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phyl1007 > Module 5: Cardiovascular > Flashcards

Module 5: Cardiovascular Flashcards

1
Q

During ventricular contraction, what happens to the AV valve?

A

It remains closed

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2
Q

Two valves of the heart?

A

Atrioventricular and semilunar valves

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3
Q

What are the two types of atrioventricular valves and where are they found?

A

Both between the atria and ventricles: Tricuspid valve on the right side, Bicuspid valve (or mitral) on the left

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4
Q

Where are the semilunar valves? What are the main two in the heart?

A

Between ventricles and arteries. In the heart, they are the aortic and pulmonary valves

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5
Q

Characteristics of myocardial muscle cells?

A

Myocardial muscle cells are branched, have a single nucleus, and are attached to each other by specialised junctions

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6
Q

What are the specialised junctions of myocardial cells?

A

Intercalated disks

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7
Q

What are so special about intercalated disks?

A

They contain desmosomes that transfer force from cell to cell, and gap junctions that allow electrical signals to pass rapidly between cells

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8
Q

Two types of cardiac muscle cells?

A

Contractile cells and autorythmic cells

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9
Q

How to distinguish an auto-rhythmic cell?

A

Has no organised sarcomeres and fewer contractile fibres

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10
Q

Mean arterial pressure equation?

A

MAP = CO (A-V) x total peripheral resistance

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11
Q

What units does flow rate use?

A

Ml/min

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12
Q

What happens when blood pressure is too low?

A

Hypotension. Shock if blood pressure is severely low

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13
Q

What happens when blood pressure is too high?

A

Hypertension

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14
Q

What is the major parameter controlled by the cardiovascular system?

A

Systemic mean arterial pressure

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15
Q

Difference between short and long term feedback loops that effect MAP?

A

Short term via neural pathways Long term via the vasculature and kidneys

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16
Q

Challenges for blood pressure regulation?

A

Posture Dehydration Haemorrhage Surgery Exercise Abnormal hormonal regulation

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17
Q

What do short feedback loops require? (five things)

A

A detector Afferent pathways Co-ordinating centre Efferent pathways Effector mechanisms

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18
Q

Where does the heart normally receive parasympathetic nervous system signals from?

A

The vagus nerve

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19
Q

Major difference in MAP between parasympathetic and sympathetic pathways?

A

Parasympathetic only effects the heart, while sympathetic stimulation effects both the heart and vasculature

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20
Q

What is the reflex that occurs when cardiac output and arterial pressure declines?

A

The arterial baroreceptor reflex

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21
Q

What is the predominate regulator of long-term regulation of MAP? What organ is mostly responsible?

A

The extracellular fluid volume can be influenced by both changes in input (thirst) or output (excretion). The kidneys are the predominant organ as the extracellular fluid volume

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22
Q

What is the difference between diastole and systole?

A

Diastole: cardiac muscle relaxes Systole: cardiac muscle contracts

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23
Q

When is the beginning of a cardiac cycle?

A

When the heart is at rest and artial and ventricular diastole

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24
Q

What is responsible for the first heart sound?

A

Early ventricular contraction and AV valves closing Vibrations (lub) following closure of the AV valves

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25
Q

What is atrial diastole?

A

All valves shut, isometric contraction of the heart, atria relax and blood flows in the atria

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26
Q

What is ventricular systole?

A

Ventricles finish contracting pushing semilunar valves open and blood is ejected in arteries

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27
Q

What is ventricular diastole?

A

Ventricular relaxation and pressure drops, still higher than atrial pressure (isovolumic)

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28
Q

What is responsible for the second heart sound?

A

Arterial blood flows back pushing semilunar valves shut Vibrations (dup) created by closing of semilunar valves

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29
Q

When do AV vales open?

A

When ventricular pressure drops below atrial pressure

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30
Q

What can be used as an indicator of diastolic dysfunction?

A

Isovolumic relaxation

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31
Q

What is isovolumic relaxation?

A

Isovolumic relaxation time (IVRT) is an interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve.

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32
Q

What is the action of listening to the heart through the chest wall with a stethoscope?

A

Auscultation

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33
Q

Average ml of stroke volume?

A

70ml

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34
Q

What is stroke volume the difference of?

A

The end diastolic volume (EDV) and the end systolic volume (ESV) or The volume of blood before contraction - volume of blood after contraction = amount of blood pumped by one ventricle during a contraction

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35
Q

What receptors in heart do sympathetic neurons innervate?

A

β1-adrenergic receptors on the autorhythmic cells

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36
Q

What causes the heart to stretch more?

A

Increased venous return stretches the ventricle and makes the next contraction stronger

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37
Q

What is venous return affected by?

A

Skeletal muscle pump Respirator pump Sympathetic innervation of veins

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38
Q

What happens to thoracic veins and intra-thoracic pressure during inhalation?

A

Inhalation increases blood flow into the thoracic veins and decreases intra-thoracic pressure

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39
Q

What happens to thoracic veins and intra-thoracic pressure during exhalation?

A

Inhalation increases blood flow into the heart and abdominal veins and increases the intra-thoracic pressure

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40
Q

What is a chemical that affects contractility?

A

An inotropic agent

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41
Q

What is a chemical that has a negative inotropic effect?

A

Lusitropy

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42
Q

What type of hormones increase contractility?

A

Catecholamines, from the adrenal cortex

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43
Q

What is the force of contraction affected by?

A

The length of a muscle fibre Contractility of heart Stretch of ventricular wall

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44
Q

What is preload? (in regards to stroke volume)

A

The degree of myocardial stretch before contraction

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45
Q

What is afterload and ejection fraction?

A

Afterload is the load that the heart must eject blood against and ejection fraction is the percentage of EDV ejected with one contraction

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46
Q

What is the ejection fraction calculation?

A

Stroke volume/EDV

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47
Q

Where does an action potential start in the heart?

A

With pacemaker (autorythmic) cells in the SA node

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48
Q

What happens when an action potential innervates a pacemaker cell?

A

Voltage-gated L-type Ca^2+ channels in the cell membrane open Ryanodine receptors open in the sarcoplasmic reticulum Calcium binds to troponin (and cross-bridge cycle initiates)

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49
Q

What happens during a heart relaxation?

A

Calcium is removed from the cytoplasm back into the SR with Ca^2+ATPase and out of the cell through a sodium-calcium exchanger

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50
Q

What is the force generated by the heart proportional to?

A

The number of active cross-bridges and thus how much calcium is bound to troponin. Sarcomere length is also important

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51
Q

Where does an action potential in the heart originate?

A

At the SA node

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52
Q

How can an action potential pass from an atria into the ventricles?

A

Via the AV node, after a brief delay

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53
Q

In which directions does an action potential spread in the heart, beginning from the SA node?

A

Right to left atria, then left ventricle

54
Q

Why is there a brief delay between the atria and ventricle action potential?

A

It allows atrial contraction to complete ventricular filling before ventricular contraction begins

55
Q

Where does an action potential go from the AV node?

A

It travels rapidly down the inter-ventricular septum via Bundle of His, then rapidly throughout myocardium through Purkinje fibres

56
Q

In what direction does a ventricle contract?

A

From base, upwards

57
Q

Myocardium cells not directly linking with a Purkinje fibre are stimulated by

A

Action potentials moving through gap junctions

58
Q

What sets the pace of the resting heart rate?

A

Sinoatrial (SA) node

59
Q

What pace do the AV nodes and Purkinje fibres set under certain conditions?

A

AV node (50bpm) Purkinje fibres (25-40bpm)

60
Q

How is AV node delay accomplished?

A

By slower conductional signals through nodal cells

61
Q

How is an action potential measured scientifically?

A

Via a patch pipette

62
Q

What is an ECG a measurement of?

A

The average electrical changes across two electrodes

63
Q

What waves do an ECG give?

A

PQRST

64
Q

Myocardial contractile cells use normal voltage-gated action potentials. How do myocardial autorhythmic cells differ?

A

Depolarisation is due to Ca^2+ channels opening

65
Q

What is the unstable membrane potential of a myocardial autorhythmic cell called?

A

The pacemaker potential (called the funny current)

66
Q

Two ways a parasympathetic stimulation occurs?

A

A larger hyper-polarisation or a slower depolarisation

67
Q

What is a P wave?

A

Atrial depolarisation

68
Q

What is a P-R segment?

A

Conduction through AV node and AV bundle

69
Q

What is the QRS complex?

A

Ventricular depolarisation Also atrial repolarisation

70
Q

What is a T wave?

A

Ventricular repolarisation

71
Q

Three waves of an ECG?

A

P: depolarisation of the atria QRS complex: wave of ventricular depolarisation T: repolarisation of the ventricle

72
Q

Where do Purkinje fibres transmit electric signals to next?

A

Down the atrioventricular bundle (Bundle of His)

73
Q

In regards to ECG waves, what is heart rate?

A

Time between two P waves or two Q waves

74
Q

In regards to ECG waves, what is ventricular contraction? Where does it end?

A

Starts at Q wave and ends at T

75
Q

In regards to ECG waves, what is the signal that goes through AV node and AV bundle?

A

P-R segment

76
Q

What does an ECG begin with?

A

At the beginning of the P wave; atrial depolarisation and atrial contraction at the end of the P wave

77
Q

Relationship between ECG and mechanical events in the heart?

A

Mechanical events lag behind electrical events

78
Q

What receptor does the parasympathetic neuron act upon in the heart?

A

ACh on M receptor

79
Q

What is the law that states the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles?

A

The Frank-Starling law

80
Q

What factors to take into consideration for the Frank-Starling law?

A

The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant

81
Q

Responses to reduced tissue perfusion in order of time of response?

A

Arterial baroreceptor reflex Activation of autonomic response (SNS/PSNS) Activation of renin/angiotensin system Stimulation of aldosterone Stimulation of vassopressin Increased anthropometry production

82
Q

What bundle of nerves makes the right atrium contract?

A

Bachmann’s Bundle

83
Q

What is the ST complex?

A

Following the QRS complex (ventricular depolarisation/atrial repolarisation), the ventricles contract during this ST phase

84
Q

Why is the T wave fatter and longer than the QRS complex?

A

Because repolarisation is a slower process than depolarisation

85
Q

Why is the PR interval called the PR interval when it goes from the P to the Q wave?

A

Ventricular depolarisation is the start of the R wave, and sometimes the Q wave is not present

86
Q

Why are R wave and T wave both in the positive direction despite one being ventricular depolarisation and one being ventricular repolarisation?

A

The EKC is a difference in charge (of potential). The epicardial cells depolarise after the endocardial cells. However, the epicardial cells also repolarise before endocardial cells; thus the EKC reads it as a positive (though it’s truly negative)

87
Q

What is the notch in systolic pressure?

A

The dicrotic notch

88
Q

What is the dicrotic notch a result of?

A

The dicrotic notch occurs due to closure of the aortic semilunar valve

89
Q

When an action potential is moving down an axon, what stops the axon potential from going backwards?

A

The refractory period! - K+ leaving the cell

90
Q

>Difference between cardiac muscle’s resting membrane potential and the membrane potential of an axon?

A

An axon is usually around -70mV; however, the cardiac muscle rests around -90! Peaks at ~+20mV when sodium depolarises

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phyl1007 (7 decks)

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