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Case 4 > Pcs Background > Flashcards

Pcs Background Flashcards

1
Q

Frank starling mechanism

A

Ability of the heart to change its force of contraction and stroke volume in response to change in venous return to maintain blood pressure levels

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2
Q

what is Left ventricular end diastolic pressure determined by / definition

A

Determined by left ventricular preload - pressure at the end of diastole normally 0-140 ml

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3
Q

Stroke work =

A

Stroke volume x mean arterial pressure

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4
Q

what is Preload

A

Initial stretching of sarcomeres in cardiomyocytes prior to contraction

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5
Q

Factors affecting preload

A

Decreased HR caused by increased ventricular filling time lowering VEPD

Increased atrial contractility

Increased central venous pressure caused by increased blood volume leading to increase VEPD

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6
Q

Positive inotropic effect

A

Increased strength of heart contractions so the heart can pump more blood with fewer beats

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7
Q

Negative inotropic effect

A

Weakening of heart contractions and slowing of HR

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8
Q

Myocardial contractility

A

Intrinsic ability of heart and myocardium to contract at given prevailing afterload

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9
Q

Chronotrophy definition

A

Affect on heart rate

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10
Q

Dromotrophy definition

A

Rate of conduction through AV nodes

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11
Q

Inotrophy definition

A

Contractility of the heart

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12
Q

Lusitrophy definition

A

Removal of Ca2+ to the endoplasmic reticulum prompting myocardium relaxation following excitation-contraction coupling

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13
Q

Effect of epinephrine on the heart

A

POSITIVE
Increase in heart rate and dilation of blood vessels causing GDP to GTP activating Gs alpha subunits causing the cAMP cascade resulting in the heart becoming more responsive to Ca2+

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14
Q

Effect of caffeine on the heart

A

POSITIVE

Inhibitor of cAMP PDE (breakdown enzyme) so the cAMP remains active for longer - mimicking effect of epinephrine

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15
Q

Calcium channel antagonist mechanism

A

NEGATIVE

Bonds to L type calcium channels causing vasodilation decreased HR and decreased conduction velocity

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16
Q

Side effects of beta adrenoreceptors

A

Cold hands
Nausea
Diarrhoea

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17
Q

Side effects of calcium channel antagonists

A

Flushed face
Headaches
Skin rash

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18
Q

Phosphodiesterase mechanism

A

POSITIVE

PDE 3 inhibitor of cAMP PDE like caffeine causing reduced arterial pressure

PDE 5 causing increased cGMP leading to vasodilation
Increasing inotrophy chronotrophy and dromotrophy

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19
Q

Digitalis mechanism

A

POSITIVE

inhibitor of the Na K ATPase channel leading to increased Na outside the cell and increased K inside the cell leading to increased calcium inside the cell so more is available to the muscles to bind to troponin C leaving to increased contractility

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20
Q

Phospholamban

A

Reversible inhibitor of sarcoplasmic reticulum calcium pump leading to increased Ca uptake speed a lusitrophic response

Mutation - dilated cardiomyopathy and heart failure

21
Q

Troponin 1 relaxed function

A

Blocks actin attatchment site preventing contraction - can be moved by Ca2+

22
Q

Afterload definition

A

Pressure against which the heart must work to eject blood during systole (systolic pressure)

23
Q

Factors affecting afterload

A

Internal radius of boood vessels
Whole body blood pressure
Volume of blood

24
Q

Pheochromocytoma

A

Neuroendocrine tumor of the medulla which secreted lots of cutecholamines

Symptoms - sweating
Abdominal pain
Rapid HR
Increased blood pressure

25
Q

Affect of increased afterload on preload

A

Increased afterload
Decreased stroke volume
Increased LVEDP
increased preload

26
Q

Vagal withdrawal definition

A

Deactivation of the parasympathetic system to permit HR to rise to SA nose natural rhythm of 100bpm

27
Q

P wave?

A

Depolarisation of atria in response to SA node

Atrial fibrillation- p waves not seen on ECG as they are too rapid

28
Q

PR interval

A

Ventricle filling
Normally 0.12-0.20 seconds
Decrease. Pre excitation syndrome
Increase. Conduction blocks

29
Q

QRS complex

A

Depolarisation of ventricles

Atrial fibrillation. Irregular and narrow

30
Q

ST segment

A

Beginning of ventricle repolarisation

31
Q

T-wave

A

Ventricular repolarisation

32
Q

Pacemaker potential

A

Funny current
Slow positive increase in membrane potential occurring between end and start of action potentials that activates upon hyperpolarisation

33
Q

Parasympathetic affect on pacemaker potential

A

Hyper polarisation (decreased cAMP) and slower depolarisation causing decreased heart rate

34
Q

Sympathetic affect on pacemaker potential

A

Reduced repolarisation and more rapid repolarisation (increased cAMP) causing increased heart rate

35
Q

Effective sympathetic stimulation on AVN node

A

Increase conduction velocity by increasing the polarisation rate therefore action potential conducts rapidly shortening PR interval

36
Q

Conduction rate comparison

A

AVN Slow conduction allowing depolarisation and contraction time

Bundle of hiss rapid induction

Purjinke fastest conduction long distance so need to increase diameter and increase conduction speed

37
Q

Total peripheral resistance

A

Resistance that must be overcome to push blood through circulatory system

Calculated by aterial pressure / cardiac output

38
Q

Pulmonary circuit definition and reason

A

Decreased resistance with increased lumens so no capillaries exchange occurs but there is enough time for gas exchange

39
Q

Parasympathetic stimulation of pacemaker cells mechanism

A

ACh released increases permeability of the membrane to potassium ions this decreases membrane potential so long it is needed to reach threshold potential decreasing action potentials per unit time

40
Q

Action potential of cardiac muscle steps phase 4

Phase 0

A

Phase 4
Calcium and sodium channels closed
Potassium channels open and stable depolarisation occurs
T type calcium channels

Phase 0
Rapid sodium influx through open fast sodium channels
L-type calcium channels open

41
Q

Action potential of cardiac muscles steps

Phase 1 2 3

A

1
Transient potassium channels open potassium Efflux = 0mv

2
Influx of calcium through L type channels balance by potassium efflux by delayed rectifier K+

3
Calcium channels close but delayed rectifier potassium channels remain open to return membrane potential to -90 mV

42
Q

Conduction through the heart steps

A

1 the AV node generates the action potential
2 the wave of excitation travels through atria walls causing contraction travels to do the left side through Bachman bundle
3.the AV node causes the delay to allow complete ejection of blood from the ventricles
4. The excitation travels down bundles of his
5. Contraction of the ventricles
The SA node = pacemaker cells that create an excitation which travels via gap junctions

43
Q

sarcomere length normal vs stretched

A

2.3 nanometers vs 2.6 nanometers

44
Q

What if the Frank Starling mechanism wasn’t true

A

Pressure changes = back flow of blood = oedema
Stagnation of blood = tissue fluid leakage
Heart transplant patients could not exercise

45
Q

Polycythemia

A

Increased red blood cells in blood (slow moving) condition caused by anabolic steroids = headache dizziness / cyanosis

46
Q

atrial compliance definition

A

how easily a chamber of the heart or vessel lumen expands when filled with a volume of blood (increased age = increased compliance)

47
Q

physical factors affecting arterial blood pressure

A

arterial blood volume

compliance

48
Q

physiological factors affecting arterial blood pressure

A

cardiac output

total peripheral resistance

49
Q

Mechanisms for blood pressure maintenance (x3)

A 
baroreceptors (stetch mediated)
constriction and dilation of blood vessels 
blood volume (hydration state)

Case 4 (2 decks)

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