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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

what is autorhythmia?

A

the heart’s ability to beat without the need for an external stimulus

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2
Q

where does the electrical conduction of the heart originate from and what is this rhythm calles

A

Sino-Atrial Node (SAN)

sinus rhythm

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3
Q

what type of cells are there in the SAN

A

pacemaker cells

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4
Q

what do pacemaker cells do

A

generate pacemaker potential (depolarisation of membrane potential to threshold)

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5
Q

how is a pacemaker potential generated

A

decrease of K+ efflux, K+ & Na+ influx, transient Ca++ influx

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6
Q

once threshold of membrane potential is reached, how does depolarisation occur?

A

activation of long-lasting Ca++ channels= Ca++ influx

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7
Q

how does re-polarisation occur

A

inactivation of L-type Ca channels, K+ influx

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8
Q

other terms for depolarisation & re-polarisation

A

rising phase of AP, falling phase of AP

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9
Q

how does the excitation wave spread across the heart

A

gap junctions & internal pathways

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10
Q

what 2 structures are involved in conduction through the AVN

A

bundle of His, Purkinje Fibres

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11
Q

True/False

conduction through AVN is delayed

A

True

is delayed to allow atrial contraction to precede ventricular contraction

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12
Q

what are the 2 main types of cell in cardiac tissue

A

myocytes & pacemaker cells

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13
Q

what is the resting membrane potential (RMP) for myocytes

A

-90mV

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14
Q

describe the 5 phases of the action potential of myocytes?

A

Phase 0: fast Na+ influx
phase 1: Na+ channels close, transient efflux of K+
Phase 2: Ca++ influx
Phase 3: Ca channels close, activation of K+ channels
Phase 4: resting membrane potential achieved- maintained near peak AP

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15
Q

what does phase 0 of myocyte AP cause the voltage to become?

A

+20mV

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16
Q

what is another name given to phase 4 which is also unique to myocytes?

A

plateau phase

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17
Q

what causes changes in heart rate?

A

autonomic nervous system (ANS)

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18
Q

how does the parasympathetic system affect HR?

A

vagus nerve supplies both nodes- acts by inc AVN delay (slope of PacMPot dec)

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19
Q

True/False:

Parasympathetic system exerts constant influence on SAN

A

True..

this is to maintain ‘normal’ HR

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20
Q

which neurotransmitter acts on Parasympathetic & sympathetic systems

A
  • Ach which binds to muscarinic receptors

- noradrenaline binds to B1 ADRs

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21
Q

how does sympathetic system affect HR?

A

dec AVN delay (slope of pp inc)- inc HR & force of contraction

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22
Q

State different types of HR ranges…

A

Normal: 60-70
Bradycardia: <60
Tachycardia: >100

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23
Q

describe the anatomy of cardiac muscle

A

myofibrils> myofibrils have actin & myosin which are arranged in sarcomeres

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24
Q

what 2 things are needed to activate myofibrils

A 
ATP= energise myosin heads to form cross-bridges
Ca= cross-bridge formation by binding to troponin/tropomyosin revealing myosin binding site
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25
Q

what law do gap junction ensure?

A

that each electrical excitation reaches all myocytes

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26
Q

Using this knowledge how does an AP cause muscle contraction?

A

Phase 2 causes a huge influx of Ca++ which is needed to from cross-bridges

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27
Q

what happens to Ca++ after the AP passes

A

it is re-sequestered in SR by Ca++ ATPase

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28
Q

what is vital in normal cardiac function and what is it

A

Refractory Period; period following an AP in which it isn’t possible to produce another AP

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29
Q

why does the refractory period occur?

A

K+ influx in falling phase of AP (depolarisation)

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30
Q

why is the refractory period important?

A

prevents generation of overlapping (tetanic) contractions

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31
Q

define stroke volume

A

vol of blood ejected by each ventricle per heartbeat

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32
Q

what 2 mechanisms regulate SV?

A

intrinsic & extrinsic

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33
Q

describe the intrinsic control of SV

A

changes in SV occur due to changes in diastolic length or stretch of myocardial fibres

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34
Q

define the Frank-Starling Mechanism

A

describes the relationship between VR, EDV & SV

states that the more ventricle is filled in diastole, the greater the vol ejected during systole

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35
Q

describe the Frank-Starling Mechanism in the pathophysiological response to inc afterload

A

after load= resistance into which heart in pumping

heart unable to eject full SV so EDV inc= inc contraction force

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36
Q

What happens if inc after load persists

A

ventricular hypertrophy to overcome resistance

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37
Q

how do sympathetic nerves affect SV

A

inc HR & contractility, rate of pressure change during systole inc

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38
Q

True/False..

Frank-Starling Curve moves right with sympathetic activity

A

False..

moves left

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39
Q

True/False…

Parasympathetic nerves have big effects on SV

A

False…

little vagus innervation of ventricles so small parasympathetic effect

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40
Q

what is the main hormone that affects SV

A

adrenaline

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41
Q

what is the formula for Cardiac Output?

A

CO= SV x HR

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42
Q

define the term ‘Cardiac Cycle’

A

orderly depolarisation and depolarisation which causes cardiac muscle contraction and relaxations

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43
Q

how long is a regular heartbeat

A

0.8sec

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44
Q

Name and describe the 5 phases of the cardiac cycle

A

passive filling: low pressure in As & Vs, high pressure is aorta. AV valves open, aortic/pulmonary valve closed. ventricles filled
atrial contraction: As depolarise
isovolumetric ventricular contraction: V pressure inc, AV valves shut, aortic/pulm valves closed. tension rises
ventricular ejection: V pressure further inc> aortic/pulm valves opens ejecting SV, aortic pressure rises, V pressure drops= aortic valve shuts
Isovolumetric Ventricular Relaxation: AV valve shut (tension falls around closed vol), V pressure falls below aortic pressure, AV valves open= new cycle

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45
Q

True/False..

during passive filling the aortic pressure is 60mmHg

A

False…

80mmHg

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46
Q

in a cardiac pressure curve there is an ECG, pressures and..?

A

blood volume of left ventricle

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47
Q

When do the heart sounds occur?

A

1st= closure of AV (mitral/tricuspid valves)= start of systole (isovolumetric vent contraction)
2nd heart sound= closure of aortic/pulm valves (start of diastole- ventricular ejection)

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48
Q

how is arterial pressure maintained during ventricular systole & diastole

A

arteries stretch and recoil

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49
Q

Why is Jugular venous pressure measured?

A

gives an estimate of the central venous pressure- may indicate pathology such as congestive heart failure

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50
Q

define blood pressure

A

outward pressure exerted by blood on blood vessel walls

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51
Q

what is a hypertensive reading?

A

140/90 with day time average of 135/85

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52
Q

What is pulse pressure & it’s normal range

A

difference between diastolic and systolic pressures (30-55mmHg)

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53
Q

How many Korotkoff sounds are there?

A 
5
1st= peak systolic pressure
2nd= regular swooshing
3rd= loudest sound
4th= muffled sound (almost diastole)
5th= laminar flow (diastolic)
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54
Q

what is MAP & its range

A

driving force of blood around body

70-105mmHg

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55
Q

how to measure MAP?

A 
MAP= CO x SVR / 
MAP= HR x SV x SVR
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56
Q

what are the average ABP readings

A

<140 systolic, <90 diastolic

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57
Q

how to estimate ABP

A

(2x diastolic pressure + systolic pressure) / 3

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58
Q

What reflex control the short term control of MAP

A

baroreceptor reflex

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59
Q

where are the baroreceptors for short term regulation of MAP?

A

carotids & aorta

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60
Q

what happens when BRs are activated in short term regulation of MAP

A

ABP inc, vagal nerve activity inc, sympathetic efferent nerve activity dec= vasodilation

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61
Q

what is short term response to dec BP?

A

dec BR firing> medulla> dec vagal activity, inc sympathetic activity, inc constrictor tone> inc HR, CO, ABP, SV, vasoconstriction so inc SVR

62
Q

what is short term response to increased BP?

A

inc BR firing > medulla> inc vagal activity, dec sympathetic activity, dec constrictor tone> dec HR, CO, ABP, SV, vasodilation so dec SVR

63
Q

True/ False…

baroreceptors keep firing even with hypertension

A

False…
firing dec if hypertension is sustained, they re-set and only fire again once an acute change in MAP occurs above new steady level

64
Q

why does postural hypertension occurs

A

person stands then venous return dec to heart so dec MAP > dec BR firing > sympathetic tone inc> vasoconstriction > inc SVR so inc VR > inc SV & BP

65
Q

how does long term control of MAP occur

A

by controlling extracellular fluid volume (EFV=plasma volume & interstitial volume)

66
Q

how is EVF controlled?

A

water excess/deficit?

Na+ excess/deficit?

67
Q

how are water and Na+ controlled?

A

Renin Angiotensin-Aldosterone System (RAAS), Niuretic peptides, antidiuretic hormone

68
Q

what does RAAS do

A
  • regulates plasma vol
69
Q

what is renin?

A
  • released from kidneys
  • stimulates release of angiotensin
  • released if dec Na+, renal artery hypotension
70
Q

what is angiotensin?

A

-AG1> AG2 by ACE causing release of aldosterone from adrenal cortex

71
Q

what is aldosterone?

A

acts on kidneys to inc Na+ & H2O retention

72
Q

what do Natriuretic peptides do?

A

counter acts RAAS
peptide hormone released by heart> causes excretion of Na+ & H2O in kidneys (dec blood vol)> dec renin release (less H20 & Na+ retention)> vasodilators released (dec SVR & BP)

73
Q

what 2 types of natriuretic peptides are there?

A

atrial NP (ANP) & brain NP (BNP)

74
Q

True/False…

ANP is synthesised in ventricles & brain

A

False…
ANP is synthesised in atrial myocytes
BNP synthesised in ventricles and brain

75
Q

True/False…

BNP is a sign of heart failure

A

True

76
Q

why is antidiuretic hormone (ADH) released?

A

if there is inc plasma osmolarity

77
Q

why is ADH released?

A

reduced EFV or inc EF osmolarity - regulated by osmoreceptors in brain

78
Q

what does ADH act on

A

kidney tubules to inc H2O absorption (inc EVF so CO & BP) which causes vasoconstriction (inc SVR so BP)

79
Q

where is ADH synthesised?

A

hypothalamus and stored in pituitary gland

80
Q

how is SVR generally affected

A

SM of arterioles

81
Q

what nerves and hormones (extrinsic factors) affect smooth muscle

A

nerves: sympathetic nerves
hormones: adrenaline

82
Q

how do sympathetic nerves affect SM

A

tonic discharge resulting in continuous release of noradrenaline

83
Q

what is vasomotor tone

A

sympathetic nerves release tonic discharge causing a partial constriction at rest

84
Q

True/False…
the sympathetic nerves are responsible for both contraction & relaxation of vascular SM
ie. there is NO parasympathetic innervation

A

True…

there- they can inc/ dec tonic discharge which in turn inc/dec vasomotor tone= vasoconstriction/ vasodilation

85
Q

where are a-receptors and what do they cause…

A

Gut, Skin, Kidney arterioles

vasoconstriction

86
Q

where are b-receptors and what do they cause…

A

cardiac & skeletal muscle arterioles

vasodilation

87
Q

what is important about intrinsic mechanisms of SVR regulations

A

can over-ride extrinsic mechanisms

88
Q

what are the chemical and physical factors of intrinsic mechanism

A

chemical: local metabolites, local humoral agents
physical: temp, myogenic response to stretch, stress

89
Q

give an example of when ASM relaxes due to metabolic changes

A

if PO2 dec, inc PCO2 (hence inc H+ [ ] & inc K+ [ ])

90
Q

True/ False…

histamine, bradykinin, NO are vasodilators

A

True…

serotonin, thromboxane A2, endothelin are all vasoconstrictors

91
Q

True/False…

resistance to blood flow is directly proportional to radius of blood vessel to power of 4

A

False..
DIRECTLY proportional to blood viscosity & length of vessel
INDIRECTLY proportional to radius of blood vessel to power of 4

92
Q

give 3 properties of endothelin?

A

anti-thrombotic, anti-inflammatory, anti-oxidant

93
Q

give 4 factors that affect venous return?

A
  1. inc venomotor tone
  2. inc blood volume
  3. inc respiratory pump
  4. inc skeletal pump
94
Q

what is the acute response to exercise

A
  1. inc sympathetic nerve activity (inc CO) & vasoconstriction in peripheral organs e.g. gut
  2. inc CO =inc SBP & inc metabolic hyperaemia= dec SVR & DBP & causes vasodilation in muscles
95
Q

what is chronic response to exercise

5 points

A
  1. reduced sympathetic tone/ inc parasympathetic tone & 2. dec adrenaline levels
  2. cardiac remodelling
  3. reduced renin
  4. inc VDs
96
Q

what is shock

A

abnormality of circulatory system resulting in inadequate tissue perfusion/ oxygenation

97
Q

name the 4 types of shock

A

hypovolaemic, cardiogenic, obstructive, distributive

98
Q

describe the pathophysiology of hypovolaemic shock

A

loss of blood vol > dec VR > dec EDV > dec CO & BP

99
Q

causes of hypovol. shock

A

haemorrhage

100
Q

main signs of hypovol. shock

A

vomiting & diarrhoea

101
Q

describe the pathophysiology of cardiogenic shock

A

dec cardiac contractility > dec SV > dec CO & BP

102
Q

main cause of cardiogenic shock?

A

MI

103
Q

describe the pathophysiology of obstructive shock

A

inc intrathoracic pressure > dec VR > dec EDV> dec SV> dec CO & BP

104
Q

causes of obstructive shock

A

tension pneumothorax

105
Q

what are the 2 types of distributive shock

A

neurogenic & vasoactive

106
Q

describe the pathophysiology of neurogenic distributive shock

A

loss of sympathetic tone in vessels & heart > vessel dilation > dec SVR, VR, HR> dec CO & BP

107
Q

causes of neurogenic shock

A

injury to spinal cord

108
Q

describe the pathophysiology of vasoactive distributive shock

A

release of vasoactive mediators > vessel dilation> dec SVR, VR, > dec CO & BP

109
Q

what is a cause of vasoactive shock?

A

sepsis

110
Q

Mx of shock

A

General: ABCDE, high O2, vol replacement

& then treat specifically e.g. cardiogenic shock= inotropes. vasoactive= vasopressors. obstructive= chest drain

111
Q

In what type of shock do you not give volume replacement therapy?

A

Hypovolaemic

112
Q

what is syncope

A

transient loss of consciousness due to cerebral hypo perfusion

113
Q

what are characteristics of syncope

A

amnesia, unconsciousness, loss of motor control, short duration

114
Q

causes of transient loss of consciousness (TLOC)

A

head trauma, seizures

115
Q

what are 3 types of syncope?

A

reflex, postural, cardiac

116
Q

what is reflex syncope

A

syncope in which neural reflexes modify HR & vessel tone = dec in MAP = cerebral hypo perfusion

117
Q

what are 3 types of reflex syncope

A

vasovagal, situational, carotid sinus

118
Q

Vasovagal syncope…

A

trigger: emotional distress
tx: horizontal position, hydration

119
Q

Situational syncope…

A

trigger: fainting after cough, swallowing etc
tx: treat cause, lie down, hydration

120
Q

Carotid Sinus syncope…

A

trigger: manipulation of neck
tx: cardiac permanent pacing
risk factors: frequent syncope, CAD, fhx of SCD

121
Q

what is postural HYPOtension

A

syncope due to failure of baroreceptor response to gravitational shift

122
Q

what is the no1 indication for postural hypotension

A

drop in
. systolic BP by 20mmHg
. diastolic BP by 10mmHg
+ symptoms within 3 mins of postural change

123
Q

what is cardiac syncope

A

syncope due to cardiac event resulting in sudden drop in CO

124
Q

cause of cardiac syncope?

A

arrhythmias, acute MI, CVD e.g. PE

125
Q

name the 4 independent adaptive circulations of the body?

A

coronary, cerebral, pulmonary, skeletal muscle

126
Q

how many coronary arteries are there?

A

2

127
Q

what are the special adaptations of coronary system

A

high capillary density, high basal flow, high O2 excretion, inc O2 demand

128
Q

how can O2 demand be met & why is this a problem?

A

by coronary blood flow- if HR is very fast then there is dec coronary flow (so dec O2 reaches heart muscle) as coronary flow peaks during diastole

129
Q

give an explanation of the adaptations of coronary circulation…

A

systemically, sympathetic nerves cause vasoconstriction & inc HR resulting in metabolic hyperaemia.
this metabolic hyperaemia overrides the small sympathetic activity on coronary artery hence causing vasodilation of the CA along with adrenaline, metabolites etc allowing inc blood flow to heart muscle to match metabolic needs

130
Q

what is the brain supplied by

A

internal carotids and vertebral arteries

131
Q

what are the special adaptations of cerebral circulation…

A
  • basilar and carotid arteries anastomose to create circle of willis
  • cerebral blood flow is auto regulatory: resistance vessels constrict/dilate
  • inter cranial pressure
  • blood-brain barrier
132
Q

what is a good inter cranial pressure range

A

8-13mmHg

133
Q

what is cerebral perfusion pressure?

A

CPP=MAP-ICP

hence CPP dec in presence of inc ICP e.g. brain tumour

134
Q

what are the tight intercellular junctions of the BBB permeable to?

A

O2 & CO2, glucose

135
Q

what is BBB impermeable to?

A

hydrophilic particles (ions, proteins etc)

136
Q

what is a unique adaptive feature of the pulmonary circulation?

A

very low resistance compared to systemic circulation

137
Q

what are special adaptation of pulmonary circulation

A
  • capillary pressure is lower
  • absorptive forces exceed filtration forces
  • hypoxia causes vasoconstriction of pulmonary arterioles (pushes blood away from poorly ventilated areas of lung towards better ventilated lung)
138
Q

give the 3 adaptations of skeletal muscle circulation

A
  • during activity local metabolic hyperaemia overrides vasoconstriction & adrenaline
  • inc CO inc skeletal blood flow
  • contraction of muscle aids venous return
139
Q

what is the largest fluid type that makes up extracellular fluid

A

interstitial fluid (IF)

140
Q

what 3 factors allow arterioles to effectively exchange nutrients between blood and IF

A
  • terminal arterioles regulate blood flow to capillary beds
  • pre-capillary sphincters regulate the flow
  • blood flow is slow to allow exchange
141
Q

True/False…

proteins can pass through capillary walls

A

False…

fluids can follow gradients, gases can follow diffusion etc but large molecules e.g. proteins cannot pass

142
Q

Transcapillary fluid flow is passively driven by pressure gradients- what is the equation for this?

A

net filtration pressure= forces favouring filtration- forces opposing filtration

143
Q

what is the name given to the forces that favour/oppose filtration?

A

starling forces

144
Q

give 2 examples of starling forces favouring filtration

A

capillary hydrostatic pressure, IF osmotic pressure

145
Q

give 2 examples of starling forces favouring absorption

A

capillary osmotic pressure, IF hydrostatic pressure

146
Q

which is stronger; capillary pressures or interstitial fluid pressures?

A

capillary pressures

147
Q

What is the overall starling forces rule?

A

starling forces favour filtration @ arteriolar end

favour reabsorption @ venular end

148
Q

True/False…

in capillaries, filtration exceeds absorption

A

True

149
Q

what is the pathological complication of oedema?

A

diffusion distance inc so more difficult for gas exchange to occur

150
Q

what are 4 main pathophysiological causes of oedema…

A

raised capillary pressure, reduced plasma osmotic pressure, lymphatic insufficiency, changes in capillary permeability

151
Q

True/False…

Left-ventricular failure causes peripheral oedema

A

False…
LV-failure= pulmonary oedema
RV-failure= peripheral oedema

Cardiovascular (12 decks)

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