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Cardiovascular - step > Physiology > Flashcards

Physiology Flashcards

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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
when does viscosity decrease?
anaemia
26
describe the result on the vardiac and vascular function cruevs if inotropy
changes in contractility - altered CO for a ive RA pressure
27
describe the result on the cardiac and vascular function curves of venous rerun
changes in circulating colume or venous tone - altered RA for a given CO
28
describe the result on the cardiac and vascular function curves of TPR
changes in TPR - altered CO at a five RA pressure, however the mean systemic pressure is unchangesd
29
qhat causese the mean systemic pressure to change?
altered blood volume or venous tone
30
what is S3?
early diastolic normal in chidren and pregnancy abnormal when have increased filling pressures ie mitral regurgitation, HG, dilated ventricles (systolic dysfunction)
31
what is the a wave?
atrial contraction | absent in atrial fibrillation
32
when does the mitral valve close in relation to the jugular venous pulse wave?
low pressure point between a and c wave
33
what is the c wave?
rapid ejection of ventricular systole and tricuspid pushed up int othe atrium
34
what is the x descent
ventricle is platuea - occurs beore the t wave blood still leaving ventricle, but its not squeezing at max no tricuspid buldge
35
what is the v wave?
atrila is filling and the ventricle is relaxed, | mitral valve is closed
36
when does the mitral valve open in relation to the jugular venous pulse wave?
between the v and y wave
37
what is the y descent?
when mitral valve opens and blood enters the ventricle from the atrium
38
describe the phases of the myocardial action potential that occurs at the myocardium, bundle of HIs and purkinje fibres
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
describe the action potential phases in the pacemaker
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
what determines heart rate
the slow of phase 4.
41
p wave?
atrial depol
42
PR interval
3 small squares to 5 small squares 0.12-0.2 sec atrial depol start to start of ventricular depol
43
QRS complex
2 small squares to 2.5 small squares 0.8-0.1 sec ventricular depolarization normally >120 msec
44
QT interval
ventricular depolarization, mechanical contraction of the ventricles, nventricular repolarization 8 small squares to 11 small squares 0.32 sec to 0.40 seconds
45
J point
junction between end of QRS complex, and start fo ST segment
46
ST segment
isoelectic | ventricles depolarized
47
U wave
caused by hypokalenima and bradycardia
48
what effect does hypokalemia have on the ECG?
U wave appearance (also occurs in bradycardia)
49
what predisposes to torsades de pointes?
increased QT interval | normal 8-12 small squares/0.32-0.4 sec
50
list specific causes of increased QT interval and risk fo trades de pointes
antiatthythmics A (class IA and III, antibiotics B (macrolides), anticycholites C (haloperidol), antidepressnats D (TCAs), antiemetics E (ondansetron) low potassium low magnesium
51
how to treat torsades de pointes
magnesium sulfate
52
Romano-Ward SYndrome
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
Jervell and Lange-Nielsen syndrome
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
Brugada SYndrome
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
Wolff-Parkinson-White Syndrome
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
what is associated with atrial fibrillation
``` hypertension coronary artery disease rheumatic heart disease binge drinking HF valvular disease hyperthyrodisin atrial stasis -- cardioembolic events ```
57
list the irregular ECG tracings
atrial fibrillation ventricular fibrillation second degree, Mobitz I aka Wenckebacj
58
list the regular ECG tracings
atrial flutter 1st degree AV block mobitz II 2nd degree AV block 3rd degree, complete
59
lyme disease arrhtymia plase
3rd degree block
60
regulary irregular
2nd degree block Mobitz I
61
describe role of ANP
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
describe role of BNP
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
aortic arch baroreceptors respond to?
increased BP only
64
carotic body baroreceptors respond to?
increased and decreased BP
65
how does cartodi massage work?
increased pressure on carotid body - mimics increased bp by stretching - increased afferent baroreceptor firing - increased AV node refractory period - decreased HR
66
what is cushing reaction
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
peripheral chemoreceptors are stimulated by?
<60 mmHg of PO2 | increased PCO2 and decreased pH
68
central chemoreceptors are stimulated by?
increasd PCO2 and decreased pH
69
PCWP measures?
left atrial pressure
70
pressure in RA?
< 5 mmHg
71
pressue in RV?
25/5 mmHg
72
pressure in pulmonary circulation
25/10 = mmHg
73
PCWP should be what?
<12 mmHg
74
Pressure in LA
<12 mmHg
75
pressure in LV
130/10 mmHg
76
pressure in aorta
130/90
77
when will PCWP > LV diastolic pressure?
mitral stenosis
78
autoregulatio in heart
adenosine, NO, CO2, decreased O2
79
autoregulation in brain
CO2
80
autoregulation in kidneys
myogenic and tubuloglomerular feedback
81
autoregulation in lungs
hypoxia causes vasoconstriction **unique shunts blood to hyperox areas
82
autoregulation in skeletal muscle
@ exercise - H, K, lactate, adenosine | @ rest - sympathetic tone
83
autoregulation in skin
sympathetic control for temperature control is most importnat
84
causes of oedema
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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