Gsse Cardiac Physiology

Front 1

The influx of what ion causes CARDIAC muscle contraction?

Back 1

Calcium

Front 2

The efflux of what ion causes CARDIAC muscle relaxation?

Back 2

calcium

Front 3

Depolarization of the cardiac myocyte opens what receptor, exactly?

Back 3

L type (long acting), voltage gated (hence depolarization) calcium chanels open to allow calcium influx.

Front 4

The influx of calcium from outside the cell into the cytoplasm of a cardiac myocyte triggers what?

Back 4

Calcium induced calcium release (from the sarcoplasmic reticulum)

Front 5

What receptor is responsible for calcium induced calcium release? Is it voltage of ligand gated?

Back 5

Ranyodine receptor, its ligand gated (Calcium IS the ligand)

Front 6

After the Calcium induced calcium release, what is the next thing that happens in the excitation contraction process or CARDIAC myocytes?

Back 6

Intracellular calcium binds with troponin.

Front 7

Calcium binding with troponin in CARDIAC myocytes causes

Back 7

actin and myosin binding.

Front 8

What are the 3 mechanisms through which calcium leaves the cardiac myocyte, allowing it to relax?

Back 8

1. Ca2+/Na+ exchanger

2. ca/atp pump cell

3. ca/atp pump sarc reticulum

Front 9

When Ca2+ binds to troponin, why does that allow actin-myosin to contract?

Back 9

conformational change removes tropomysin inhibition of

Front 10

1. Name the receptor for the L type, voltage gated calcium receptor on the cell membrane?

2. Name the receptor for the ligand gated calcium receptor on the sarcoplasmic reticulum

Back 10

1. Dihydropyridine Receptor

2. Ryanodine Receptor

Front 11

Are cardiac myocytes seperate free of one another or fused?

Back 11

They are fused together! Syncitium!

Front 12

What feature identifies cardiac myocytes under the microscope?

Back 12

They have intercalated disks, which appear as dark bands between cells.

Front 13

How do cardiac myocytes communicate with one another?

Back 13

Through GAP junctions in the intercalated disks

Front 14

Where on the cell membrane are the majority of the calcium channels located?

Back 14

In the T-TUBULE - invagination of the sarcolemma (the cell membrane of striated muscle)

Front 15

Does the heart have nicotinic or muscarinic parasympathetic receptors, and exactly what receptor subclass is it?

Back 15

m2 muscarinic

Front 16

Does the parasympathetic innervation have a greater effect on the atria or ventricles?

Back 16

It has very little effect on the ventricles,

the strongest innervation is sa node and av node, so it slows atrial firing.

Front 17

Which can "override", the other, parasympathetic or sympathetic activity in the heart?

Back 17

Parasympathetic, as it has prejunctional receptors on the sympathetic neurons that regulate noradrenaline release

Front 18

What branches of the vagus contribute to the cardiac plexus?

Back 18

Superior cervical cardiac branch

inferior cervical cardiac branch

thoracic cardiac branch

Front 19

Describe the different origins of the left and right inferior cervical cardiac branches

Back 19

Left recurrent laryngeal nerve

right main vagus

Front 20

What nucleus provides parasympathetic innervation for the heart?

Back 20

dorsal vagal nucleus

Front 21

Right vagus vs left vagus which node

Back 21

Right vagal trunk gives off branches for SA node

Left vagus has branches does AV node

Front 22

Superficial cardiac plexus location

Deep cardiac plexus location

Back 22

Superficial - is superficial to aortic arch (sits on it)

Deep - is deep to aortic arch (sits on carina)

Front 23

What makes up the superficial cardiac plexus?

Back 23

Left sympathetic trunk + left vagus trunk (think - right goes deep because theres nothing in the way, just slips down)

left Sympthatetic - superior cervical cardiac branch

left vagus - inferior cervical cardiac branch

Front 24

The superficial cardiac plexus sends branches to?

Back 24

(remember its superficial, so its anterior)

anterior cardiac plexus

anterior left anterior pulmonary plexus

deep plexus

Front 25

What is the resting potential of sinoatrial node cells?

Back 25

THEY HAVE NO TRUE RESTING POTENTIAL!

Front 26

In what phase of the action potential do the PACEMARKET myocytes depolarise? Do they depoarlise in the same phase as the other cells

Back 26

NO DIFFERENT TIME - PACEMAKERS ARE IN PHASE 4!

Front 27

The influx of which ion causes the depolarization of the pacemaker cells?

Back 27

SLOW CALCIUM INFLUX (not fast, and not Na)

Front 28

16. Which of the following does NOT show rapid initial depolarization at the start of an action potential?

A. SA node.B. Atrial muscle.C. Purkinje fibers.D. Ventricular muscle.E. Bundle of His.

Back 28

SA node - the pacemaker cells are relatively slowly depolarized, with slow calcium influx

Front 29

What causes sodium efflux in cardiac myocytes?

Back 29

Still just the na-k pump

Front 30

What happens if you reduce the outward current efflux in cardiac myocyte?

Back 30

Longer action potential

Front 31

What is responsible for starting the diastolic depoloarization phase of the action potential of cardiac myocytes?

Back 31

The funny current

Front 32

What is different about phase 4 of the action potential of pacemaker vs non pacemaker cells?

Back 32

Phase 4 is the resting membrane potential. So for non pacemaker cells its a flat line.

For pacemaker cells its wandering.

Front 33

Describe the 3 currents that contribute to diastolic depolarization in pacemaker cells.

Back 33

1. At -60, funny current

2. At -55 its slow Ca+

3. K+ outflow, which tries to repolarize, is decreased

Front 34

Funny channel sare mediated by ...

Back 34

Slow Na +

Front 35

What is the effective refractory period?

Back 35

period when a new actional potential cannot be generated

Front 36

why does the effective refractory period occur?

Back 36

Because the fast sodium channels are closed until cell fully repolarises

Front 37

What is the absolute refractory period

Back 37

no stimulous is great enough to depolarise the cells

Front 38

What is the duration of cardiac action potential vs skeletal muscle action potential

Back 38

cardiac is at least 200ms

skeletal is 2ms!!!!

Front 39

Where are gap junctions most prevalent

Back 39

In atria and ventricles, as opposed to nodes (so the current spreads)

Front 40

What are gap junctions composed of?

Back 40

2 connexins

Front 41

What are early after depolarizations?

Back 41

They are abnormal depolarizations, early ones occur in phase 2 or 3 of cardiac action potential

Front 42

what can early after depoliarzations cause?

Back 42

Torsades, tachycardia

Front 43

In which of the following do Early After Depols occur more frequently and why?

A. Atrial fibers.

B. SA node

C. AV node

D. Purkinje fibers.

Back 43

Purkinje because of long action potential

Front 44

Aetiology of early after depolarization in phase 2, and phase 3? Clinical Causes?

Back 44

2 - calcium channels opening pathological

3 - na channels opening pathological

hypokalaemia,

any drug extending qr

Front 45

Definition, aetiology and clinical cause of delayed after depolization?

Back 45

When depolarization happens in phase 4 of action potential. Causes by to much cytosolic (in the cell calcium!) ER randomly releases calcium! Most common cause is digoxin toxicity.

Classic presentation bidirectional VT

Front 46

What is calciquestrin?

Back 46

Best name ever.

its a protein in the SR that helps keep calcium there. Hence its name...

CALCIum seQUESTRATION

Front 47

How does an ECG measure the action potential duration of the ventricle myocytes?

Back 47

Thats what QT interval is

Front 48

Whats the difference between isometric and isotonic cardiac contractions?

Back 48

Isometric - no change in length

isotonic - get shorter

Front 49

What explains the positive length-tension relationship?

Back 49

Greater sarcomere length, more actin-myosin cross bridges formed.

Front 50

How do compliant vessels reduce blood pressure?

Back 50

Because as they expand, they dissipate some of the pressure. If stiff, it all remains as blood pressure.

Front 51

Why do we need a coronary circulation?

Back 51

Because straight up diffusion of blood from left ventricle to underlying myocytes would take 15 hours!!!!

Front 52

What percentage of the blood do the kidneys get, and what percentage of oxygen consumption?

Back 52

20% blood, 6% oxygen

Front 53

myocardium, what percentage of blood flow does it get, what percentage of o2 does it consume?

Back 53

Gets only 4% consumes 10% of the o2

Front 54

Why does the pulmonary system have a much lower resistance than the systemic circulation?

Back 54

Shorter circuit needs less pressure has less resistance. (around 15% of SVR)

Front 55

How does lung disease cause pulmonary hypertension?

Back 55

Pulm vasc resistance is lowest at residual capacity. When lungs hyperinflated, stretch the extra-alveolar vessel, narrows diameter, increases the resistance, increases the pressure!

Front 56

Which is higher, brachial artery systolic pressure or aortic artery systolic pressure?

BA MAP or aorta MAP higher?

Back 56

Aorta MAP higher.

But Brachial artery systolic higher, as pressure waveform changes!!!

Front 57

Vessels like the aorta have lots of what to be elastic for the stroke volume?

Back 57

Elastin in walls!

Front 58

What defines the 3 layers of a blood vessel

Back 58

There are 2 interlying sheets of elastin!

external and internal elastic lamella

Front 59

How does the structural makeup at a protein level of the capillary differ from the other blood vessels?

Back 59

They all contain types 1-4 collagen,

capillaries only contain type 4

Front 60

Which layer of an arteriole has the smooth muscle?

Back 60

tunica media

Front 61

Blood flow is slowest through which vessels?

Back 61

Capillaries, even slower than venules

Front 62

veins: arteries, distribution of total blood at anyone time?

Back 62

2/3 : 1/3

Front 63

What 2 anatomical pathways help shunt blood form

Back 63

Atria - fossa ovalis

pulmonary trunk - ductus arteriosis

Front 64

When does the 1st heart sound occur in terms of the heart cycle?

Back 64

The m and t valves shut at the beginning or isovolumetric contraction

Front 65

How much of the blood normally leaves the left ventricle

Back 65

Ejection fraction is 2/3's

Front 66

When does ventricular filling begin in terms of heart cycle?

Back 66

When the M and T valves open = at the End of the isovolumetric relaxation phase!

Front 67

Do both ventricles have the same stroke volume?

Back 67

Yes

Front 68

What is the oxygen saturation of venous compared to arterial blood?

Back 68

Its about 3 quarters. Unbelieve!

Front 69

Pulmonary circulation blood pressure?

Back 69

Systolic around 25mmhg!

Front 70

Ok, what does isovolumetric contraction mean?

Back 70

That both inlet and outlet coronary valves are closed!!!!

Front 71

Isovolumetric contraction is associated with?

3 things

Back 71

1. First heart sound

2. Falling pressure in the aorta

3. c wave in the right atrium

Front 72

Name the 7 parts of the cardiac cycle

Back 72

atrial contraction

isovolumetric contraction

rapid ejection

reduced ejection

isovolumetric relaxation

rapid filling

reduced filling

Front 73

Which increases ventricular pressure faster? Isovolumetric contraction or rapid ejection?

Back 73

Isovolumetric contraction- the pressure is rising against a closed valve

Front 74

T/F - the aortic valve stays open for some time after the ventricular pressure has fallen below aortic pressure?

Back 74

TRUE: because the escaping blood has to be decelerated to zero before the valves close

Front 75

What is the ventricular end diastolic volume and end diastolic pressure?

Back 75

120mls and 12mmHG

Front 76

What causes a 4th heart sound

Back 76

Its the vibration of the atrial contraction, transmitting to a stiff ventricle

(think about how a loose guitar string doesn't make a noise, then you tighten it to produce a noise)

Front 77

end diastolic volume is recorded during which phase of cardiac cycle?

Back 77

PHASE 1 - atrial contraction

after atria contracts, the pressure gradient over av valves flips, ventricles are sucked upwards and this is the end diastolic volume (think, they're just about to contract)

Front 78

Where in the cardiac cycle is the T wave?

Back 78

REDUCED EJECTION

- repolarization means reduced tension

- lower tension means lower rate of ejection

Front 79

During Reduced Ejection, what happens to atrial pressure?

Back 79

Its gradually rising, ongoing return from lungs

Front 80

When do the heart sounds occur?

Back 80

S1 - Begining of isovolumetric contraction

S2 - beginning of isovolumetric relaxation

Front 81

End systolic Volume is record during which phase of the cardiac cycle? and what is it?

Back 81

the 2 "isometrics" occur with the 2 heart sounds and with the 2 "volumes"

end systolic occurs at stage 5, isovolumetric relaxation. its about 50mls

Front 82

When does the v wave occur in cardiac cycle?

Back 82

V wave occurs because of V for Venous inflow from lungs, against a CLOSE AV valve. So stage 5, isovolumetric relaxation

Front 83

Y descent occurs during?

Back 83

Rapid Filling, because the AV valves open

Front 84

in relation to the heart sounds the palpated pulse occurs....

Back 84

in between s1 + s2

Front 85

ventricular contraction coincides with what section of the ecg?

Back 85

sT segmenet

Front 86

During the rapid filling phase, are there any valves opening?

Back 86

AV valves

Front 87

When does the aortic valve close?

Back 87

onset of isometric relaxation

Front 88

What are valves made of?

Back 88

Fibrous tissue covered by endothelium

Front 89

Why is splitting heart sound increased by inspiration?

Back 89

ups right, lowers left ventricular filling

Front 90

T/F pacemaker cells are the only cells that depolarize spontaneously?

Back 90

Purkinje cells can do it too!!!

Front 91

The myocardium conducts electrical current straight from a to v?

Back 91

The fibrotendinous ring blocks that

Front 92

whats "dominance" in cardiac physiology?

Back 92

faster cells dominate other pacemakers

Front 93

What causes muscle striations?

Back 93

These light and dark bands on microscopy are caused by the orderly overlapping of actin and myson

Front 94

Whats the thick filaments made of?

Back 94

400 myosins

Front 95

What are thin filaments made of?

Back 95

Actually 3 things!

Chains of F actin, with random bits of G actin that contain the myosin binding site. With the troponomysin (blocking) and troponin (unblocking)

Front 96

Describe the troponin complex

Back 96

3 troponin subunits

t - binds to tropomysin

i - is the actually inhibitor troponin of a-m binding

c - is the calcium binding site

Front 97

What is digoxins main mode of action, how does it cause DAD's?

Back 97

It blocks the na+k atpase pump, so increases sodium concentration.

Hence reduces gradient driving na-ca exchanger, so calcium increases too

Front 98

In non pacemaker, ventricular myocyte, the resting membrane potential is generated chiefly by?

Back 98

K+ efflux, diffusion.

Front 99

What causes the long plateau of the cardiac myocyte non pacemaker action potential?

Back 99

Calcium channels and the na-ca calcium exchanger

Front 100

Describe major anion movement at

4

1

0

2

3

Back 100

4 - K influx

0 - na influx

1 - k efflux, cl out

2- k efflux, ca influx

3 - k efflux

Front 101

MIND BLOWN: WHY IS THE T WAVE UPRIGHT

Back 101

double negative.

depolarises down axis then

repolarise up axis.

as subepicardial have shorter action potential than subendocardial myocytes!

Front 102

How does beta adrenergic stimulation affect non pacemaker cardiac myocyte?

Back 102

increases plateau calcium influx, so that the action potential has a hump

Front 103

What causes repolarisation in non-pacemaker cardiac myocytes?

Back 103

Passive outward k current

Front 104

What affect does adrenergic stimulation have on calcium in the cardiac myocyte?

Back 104

stimulates sr pump

increases calcium through ca channels of sarcolemma

Front 105

how does caffeine work?

Back 105

inhibits phosphodiesterase 3, normally breaks down camp. Increased cystostolic camp increased

Front 106

do cells depolarize faster at 39 or 37 degrees?

Back 106

39, hence fever causes tachycardia

Front 107

Why does the Sa node have a resting membrane potential of -60, whereas other atrial and ventricular non-pacemaker cardiac myocytes have a resting membrane potential of -80?

Back 107

no inward rectifier K+ channels

Front 108

In diastole is the pacemaker cardiac myocyte membrane more permeable to na+ or k+

Back 108

Its negative potential in diastole. k+ is negative potential, na is positive. Nernst says, if negative equilibrium potential, must be closer to K+ equilibrium potential, hence must be more permeable to k+

Front 109

Pacemaker cells and potassium rectifier channels.

Back 109

Pacemakers do have a delayed rectifier (this kicks the depolarization off). They don't have an inward rectifier K+ channel)

Front 110

What is funny about the funny sodium channels of the pacemaker cells?

Back 110

its activated by hyperpolarizing, not depolarizing the membrane!

Front 111

What causes the action potential of the pacemaker cells of the cardiac myocytes?

Back 111

inward calcium influx. These are through voltage gated L and T types (hence require the funny na+ first.

Front 112

delayed rectifier k+ channel, how does it get its name?

Back 112

Once the cardiac pacemaker myocytes are depolarizes, the "rectifing" voltage-gated K+ chanel starts to work. Very slowly, hence its effective is delayed.

Front 113

Where is the AV node?

Back 113

In the atria, in the atrial septum

Front 114

Purkinje cells:

wide or narrow

fast or slow conduction

what do they excite first?

Back 114

widest cells, makes them incredibly fast

They excite intraventricular septum

Front 115

Desmosomes vs Gap junctions

Back 115

desmosomes - nonconducting rivets

gap junctions, are conducting

Front 116

lusitropic effect

"loosey" tropic effect is what?

Back 116

how sympathetic fibres, increase the rate of cardiac relaxation!

by inhibiting phospholamban to disinhibit the sr calcium store

Front 117

What is maximum normal human heart rate?

Back 117

200

Front 118

atropine mode of action? (you saw it used when the hR went to 30 the other day)

Back 118

it blocks vagal stimulation.

blocks acetyl choline

it blocks m2 muscarinic ACh receptors

Front 119

Acetylcholine effect on heart

Back 119

hyperpolarises membrane potential of sa node, via its own ligand gated Kach channel

Front 120

what causes sinus arythmia

Back 120

cardiac vagal neuron control is modulated by the neurons controlling breathing. Expiration slows the heart rate!!!!! (remember for arrythmia)

Front 121

how does hyperkalaemia affect the heart?

Back 121

it makes the resting membrane potential less negative. That partial depolarization, locks a portion of the voltage gated na+ channels to reduce the amplitude of the action potential

Front 122

increased blood co2, effect on BP?

Back 122

Increases! carbonic anydride inhibitor for retrinal artery stroke remember!

Front 123

fick's principle

Back 123

cardiac output = o2 consumption/a-v difference

Front 124

a wave

Back 124

Atrial contraction

Front 125

C wave

Back 125

TriCuspid bulging into atria from Vent Contraction

caused by isovolumetric contraction of ventricle

Front 126

x wave

Back 126

atrial relaXation

Front 127

v wave

Back 127

venous filling

Front 128

y wave -

Back 128

rapid emypting, tricupsid "y"-ed open

Front 129

Fastest conduction in heart?

Back 129

purkinje fibres

Front 130

dicrotic notch

Back 130

closure of the aortic valve

Front 131

how do you calculate resistance in vessels?

What is learn from this?

Back 131

reciprocal of the total = sum of recipirocal of individuals

explains how parallel vessels together have very low resisance

Front 132

What increases cerebral blood flow:

a) exercise

b) strenuous mental activity

Back 132

a) mental activity

exercise does nothing!

Front 133

What two factors influence pulse pressure

Back 133

stroke volume and aortic compliance

Front 134

Cause of low pulse pressure

Back 134

decreased stroke volume, (decreased preload)

Front 135

Effect of exercise on pulse pressure

Back 135

increases it as stroke volme increases

Front 136

total peripheral resistance and exercise

Back 136

tpr decreased whilst exercising

Front 137

Systemically administered norepinephrine

Back 137

reflex bradycardia

α-adrenergic effects on systemic vasculature exceed the effects of β1-adrenergic effects on the heart

Front 138

what happens to renal blood flow during exercise?

Back 138

reduces

Front 139

What causes the cardiac action potential (non-pacemaker)

Back 139

fast sodium, slow calcium

Front 140

why is the cardiac action potential so long?

Back 140

slow calcium, depol immediately stops k+ efflux

Front 141

What stimulates vasopressin?

Back 141

DECREASES right atrial pressure

Front 142

whats the range for pr interval?

Back 142

.16-.20

Front 143

AV nodal delay is caused by?

Back 143

increased resting membrane potential (-85)

Front 144

first physiology conduction change in myocardium just seconds after ami?

Back 144

rapid repolarisation

Front 145

fast response action potential is seen in which type of cardiac myocyte?

Back 145

ventricular myocyte

Front 146

Bundle branch block is caused by damage do which cell types of cardiac myocytes?

Back 146

purkinje fibres

Front 147

do pulse waves travel at the same speed as the blood flow?

Back 147

No about ten times faster

Front 148

Purkinje fibres go base or apex first for spread of conductance?

Back 148

apex, then base

Front 149

3 things that increase turbulence in blood

Back 149

increased flow

increased vessel diameter

increased density (decreased viscosity)

Front 150

why do you get bruits with anaemia?

Back 150

decreased viscosity

increased velocity!

INCREASED TURBULENCE

Front 151

True or false, the further from the heart, the more turbulent the blood flow?

Back 151

with decreasing vessel diameter and decreasing flow it decreases. False

Front 152

Adrenaline vs noradrenaline administration.

effect on skletal blood flow

effect on renal blood flow

effect on pulse rate

effect on diastolic pressure

effect on skin blood flow

Back 152

reduce renal and skin blood flow

adrenaline increases heart rate

noradrenaline decreases heart rate

norad raises diastolic pressure

adrenaline lowers diastolic pressure

adrenaline inc. muscle blood flow

noradrenaline red. muscle blood fow

Front 153

Chronic hypoxia causes hypertension?

Back 153

causes pulmonary hypotension, and systemic vasodilation

Front 154

Aldosterone increases or decreases blood pressure?

Back 154

inc: salt and water retention

Front 155

Right ventricle hypertrophy ECG

Back 155

high voltage R waves

Front 156

What pulmonary capillary pressure is required for pulmonary oedema?

Back 156

Pressure has to rise from 5-15mmhg to 25mmhg to overcome the plasma oncotic pressure

Front 157

Hypoxia and hypercarbia (t1 resp failure). Vasoconstricts or vasodilates pulmonary vessels? Systemic vessels?

Back 157

Hypoxia Vasoconstricts pulm! Hypercarbia dilates systemically

Front 158

Which valve causes a huge pulse pressure

Back 158

Aortic Incompetence

Front 159

What happens to coronary vascular resistance during exercise?

Back 159

It falls

Front 160

Ventricular extrasystole - why does it fail to produce a pulse at the risk

Back 160

if it occurs during diastole,

poor filling, no pulse

Front 161

Atherosclerosis, hardening of the arterial walls, affects the bp how?

Back 161

Increases the systolic blood pressure -> less absobred

Decreases the diastolic blood pressure, no rebound

-> widens the pulse pressure

Front 162

What happens to the jvp in complete heart block?

Back 162

The A and C pulses occur together - atrial and ventricular contraction

Front 163

Why does orthopnea occur?

Back 163

Because theres an increase in venous return, worsens venous congestion

Front 164

Hyperventilation does what to cerebral vascular resistance?

Back 164

Increases it. Decreases cerebral capilary pressure so less cerebral oedema.

Front 165

Where does the baroreceptor reflex increase the peripheral vascular resistance the most?

Back 165

Splanchnice circulation

Front 166

What determines flow of liquid through a tube?

Back 166

Pressure gradient and resistance

Front 167

What determines resistance of liquid through a tube?

Back 167

viscosity, radius and length

Front 168

What happens to 2-3 dgp in transfusion red blood cells

Back 168

fall, not undergoing any glycolysis

Front 169

Why is the MAP calculated with 1/3 of systolic bp?

Back 169

cause its only in systole 1/3 ;)

Front 170

What percentage of oxygen does the cardiac myocytes extract from blood

Back 170

70%