 100 msec delay –> time for ventricular filling

43
Q

drugs that cause long QT?

A

ABCDE:

anti-arrhythmics (IA, III)

anti-biotics (macrolides)

anti-Cychotics

anti-depressants

anti-emetics (ondansetron)

44
Q

congenital long QT, AD, purely cardiac?

A

Romano Ward

45
Q

congenital long QT, AR, deaf?

A

Jervell and Lange-Nielsel

46
Q

Asian, AD, pseudo-RBBB and V1-V3 ST elevations?

A

Brugada

** increased risk of VT and SCD

** give ICD

47
Q

what’s the bundle of Kent?

A

accessory pathway in WPW

48
Q

causes of Afib?

A

HTN

CAD

rheumatic heart dz

binge drinking

HF

valvular dz

hyperthyroidism

49
Q

MOA of ANP/BNP?

A

increase cGMP

–> vasodilation and decreased Na reabs in collecting tubule

–> vasodilation of afferent arteriole

–> vasoconstriction of efferent arteriole

** aldosterone escape

50
Q

how does aortic arch transmit info to brain?

A

vagus –> solitary nucleus of medulla

51
Q

how does carotid sinus transmit info to brain?

A

glossopharyngeal –> solitary nucleus of medulla

52
Q

does hypoT cause increase or decrease in baroreceptor firing?

A

causes DECREASE in firing (b/c of DECREASED stretch)

53
Q

how does decreased baroreceptor firing affect the heart?

A

vasocontriction

increased HR, contractility, BP

54
Q

how does increased baroreceptor firing affect the heart?

A

increased AV refractory period

55
Q

what stimuli do the carotid and aortic bodies respond to?

A

PO2 decrease (once below 60 mmHg)

increased PCO2

decreased pH

56
Q

what stimuli do central chemoreceptors respond to?

A

ONLY changes in pH and PCO2 of interstitial fluid of brain

** no direct response to PO2

57
Q

what factors affect autoreg of blood flow to heart?

A

adenosine

NO

CO2

decreased O2

** all vasodilatory

58
Q

what factors affect autoreg of blood flow to brain?

A

CO2, pH - vasodilatory

59
Q

what factors affect autoreg of blood flow to kidneys?

A

myogenic and tubuloglomerular feedback

60
Q

what factors affect autoregulation of blood flow to lungs?

A

hypoxia –> VASOCONSTRICTION

** opposite of other vasculature - prevents perfusion of poorly ventilated area

61
Q

what factors affect autoregulation of blood flow to skeletal mm?

A

local metabolites during exercise: lactate, adenosine, K, H, CO2 –> vasodilation

at rest: sympathetic tone

62
Q

what factors affect autoregulation of blood flow to skin?

A

sympathetic stimulation –> temperature control

63
Q
A

step 1 - physiology (8 decks)

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