Physiology Flashcards

1
Q

intrinsic control of SV

A

changes brought about by changes in diastolic length/ diastolic stretch of myocardial fibres

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2
Q

EDV

A

volume of blood within each ventricle at the end of diastole

determines the cardiac preload

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3
Q

cardiac afterload

A

the resistance into which the heart is pumping

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4
Q

increase in afterload

A

at first: heart unable to eject full SV, so SV decreases > increase in EDV > force of contraction increase
eventually causing ventricular hypertrophy

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5
Q

hormones that regulate extracellular fluid volume

A

the renin-angiotensin aldosterone system
natriuetic peptides
antidiuretic hormones

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6
Q

rate liming step for RAAS

A

Renin secretion

RAAS regulated by mechanisms which stimulates renin release from juxtaglomerular apparatus in kidneys

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7
Q

Juxtaglomerular apparatus

A

region comprising of the macula densa, extraglomerylar mesangial cells and granular cells

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8
Q

Natriuretic peptides

A

peptide hormones synthesised by the heart and released in response to cardiac distension or stimuli

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9
Q

NPs function

A

Cause excretion of salt and water in kidneys > reducing blood volume and BP

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10
Q

decrease renin release =

A

decrease BP

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11
Q

two types of NPs released by the heart

A

atrial peptide

brain-type natriuretic peptide

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12
Q

shock

A

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

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13
Q

causes of shock

A

loss of blood
sudden severe impairment of heart function
physical obstruction to circulation
excessive vasodilation and abnormal distribution of blood flow

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14
Q

4 types of shock

A

hypovolaemic shock
cardiogenic shock
obstructive shock
distributive shock

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15
Q

hypovolaemic shock

A

caused by loss of blood volume

haemorrhagic or non-haemorrhagic

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16
Q

cardiogenic shock

A

caused by sudden severe impairment of cardiac function

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17
Q

obstructive shock

A

caused by physical obstruction to circulation either in or out the heart
- PE, pneumothorax

18
Q

Distributive shock

A

caused by excessive vasodilation and abnormal distribution of blood flow
neurogenic or vasoactive

19
Q

Systemic vascular resistance

A

sum of resistance of all vasculature in the systemic circulation

20
Q

Resistance to blood flow

A

characteristics of blood, length of blood vessel, radius of blood vessel (inversely proportional to the power of 4)

21
Q

nerve control of vascular smooth muscle

A

sympathetic nerves
noradrenaline acting on alpha receptors
- constrict

22
Q

Vasomotor tone

A

means the vascular smooth muscle is partially constricted at rest
caused by tonic discharge of sympathetic nerves > continuous release of noradrenaline

23
Q

Main hormone control of vascular smooth muscle

A

Adrenaline from the medulla

  • acting on alpha (skin, gut, kidney arterioles) receptors causes vasoconstriction
  • acting on beta2 (cardiac and skeletal) receptors causes vasodilatation
24
Q

other hormones involved in control of vascular smooth muscle

A

angiotensin II- causes vasoconstriction

antidiuretic hormone- causes vasoconstriction

25
intrinsic control of vascular smooth muscles
match the blood flow of different tissues to their metabolic needs can over-ride extrinsic controls chemical and physical factors
26
chemical local metabolite factors causing relaxation of arteriolar smooth muscle
decreased PO2 | increased PCO2
27
examples of chemical local humoral agents that cause vasodilation
histamine bradykinin NO
28
Nitric oxide
continuously produced by vascular endothelium from amino acid L-arginine through enzymatic action of nitric oxide synthase potent vasodilator
29
examples of chemical local humoral agents that cause vasoconstriction
serotinin thromboxane A2 leukotrienes endothelin- potent vasoconstrictor, released from endothelial cells
30
factors influencing venous return
increased venomotor tone increased blood volume increased "skeletal muscle pump" increased "respiratory pump"
31
Venomotor tone
increased venomotor tone increases venous return
32
what is an ECG
recording of potential changes, detected by electrodes that allow the electrical activity of the heart to be monitored
33
12 leads of the ECG
3 standard limb leadds 3 augmented voltage leads 6 chest leads- horizontal
34
Lead II
sees the heart from inferior view
35
PR interval
time for the SA node impulses to reach the ventricles
36
Leads I and aVL
lateral leads | views the heart from the left
37
Leads II, III, and aVF
inferior leads
38
V1 and V2
coming from right | look at interventricular septum
39
V3 and V4
lateral aspect
40
3 types of syncope
reflex syncope orthostatic hypotension cardiac syncope
41
physiological role of troponin I
binds to actin to hold the troponin-tropomyosin complex in place