Physiology Flashcards Preview

Cardiovascular > Physiology > Flashcards

Flashcards in Physiology Deck (288):
1

what is the name for the mechanism of the heart beating rhythmically in the absence of external stimuli?

autorhythmicity

2

where does excitation of the heart normally originate?

pacemaker cells in the sino-atrial node

3

where is the SA node located?

upper right atrium
(close to where the SVC enters the RA)

4

what is it called when a heart is controlled by the sino-atrial node?

sinus rhythm

5

why do cells within the SA node have spontaneous pacemaker potential?

they do not have a stable resting membrane potential so the drift through depolarisation spontaneously

6

what is the name of the slow depolarisation of membrane potential, that takes the potential to a threshold for the AP to occur?

pacemaker potential

7

what is the pacemaker potential (ie the slow depolaristation to a threshold) due to?

decreasing in K+ efflux
slow Na + influx
(resulting in an increasingly positive membrane potential)

8

what happens in a pacemaker cell once the threshold has been reached?
(the rising phase of action potential)

activation of voltage-gated Ca++ channels causing an Ca++ influx

9

what is the falling phase of the pacemaker action potential caused by?

activation of K+ channels
resulting in K+ efflux

10

why is there a short pause of the electrical impulse at the AV node?

to allow time for both atria to contract in order for co-ordination of systole

11

from SA node to the atria what is the process of excitation spread?

cell-to-cell spread of excitation via gap junctions

12

what are gap junctions?

low resistance protein channels

13

within the ventricles, what is the process of excitation spread?

cell-to-cell spread of excitation via gap junctions

14

where is the AV node located?

at the base of the right atrium
(just above the junction of atria and ventricles)

15

what should be the only point of electrical contact between atria and ventricles?

AV node

16

how do the cells within the AV node facilitate the pause that allows co-ordination of systole?

slow conduction velocity between them

17

what are the pathways by which the electrical impulse is spread from the SA node to the AV node?

internodal pathways
cell-to-cell spread (gap junctions)

18

what is the function of the bundle of his and the purkinje fibres?

allow rapid spread of action potential to the ventricles

19

what is the resting potential of ventricular muscle action potentials?

-90mV (until cell is excited)

20

what causes the rising phase of action potential within the ventricular muscle cell?

fast Na+ influx

21

what does the fast influx of sodium reverse the ventricular muscle action potential to?

+30mV
(from -90mV)

22

what phase is the rising phase of action potential within the ventricular muscle cell?

phase 0

23

what causes phase 1 of the ventricular muscle action potential?

closure of Na+ channels and transient K+ efflux

24

what phase is the plateau phase of the ventricular muscle action potential?

phase 2

25

what causes phase 2 (plateau phase) of the ventricular muscle action potential?

opening of Ca++ voltage gated channels and Ca++ influx
(with background K+ efflux causing it to balance out)

26

what causes phase 3 of the ventricular muscle action potential?

closure of voltage gated Ca++ channels and K+ efflux

27

what is phase 4 of the ventricular muscle action potnential?

membrane rests at resting membrane potential
(-90mV)

28

what is the unique characteristic of contractile cardiac muscle cell's action potential?

the plateau phase

29

what part of the nervous system influences the heart rate?

autonomic nervous system

30

what does sympathetic stimulation do to the heart rate?

increases heart rate

31

what does parasympathetic stimulation do to the heart rate?

decreases the heart rate

32

what nerve supplies parasympathetic innervation to the heart?

vagus nerve

33

under normal resting condition what autonomous tone dominates in control to the heart?

vagal tone

34

what is the intrinsic heart rate? (ie without vagal tone)

100bpm

35

what is the name for a resting heart rate below 60bpm?

bradycardia

36

what is the name for a resting heart rate more than 100bpm?

tachycardia

37

what areas of the heart does the vagus nerve supply?

SA and AV node

38

what does vagal stimulation of the AV node cause?

increases AV nodal delay

39

what muscarinic receptors in the heart are acted on by the parasympathetic system?

M2 muscarinic receptors
(ACh)

40

why is atropine used in extreme bradycardia to speed up the heart?

atropine is a competitive inhibitor of acetylcholine so blocks the slowing down effect of the parasympathetic system

41

what is a negative chronotropic effect?

decreases the heart rate

42

what is a positive chronotrophic effect?

increases the heart rate

43

what does vagal stimulation do to the slope of the pacemaker potential?

decreases slope of pacemaker potential
(and so frequency of AP decreases)

44

what does sympathetic stimulation do to the slope of the pacemaker potential?

increases slope of pacemaker potential
(and so frequency of AP increases)

45

explain effect of parasympathetic system and sympathetic system on heart rate in terms of chronotropic effect?

sympathetic- positive chronotropic effect

parasympathetic- negative chronotropic effect

46

what areas of the heart do sympathetic nerves supply?

SA node
AV node
myocardium

47

what effect does the sympathetic system have on the myocardium?

increases force of contraction
(positive inotropic effect)

48

what receptors in the heart does the sympathetic system act through?

B1 adrenoceptors

49

what does the sympathetic system do to the rate of K+ efflux during pacemaker potential?

decreases the rate of K+ efflux
(allowing membrane potential to depolarise and reach threshold faster)

50

what does the parasympathetic system do to the rate of K+ efflux during pacemaker potential?

increases the rate of K+ efflux
(causing membrane potential to take more time to depolarise and reach threshold)

51

what does the sympathetic system do to the rate of Na+ influx during pacemaker potential?

increases the rate of Na+ influx
(allowing membrane potential to depolarise and reach threshold faster)

52

what does the parasympathetic system do to the rate of Na+ influx during pacemaker potential?

decreases rate of Na+ influx
(causing membrane potential to take more time to depolarise and reach threshold)

53

what does the parasympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?

decreases the rate of Ca++ influx
(slowing the impulse down)

54

what does the sympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?

increases the rate of Ca++ influx
(speeding the impulse up)

55

what are the wires that make up Lead I in an ECG?

RA- LA

56

what are the wires that make up Lead II in an ECG?

RA- LL

57

what are the wires that make up Lead III in an ECG?

LA- LL

58

what does the p wave on an ECG correspond to?

atrial depolarisation

59

what does the QRS complex on an ECG correspond to?

ventricular depolarisation

60

what does the T wave on an ECG correspond to?

ventricular repolarisation

61

what makes up most of the PR interval of an ECG?

AV node delay

62

what occurs in the ST segment of an ECG?

ventricular systole

63

what occurs in the TP interval of an ECG?

diastole

64

what type of muscle is the cardiac muscle?

smooth and striated

65

how are the cardiac myocytes electircally coupled?

gap junctions which allow APs to spread from one cell to the next

66

whats the difference between skeletal muscle and cardiac muscle in terms of nerve supply?

each skeletal muscle cell needs a nerve supply so contain neuromuscular junctions
cardiac myocytes dont

67

what are desmosomes?

mechanical adhesions between adjacent cells that ensure the tension developed by one is transmitted to the next

68

myofibrils contain alternating segments of thick and thin protein filaments, what are the names of the filaments?

myosin: thick filaments- causes the darker appearance
actin: thin filaments- causes the lighter appearance

69

what is the name of the band of muscle fibre that is arranged of actin and myosin?

sarcomere (the functional unit of the muscle)

70

how is muscle tension produced?

by sliding of actin filaments on myocin filaments

71

within a muscle cell cycle what is ATP used for?

contraction and relaxation

72

what happens to an energized myosin filament if no calcium is present?

it goes into the resting phase

73

what happens to an energized muscle filament if calcium is present?

binding of the myosin filament to the actin filament

74

once a myosin filament as binded to an actin filament what occurs?

bending (the power stroke where myosin and actin overlap)
-energy is released

75

once bending has occured, what happens to the myosin and actin if there is fresh ATP available?

detachment

76

once bending has occured, what happens to the myosin and actin if there is no ATP available?

forms a rigor complex
(which can no longer be used)

77

what does the detached myosin do with the ATP'?

becomes energised, now it can either go onto resting phase, or it can go onto binding phase and then contraction again

78

within a muscle cell cycle what is ATP used for?

contraction (energy released) and relaxation (ATP itself attached to myosin)

[same ATP molecule, different actions required for contraction and relaxation]

79

why in the absence of calcium does an energised myosin go into the resting phase?

because cross-bridge binding sites are covered by troponin-tropomyosin complex
so myosin cross bridge cannot bind to actin binding sites

80

why in the presence of calcium does an energised myosin go into the binding phase? (to move onto contraction)

calcium binds to the troponin and movex the troponin-tropomyosin complex out the way thus exposing the cross-bridge binding sites.
myosin cross bridge can now bind to the actin binding sites

81

what is needed to switch on cross bridge formation?

Calcium

82

in a cardiac muscle cell, what is the release of Ca from SR dependent on?

the presence of extra-cellular Ca

83

what is needed to switch off the cross bridge formation and cause relaxation?

removal of calcium (either back into SR or out of cell)

84

when the muscle fibre is relaxed why is there no cross-bridge binding?

because the cross bridge binding site on actin is physically covered by the troponin-tropomyosin complex

85

what is the refractory period?

the amount of time it takes for an excitable membrane to be ready for a second stimuli following an exictation

86

what is a tetanic contraction?

continuous contraction

87

what does the refractory period prevent?

a tetanic contraction

88

what is the stroke volume?

the volume of blood ejected by each ventricle per heart beat

89

SV =

EDV- ESV
(end diastolic volume - end systolic volume)

90

what is the intrinsic mechanism regulating the stroke volume?

frank-starling mechanism

91

what is the extrinsic mechanism regulating the stroke volume?

nervous and hormonal control

92

what is the diastolic length of myocardial fibres determined by? (the stretch)

the end diastolic volume
(eg preload)

93

what is the end diastolic volume?

the volume of blood within each ventricle at the end of diastole

94

what is the end diastolic volume determined by?

venous return to the heart

95

as venous return increases what happens to the stroke volume?

as venous return increase
EDV increases
stretch increases
stroked volume increases (to a max force)

96

the max force of contraction by the myocytes is when the muscle fibres are at what length?

optimal length

97

what does stretch do to the affinity of troponin for calcium?

increases it

98

what is the difference between skeletal muscle and cardiac muscle in terms of optimal fibre length?

skeletal muscle: optimal fibre length is resting muscle length
cardiac muscle: optimal length is achieved by stretching the muscle

99

what does starlings law do to the stroke volumes of RV and LV?

matches them

100

what is the afterload?

the resistance into which heart is pumping

101

at first, what partially compensated for the increased afterload?

frank starling mechanism
incresed afterload causes decreased stroke volume causing increased EDV causing increased contractile force cause stroke volume to return to normal

102

if increased afterload persists (eg untreated hypertension) what happens to the ventricle?

ventricular hypertrophy in order to overcome the resistance (and provide a constant higher contractile force)

103

what are the intrinsic factors of SV?

preload/venous return
afterload (determined by resistance)
contractility of the muscle itself

104

what does an inotropic effect (such as sympathetic nerve stimulation) do to the frank-starling curve?

shift it to the left

105

CO =

SV x HR

106

what is the cardiac output?

the volume of bloof pumped by each ventricle per minute

107

what is the normal CO in a resting adult?

5L

108

at a heart rate of 75, what is the average time taken for diastole?

0.5s

109

at a heart rate of 75, what is the average time taken for systole?

0.3s

110

what are the 5 main events during the cardiac cycle?

1. passive filling
2. atrial contraction
3. isovolumetric ventricular contraction
4. ventricular ejection
5. isovolumetric ventricular relaxation

111

how does passive filling of the ventricles come about?

the pressure gradient allows passive filling of ventricles from high pressure atria to lower pressured ventricles

112

how much of the ventricles become full by passive filling?

80%

113

when do the AV valves shut?

when the ventricular pressure exceeds the atrial pressure

114

what produced the first heart sound? (lub)

AV valves shutting

115

what is isometric contraction of the ventricles?

the period of the cardiac cycle where both valves are closed creating a closed volume, but the pressure is increasing due to the contraction of the ventricles

116

when do the AV valves open?

when the atrial pressure (which is filling with blood) exceeds the ventricular pressure (which is rapidly falling due to relaxation)

117

what produces the first heart sound? (lub)

AV valves shutting

118

when do the aortic/pulmonary valves open?

when the pressure the pressure within the ventricles exceeds aorta/pulmonary artery pressure

119

when do the aortic/pulmonary valves close?

when the ventricular pressure falls below aortic pressure
(remember ventricles are relaxing now)

120

what produces the second heart sound? (dub)

the closing of the aortic/pulmonary valves

121

what does the vibration of the valve closure cause in the aortic pressure curve?

dicrotic notch

122

what is isometric relaxation of the ventricles?

the valves are both closed causing a closed volume, and the pressure is decreasing due to the relaxation of the ventricles

123

what are the 4 areas that must be auscultated in a cardiac exam?

aortic
pulmonary
tricuspid
mitral

124

why do arterial pressures not fall to zero during diastole?

due to the arterial stretch and recoil

125

what does the a wave of the right atrial pressure/JVP correspond to?

atrial contraction

126

what does the c wave of the right atrial pressure/JVP correspond to?

bulging of tricuspid valve into atrium during ventricular contraction

127

what does the 'v' wave of the right atrial pressure/JVP correspond to?

the rise of atrial pressure during atrial filling

128

when do the JVP waves occur in releation to the right atrial pressure waves?

JVP occurs AFTER right atrial pressure waves

129

how does blood flow through the arteries under normal circumstances?

laminar fashion

130

when is sound audible through a stethoscope?

when there is turbulent flow and not laminar flow

131

how is turbulent flow in the arteries produced?

occluding an artery but not fully blocking it

132

what is Kortkoff sound 1?
(BP measuring)

first sound heard
occurs at peak systolic pressure

133

what are Kortkoffs sounds 2 and 3?
(BP measuring)

intermittent sounds heard due to turbulent spurts of flow cyclically exceeds cuff preeure

134

what is Kortoff sound 4?
(BP measuring)

the last sound heard
occurs at minimum diastolic pressure
(very muffled)

135

what is Kortfoff sound 5?
(BP measuring)

point where sound disappears due to uninterrupted smooth laminar flow

136

when is diastolic pressure recorded?

at 5th Kortkoff sound

137

what drives blood around the systemic circulation?

a pressure gradient between the aorta and the right atrium:
MAP - CVP
(RA pressure is close to 0 so main driving force for blood flow is MAP)

138

what is Mean Arterial Blood Pressure?

the average arterial blood pressure during a single cardiac cycle

139

MAP =
(in terms of diastolic and systolic pressure)

[2xDBP + SBP] /3

140

what is the normal range of MAP?

70-105mmHg

141

what is the minimum MAP needed to perfuse the coronary arteries, brain and kidneys?

60mmHg

142

MAP =
(in terms of cardiac output and peripheral resistance)

CO x TPR
HR x SV x TPR

143

what is total peripheral resistance?

the sum of resistance of all the peripheral vasculature in the systemic circulation

144

what are the main resistance vessels?

arterioles

145

what reflex is in control of the short-term regularion of mean arterial blood pressure?

the baroreceptor reflex

146

what type of feedback mechanism is the baroreceptor reflex?

negative feedback

147

where are the 2 group of baroreceptors?

aortic arch
carotid sinus

148

what cranial nerve do the carotid baroreceptors signal to the medulla via?

glossopharyngeal (IX)

149

what cranial nerve do the aortic baroreceptors signal to the meduall via?

vagus (X)

150

what reflex is important in the prevention of postural blood pressure changes?

baroreceptor reflex

151

what happens to the systolic blood pressure when healthy people stand from lying position?

no change
baroreceptors notice a transient change and reflex arc causes increased heart rate and TPR

152

what happens to the diastolic blood pressure when healthy people stand from lying position?

slight increase due to the increased TPR (baroreflex)

153

what is the name for the failure of baroreceptor reponses to gravitational shifts in blood when moving from horizontal to vertical position?

postural hypotention

154

what happens if high blood pressure is sustained?

baroreceptors firing decreases and they will re-set to a higher steady state level

155

what 2 types of body fluids make up the total body fluid?

intracellular fluid (2/3rds)
extracellular fluid (1/3rd)

156

what 2 types of fluid make up the extracellular fluid?

plasma volume and interstitial fluid

157

what is the interstitial fluid?

the fluid the bathes the cells and acts as a go between the blood and the body cells

158

how would you dexcribe the relationship between the plasma and he interstitial fluid?

equilibrium with each other

159

what are the 2 main factors which affect extracellular fluid volume?

water excess or deficit
Na+ ecess or deficit

160

what 3 hormones/hormone systems regulate the extracellular fluid volume?

1. Renin-Angiotensin-Aldosterone System (RAAS)
2. Atrial Natriuretic Peptide (ANP)
2. Antidiuretic Hormone ADH

161

where is renin released from?

kidneys

162

where is angiotensinogen produced?

liver

163

what is the function of renin?

stimulates the formation of angiotensinogen to angiotensin I

164

what enzyme converts angiotensin I to angiotensin II?

ACE
(angiotensin converting enzyme)

165

what 3 functions does angiotensin II have?

1. stimulates the release of aldosterone from the adrenal cortex
2. causes systemic vasoconstriction (increases TPR + BP)
[3. stimulates thirst and ADH release to increase plasma volume slightly and therfore BP]

166

where is ACE produced?

pulmonary vascular endothelium

167

what is the function of aldosterone?

acts on the kidneys to increase sodium (and therefore water) retention to greatly increase plasma volume and therefore BP

168

what is Renin usually secreted in response to?

1. hypotension
2. stimulation of renal sympathetic nerves
3. decreased [Na+] in renal tubular fluid

169

what is the rate limiting step for RAAS?

the renin secretion rate

170

where is atrial natriuretic peptide (ANP) synthesised and stored?

atrial myocytes

171

what is atrial natriuretic peptide (ANP) released in response to?

atrial distension
(hypervolaemic state)

172

what are the 4 main function of atrial natriuretic peptide (ANP)?

1. excretion of salt and water in the kidneys (reduced blood volume and BP)
2. vasodilator (decreases BP)
3. decreases renin release (decreases BP)
4. acts as a counter-regulatory mechanism for the Renin-Angiotensin-Aldosterone System

173

where is ADH synthesised and stored?

derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

174

what is ADH secreted in response to?

1. reduced extracellular fluid
2. increased extracellular fluid osmolarity

175

what is plasma osmolarity monitored by?

osmoreceptors mainly in the brain close to the hypothalamus

176

what does ADH do?

1. act in the kidney tubules to increase the reabsorption of water and concentrate urine (antidiuresis)
[increases BP]
2. vasoconstriction [increases BP]

177

when is the effect of ADH important?

in hypovolaemic shock (eg haemorrhage)

178

explain the relationship between resistance to blood flow, blood viscosity, length of blood vessel and radius of blood vessel?

resistance to blood flow is directly proportional to the blood viscosity and the length of the blood vessels
resistance to blood flow is inversely proportional to the radius of the blood vessels to the power of 4

179

what is the name for the way the vascular smooth muscle is partially constricted at rest?

vasomotor tone

180

what receptor does noradrenaline act on to constrict the blood vessels?

alpha 1 adrenoreceptors

181

what receptor does adrenaline act on to constrict the blood vessels?

alpha adrenoceptors

182

what receptors does adrenaline act on to dilate the blood vessels?

beta adrenoceptors

183

where are alpha adrenoceptors mainly found in the circulation?

skin, gut, kidney arterioles

184

where are beta adrenoceptors mainly found in the circulation?

cardiac and skeletal muscle arterioles

185

what 6 local metabolic factors cause vasodilation of systemic circulation?

decreased local PO2
increased local PCO2
increased local [H+]
increased extra-cellular [K+]
increased osmolarity of ECF
adenosine release

[all are factors of metabolically active tissues]

186

what 4 local humoral agents cause vasodilation of systemic circulation?

histamine
prostaglandins
bradykinin
nitric oxide

187

where is nitric oxide produced?

vascular endothelium

188

what enzyme catalyses the production of nitric oxide from L-argine (amino acid)?

nitric oxides synthase (NOS)

189

describe the half life of nitric oxide?

very short

190

what are the 2 functions of nitric oxide?

the regulation of blood flow
maintenance of vascular health

191

what is angiotensin II's effect on vascular smooth muscle?

vasoconstriction
(through endothelin production)

192

what is ADH's effect on vascular smooth muscle?

vasoconstriction
(through endothelin production)

193

what is flow dependent Nitric Oxide formation?

shear stress on vascular endothelium (due to increased blood flow) causes release of calcium in vascular endothelial cells and the subsequent activation of NOS

194

what is receptor stimulated Nitric Oxide formation?

vasoactive substances act through stimulation of NO formation and act as a chemical stimuli to induce NO formation

195

once released from the vascular endothelium, where does nitric oxide diffuse into?

adjacent smooth muscle cells

196

in smooth muscle cells, what does nitric oxide do?

activates the formation of cGMP (timulates smooth muscle relaxation)

197

what 4 local humoral agents cause vasoconstriction?

serotonin
thromboxane A2
leukotrienes
endothelin

198

what is the production of endothelin stimulated by?

angiotensin II
vasopressin (ADH)

199

what is thromboxane A2 released from?

platelets

200

what is endothelin released from?

endothelial cells

201

what is the local effect of cold temperature on vasculature? and why?

vasoconstriction
to conserve heat at peripheries

202

what is the local effect of warm temperature on vasculature?

vasodilation
to provide blood supply to metabolically active tissues

203

where is the myogenic response to stretch important?

brain and kidneys

204

if MAP rises what happens to the vasculature in organs with a myogenic response?

constrict to limit flow

205

if MAP falls what happens to the vasculature in organs with a myogenic response?

dilate to increase flow

206

what are the 4 factors increasing venous return?

venomotor tone
skeletal muscle pump
respiratory pump
blood volume

207

what 3 factors does venomotor tone effect?

venous return
stroke volume
MAP

208

what 2 factors does vasomotor tone effect?

TPR
MAP

209

during exercise what autonomic system dominates?

sympathetic nervous system

210

during exercise what happens to the vasculature that provides blood to kidneys and gut?

vasoconstrction to reduce flow

211

during exercise what happens to the vasculature that provides blood to the skeletal and cardiac muscle?

vasodilation to increase flow
(due to local metabolic factors and adrenalines effect on b adrenoceptors)

212

during exercise what happens to the SBP, DBP and pulse pressure?

SBP increases
DBP decreases
pulse pressure increases

213

what are 6 chronic CVS responses to exercise?

1. reduction in sympathetic tone and noradrenaline levels
2. increased parasympathetic tone to the heart
3. cardiac remodeling
4. reduction in plasma renin levels
5. improved endothelial function (ie increased vasodilators and decreased vasoconstrictors)
6. reduced arterial stiffening

214

what are the 4 different types of shock?

hypovolaemic
cardiogenic
obstructive
distributive

215

what is shock?

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

216

what are the steps from shock to cellular failure?

1. shock
2. inadequate tissue perfusion
3. inadequate tissue oxygenation
4. anaerobic metabolism
5. accumulation of metabolic waste products
6. cellular failure

217

what are the steps from hypovolaemic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)

1. loss of blood volume
2. decreased blood volume
3. decreased venous return
4. decreased end diastolic volume
5. decreased stroke volume
6. decreased cardiac output and decreased blood pressure
7. inadequate tissue perfusion

218

what is cardiogenic shock?

sustained hypotenstion caused by decreased cardiac contractibility

219

what are the steps from cardiogenic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)

1. decreased cardiac contractility
2. decreased stroke volume
3. decreased cardiac output and decreased blood pressure
4. inadequate tissue perfustion

220

what does cardiac failure do to the frank starling curve?

shifts it to the right

221

what does exercise do to the frank starling curve?

shifts it to the left

222

what type of shock would a tension pneumothorax fall under?

obstructive shock

223

what are the steps from obstructive shock to inadequate tissue perfusion?

1. increased intrathoracic pressure
2. decreased venous return (due to reduced gradient)
3. decreased end diastolic volume
4. decreased stroke volume
5. decreased cardiac output and decreased blood pressure
6. inadequate tissure perfusion

224

what are the steps from neurogenic shock to inadequate tissue perfusion?

1. loss of sympathetic tone
2. massive venous and arterial vasodilation
3. decreased venous return and decreased TPR
4. decreased cardiac output and decreased blood pressure
5. inadequate tissue perfusion

225

what type of shock is sepsis?

distributive shock

226

what are the steps from distributive (vasoactive) shock to inadequate tissue perfusion?

1. release of vasoactive mediators
2. massive venous and arterial vasodilation + increased capillary pemeability
3. decreased venous return and decreased TPR
4. decreased cardiac output and decreased blood pressure
5. inadequate tissue perfusion

227

what are the 4 steps for the treatment of shock?

1. ABCDE approach
2. high flow oxygen
3. volume replacement
4 shock specific treatment

228

after ABCDE, high flow oxygen and volume replacement, what is the next step for cardiogenic shock?

give inotropes

229

after ABCDE, high flow oxygen and volume replacement, what is the next step for a pneumothorax? (obstructive shock)

immediate chest drain for tension pneumothorax

230

after ABCDE, high flow oxygen and volume replacement, what is the next step for anaphylactic shock? (distributive shock)

adrenaline

231

after ABCDE, high flow oxygen and volume replacement, what is the next step for septic shock? (distributive shock)

vasopressors

232

what are the 2 types of hypovolaemic shock?

haemorrhagic
non-haemorrhagic

233

what are 3 causes of non-haemorrhagic shock?

vomitting , diarrhoea, excessive sweating
(causing reduced extracellular fluid volume)

234

how much blood loss can compensatory mechanisms work to maintain blood pressure?

until 30% blood loss

235

what compensatory mechanisms work to maintain blood pressure during blood loss? (up to 30%)

baroreceptor reflex
chemoreceptors

236

what does the ALTS classification quantify?

the level of haemorrhagic shock

237

where do right and left coronary arteries arise from?

base of the aorta

238

where do cardiac veins drain into?

right atrium via coronary sinus

239

what is the oxygen extraction of the coronary circulation compared to the rest of the body?

75% compared to 25% body average

240

what is the only way extra O2 can be supplied to the cardiac muscle?

increasing coronary blood flow
(cant be achieved through increasing O2 extraction since it is so high already)

241

what does local hypoxaemia of the myocardium cause?

vasodilation of the coronary arteries

242

what does local production of adenosine from the myocardium cause?

vasodilation of the coronary arteries

243

how is adenosine made?

ATP-ADP-AMP-adenosine

244

what does sympathetic stimulation of the heart result in? (in respect to the blood supply) and why?

coronary vasodilation
(due to metabolic hyperaemia overriding sympathetic vasoconstriction)

245

what is circulating adrenalines effect on the coronary arteries B2 adrenoceptors?

vasodilation

246

when does the majority of the blood flow through the coronary arteries occur?

diastole

247

in the brain what do the 2 vertebral arteries join to make?

basilar artery

248

what do the 2 internal carotid arteries join the basilar artery to make?

circle of Willis

249

where do cerebral arteries arise from?

circle of Willis

250

what does the circle of Willis allow?

cerebral perdusion to staty mainained even if one caroid artery gets obstructed

251

what are the 2 types of stroke?

haemorrhagic
ischaemic

252

what do stroked cause?

interruption of blood supply to a region of the brain

253

what causes a haemorrhagic stroke?

rupture of a damaged artery

254

what causes a ischaemic stroke?

obstruction due to emboli or atherothrombosis

255

for what range of MAP can the brain guard against changes in cerebral flow? (myogenic effect- autoregulation)

60 -160mmHg

256

what happens out with 60-160mmHg to the cerberal flow?

autoregulation fails

257

what do high levels of carbon dioxide in cerebral tissues cause on local vasculature?

vasodilation

258

what do low levels of carbon dioxide in cerebral tissues cause on local vaculature?

vasoconstriction

259

why can hyperventilation lead to fainting?

low CO2, leads to vasoconstriction of cerebral blood flow, brain doesnt get enough oxygen

260

cerebral perfusion pressure (CPP) =

MAP -ICP (intercranial pressure)

261

what happens to CPP and cerebral blood flow if there is increased ICP?

decreased CPP and so decreased cerebral blood flow

262

what makes up the blood brain barrier?

tight intercellular junctions int he cerebral capillaries

263

how does glucose cross the blood brain barrier?

facilitated diffusion using specific carrier molecules

264

how does the pulmonary circulation protect against pulmonary oedema considering it is such a low pressure system?

absorptive forces exceed filtration forces

265

what is the local effect of hypoxia on the pulmonary arterioles?

vasoconstriction
(opposite to systemic arterioles)

266

what is the purpose of the vasoconstrictive effects of hypoxia on pulmonary arterioles?

diverts blood away from poorly ventilated areas of the lungs

267

what happens during exercise to ensure the skeletal muscle get enough blood supply?

metabolic hyperaemia (and circulating adrenaline) overcomes sympathetic vasoconstrictor activity

268

what are varicose veins?

when blood pools in lower limbs because of incompetent valves

269

why do varicose veins not lead to a reduction in cardiac output?

chronic compensatory increase in blood volume

270

why is blood flow through the capillary bed slow?

to allow adequate exchange time

271

what regulates the regional blood flow to capillary beds in most tissues?

terminal arterioles
(occasionally there are precapillary sphincters)

272

how do exchangeable proteins move across the vascular bed into the interstitial fluid?

vesicular transport

273

how do lipid soluble substances get from the capillary bed to the interstitial fluid?

through endothelial cells

274

how do water soluble substances get from the capillary bed to the interstitial fluid?

through the water filled pores

275

what are the forces favouring filtration in the transcapillary fluid flow?

capillary hydrostatic pressure (Pc)
interstitial fluid osmotoic pressure (pieI)

276

what are the forces opposing filtration?

capillary osmotic pressure (pieC)
interstitial fluid hydrostatic pressure (Pi)

277

Net filtration pressure =

(PC + pieI) - (pieC + Pi)

278

at the arteriolar end of the capillary bed what force wins? (filtration or reabsorption)

filtration forces

279

at the venular end of the capillary bed what force wins? (filtrative or reabsorptive)

reabsorptive forces

280

how is excess fluid in the interstitial fluid returned to the circulation?

via the lymphatic as lymph

281

what is oedema?

accumulation of fluid in the interstitial space

282

why is gas exchange compromised in pulmonary oedema?

diffusion distance increases

283

what are the 4 causes of oedema?

1. raised capillary pressure
2. reduced plasma osmotic pressure
3. lymphatic insufficiency
4. increased capillary permeability

284

what are the 2 reasons for raised capillary pressure resulting in oedema?

arteriolar dilation
raised venous pressure

285

in left ventricular failure, where is the oedema and why?

pulmonary oedema due to back pressure causing raised pulmonary venous pressure

286

in right ventricular failure, where is the oedema and why?

peripheral oedema due to back pressure causing raised systemic venous pressure

287

what are the 3 reasons for reduced plasma osmotic pressure?

malnutrition
protein malabsorption
excessive renal excretion of protein

288

what type of oedema is caused by heart failure?

pitting oedema