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Cardio > Physiology > Flashcards

Physiology Flashcards

1
Q

definition of blood pressure

A

the outward hydrostatic pressure exerted by the blood on the blood vessel walls

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2
Q

average systolic and diatonic values?

A

systolic 140mmHg, diastolic 90mmHg

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3
Q

blood flow in arteries is in what fashion?

A

laminar flow - not audible through a stethoscope

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4
Q

diastolic pressure is heard at which one of the Korotkoff sounds?

A

5th - the point at which the sound goes away and the blood returns to laminar flow

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5
Q

what is the mean arterial pressure?

A

average arterial blood pressure during a single cardiac cycle

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6
Q

what is the lowest value of MAP that is needed to perfuse coronary arteries, brain and kidneys?

A

60mmHg - normal range is usually from around 70-105mmHg

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7
Q

how can MAP be estimated?

A

(2 x diastolic pressure) + systolic pressure
all decided by 3

OR

diastolic blood pressure plus 1/3 of the difference between DBP AND SBP

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8
Q

MAP is?

A

cardiac output x total peripheral resistance

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9
Q

definition of cardiac output?

A

the volume of blood pumped by each ventricle of the heart per minute

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10
Q

definition of the stroke volume?

A

is the volume of blood pumped by each ventricle of the heart per heart beat

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11
Q

calculation of CO

A

stroke volume x heart rate

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12
Q

definition of the total peripheral resistance?

A

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

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13
Q

where are the two important baroreceptors within the cardiovascular system?

A

the arch of the aorta and the carotid sinus

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14
Q

wha types of change in blood pressure do baroreceptors react to?

A

Only react to ACUTE changes in blood pressure - the firing decreases if high blood pressure is sustained an will not fire again uni l a new even higher BP is picked up.

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15
Q

what are the two factors that effect the extracellular fluid volume?

A

water excess or deficit

Na+ excess or deficit

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16
Q

which hormones act as effectors to regulate the extracellular volume and how do they do so?

A
  1. renin-angiotensin-aldosterone system
  2. atrial natriuretic peptide
  3. antidiuretic hormone (arginine vasopressin)

they all control the water to salt balance within the body

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17
Q

what are the components of the RAAS and what do they do?

A

RENIN:
released from the kidneys, stimulates the formation of angiotensin 1 in the blood from anginotensinogen

ANGIOTENSIN:
angiotensin 1 gets converted to angiotensin 2 by ACE - which stimulates the release of aldosterone

ALDOSTERONE:
released from adrenal cortex - causes vasoconstriction (increasing TPR) - also stipulates thirst and release of ADH - increases plasma volume

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18
Q

how is the RAAS system regulated?

A

renal artery hypotension
stimulation of renal sympathetic nerves
decreased [Na+] in renal tubular fluid

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19
Q

role of Atrial natriuretic peptide?

A

counter-regulatory mechanism to the RAAS

  • released in response to atrial distension, causes vasodilation,, release of salt and water from kidneys, decreased renin release
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20
Q

where is ADH made and stored?

A

produced in the hypothalamus and stored in the posterior pituitary body

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21
Q

role of ADH?

A

stimulated by reduced ECF or increased ECF osmolarity (main stimulus)
normal - 280 milli-osmoles/L - deviation from this will cause ADH to be released

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22
Q

where does ADH act?

A

acts on the tubules in the kidney to increase the reabsorption of water - i.e. concentrates urine - increasing the ECF and plasma volume +hence increasing the cardiac output and blood pressure
also causes vasoconstriction - increasing TPR and therefore blood pressure - effect is small in normal people but is massive in hypovoleamic shock

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23
Q

what is shock?

A

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

depends on blood pressure and adequate cardiac output

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24
Q

definition of hypovolaemic shock?

A

loss of blood leading to inadequate tissue perfusion

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25
Q

definition of cardiogenic shock?

A

decreased cardiac contractility leading to inadequate tissue perfusion

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26
Q

treatment of shock?

A 
ABCDE approach 
high flow oxygen 
volume replacement
inotropes for cariogenic shock 
immediate chest drain for pneumothorax 
adrenaline for anaphylactic shock 
vasopressors for septic shock
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27
Q

how much blood can be lost until the body no longer functions?

A

> 30%

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28
Q

what are/is the function of gap junctions within striated cardiac muscle?

A

these are protein channels which forms a low resistance electrical pathway between neighbouring myocytes - ensuring that the electrical excitation reaches all of the myocytes - ALL OR NOTHING LAW

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29
Q

function of desmosomes?

A

lie within intercalated discs - provide mechanical adhesion between adjacent cardiac muscle cells

30
Q

what are the contractile units of muscle?

A

myofibrils

31
Q

why is calcium needed for muscle contraction?

A

calcium makes the troponin slide away from the actin binding site allowing it to become available for binding with the myosin head

32
Q

how does the action potential switch on ventricular systole?

A

during the plateau phase, calcium is influxes into the cell

33
Q

Define Refractory period

A

is a period following an action potential in which it is impossible to produce another action potential - prevents tetanic contractions in cardiac muscle

34
Q

how is the refractory period achieved?

A

during the plateau phase - Na+ channels are in the depolarised closed state
during the descending phase, the K+ channels are open - do the membrane cannot be polarised

35
Q

stroke volume is regulated by which two types of mechanism ?

A

intrinsic - within the heart muscle itself

extrinsic - nervous and hormonal control

36
Q

define end diastolic volume and what determines it?

A

the volume of blood within each of the ventricles at the end of diastole
determined by the venous return to the heart

37
Q

relationship between EDV and SV - Starlings law

A

the more blood that is present within the ventricles at the end of diastole, will will result in a greater amount of blood being ejected during systole (SV)

38
Q

what is afterload?

A

the resistance into which the heart is pumping

39
Q

what occurs if an continually increased afterload is present?

A

Ventricular hypertrophy - the heart muscle has to contract as there is now a greater EDV as the full stroke volume cannot be ejected

40
Q

what type of nerve fibre are the ventricles supplied by? and which transmitter is used?

A

sympathetic - noradrenaline

41
Q

what effects do sympathetic nerve fibres have upon the heart?

A

increases the forces of contraction - positive inotropic effect
increases the heart rate - positive chronotropic effect

SHIFTS THE FRANK STARLING CURVE TO THE LEFT

42
Q

what effects do parasympathetic nerves have on the heart?

A

little to no effect upon the force of contraction of the ventricles by vagus

vagus however has a major influence upon the heart rate

43
Q

what does autorhythmicity mean?

A

the ability of the heart to beat in the absence of external stimuli

44
Q

where does the electrical activity originate?

A

from pacemaker cells within the sion-atrial node in the right atrium

45
Q

how does the electrical activity spread across all of the heart?

A

sino atrial node (mainly cell-to-cell via gap junctions), to AV node, down the bundle of his, into the purkinje fibres which branch off into right and left branches

46
Q

the is the significance of AV nodal delay?

A

it allows atrial systole precede ventricular systole

47
Q

effects of sympathetic/parasympathetic on the heart rate?

A

parasympathetic - decreases

sympathetic - increases

48
Q

what does the vagus never supply in the heart?

A

SA node and AV node - acting from M2 receptors using acetylcholine

atropine is a competitive inhibitor of acetylcholine - therefore used to speed up the heart

49
Q

what does the sympathetic nerves supply within the heart?

A

SA node, AV node and myocardium - acting through Beta1 receptors via noradrenaline

50
Q

what is an ECG?

A

a record of depolarisation and depolarisation of the cardiac cycle obtained from the skins surface

51
Q

what are the five events during her cardiac cycle?

A
  1. passive filling
  2. atrial contraction
  3. isovolumetric ventricular contraction
  4. ventricular ejection
  5. isovolumetric ventricular relaxation
52
Q

define passive filling

A

the pressure the ratio and ventricles is close to zero and blood from the venous return returns to the atria and ventricles as AV node opens
the ventricles become 80% full from passive filling

53
Q

what does the P wave signal?

A

atrial depolarisation

54
Q

what are the first and second heart sounds due to?

A

first heart sound (LUB) is due to the shutting of the AV valve as the ventricular pressure exceeds that of the atrial pressure

the second heart sound (DUB) is due to the shutting of the aortic valve, when aortic pressure exceeds that of the ventricular

55
Q

what heralds the beginning of systole and diastole?

A

S1 heralds the beginning of systole and S2 heralds the beginning of diastole

56
Q

How is the TPR controlled?

A

vascular smooth muscle - mainly in the arterioles, contraction increases the TPR and therefore MAP

57
Q

resistance formula?

A

the resistance to blood flow is; directly proportional to blood viscosity and length of blood vessel, and inversely proportional to the radius o the blood vessel to the power of 4

R ∝ η.L/ r4

58
Q

what is vasomotor tone?

A

the partial constriction of vascular smooth muscle at rest - due to the release of noradrenaline from sympathetic nerve fibres

59
Q

where does adrenaline come from? and what is it effect on vascular smooth muscle?

A

adrenaline comes from the adrenal medulla

vasoconstriction: alpha receptors (skin, gut kidney arterioles)
vasodilation: beta receptors (cardiac and skeletal muscle)

60
Q

effect of intrinsic control of smooth muscle?

A

can override the extrinsic control mechanisms - are responsible for matching blood flow of different tissues to their metabolic needs

61
Q

chemical states which cause vasodilation?

A 
decreased O2 
increased CO2
decreased pH
increased extracellular [k+]
increased osmolarity to ECF 
adenosine
62
Q

hormonal states which can cause vasodilation?

A

histamine
bradykinin
nitric oxide (NO) (continuously released by endothelial cells of arteries and arterioles)

63
Q

How is NO produced?

A

from L-arginine through the enzymatic action of nitric oxide synthase

64
Q

how does NO cause vascular smooth muscle relaxation?

A

diffuses from endothelium into adjacent smooth muscle cells which it activates the formation of cGMP that serves as a second messenger for signally smooth muscle relaxation

65
Q

hormonal states which cause vasoconstriction?

A

serotonin
thromboxane A2
leukotrienes
endothelin (potent vasoconstrictor released from endothelial cells)

66
Q

what physical features effect TPR?

A

Temperature - cold causes vasoconstriction, heat vasodilation

MAP - if the MAP increased, vessels constrict to limit flow, if MAP falls, vessels dilate (this is essential for organs like the brain and kidneys)

67
Q

what factors effect venous return?

A

skeletal muscle pump
venomotor tone
blood volume
respiratory pump

68
Q

where does most of the blood in the body lie?

A

within the veins - they are the capacitance vessels that contain most of the blood volume under resting conditions

69
Q

increased venomotor tone does what?

A

increases the venous return and therefore SV and MAP

70
Q

Give two examples of organic nitrates and when they might be used.

A

glyceryltrinitrate (GTN) and isorbide mononitrate

  • used in stable angina and acute coronary syndrome

Cardio (6 decks)

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