Cardiovascular Physiology 2-3 Flashcards

1
Q

Electrocardiogram 3 leads

A

-/- right arm
+/+ left leg
+/- left arm

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2
Q

P wave

A

Beginning of atrial contraction (systole), wave of depolarisation travels from the SA node towards the AV node

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3
Q

QRS complex

A

Beginning of ventricular contraction, the time for depolarisation to spread. Covers the wave that would be atrial repolarisation.

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4
Q

T wave

A

Ventricular repolarisation

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5
Q

P-Q interval

A

The time for the electrical excitation of the atria to reach the ventricles, usually slows through the AV node due to thicker fibers. (0.16 sec normal).`

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6
Q

Q-T interval

A

Duration of ventricular contraction (0.35 sec normal)

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7
Q

Einthoven’s triangle

A

Heart at the center, 3 electrodes from arms to legs.

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8
Q

Causes of cardiac arrhythmias

A

abnormalities in the rhythmicity conduction system of the heart:
- abnormal pacemaker activity
- ectopic pacemakers
- blocks
- abnormal pathways for impulses
- spontaneous generation of spurious impulses.

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9
Q

Sound 1

A

Closure of the AV valves

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10
Q

Sound 2

A

Closure of the pulmonary and aortic valves

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11
Q

S3 and S4

A

Early ventricular filling and atrial contraction

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12
Q

Atrial systole

A

From P-Q, atrial pressure remains low and ventricular pressure increases until the mitral valve closes.

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13
Q

Ventricular systole

A

Isovolumic contraction as blood volume remains constant until the pressure is greater than that of the aorta, opening the aortic valve.

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14
Q

Isovolumetric phases

A

Contraction - when the mitral valve has closed, until the aortic valve opens.
Relaxation - when the aortic valve closes, until the mitral valve reopens.

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15
Q

Stroke volume

A

amount of blood pushed into systemic circulation by ventricular contraction.
EDV - ESV, usually = 70mL

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16
Q

Cardiac output

A

= heart rate x stroke volume

17
Q

Ejection fraction

A

The fraction of blood that was ejected during cardiac systole.
= (EDV - ESV) / EDV ~ 50-70% but goes up with exercise.
Indicates cardiac contractility.

18
Q

Parasympathetic innervation of the SA/AV node

A

Sparse by releasing ACh on to muscarinic receptors.
Increases K efflux, and decreases Ca influx to HYPERPOLARISE the cell.

19
Q

Sympathetic innervation of the SA/AV node

A

Rich by release NE on to β1 adrenergic receptors.
Increases both NA and CA influx to DEPOLARISE the cell.

20
Q

Resting condition

A

Parasympathetic discharge dominates because ACh suppresses sympathetic activity and the release of NE from nearby nerve endings.

21
Q

Atropine

A

Muscarinic receptor antagonist - blocks parasympathetic effects and increases heart rate.

22
Q

Propranolol

A

β-adrenergic receptor antagonist that blocks sympathetic effects and decreases heart rate.

23
Q

Extrinsic control of cardiac output

A

Sympathetic innervation that increases[ both contractility and venous return.

24
Q

Frank-Starling law

A

Force (indicated by stroke volume) generated by cardiac muscle is proportional to initial length of the cardiac muscle fibers.

25
Preload
Workload imposed on cardiac muscle before the heart begins to contract.
26
Intrinsic control of stroke volume
Venous return is defined by the compression of veins by the skeletal muscle pump, and by breathing of the respiratory pump. This determines EDV which influences SV
27
Extrinsic control of stroke volume
Sympathetic innervation of veins may increase constriction, increasing venous return and EDV, therefore affecting SV.
28
Contractility
Ability of the cardiac muscle to contract and generate force for the pumping function.
29
Influencers of contractility
More intracellular Ca2+ increase the force of contraction, catecholamines increase the transport of Ca2+ into the cell
30
How do catacholamines mediate heart rate?
Phosphorylation sarcolemmal Ca2+ channels to increase flow, and bind to β1adrenergic receptors increasing phosphorylation of phospholamban and Troponin I to induce relaxation. Accelerates both contraction and relaxation of the heart.
31
After load
Workload imposed on cardiac muscle after the contraction has begun, no effect on cardiac output.
32
Heart failure
Cardiac output is insufficient to meet the needs of the body in the presence of normal venous return.
33
Continuous myocardial oxygen demand
Heart constantly need ATP and is uses a wide range of substrates to use this, mostly using fatty acid oxidation 60%, and glucose oxidation 35-40%.
34
Factors associated with myocardial oxygen demand
Wall stress, heart rate, contractility
35
Factors associated with myocardial oxygen supply
o2 content, coronary blood flow (perfusion pressure, vascular resistance)
36
Myocardial Ischemia
Depending on the site of the blockage, a wide range of tissues may be deprived of a blood supply.