CARDIAC PHYSIOLOGY Flashcards

1
Q

what does ANP do

A

released from atria in response to increased ECV
promotes water excretion:
-> increases NA excretion
-> inhibits excretion of renin and ADH

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2
Q

what responses to baroreceptors initiate following a drop in BP

A
  1. increased HR
  2. increase strength of contraction
  3. increased constriction of arterioles (except in brain)
  4. increased constriction of veins

this improve CO and raises VR

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3
Q

where are the cardiac centres in the brain

A

medulla

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4
Q

what is dracy’s law

A

Q=(P1-P2)/R

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5
Q

what is resistance dependant on in blood vessels

A

steepness of velocity gradient between the layers of fluid (NO SLIP CONDITION)

VISCOSITY of fluid
described in
POISEULLE”S LAW

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6
Q

what is the Fahraeus lindqvist effect

A

blood viscosity changes with diameter of vessels
minimal in micro vessels (bolus flow)
axial streaming in larger vessels

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7
Q

3 things which alter blood viscosity

A

fahraeus lindqvist effect

shear thinning
haematocrit

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8
Q

how do you measure mean arterial blood pressure

A

MABP=CO.TPR

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9
Q

three methods of measuring blood flow

A
  1. Kety’s clearance
  2. Venous occlusion plethymegraphy
  3. Fick’s principle
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10
Q

what are the main resistance vessels in the body

A

systemic arterioles

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11
Q

2 mechanisms of radius regulation in arteriolses under intrinsic control

A

autoregulation (myogenic/vasodilator washout)

active hyperaemia (metabolic vasodilators)

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12
Q

what happens during venous pooling in the lower extremities

A
  1. veins expand –> greater capacity (unto 600ml)

2. hydrostatic pressure forces fluid out

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13
Q

how much water is in the average adult male

A

64% (42L)

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14
Q

20:40:60 rule

A

20% ECF
40% ICF
60% TBW is water

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15
Q

what is the osmolarity of blood

A

300-310 mOsm/L

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16
Q

what is the osmolarity of 0.9% NaCl

A

308 mOsm/L

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17
Q

what is the osmolarity of intracellular fluid

A

290mOsm/L

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18
Q

what percentage of a unit of 5% dextrose would stay in the plasma after equilibration

A

7%

it has an osmolarity of 252mOsm/l

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19
Q

2 systems which regulate body fluid compartments

A

1) osmoregulation (osmoreceptors in hypothalamus sense drop in osmolarity and stimulate pituitary to secrete ADH)
2) volume regulation sensed by blood vessels –> RAAS, SNS, ANP,ADH, pressure natriuresis

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20
Q

what is starling’s hypothesis

A

capillary filtration rate is proportional to hydraulic drive minus osmotic suction

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21
Q

what is starling’s law of the heart

A

stroke volume increases in response to increased volumes of blood filling the heart

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22
Q

how long is the normal PR interval

A

120-200ms (3-5 small squares)

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23
Q

how long is the normal QRS

A

120ms (3 small squares)

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24
Q

how long should the QT interval be

A

350ms (proportional to heart rate)

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25
Q

what is the duration of a ventricular action potential

A

400msec (4 in muscle)

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26
Q

what are the differences between atrial/nodal APs and ventricular APs

A

Atrial has shorter plateau phase, upstroke and a different NA channel in depolarisation

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27
Q

in a normal axis what would you expect to see on an ECG

A
\+ve= I II aVL aVF
-ve= III aVR
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28
Q

what provides SHORT TERM control of BP

A

baroreceptor reflexes

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29
Q

what provides INTERMEDIATE control of BP

A

Transcapillary shift
Vascular stress relaxation (10-60mins)
Renin-angiotensin system (after 20mins)

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30
Q

what provides LONG TERM control of BP

A

KIDNEYS:

  • aldosterone
  • ADH
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31
Q

what is the difference between vasculogenesis and angiogenesis

A

vasculogenesis occurs in the early embryo

angiogenesis occurs during development, repair, tumour growth and in the endometrium

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32
Q

what is vasculogenesis

A

appearance of new blood cells and blood vessels

mesoderm –> haemangioblast

form dorsal aortae and cardinal veins

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33
Q

what is angiogenesis

A

formation of new blood vessels from existing ones

intussusception is the splitting of blood vessels into two

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34
Q

what happens in the initials stages of heart development in the embryo

A

vasculogenesis occurs in the caudal end of the flat embryo (blood islands around yolk sac and lateral mesoderm)

the embryo then folds laterally to form the early heart tube

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35
Q

describe the structure of the early

A

at this stage there are 3 pairs of veins at a sinus venosus
blood then goes through an early atrium, ventricle, bulbs cords and out through a truncus arteriorsus and into the paired dorsal aortae

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36
Q

how does folding occur in the heart

A

the heart is fixed at either pole by the blood vessels, growth in the middle means that folding occurs.

the ventricles grow anteriorly to cover the atrium and the great veins

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37
Q

what does the right ventricle differentiate from

A

the bulbus conus region

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38
Q

what does the truncus arteriosus become

A

bifurcation the pulmonary trunk and the aortic arches

39
Q

endocardial cushions grow into what structures

A

split the atrioventricular canal into two

40
Q

what forms the inter ventricular septum

A

proliferation from the muscular ridge at the base of the heart. This tissue is myocardium and forms the muscular inter ventricular septum
the membranous part forms from
the spiral conotruncal septum

41
Q

how is the interatrial septum forms

A

septum premium forms as a wedge of endocardium

in the top of the septum there is the osmium primum
a second curved wedge of endocardium forms - the septum secundum but does not extend all the way down to the end cardinal cushions.

42
Q

each aortic arch supplies what

A

a pharyngeal arch

each has its own cranial nerve

43
Q

what does the first aortic arch become

A

it mostly disappears

some remains to make the maxillary artery

44
Q

what does the second aortic arch become

A

most of it disappears

45
Q

what does the 3rd aortic arch become

A

the common carotid artery and start of ICA and the ECA sprouts from it

46
Q

what does the 4th aortic arch become

A

left –> arch of aorta

right –> start of right subclavian artery

47
Q

what does the 6th aortic arch become

A

the pulmonary arteries

ductus arteriosus

48
Q

the first heart sound is caused by what

A

closure of the AV valves when ventricular pressure> atrial pressure

49
Q

what causes the second heart sound

A

closure of the aortic valve when aortic pressure is greater than ventricular pressure

50
Q

what are the 5 stages of the cardiac cycle

A
atrial systole
isovolumetric contraction
ventricular ejection
isovolumetric relaxation
ventricular filling
51
Q

what happens during atrial systole

A

atria contract

ventricle receives last 30% of blood

52
Q

what happens during isovolumetric contrations

A

ventricles contract and pressure rises
volume is unchanged
AV valves shut

53
Q

what happens during isovolumetric relaxation

A

venricle relaxes

outflow valves close

54
Q

what happens during ventricular ejection

A

pressure in ventricle > aorta/pulmonary artery

55
Q

what happens during ventricular filling

A

passive filling of ventricles and atria

56
Q

what happens during the a wave of the CVP

A

atrial contraction

pathologies
no a wave –> AF
large A –> atrial hypertorphy
cannon wave –> complete heart block

57
Q

what causes the c wave on the CVP

A

bulging of tricuspid into right atrium during ventricular contraction

58
Q

what causes the x descent on the CVP

A

downward movement of the heart during ventricular systole and relaxation of the atrium

59
Q

what causes the v wave of the CVP

A

atrial filling against closed tricuspid valve

pathology:
giant V wave –> tricuspid regurg

60
Q

what causes the y descent of the CVP

A

passive ventricular filling after the opening of the tricuspid valves

61
Q

which leads of an ECG look at the anterior surface (right ventricle and septum)

A

V1,2,3,4

62
Q

which leads of an ECG look at the lateral surface of the heart (left ventricle)

A

V5,6, aVL, I

63
Q

which leads of an ECG look at the inferior surface of the heart

A

II, III and aVF

64
Q

which leads of an ECG look at the right atrium

A

aVR

65
Q

what should the paper speed be on an ECG

A

25 mm per second

66
Q

how do you calculate the ventricular rate

A

RR
300/large squares
1500/small squares

67
Q

which three things must be present on an ECG for sinus rhythm

A

p wave before every QRS
P-R normal (3-5 small squares)
PR constant

68
Q

what is sinus arrhythmia

A

normal variation

increased heart rate on inspiration

69
Q

what would you see on an ECG in atrial fibrillation

A

erratic activity in the atria - no visible p waves

irregular QRS

70
Q

what would you see on an ECG in atrial flutter

A

flutter waves give a saw-toothed appearance

can occur with a fixed degree of AV block - e.g. 3:1
or can be variable

71
Q

what is present on an ECG in first degree heart block

A
prolonged PR (>5 small squares)
constant
p before every QRS
72
Q

what is the Wenckebach phenomenon

A

Mobitz type I 2nd degree heart block

progressive lengthening of PR until non-conduction of p wave which resets the rhythm

73
Q

what is the pathology is an ECG shows:
consistant PR interval
p waves with no associated QRS

A

Mobtiz type II 2nd degree heart block

74
Q

which type of heart block has fixed degree of atrioventricular block

A

2 nd degree

75
Q

which syndrome has shortened PR interval with delta waves on ECG

A

Wolff-Parkinson-White syndrome

76
Q

what happens on an ECG in third degree heart block

A

dissociation between p waves and QRS

QRS are firing off intrinsic pacemaker

77
Q

what describe tall peaked P waves (> 2.5 small squares) on an ECG

A

p pulmonale (enlarged right atria)

78
Q

what describes bifid p waves on an ECG

A

p mitrale –>left atrial enlargement owing to mitral stenosis

79
Q

what causes small QRS complexes

A

pericardial effusions
pericarditis
emphysematous lungs

80
Q

what is the normal duration for a QRS

A

no more than 3 small square wide

wide QRS indicates abnormal conduction through the ventricles

81
Q

what conclusions can you draw from an ECG in the presence of LBBB

A

none! it can distort the ECG therefore no inferences can be made about ST segments

however if it is new onset LBBB may be indicative of acute MI

82
Q

what would an RSR in V6 indicate

A

LBBB

WiiLLiamM

83
Q

what would an RSR in V1 indicate

A

RBBB

MaRRoW

84
Q

what is a CONCAVE ST elevation associated with

A

pericarditis

85
Q

what is a downwards sloping ST depression associated with

A

aka reverse tick

digoxin

86
Q

how tall should a normal T wave be

A

no more than 2 large squares

87
Q

in which leads are inverted T waves normal

A

aVR III (V1+/-V2)

not V2 alone

pathological inversion can be a sign of cardiac ischaemia

88
Q

what are:

  • tall tented T waves
  • loss of p waves
  • QRS broadening
  • sine wave ECG

signs of

A

hyperkalaemia

89
Q

what are :

  • flat broad T waves
  • ST depression
  • long QT
  • ventricular dysrhythmias
A

hypokalaemia

90
Q

what are the shockable rhythms

A

VF
pulseless VT

non-shock
PEA
asystole

91
Q

what is kissmauls sign

A

raised JVP on inspiration due to pericardial tamponade

92
Q

What is Dressler’s syndrome

A

a pericarditis which develops 2 to 10 weeks after a MI or heart surgery

Signs of this:
- low grade fever
- chest pain
- pericardial friction rub
(pericardial effusion)
93
Q

A 65-year-old female presents six weeks after a myocardial infarction with deteriorating shortness of breath of relatively recent onset. On examination, there is a soft first heart sound followed by a mid-systolic murmur which is loudest at the apex and in expiration. What is the most likely diagnosis

A

This is likely to be mitral valve prolapse or dysfunction of the papillary muscles following MI, which has resulted in mitral regurgitation

94
Q

A 72-year-old female presents with a deteriorating shortness of breath. On auscultation of the heart there is a loud first heart sound and a rumbling diastolic murmur. What is the most likely diagnosis

A

A classic description of mitral stenosis with the rumbling mid diastolic murmur and loud first heart sounds.

Other features include an opening snap (tapping apex beat is the palpable first heart sound) which signifies mobile leaflets, and in sinus rhythm a pre-systolic accentuation can be heard.