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4 - Med > Cardiology - Physiology > Flashcards

Cardiology - Physiology Flashcards

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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 atria 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 SV ?

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
what is laminar flow ? describe it
velocity is highest in centre of vessel and lower closer to vessel wall (due to increased resistance)
26
where is turbulent blood flow more likely ?
when vessel branched/constricted => rougher flow (bifurcations, atheroslecrotic)
27
What is resistance to blood flow dependant on ? (3) high or low of each of these increase resistance ? what law ?
dependant on - radius (increase) - viscosity (decrease) - vessel length (decrease)
28
what is virchows triad ? what are the 3 factors ?
3 factors that reduce flow => increase thrombus risk - stasis of blood flow - hypercoagulability - vessel wall injury
29
What is BP equal to ?
CO x TPR (flow x resistance)
30
what is short term BP regulation controlled by ? detected by what ?
controlled by autonomic NS - baroreceptors detect BP
31
What happens when there is increased baroreceptor firing ? what innervation ? what affect on BP does this have ?
increased firing => (medulla oblongata) PSNS via X nerve => reduce HR => reduce CO => reduce BP
32
what is involved in long term BP regulation ? (2) explain a bit
- RAAS: reinin is released in response to SNS stimulation - ADH: produced in hypothalamus + stored/released from AP => increased water reabsorption
33
what are some of the complications of long term high BP ? (3)
- Macrovasc (storke, MI) - Microvasc (neph/retinopathy) - Heart (increase afterload => LV hypertrophy, dilated cardiomyopathy => HF)
34
What is Ficks law ?
rate of diffusion is proportional to conc difference + area available (capillary exchange) - capillaries have large SA + steep conc gradient + short diffusion pathway
35
what are starling forces ? name the 4
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
what is kwashiorkor ? pathophys explain
malnutrition + low albumin => low oncotic pressure => muscles wasting + oedema (thin extremities + distended albumin)
37
what cells regulate arteriolar tone ?
smooth muscles cells in tunica media
38
describe the pressure in veins vs arteries ?
- Veins: low pressure, low resistance - Arteries: high pressure, high resistance
39
do veins or arteries have higher capacitance ? what does this mean ?
veins have high capacitance (can distend with increasing BP)
40
what is CVP ? where is is measured from ?
Central venous pressure (CVP) is the BP in the vena cava (near RA)
41
What does coronary vessel perfusion occur during cardiac cycle ? where does blood enter through ?
occurs during diastole - enters through aortic sinuses (openings behind the aortic valve leaflets)
42
What is the clever things about circle of willis being a circle ?
anastomoses between basilar _ internal carotid arteres (this provides collateral flow in case one artery is blocked)
43
describe Cushings triad ? what does this indicate ?
- hypertension - bradycardia - irregular breathing (indicates acute elevated ICP)
44
What are the actions of ANP (atrial naturieretic peptide)
- promotes excretion of NA (natriuretic) - reduce BP - Antagonise angiotensin II
45
What is endothelin ?
- potent long-acting vaso + bronchoconstrictor - thought to be involved in pathogenesis of: primary HTN, HF, Raynaud's
46
What vessel do the coronary arteries branch off from ?
branch off from the aorta
47
what are the branches from the aorta ? (3)
- brachiocephalic - L common carotid - L subclavian
48
at what vertebral level does the pulmonary truck split ? into what ?
splits at T5-6 into R + L pulmonary arteries
49
SVC is formed by the merging of which veins ?
brachiocephalic veins
50
what forms the R border of the heart ?
RA
51
what is the coronary sinus ? opens into where ?
recieves blood form the coronary veins and opens into RA
52
what forms majority of anterior border of the heart ?
RV
53
what are papillary muscles ? pull on what ?
papillary muscles pull on cord tendinae to prevent valve prolapse
54
Describe overview of conducting system of the heart ?
AP is created in SAN => wave of excitation spreads across atria => deli at AVN => conduction down bundle of His => purkinje fibres
55
what is the SAN ? where located ? what impact does SNS input have ?
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
how long AVN delay ? why have this delay ?
node delays impulses by 120ms which allows time for atria to fully eject blood before ventricular systole (lies near coronary sinus)
57
what is bundle of His ?
continuation of AVN dividing into 2 main bundles (RBB conducts impulse to purkinje fibres of RV)
58
which part of the heart has fastest conduction rate ?
purkinje fibres
59
What is the pericardium ?
fibroserous, fluid filled sack that surrounds the hearts + roots of the great vessels
60
describe the two layers to the pericardium ?
- 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
functions of the pericardium ? (4)
- fixes the heart in places - prevents overfilling - lubrication - protection from infection
62
what is the innervation of the pericardium ? where referred pain ?
phrenic nerve (C3,4,5) - referred pain: shoulder pain
63
how many cusps does the pulmonary valve have ? aortic valve ?
semilunar valves - pulm valve (3 cusps) - aortic valve (3 cusps)
64
where do the Coronary arteries arise from ? when do they fill ?
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
describe the veinous drainage of the heart ?
venous drainage mostly through coronary sinus - cardiac veins => coronary sinus => RA
66
ECG changes ssen in II, III, aVF. what artery occluded ?
RCA (inferior)
67
ECG changes ssen in V3 + V4. what artery occluded ?
Distal LAD (anteroapical)
68
ECG changes ssen in V1 + V2. what artery occluded ?
LAD (anteroseptal)
69
ECG changes ssen in I, aVL, V5, V6. what artery occluded ?
circumflex artery
70
describe the ECG changes ? (like slow mo described)
V1-2: septal V3-4: anterior V5-6: Lateral II,III, aVF: Inferior I, aVL: Lateral
71
give examples for each of these categories of tachycardia: - narrow regular - narrow irregular - wide regular - wide irregular
- 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
normal PR interval ?
<200ms
73
what class drug is amiodarine ? what does it do ?
class III anti-arryhtmic - prolongs cardiac action potential

4 - Med (21 decks)

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