CVS Flashcards

1
Q

What is the maximal ejection fraction in ventricles?

A

Maximal ejection is around 70%, so around 30% remains in the ventricles.

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2
Q

What is shown by the T-wave on an ECG?

A

Ventricular Repolarisation

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3
Q

What happen during the PR interval?

A

There is the delay at the AV node for electrical conduction to allow the ventricles to fill.

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4
Q

What is isovolumetric contraction?

A

When ventricles are contracting but the valve doesn’t open so pressure builds in the ventricle but volume stays the same. There is no ejection of blood yet.

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5
Q

What is preload?

A

(Pressure/Volume) Load present before ventricular contraction has started. Equivalent to the end diastolic (left ventricular) volume. Relates to the stretch in heart muscle sarcomeres before contraction.

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6
Q

What may cause increased preload?

A

Aortic stenosis, ventricular systolic failure

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7
Q

Define contractility

A

Inotropic state - The state if the heart which enables it to increase its contraction velocity to achieve higher pressure when contractility is increased. This is independent of load.
This is reflected in the end systolic pressure-volume relationship.

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8
Q

Define elasticity

A

The myocardial ability to recover its normal shape after removal of systolic stress.

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9
Q

Define Compliance

A

The relationship between the change in stress the resultant strain. This is reflected in the end diastolic pressure-volume relationship

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10
Q

Define Diastolic Distensibility

A

Pressure required to fill the ventricle to the same diastolic volume.

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11
Q

What is the Frank-Starling Law?

A

As stretch increases that contraction will increase. Stroke volume will increase in response to an increased end diastolic volume the other factors remain constant.

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12
Q

What is the equation of Stroke Volume

A

Stroke volume = End diastolic volume - End systolic volume

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13
Q

Mean arterial pressure equation

A

MAP =(Cardiac Output * Systemic vascular resistance) + Central venous pressure

MAP = Diastolic pressure + 1/3*pulse pressure

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14
Q

Pulse pressure equation

A

Pulse pressure=Systolic - Diastolic Pressure

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15
Q

Cardiac Output equation

A

CO= Stroke volume * Heart Rate

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16
Q

Ohms Law =

A

Flow = Pressure Gradient/ Resistance

17
Q

Poiseuille’s Law =

A

Flow is proportional to radius^4

This equation is good as it is about flow in a tube - vessels are tube like

18
Q

What is positively chronotropic?

A

Sympathetic stimulation to the heart. (Chronotropic = effecting heart rate)

19
Q

What is negatively intropic?

A

Parasympathetic stimulation (force of contraction)

20
Q

List the electrical pathway of the heart

A

Sino Atrial Node - (Bachmann’s Bundle) and Internodal Pathways - (100-200ms delay) Atrio Ventricular Node - Bundle of His - R and L bundle branches (L activated b4) - Ant and post fascicles - Purkinje fibres

21
Q

What does increased sympathetic stimulation do?

A

+ve chronotropic HR up to 180-250 bpm,
+ve inotropic,
greater Cardiac output up to 200% increase .

22
Q

What neurotransmitters and are released at the heart and receptors at heart

A

Controlled by adrenaline, noradrenaline and Beta 1 - adrenoreceptors

23
Q

What are the parasympathetic neurotransmitters and receptors and how it effects the heart.

A

Parasympathetic controlled by acetylcholine (ACh) and M2 receptors.
They inhibit adenyl cyclase which reduces cAMP, so decreasing heart rate/ pausing it.
-ve inotropic, up to 50% reduction in Cardiac Output.
Each causes K+ channels to open so K+ moves out prolonging pacemaker potential- reducing HR

24
Q

How do pacemaker potentials/ diastolic depolarisation work

A

K+ channels close slowly (after it was open for repolarisation)
HCN channels open (-60mV_ allows slow influx of Na+
Around -40mV voltage gated Ca2+ channels open for Ca2+ influx briefly. (Then it reaches threshold level)

25
Q

What are HCN channels affected by

A

HCN channels
-ve effect by ACh
+ve effect by catecholamines (noradrenaline)

26
Q

What are the steps in Myocardial Action Potential

A

1) Rapid depolarisation once activated, huge influx of Na+
2) Partial Repolarisation, K+ moves out and influx of Na+ stops
3) Plateau as Ca2+ slow influx and K+ channels close
4) Repolarisation as K+ out influx of Ca2+ stops

27
Q

How long is the refractory period (absolute and relative) last

A

200 - 300 msec

28
Q

What are the benefits of a long refractory period?

A

Allows heart to fill
Prevents summation
Prevents tetanus
Myocardial contraction last 15x longer than skeletal contraction

29
Q

How does a Beta-blocker work

A

Block Beta1 adrenergic receptors which reduces adenyl cyclase which reduces cAMP reduces HR

30
Q

What is the duration of normal systole?

A

0.3s

31
Q

What is the duration of normal diastole?

A

0.5s