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
what law do gap junction ensure?
that each electrical excitation reaches all myocytes
26
Using this knowledge how does an AP cause muscle contraction?
Phase 2 causes a huge influx of Ca++ which is needed to from cross-bridges
27
what happens to Ca++ after the AP passes
it is re-sequestered in SR by Ca++ ATPase
28
what is vital in normal cardiac function and what is it
Refractory Period; period following an AP in which it isn't possible to produce another AP
29
why does the refractory period occur?
K+ influx in falling phase of AP (depolarisation)
30
why is the refractory period important?
prevents generation of overlapping (tetanic) contractions
31
define stroke volume
vol of blood ejected by each ventricle per heartbeat
32
what 2 mechanisms regulate SV?
intrinsic & extrinsic
33
describe the intrinsic control of SV
changes in SV occur due to changes in diastolic length or stretch of myocardial fibres
34
define the Frank-Starling Mechanism
describes the relationship between VR, EDV & SV | states that the more ventricle is filled in diastole, the greater the vol ejected during systole
35
describe the Frank-Starling Mechanism in the pathophysiological response to inc afterload
after load= resistance into which heart in pumping | heart unable to eject full SV so EDV inc= inc contraction force
36
What happens if inc after load persists
ventricular hypertrophy to overcome resistance
37
how do sympathetic nerves affect SV
inc HR & contractility, rate of pressure change during systole inc
38
True/False.. | Frank-Starling Curve moves right with sympathetic activity
False.. | moves left
39
True/False... | Parasympathetic nerves have big effects on SV
False... | little vagus innervation of ventricles so small parasympathetic effect
40
what is the main hormone that affects SV
adrenaline
41
what is the formula for Cardiac Output?
CO= SV x HR
42
define the term 'Cardiac Cycle'
orderly depolarisation and depolarisation which causes cardiac muscle contraction and relaxations
43
how long is a regular heartbeat
0.8sec
44
Name and describe the 5 phases of the cardiac cycle
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
45
True/False.. | during passive filling the aortic pressure is 60mmHg
False... | 80mmHg
46
in a cardiac pressure curve there is an ECG, pressures and..?
blood volume of left ventricle
47
When do the heart sounds occur?
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)
48
how is arterial pressure maintained during ventricular systole & diastole
arteries stretch and recoil
49
Why is Jugular venous pressure measured?
gives an estimate of the central venous pressure- may indicate pathology such as congestive heart failure
50
define blood pressure
outward pressure exerted by blood on blood vessel walls
51
what is a hypertensive reading?
140/90 with day time average of 135/85
52
What is pulse pressure & it's normal range
difference between diastolic and systolic pressures (30-55mmHg)
53
How many Korotkoff sounds are there?
``` 5 1st= peak systolic pressure 2nd= regular swooshing 3rd= loudest sound 4th= muffled sound (almost diastole) 5th= laminar flow (diastolic) ```
54
what is MAP & its range
driving force of blood around body | 70-105mmHg
55
how to measure MAP?
``` MAP= CO x SVR / MAP= HR x SV x SVR ```
56
what are the average ABP readings
<140 systolic, <90 diastolic
57
how to estimate ABP
(2x diastolic pressure + systolic pressure) / 3
58
What reflex control the short term control of MAP
baroreceptor reflex
59
where are the baroreceptors for short term regulation of MAP?
carotids & aorta
60
what happens when BRs are activated in short term regulation of MAP
ABP inc, vagal nerve activity inc, sympathetic efferent nerve activity dec= vasodilation
61
what is short term response to dec BP?
dec BR firing> medulla> dec vagal activity, inc sympathetic activity, inc constrictor tone> inc HR, CO, ABP, SV, vasoconstriction so inc SVR
62
what is short term response to increased BP?
inc BR firing > medulla> inc vagal activity, dec sympathetic activity, dec constrictor tone> dec HR, CO, ABP, SV, vasodilation so dec SVR
63
True/ False... | baroreceptors keep firing even with hypertension
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
why does postural hypertension occurs
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
how does long term control of MAP occur
by controlling extracellular fluid volume (EFV=plasma volume & interstitial volume)
66
how is EVF controlled?
water excess/deficit? | Na+ excess/deficit?
67
how are water and Na+ controlled?
Renin Angiotensin-Aldosterone System (RAAS), Niuretic peptides, antidiuretic hormone
68
what does RAAS do
- regulates plasma vol
69
what is renin?
- released from kidneys - stimulates release of angiotensin - released if dec Na+, renal artery hypotension
70
what is angiotensin?
-AG1> AG2 by ACE causing release of aldosterone from adrenal cortex
71
what is aldosterone?
acts on kidneys to inc Na+ & H2O retention
72
what do Natriuretic peptides do?
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
what 2 types of natriuretic peptides are there?
atrial NP (ANP) & brain NP (BNP)
74
True/False... | ANP is synthesised in ventricles & brain
False... ANP is synthesised in atrial myocytes BNP synthesised in ventricles and brain
75
True/False... | BNP is a sign of heart failure
True
76
why is antidiuretic hormone (ADH) released?
if there is inc plasma osmolarity
77
why is ADH released?
reduced EFV or inc EF osmolarity - regulated by osmoreceptors in brain
78
what does ADH act on
kidney tubules to inc H2O absorption (inc EVF so CO & BP) which causes vasoconstriction (inc SVR so BP)
79
where is ADH synthesised?
hypothalamus and stored in pituitary gland
80
how is SVR generally affected
SM of arterioles
81
what nerves and hormones (extrinsic factors) affect smooth muscle
nerves: sympathetic nerves hormones: adrenaline
82
how do sympathetic nerves affect SM
tonic discharge resulting in continuous release of noradrenaline
83
what is vasomotor tone
sympathetic nerves release tonic discharge causing a partial constriction at rest
84
True/False... the sympathetic nerves are responsible for both contraction & relaxation of vascular SM ie. there is NO parasympathetic innervation
True... | there- they can inc/ dec tonic discharge which in turn inc/dec vasomotor tone= vasoconstriction/ vasodilation
85
where are a-receptors and what do they cause...
Gut, Skin, Kidney arterioles | vasoconstriction
86
where are b-receptors and what do they cause...
cardiac & skeletal muscle arterioles | vasodilation
87
what is important about intrinsic mechanisms of SVR regulations
can over-ride extrinsic mechanisms
88
what are the chemical and physical factors of intrinsic mechanism
chemical: local metabolites, local humoral agents physical: temp, myogenic response to stretch, stress
89
give an example of when ASM relaxes due to metabolic changes
if PO2 dec, inc PCO2 (hence inc H+ [ ] & inc K+ [ ])
90
True/ False... | histamine, bradykinin, NO are vasodilators
True... | serotonin, thromboxane A2, endothelin are all vasoconstrictors
91
True/False... | resistance to blood flow is directly proportional to radius of blood vessel to power of 4
False.. DIRECTLY proportional to blood viscosity & length of vessel INDIRECTLY proportional to radius of blood vessel to power of 4
92
give 3 properties of endothelin?
anti-thrombotic, anti-inflammatory, anti-oxidant
93
give 4 factors that affect venous return?
1. inc venomotor tone 2. inc blood volume 3. inc respiratory pump 4. inc skeletal pump
94
what is the acute response to exercise
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
what is chronic response to exercise | 5 points
1. reduced sympathetic tone/ inc parasympathetic tone & 2. dec adrenaline levels 3. cardiac remodelling 4. reduced renin 5. inc VDs
96
what is shock
abnormality of circulatory system resulting in inadequate tissue perfusion/ oxygenation
97
name the 4 types of shock
hypovolaemic, cardiogenic, obstructive, distributive
98
describe the pathophysiology of hypovolaemic shock
loss of blood vol > dec VR > dec EDV > dec CO & BP
99
causes of hypovol. shock
haemorrhage
100
main signs of hypovol. shock
vomiting & diarrhoea
101
describe the pathophysiology of cardiogenic shock
dec cardiac contractility > dec SV > dec CO & BP
102
main cause of cardiogenic shock?
MI
103
describe the pathophysiology of obstructive shock
inc intrathoracic pressure > dec VR > dec EDV> dec SV> dec CO & BP
104
causes of obstructive shock
tension pneumothorax
105
what are the 2 types of distributive shock
neurogenic & vasoactive
106
describe the pathophysiology of neurogenic distributive shock
loss of sympathetic tone in vessels & heart > vessel dilation > dec SVR, VR, HR> dec CO & BP
107
causes of neurogenic shock
injury to spinal cord
108
describe the pathophysiology of vasoactive distributive shock
release of vasoactive mediators > vessel dilation> dec SVR, VR, > dec CO & BP
109
what is a cause of vasoactive shock?
sepsis
110
Mx of shock
General: ABCDE, high O2, vol replacement | & then treat specifically e.g. cardiogenic shock= inotropes. vasoactive= vasopressors. obstructive= chest drain
111
In what type of shock do you not give volume replacement therapy?
Hypovolaemic
112
what is syncope
transient loss of consciousness due to cerebral hypo perfusion
113
what are characteristics of syncope
amnesia, unconsciousness, loss of motor control, short duration
114
causes of transient loss of consciousness (TLOC)
head trauma, seizures
115
what are 3 types of syncope?
reflex, postural, cardiac
116
what is reflex syncope
syncope in which neural reflexes modify HR & vessel tone = dec in MAP = cerebral hypo perfusion
117
what are 3 types of reflex syncope
vasovagal, situational, carotid sinus
118
Vasovagal syncope...
trigger: emotional distress tx: horizontal position, hydration
119
Situational syncope...
trigger: fainting after cough, swallowing etc tx: treat cause, lie down, hydration
120
Carotid Sinus syncope...
trigger: manipulation of neck tx: cardiac permanent pacing risk factors: frequent syncope, CAD, fhx of SCD
121
what is postural HYPOtension
syncope due to failure of baroreceptor response to gravitational shift
122
what is the no1 indication for postural hypotension
drop in . systolic BP by 20mmHg . diastolic BP by 10mmHg + symptoms within 3 mins of postural change
123
what is cardiac syncope
syncope due to cardiac event resulting in sudden drop in CO
124
cause of cardiac syncope?
arrhythmias, acute MI, CVD e.g. PE
125
name the 4 independent adaptive circulations of the body?
coronary, cerebral, pulmonary, skeletal muscle
126
how many coronary arteries are there?
2
127
what are the special adaptations of coronary system
high capillary density, high basal flow, high O2 excretion, inc O2 demand
128
how can O2 demand be met & why is this a problem?
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
give an explanation of the adaptations of coronary circulation...
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
what is the brain supplied by
internal carotids and vertebral arteries
131
what are the special adaptations of cerebral circulation...
- 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
what is a good inter cranial pressure range
8-13mmHg
133
what is cerebral perfusion pressure?
CPP=MAP-ICP | hence CPP dec in presence of inc ICP e.g. brain tumour
134
what are the tight intercellular junctions of the BBB permeable to?
O2 & CO2, glucose
135
what is BBB impermeable to?
hydrophilic particles (ions, proteins etc)
136
what is a unique adaptive feature of the pulmonary circulation?
very low resistance compared to systemic circulation
137
what are special adaptation of pulmonary circulation
- 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
give the 3 adaptations of skeletal muscle circulation
- during activity local metabolic hyperaemia overrides vasoconstriction & adrenaline - inc CO inc skeletal blood flow - contraction of muscle aids venous return
139
what is the largest fluid type that makes up extracellular fluid
interstitial fluid (IF)
140
what 3 factors allow arterioles to effectively exchange nutrients between blood and IF
- terminal arterioles regulate blood flow to capillary beds - pre-capillary sphincters regulate the flow - blood flow is slow to allow exchange
141
True/False... | proteins can pass through capillary walls
False... | fluids can follow gradients, gases can follow diffusion etc but large molecules e.g. proteins cannot pass
142
Transcapillary fluid flow is passively driven by pressure gradients- what is the equation for this?
net filtration pressure= forces favouring filtration- forces opposing filtration
143
what is the name given to the forces that favour/oppose filtration?
starling forces
144
give 2 examples of starling forces favouring filtration
capillary hydrostatic pressure, IF osmotic pressure
145
give 2 examples of starling forces favouring absorption
capillary osmotic pressure, IF hydrostatic pressure
146
which is stronger; capillary pressures or interstitial fluid pressures?
capillary pressures
147
What is the overall starling forces rule?
starling forces favour filtration @ arteriolar end | favour reabsorption @ venular end
148
True/False... | in capillaries, filtration exceeds absorption
True
149
what is the pathological complication of oedema?
diffusion distance inc so more difficult for gas exchange to occur
150
what are 4 main pathophysiological causes of oedema...
raised capillary pressure, reduced plasma osmotic pressure, lymphatic insufficiency, changes in capillary permeability
151
True/False... | Left-ventricular failure causes peripheral oedema
False... LV-failure= pulmonary oedema RV-failure= peripheral oedema