Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RB Y1 Cardiology > physiology > Flashcards

physiology Flashcards

1
Q

where is the SA node found

A

in the right atrium close to where the SVC enters it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what rhythm is a heart controlled by the SA node said to be in

A

sinus rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what type of potential to the cells in the SA node exhibit

A

spontaneous pacemaker potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does the pacemaker potential do

A

takes the membrane potential to a threshold to generate an action potential in the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

waht is the pacemaker potential due to

A

decrease in K efflux

funny current (Na and K influx)

transient Ca influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the ion movement during the phases of the SA node cell AP

A

note Ca influx via L type Calcium channels during depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the spread of conduction through the heart

A

SA node initiates an impulse that is conducted to atrial muscle fibres causing them to contract. impulse spread to AVN by myogenic (cell to cell) conduction

bundle of His

left and right branches in muscular interventricular septum

branches ramify into subendocardial branches (Purkinje fibres) which extend into the walls of the respective ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does excitation spread through cells in the heart

A

gap junctions- these are protein channels which form low resistance electrical communication pathways between neighbouring myocytes

  • across the atria via cell to cell conduction
  • there are some internodal pathways between SAN and AVN
  • within ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe the structure of a gap junction

A

the desmosomes provide mechanial adhesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the only point of electrical contact between the atria and ventricles

A

AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where is the AV node located

A

base of the RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why is conduction delayed in the AV node

A

to allow atrial systole to precede ventricular systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the phases of venticular muscle AP

what is the resting mp?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where does the CNX supply in the heart

vagal stimulation

A

SA and AV node

vagal stimulation slows heart rate and increases AV nodal delay - negative chronotropic effect

on an ECG this causes decreased slope of pacemaker potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

vagal tone

A

CNX exerts a continuous influence on the SAN under resting conditions - this dominates and slows the intrinsic HR from 100bpm to around 70bpm in resting conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

neurotransmitter for parasympathetic supply to the heart

A

neurotransmitter is ACh through M2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

atropine

A

inhibitor of ACh - used in severe bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cardiac sympathetic nerves

  • where do they supply
  • effect
  • neurotransmitter
A

as they supply the SAN, AVN and myocardium, they have a positive inotropc effect (force) and chronotropic effect (rate)

slope of pacemaker potential increases

neurotransmitter is noradrenaline through ß1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the sarcolemma

A

the cell membrane of a striated muscle fibre cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

outline actin and myosin crossbridge action

A

ATP is broken down into ADP and Pi on myosin – myosin extends and can attach to binding sites on actin to form cross bridges.

Power stroke – myosin pulls the actin towards the M-line shortening the sarcomere.

ADP and Pi are released during power stroke.

Myosin remains attached to actin until ATP binds again – contract again or relax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

rigor complex

A

ATP is needed for contraction and relaxation

a rigor complex is formed when the myosin head is bent and bound to actin

  • this explains rigor mortis after death
  • muscle cramps may be due to development of rigor complex due to lack of ATP or inability to remove calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe the action of tropomyosin and troponin

A

when muscle is relaxed tropomyosin blocks the cross bridge binding sites on actin

when Ca levels are high enough, Ca ions bind to troponin which displaces tropomyosin exposing myosin binding sites on actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

muscle contraction

A

Ca++ ions stored in sarcoplasmic reticulum and are released in response to signals from the nervous system to contract.

Neurotransmitter molecules released from neurone and bind to receptors which depolarises the muscle fibre membrane, electrical impulse travels down T tubules and opens Ca stores in sarcoplasmic reticulum.

These travel to myofibrils – muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does long refractory period prevent and what is the significance of this

A

generation of tetanic contraction

excessive heart rate provides insufficient time for cardiac filling, problems with insufficient oxygen and blood etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how is the refractory period generated in ventricular cells and AP

A

ventricular: during the plateau phase the Na channels are closed

AP: during the descending phase the K channels are open and so membrane cant be depolarised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

define SV and its regulation

A

volume of blood ejected by each ventricle per heart beat

= EDV - ESV

changes in SV are brought about by changes in the diastolic length of the myofibrils - this is determined by the volume of blood within each ventricle by the end of diastole (EDV) = cardiac preload

the EDV is determined by the venous return to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

when is maximal force generated by myofibrils

A

at optimal fibre length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does the frank starling law state

A

the larger the VR, the larger the EDV and the larger the SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what effect does stretch have on the affinity of troponin for Ca++

A

increases it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

in skeletal muscle when is the optimal fibre length

A

at resting muscle length - maximum overlap of actin and myosin filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

define afterload

A

the resistance into which the heart is pumping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how does the frank starling mechanism compensate for increased afterload causing decreased SV

A

with increased afterload, at first the heart won’t be able to eject full SV, so EDV increases

this causes FS mechanism to increase the force of contraction and SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what happens in longterm causes of increased afterload

A

eg untreated hypertension

eventually the ventricular muscle mass increases (hypertrophy) to overcome the resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how do inotropes increase force of contraction

A

activate Ca channels resulting in greater Ca influx - this causes the peak venticular pressure to rise, and the rate of pressure change during systole to increase - thus reducing the duration of systole

(inotropic and chronotropic)

rate of ventricular relaxation also increases, reducing the duration of diastoe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what mediates the positive inotropic effect that sympathetic stimulation has on the heart

A

cAMP - controls Na and Ca influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how does sympathetic stimulation affected the Frank Starling Curve

A

shifts it to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what effect does a rise in peak ventricular pressure have on the contractility of the heart at a given EDV

A

increases it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how does heart failure effect the curve

A

shift to right

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the resting CO in adults

A

5l per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the ligamentum arteriosus

A

remnant of the fetal shunt ( ductus arteriosus)

a persistent ductus arteriosus produces a machine like murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what are the principles of valves

A

AV valves are open when atrial pressure exceeds ventricular pressure

semilunar valves are open when ventricular pressure exceeds aortic/pulmonary pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

passive filling and atrial contraction

A

pressure in atria and ventricles is close to 0, AV valves are open so venous return flows into the ventricles - 80% passive filling

atrial depolarisation (P wave), atria contract and pressure increases forcing the remaining blood into the ventricles

as AC completes, the pressure in the atria falls and the valves shutl producing the first heart sound - S1 (LUB)

this signifies the beginning of ventricular systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

normal EDV in resting adult

A

around 130ml

45
Q

isovolumetric ventricular contraction

A

early systole, for a short time all the valves are shut and the ventricles depolarize and contract, increasing pressure in the ventricles without a change in volume

the increase in ventricular pressure is sharp

this happens until the pressure in ventricles exceeds that in pulmonary artery/aorta and the semilunar valves open - ventricular ejection

ventricular repolarization occurs, the ventricles relax, pressure falls and the semilunar valves shut - S2 (DUB). this signifies the end of systole

46
Q

what are the normal values for SV, EDV and ESV

A

SV = EDV -ESV

70 = 135-60ml

47
Q

dicrotic notch

A

coincides with aortic valve closure, caused by the valve vibration

48
Q

Isovolumetric Ventricular relaxation

A

Tension falls in ventricles in a closed volume, until ventricular pressure falls below that of atrial, and AV valves open to start cycle again

49
Q

heart sounds

A
  • S1 (LUB) is caused by the tricuspid and mitral valves closing and signifies the beginning of systole
  • S2 (DUB) is caused by the closure of aortic and pulmonary valves and signifies the beginning of diastole
50
Q

how does arterial pressure not fall to 0 during diastole?

A

i do not know

51
Q

explain JVP

A

it is a biphasic pulse along the sternocleidomastoid

when the pressure in the RA increases, a pressure is exerted outwards onto the IJV

  • a wave signifies increase in atrial pressure due to atrial contraction
  • c wave signifies increase in atrial pressure due to bulging of tricusped valve into atrium during ventricular contraction
  • v wave signifies increase in atrial pressure due to atrial filling, it releases as the AV valve opens
52
Q

define BP

A

the outwards pressure that is exerted by the blood on blood vessel walls

53
Q

Kortkoff sounds

A
  • no sound is heard above systolic pressure eg 120/80*
    1. heard at peak systolic pressure

2-3: intermittent sounds heard between 80 and 120

4: muffled sound heard at minimunm/diastolic pressure
5: no sound heard below diastolic (80) as the flow is laminar
* diastolic pressure is measured at the 5th sound as this is more reproducible*

54
Q

what drives the blood around the systemic circulation

A

pressure gradient between aorta and right atrium

55
Q

define MAP

A

the average arterial blood pressure during a single cardiac cycle

as D is twice as long as S:

MAP = (2xDP + SP) / 3

56
Q

normal range of MAP

and minimum MAP to perfuse

A

70-105mmHg

60mmHg

57
Q

define cardiac output

A

volume of blood pumped by each ventricle per minute

58
Q

explain the effect of the sympathetic nervous system on MAP

A
59
Q

baroreceptor reflex

A

Short term regulation of MAP

  • the baroreceptors are pressure sensors, they are located in the carotid sinus (carotid ones - CNIX) and aortic area (aortic ones - CNX)
  • send signals to medulla via CN
  • if there is a drop in BP (eg standing up), they will detect the decrease in tension and stop firing, this allows uninhibited symapthetic activity on the heart
  • if there is an increase in BP, they will be stretched and fire, inhibiting sympathetic activity and increasing vagal tone on the heart
  • have the ability to reset, eg after one day of increased BP
60
Q

when does postural hypotension occur

A

failure of baroreceptor to respond to gravitational shifts in blood (which decrease venous return to heart)

61
Q

how much of total body fluid is intracellular and extracellular

A

2/3 intracellular

1/3 extracellular

62
Q

explain RAAS

A

note, aldosterone causes sodium retention, and water follows

63
Q

what is the rate limiting step for RAAS

A

renin production

64
Q

activation of RAAS

A
  • renal artery hypotension caused by systemic hypotension
  • stimulation of renal sympathetic nerves
  • decreased sodium concentration in renal tubular fluid (sensed by macula densa in kidney tubules)
65
Q

role of ANP

A

released in response to atrial distension in hypervolaemic states:

  • excretion of salt and water in the kidneys, therefore reducing blood volume and pressure
  • vasodilation
  • decrease renin release - counter regulate RAAS
66
Q

how many amino acids does ANP have

A

28

67
Q

what is ADH secretion stimulated by

A

dec extracellular fluid or inc extracellular fluid osmolarity (detected by osmoreceptors in the brain near they hypothalamus)

68
Q

what is the normal osmorality of extracellular fluid

A

280 mili osmoles

69
Q

when is ADH important

A

hypovolaemic shock

70
Q

what are the major resistance vessels

A

arterioles

71
Q

what contains most of blood volume during rest

A

veins - they are capacitance vessels

72
Q

resistance to flow equation

A
73
Q

vasomotor tone of vascular smooth muscle

A

blood vessels are partially constricted at rest - tonic discharge of sympathetic nerves, resulting in continuous noradrenaline release, acting on alpha receptors

74
Q

which smooth muscles have significant parasympathetic innervation

A

penis and clitoris

75
Q

describe the organ specific effect of adrenaline and its advantages

A
  • acting on alpha receptors in skin, gut and kidney arterioles, causes vasoconstriction
  • acting on ß2 receptors in cardiac and skeletal muscle causes vasodilation
  • this allows for the strategic distribution of blood eg during exercise
76
Q

simply, what comprises extrinsic control of vascular smooth muscles

A

nerves and hormones

77
Q

which chemical factors cause vasodilatation and metabolic hyperaemia

A
  • Decreased local PO2
  • Increased local PCO2
  • Increased local [H+] (decreased pH)
  • Increased extra-cellular [K+]
  • Increased osmolality of ECF
  • Adenosine release (from ATP)
78
Q

bradykinin

A

an inflammatory mediator that causes vasodilatation

it is increased by ACE inhibitors, and causes a dry cough

79
Q

formation of NO

A
  • it is continuously produced by the vascular endothelium from the amino acid L-arginine through the enzymatic action of NOS
  • acts in the smooth muscle
80
Q

nitric oxide

A

NO is a potent vasodilator - activates the formation of cGMP in the smooth muscle cells which signals smooth msucle relaxalation

  • shear stress on vascular endothelium as a result of increased flow, causes calcium release which activates NOS
  • chemical stimuli can stimulate NO formation
81
Q

what do serotonin, thromboaxane A2 and leukotrienes cause

A

vasocontriction

82
Q

endothelin

A

vasoconstrictor released from endothelial cells

83
Q

sheer stress

A

dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate - increases blood flow to metabolically active tissues

84
Q

can local control of TPR override extrinsic control?

A

yes, it responds to immediate demands of particular tissues, can overide the nerves that control these tissues

85
Q

how is blood flow to skeletal and cardiac muscles increased during exercise

A

local hyperaemia overcomes vasomotor drive, resulting in vasodilatation

86
Q

what happens to pulse pressure during exercise

A
  • decrease in SVR during exercises increases the flow to tissues and increases VR
  • this increase CO and systolic BP
  • diastolic BP is decrease because TPR decreases
87
Q

define shock

A
  • abnormality of the circulatory system resulting in inaequate tissue perfusion and oxygenation
  • this results in anaerobic metabolism, and accumulation of metabolic waste products
88
Q

cardiogenic shock

A

sustained hypotension caused by decreased cardiac contracility

89
Q

how does a tension pneumothorax cause obstructive shock

A

increased intrathoracic pressure results in decreased venous return (increased resistance in vena cava)

90
Q

how does neurogenic shock casue inadeqaute tissue perfusion

A

loss of sympathetic tone, leading to massive venous and arterial vasodilatation

91
Q

vasoactive shock

A

release of vasoactive mediators - massive venous and arterial vasodilatation

increased capillary permeability

92
Q

during haemorrhagic shock, up to which point can compensatory mechanisms maintain blood pressure

A

up to 30% blood loss

93
Q

what are capillaries formed from

A

a single layer of endothelial cells

94
Q

what is interstitial fluid

A

component of the extracellular fluid (70%) that surrounds cells in the body - go between blood and body cells

95
Q

describe the functions of capillaries

A
  • allow rapid exchange of gases, water and solutes with interstitial fluid
  • delivery of nutrients and O2 to cells
  • removal of metabolites from cells
96
Q

how is blood flow to capillaries determined

A
  • the contractile state of terminal arterioles regualte regional blood flow to the capillary bed in most tissues
  • precapillary sphincters regulate the flow in a few tissues
97
Q

describe the blood flow through CB

A

very slow to allow for adequate time for exchange

98
Q

name a tissue that has precapillary sphincters

A

mesentery

99
Q

how do lipid soluble and water soluble substances pass throughcapillary wall

A
  • lipid soluble pass through endothelial cells
  • water soluble pass through water filled pores
  • large molecules generally cannot cross the capillary wall eg plasma proteins
100
Q

starling forces

A

the forces involved in transcapillary fluid flow

101
Q

define NFP

A

(PC + πi) - (pC + πi)

102
Q

what do starling forces favour at the arteriolar and venular end

A

favour filtration at the arteriolar end and reabsorption at the venular end

103
Q

what happens to excess fluid

A

it is returned to the circulation via lymphatics as lymph

104
Q

how are the lungs generally kept dry

A
  • they need to be to facilitate gas exchange
  • pulmonary resistance is 9x less than systemic
  • they have a low capillary hydrostatic pressure and a high capillary osmotic pressure - minimise fluid loss into interstitium
  • efficient lymphatic drainage removes any filtered fluid thus preventing accumulation of interstitial fuid
105
Q

define oedema

A

accumulation of fluid in the interstitial space

106
Q

decribe the effect of pulmonary oedema on gas exchange

A

increases the diffusion distance, compromising gas exchange

107
Q

name 4 causes of oedema

A
  • raised capillary pressure
  • reduced osmotic pressure
    • malnutrition, protein malabsorption, hepatic failure
  • lymphatic insufficiency
  • changes in capillary permeability
    • eg inflammation, histamine increases leakage of protein
108
Q

what can filariasis cause

A

elephantiasis

RB Y1 Cardiology (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions