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Case 4 > Pcs Background > Flashcards

Pcs Background Flashcards

(49 cards)

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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

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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

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A

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

22
Q

Afterload definition

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A

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

23
Q

Factors affecting afterload

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A

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

24
Q

Pheochromocytoma

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A

Neuroendocrine tumor of the medulla which secreted lots of cutecholamines

Symptoms - sweating
Abdominal pain
Rapid HR
Increased blood pressure

25
Affect of increased afterload on preload
Increased afterload Decreased stroke volume Increased LVEDP increased preload
26
Vagal withdrawal definition
Deactivation of the parasympathetic system to permit HR to rise to SA nose natural rhythm of 100bpm
27
P wave?
Depolarisation of atria in response to SA node Atrial fibrillation- p waves not seen on ECG as they are too rapid
28
PR interval
Ventricle filling Normally 0.12-0.20 seconds Decrease. Pre excitation syndrome Increase. Conduction blocks
29
QRS complex
Depolarisation of ventricles Atrial fibrillation. Irregular and narrow
30
ST segment
Beginning of ventricle repolarisation
31
T-wave
Ventricular repolarisation
32
Pacemaker potential
Funny current Slow positive increase in membrane potential occurring between end and start of action potentials that activates upon hyperpolarisation
33
Parasympathetic affect on pacemaker potential
Hyper polarisation (decreased cAMP) and slower depolarisation causing decreased heart rate
34
Sympathetic affect on pacemaker potential
Reduced repolarisation and more rapid repolarisation (increased cAMP) causing increased heart rate
35
Effective sympathetic stimulation on AVN node
Increase conduction velocity by increasing the polarisation rate therefore action potential conducts rapidly shortening PR interval
36
Conduction rate comparison
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
Total peripheral resistance
Resistance that must be overcome to push blood through circulatory system Calculated by aterial pressure / cardiac output
38
Pulmonary circuit definition and reason
Decreased resistance with increased lumens so no capillaries exchange occurs but there is enough time for gas exchange
39
Parasympathetic stimulation of pacemaker cells mechanism
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
Action potential of cardiac muscle steps phase 4 | Phase 0
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
Action potential of cardiac muscles steps | Phase 1 2 3
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
Conduction through the heart steps
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
sarcomere length normal vs stretched
2.3 nanometers vs 2.6 nanometers
44
What if the Frank Starling mechanism wasn't true
Pressure changes = back flow of blood = oedema Stagnation of blood = tissue fluid leakage Heart transplant patients could not exercise
45
Polycythemia
Increased red blood cells in blood (slow moving) condition caused by anabolic steroids = headache dizziness / cyanosis
46
atrial compliance definition
how easily a chamber of the heart or vessel lumen expands when filled with a volume of blood (increased age = increased compliance)
47
physical factors affecting arterial blood pressure
arterial blood volume | compliance
48
physiological factors affecting arterial blood pressure
cardiac output | total peripheral resistance
49
Mechanisms for blood pressure maintenance (x3)
``` baroreceptors (stetch mediated) constriction and dilation of blood vessels blood volume (hydration state) ```

Case 4 (2 decks)

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