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4 - Med > Cardiology - Physiology > Flashcards

Cardiology - Physiology Flashcards

1
Q

What is CO equal to ? typical CO ?

A

CO = HR x SV
typical CO: 5L/min

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2
Q

What structures in heart have pacemaker potential ? (4) what determines which is the one that the heart follows?

A

heart follows rhythm of fastest pacemaker
- usually SAN, can be AVN, ventricular myocytes, purine fibres

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3
Q

What is chronotropy ? inotropy ?

A

Chronitropy: affecting HR
inotropy: alter force/energy of contraction

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4
Q

What is normal HR? what is the structure that normally controls this ?

A

normal HR 60-100 usually controlled by SAN (cluster of pacemaker cells in RA)

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5
Q

what is normal SAN pacing? what innervation brings it down ?

A

SAN pacing normally around 100 bpm but para innervation at rest brings it down
(has natural automaticity)

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6
Q

what is AVN function ?

A

pass on impulse from A => V (but with small delay due to lower conduction velocity (0.5s) => allows atresia to finish contraction + AV valve to shut

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7
Q

describe the para effect on heart ? (chronic/ino)

A

para via vagus nerve (to SAN + AVN) => negative chronitropic effects (decrease HR)

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8
Q

describe the sympathetic effect on heart ? (chronology/ino)

A

via superical + deep cardiac plexus => +ve chrono + inotropic effects (increase HR and SV)

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9
Q

what are baroreceptors sensitive to ? where are they located ? what does increased firing mean ? what does this cause ?

A

baroreceptors (located in carotid sinus and aortic arch): sensitive to change in stretch + tension in arterial walls (then communicated to medulla)
- increased barorecepot firing => means increased arterial pressure detected => PSNS innervated => reduced HR + vasodilation

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10
Q

What is SV equal to ? (what blood in heart)

A

difference between end diastolic vol + end systolic vol

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11
Q

what is central venous pressure (CVP)

A

BP in vena cava, reflects amount of blood returning to RA)

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12
Q

how does increased CVP affect SV ?

A

increase CVP => increased diastolic filling => stretch myocytes => increase preload => increase SV

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13
Q

What is starlings law?

A

the more the hear chamber fills, the stronger the ventricular contraction => increase SV

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14
Q

How does increased TPR affect HR ?

A

increased TPR => increased after load = > reduce SV

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15
Q

How much blood does the heart pump around the body at rest ?

A

5L

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16
Q

when does most filling of the ventricles take place ?

A

ventricles fill during diastole and atrial systole (most filling is in diastole)

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17
Q

what is is-volumetric contraction ?

A

ventricles contract, hert valves remain shut => increase pressure

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18
Q

What is the outflow phase of the cardiac cycle ?

A

(systole)
ventricles contract further, valves open, blood exit

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19
Q

What are the phase 0 - 4 of cardiac muscle contraction ?

A

Phase 0: rapid depolarisation (rapid sodium influx)
Phase 1: early depolarisation (efflux of K)
Phase 2: plateau (slow influx of Ca)
Phase 3: Final depolarisation (efflux of K)
Phase 4: restoration of ionic concs (NA+/K+ ATPase)

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20
Q

Where is the AVN located ?

A

within AV septum - near opening of coronary sinus

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21
Q

what are the 2 AV bundles? where supply to ?

A

AV bundle (bundle of His)
- Right bundle branch (conducts impulse to RV)
- Left bundle branch (conducts impulse to LV)

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22
Q

What are gap junctions ? located where in cardiac context ? What does it allow for ?

A

regulated pores that connect adjacent cardiac myocytes
- located at the intercalated discs (at either end of the myocytes)
- allows for cell coupling => quick AP spread from cell to cell => unidirectional and synchronicity

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23
Q

What is the ventricular resting membrane potential

A

-70mV

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24
Q

What is blood flow ? and what is it equal to ?

A

vol of fluid passing a point per unit time
Flow = pressure / resistance

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25
Q

what is laminar flow ? describe it

A

velocity is highest in centre of vessel and lower closer to vessel wall (due to increased resistance)

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26
Q

where is turbulent blood flow more likely ?

A

when vessel branched/constricted => rougher flow
(bifurcations, atheroslecrotic)

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27
Q

What is resistance to blood flow dependant on ? (3) high or low of each of these increase resistance ?
what law ?

A

dependant on
- radius (increase)
- viscosity (decrease)
- vessel length (decrease)

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28
Q

what is virchows triad ?
what are the 3 factors ?

A

3 factors that reduce flow => increase thrombus risk
- stasis of blood flow
- hypercoagulability
- vessel wall injury

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29
Q

What is BP equal to ?

A

CO x TPR
(flow x resistance)

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30
Q

what is short term BP regulation controlled by ? detected by what ?

A

controlled by autonomic NS
- baroreceptors detect BP

31
Q

What happens when there is increased baroreceptor firing ? what innervation ? what affect on BP does this have ?

A

increased firing => (medulla oblongata) PSNS via X nerve => reduce HR => reduce CO => reduce BP

32
Q

what is involved in long term BP regulation ? (2) explain a bit

A
  • RAAS: reinin is released in response to SNS stimulation
  • ADH: produced in hypothalamus + stored/released from AP => increased water reabsorption
33
Q

what are some of the complications of long term high BP ?

A
  • Macrovasc (storke, MI)
  • Microvasc (neph/retinopathy)
  • Heart (increase afterload => LV hypertrophy, dilated cardiomyopathy => HF)
34
Q

What is Ficks law ?

A

rate of diffusion is proportional to conc difference + area available
(capillary exchange)
- capillaries have large SA + steep conc gradient + short diffusion pathway

35
Q

what are starling forces ? name the 4

A

physical forces that determine the movement of fluid between capillaries and tissue fluid
- blood hydrostatic (pressure exerted by blood in capillaries against vessel wall)
- oncotic (pressure exerted by proteins in blood (pull fluid into blood))
- interstitial hydrostatic pressure
- interstitial oncotic pressure

36
Q

what is kwashiorkor ? pathophys explain

A

malnutrition + low albumin => low oncotic pressure => muscles wasting + oedema (thin extremities + distended albumin)

37
Q

what cells regulate arteriolar tone ?

A

smooth muscles cells in tunica media

38
Q

describe the pressure in veins vs arteries ?

A
  • Veins: low pressure, low resistance
  • Arteries: high pressure, high resistance
39
Q

do veins or arteries have higher capacitance ? what does this mean ?

A

veins have high capacitance (can distend with increasing BP)

40
Q

what is CVP ? where is is measured from ?

A

Central venous pressure (CVP) is the BP in the vena cava (near RA)

41
Q

What does coronary vessel perfusion occur during cardiac cycle ? where does blood enter through ?

A

occurs during diastole
- enters through aortic sinuses (openings behind the aortic valve leaflets)

42
Q

What is the clever things about circle of willis being a circle ?

A

anastomoses between basilar _ internal carotid arteres
(this provides collateral flow in case one artery is blocked)

43
Q

describe Cushings triad ? what does this indicate ?

A
  • hypertension
  • bradycardia
  • irregular breathing
    (indicates acute elevated ICP)
44
Q

What are the actions of ANP (atrial naturieretic peptide)

A
  • promotes excretion of NA (natriuretic)
  • reduce BP
  • Antagonise angiotensin II
45
Q

What is endothelin ?

A
  • potent long-acting vaso + bronchoconstrictor
  • thought to be involved in pathogenesis of: primary HTN, HF, Raynaud’s
46
Q

What vessel do the coronary arteries branch off from ?

A

branch off from the aorta

47
Q

what are the branches from the aorta ? (3)

A
  • brachiocephalic
  • L common carotid
  • L subclavian
48
Q

at what vertebral level does the pulmonary truck split ? into what ?

A

splits at T5-6 into R + L pulmonary arteries

49
Q

SVC is formed by the merging of which veins ?

A

brachiocephalic veins

50
Q

what forms the R border of the heart ?

A

RA

51
Q

what is the coronary sinus ? opens into where ?

A

recieves blood form the coronary veins and opens into RA

52
Q

what forms majority of anterior border of the heart ?

A

RV

53
Q

what are papillary muscles ? pull on what ?

A

papillary muscles pull on cord tendinae to prevent valve prolapse

54
Q

Describe overview of conducting system of the heart ?

A

AP is created in SAN => wave of excitation spreads across atria => deli at AVN => conduction down bundle of His => purkinje fibres

55
Q

what is the SAN ? where located ? what impact does SNS input have ?

A

collection of specialised pacemaker cells (in RA where SVC enters) which spontaneously generate electrical impulses
- excitation spreads across both atria via gap junctions (atrial systole)
- SNS => increased San firing rate

56
Q

how long AVN delay ? why have this delay ?

A

node delays impulses by 120ms which allows time for atria to fully eject blood before ventricular systole
(lies near coronary sinus)

57
Q

what is bundle of His ?

A

continuation of AVN dividing into 2 main bundles
(RBB conducts impulse to purkinje fibres of RV)

58
Q

which part of the heart has fastest conduction rate ?

A

purkinje fibres

59
Q

What is the pericardium ?

A

fibroserous, fluid filled sack that surrounds the hearts + roots of the great vessels

60
Q

describe the two layers to the pericardium ?

A
  • tough external fibrous pericardium
  • internal serous pericardium (sub divided into visceral + parietal layers with pericardial cavity in between which contains small amount of lubricating serous fluid to minimise heart friction)
    (fibrous layer => serous parietal layer => serous fluid => serous visceral layer)
61
Q

functions of the pericardium ? (4)

A
  • fixes the heart in places
  • prevents overfilling
  • lubrication
  • protection from infection
62
Q

what is the innervation of the pericardium ? where referred pain ?

A

phrenic nerve (C3,4,5)
- referred pain: shoulder pain

63
Q

how many cusps does the pulmonary valve have ? aortic valve ?

A

semilunar valves
- pulm valve (3 cusps)
- aortic valve (3 cusps)

64
Q

where do the Coronary arteries arise from ? when do they fill ?

A

L + R coronary arteries arise form the L + R aortic sinuses (small openings behind the L + R flaps of the aortic valve)
- fill during diastole

65
Q

describe the veinous drainage of the heart ?

A

venous drainage mostly through coronary sinus
- cardiac veins => coronary sinus => RA

66
Q

ECG changes ssen in II, III, aVF. what artery occluded ?

A

RCA (inferior)

67
Q

ECG changes ssen in V3 + V4. what artery occluded ?

A

Distal LAD (anteroapical)

68
Q

ECG changes ssen in V1 + V2. what artery occluded ?

A

LAD (anteroseptal)

69
Q

ECG changes ssen in I, aVL, V5, V6. what artery occluded ?

A

circumflex artery

70
Q

describe the ECG changes ? (like slow mo described)

A

V1-2: septal
V3-4: anterior
V5-6: Lateral
II,III, aVF: Inferior
I, aVL: Lateral

71
Q

give examples for each of these categories of tachycardia:
- narrow regular
- narrow irregular
- wide regular
- wide irregular

A
  • Narrow regular: sinus tachycardia, atrial flutter, paroxysmal SVT
  • narrow irregular: AFib, AFlut with variable block
  • Wide regular: monomorphic Vent tachycardia
  • Wide irregular: Polymorphic Vent tachycardia (TdP), ventricle fib
72
Q

normal PR interval ?

A

<200ms

73
Q

what class drug is amiodarine ? what does it do ?

A

class III anti-arryhtmic
- prolongs cardiac action potential

4 - Med (12 decks)

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