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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

What hormones control the extracellular fluid?

A

RAAS, ANP, ADH

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2
Q

What is ECF Volume?

A

Interstitial fluid + plasma volume

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3
Q

Describe the RAAS pathway

A

Renin–Angiotensin 1- Angiotensin 11-Aldersterone

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4
Q

What does RAAS do to the arteries?

A

vasoconstriction

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5
Q

What does RAAS do to Blood pressure and plasma volume?

A

Increases them

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6
Q

What does ANP do to the arteries?

A

vasodilation

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7
Q

What does ANP do to blood pressure and renin production

A

Decreases them

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8
Q

What does ADH do to blood vessels?

A

Vasoconstriction

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9
Q

What regulates ADH?

A

Hypothalamus

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10
Q

What does ADH do to blood vessels, TPR and BP

A

Vasoconstriction and increases TPR and blood pressure

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11
Q

How is MAP regulated in the short term?

A

Baroreceptor complex

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12
Q

How is MAP regulated in the long term?

A

Blood volume by hormones, RAAS

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13
Q

What are the major resistance blood vessels?

A

Arterioles

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14
Q

When adrenaline acts on alpha receptors, what happens?

A

Vasoconstriction

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15
Q

When adrenaline acts on beta receptors what happens?

A

Vasodilatation

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16
Q

What are the chemical metabolites which stimulate vasodilatation to occur?

A

decreased Po2, PCO2, increased [H]

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17
Q

What is the main intrinsic dilator?

A

NO

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18
Q

What is the main intrinsic vasoconstrictor?

A

Endothelin

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19
Q

What are the intrinsic physical factors?

A

temperature, myogenic response to stretch (MAP), sheer stress

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20
Q

Where is NO synthesised?

A

Endothelium

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21
Q

What controls venous return?

A

increased: blood volume, atrial pressure, EDV, SV, respiratory pumps, skeletal muscle action

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22
Q

What is vasomotor control controlled by?

A

increased: venous return, TPR and MAP, venous return

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23
Q

What happens during acute exercise?

A

Hyperanaemia overrides

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24
Q

Describe the course of the pacemaker potential

A

There is a slow Na influx and a and a K efflux until threshold is reached. Ca channels then open during the rising phase (depolarisation) and during falling phase depolarisation occurs.

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25
Q

What are the 2 gap junctions that allow cell to cell conduction to flow?

A

Intercalated discs and desmosomes

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26
Q

What is the resting membrane potential of a Ventricular muscle action potential cell?

A

-90mV

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27
Q

What is the new ventricular muscle membrane potential following fast Na influx?

A

+30mV

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28
Q

Describe the 4 phases of the ventricular muscle action potential

A 
0= fast rising Na influx
1= cells start to repolarise due to K efflux
2= plateau phase
3= closure of Ca, K efflux
4= -90mV
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29
Q

What is the plateau phase?

A

It is unique to contractile cardiac muscle and is a Ca influx

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30
Q

What does sympathetic stimulation supply?

A

SAN, AVN and myocardium

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31
Q

What effect does the sympathetic stimulation on pacemaker potential slope and what is the name?

A

Slope increases, chronotrophic effect

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32
Q

Name an active inhibitor of Ach and what does it do?

A

Atropine speeds up HR

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33
Q

What effect does the parasympathetic stimulation effect have?

A

Negative chronotrophic

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34
Q

What is an ECG?

A

A record of depolarisation and hyper polarisation as it moves across the heart from skin cells

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35
Q

State what occurs at the PQRS wave

A 
P= atrial depolarisation
QRS= ventricular depolarisation
T= ventricular depolarisation 
PR= AVN delay
TP= diastole
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36
Q

Where are intracellular stores of Ca found?

A

Sarcoplasmic Reticulum

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37
Q

What is a sarcomere?

A

The smallest functional unit capable of carrying out function

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38
Q

What complex exposes the myosin binding site and is stimulated by Ca?

A

Tropomyosin

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39
Q

What is the Refractory period?

A

A period following an action potential in which it is not possible to produce another action potential

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40
Q

What does the Refractory Period do?

A

It protects the heart by preventing generation of tetanic conditions

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41
Q

How is stroke volume calculated?

A

EDV-ESV

42
Q

What is SV?

A

The volume of blood ejected by each ventricle per heart beat

43
Q

What are the 3 factors that affect SV?

A
  1. Preload/venous return
  2. Afterload/resistance
  3. Contractility
44
Q

What is the Frank Starling Law?

A

Increased Venous return= increased EDV= increased SV

45
Q

What is the name of the effect where stimulation of sympathetic nerves and increased force of contraction takes place?

A

Positive Inotropic effect

46
Q

What do parasympathetic nerves do to SV?

A

Nothing, they do not affect force of contraction

47
Q

What is Cardiac Output?

A

The volume of blood pumped by each ventricle per minute

48
Q

What is the CO relationship?

A

CO= SVxHR

49
Q

What is a healthy CO

A

5L

50
Q

What is the cardiac cycle?

A

A sequence of depolarisation and reploarisation

51
Q

What is depolarisation and depolarisation in terms of systole and diastole?

A 
Depolarisation= systole
Repolarisation= diastole
52
Q

What are the events during the cardiac cycle?

A
  1. Passive filling
  2. Atrial contraction
  3. Isometric Ventricular Contraction– LUB
  4. Ventricular Ejection (EDV of 70ml is left)
  5. Isovolumetric Ventricular Relaxation (cycle starts again)
53
Q

Why does the atrial pressure not fall to zero during diastole?

A

Due to recoil of the arteries

54
Q

How does blood flow in a normal artery?

A

In laminar fashion

55
Q

What happens when cuff pressure>BP

A

the artery is occluded and no sound is heard

56
Q

What happens when BP>cuff pressure?

A

This is called Turbulent flow and can be heard

57
Q

What is the significance of the first and 5th Korotkoff sounds?

A 
1st= systolic BP
5th= Disatolic
58
Q

What is pressure gradient?

A

MAP- Central venous pressure

59
Q

Define MAP

A

the average arterial BP during a single cardiac cycle

60
Q

How do we calculate MAP (both ways)

A

[2xdiastolic BP] = systolic BP/3

OR

DBP+ 1/3 pulse pressure (difference between SBP & DBP)

61
Q

What is the average MAP?

A

70-105mmHg

62
Q

How is MAP calculated?

A

COx TPR

63
Q

Describe the baroreceptor pathway

A

Pressure sensors–control centre–Effectors

Baroreceptors–Medulla–HR,SV<TPR

64
Q

What do stretch receptors do when BP increases in aortic arch and carotid sinus?

A

Stretch receptors increase firing through vagus and glossopharyngeal nerves

65
Q

What is the significance of the baroreceptor in postural hypotension?

A

suddenly stand up–decreased: venous return, MAP, baroreceptor firing, vagal tone, increased: sympathetic, HR, SV, TPR

Failure of baroreceptor reflexes

66
Q

What changes to baroreceptors respond to?

A

Acute changes

67
Q

What is shock?

A

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

68
Q

What is the primary cause of hypovolaemic shock and the subtypes?

A

Decreased preload

haemorrhage and non haemorrhage

69
Q

Primary cause of cariogenic shock and eg

A

Decreased cardiac contractility and acute MI

70
Q

Primary cause of shock in tension pneumothorax and what type is it?

A

Rise in intrapleural pressure with pressure in atrium exceeding pressure in ventricle.

71
Q

Name some obstructive types of shock

A

cardiac tamponade, tension pneumothorax, PE, severe aortic stenosis

72
Q

What is the primary cause of neurogenic shock (e.g. spinal cord injury)?

A

loss of vasomotor control (sympathetic)

73
Q

What is the primary cause of vasoactive distributive shock (e.g. septic shock or anaphylaxis)?

A

Release of vasoactive mediators (vasoconstrictors)

74
Q

What stimulates the peripheral chemoreceptors to increase R.R?

A

Release of lactic acid

75
Q

What should you look for in a patient who has gone into shock?

A

cold peripheries, inadequate capillary refill, tachycardia, decreased BP

76
Q

How is shock managed?

A

ABCDE
High flow O2
Volume replacement
Inotropes for cardiogenic shock to increase contractility
Immediate chest drain for tension pneumothorax
adrenaline for anaphylaxis
vaspressor for septic shock

77
Q

What is the CV response to hypovolaemic shock?

A

decreased: MABP, CO, BV

78
Q

What is the range of shock classification?

A 
class I- body can cop well without much physiological compensation
class IV- life threatening- no urine output, confused and lethargic
79
Q

Where does the coronary circulation arise from

A

The base of the aorta

80
Q

How can 02 be increased in the coronary circulation during demand?

A

By increasing coronary blood flow through intrinsic and extrinsic regulation

81
Q

What special adaptations does the heart make to supply more 02 to the coronary circulation?

A

High capillary density and high basal blood flow

82
Q

What are the intrinsic mechanisms which regulate coronary blood flow?

A

decreased 02–> vasodilation
Metabolic hyperaemia
Adenosine from ATP is a potent vasodilator

83
Q

What are the extrinsic mechanisms which regulate coronary blood flow?

A

adrenaline acts on the beta2 receptors causing vasodilation

84
Q

Describe the pathway of increasing coronary blood flow

A

sympathetic–> increased HR and SV–> increased Cardiac output–> incr Metabolism–> incr adenosine–> incr metabolites eh K,PCO2, H–> increased circulating adrenaline

85
Q

When does the major of coronary blood flow take place?

A

During diastole

86
Q

What happens if diastole is reduced?

A

decreased coronary blood flow, rapid incr in HR and tachycardia, chest pain

87
Q

What 2 factors regulate the cerebral circulation and what is their combined name?

A

Internal carotid arteries, Basilar (vertebral bodies) = Circle of Willis

88
Q

What happens when grey matter undergoes hypoxia?

A

Consciousness is lost after a few seconds of ischemia and the damage is irreversible therefore special adaptations take place

89
Q

What are the two subtypes of stroke?

A

Ischaemia and hemorrhagic

90
Q

What are the pressure values at which auto regulation kicks in when MAP changes in the cerebral circulation?

A

-60mmHg or 160mmHg

91
Q

What happens when MAP value in the cerebral circulation falls below 50mmHg?

A

Auto regulation fails and the patient is confused, faints and suffers from brain damage

92
Q

What happens when MAP is increased and decreased in the cerebral circulation?

A

MAP increased: constriction

MAP decreased: dilation

93
Q

What happens to cerebral MAP when PCO2 is increased and decreased?

A

PCO2 increased= vasodilation

PCO2 decreased= vasoconstriction

94
Q

What is normal intracranial pressure? (ICP)

A

8-13mmHg

95
Q

What is the cerebral perfusion pressure? (CPP)

A

MAP-ICP

96
Q

What happens when ICP is increased?

A

decr CPP, decr cerebral blood flow

97
Q

What special adaption in the pulmonary circulation prevents oedema?

A

Absorptive forces. filtration

98
Q

What happens to the arterioles in the pulmonary and systemic circulation when there is a decrease in 02?

A

Pulmonary: vasoconstriction
Systemic: vasodilation

99
Q

Why does varicose veins not affect the cardiac output?

A

It is a chronic development and so the body can compensate and the blood volume will not fall

100
Q

What happens during exercise that overcomes the sympathetic vasocontrictor activity?

A

Metabolic hyperaemia

101
Q

What is retrograde conduction?

A

When the conduction comes from the ventricle or the AVN to the atria

Cardiovascular (8 decks)

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