Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Module Three > Cardiac physiology + pathology > Flashcards

Cardiac physiology + pathology Flashcards

1
Q

What two types of cells exist in the heart?

A

Cardiomyocytes (99%) and pacemaker cells (1%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is the AV node located?

A

Base of the right atrium, superior to the atrioventricular junction. At the apex of the triangle of Koch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three layers of heart wall called?

A

Epicardium, myocardium and endocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What two sections of the myocardium are important in understanding an ECG?

A

Subendocardial and subepicardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which section of the myocardium will depolarise first?

A

Subendocardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

At an electrical level, what do the lines on an ECG represent?

A

The difference in electrical activity between the subendocardial section and the subepicardial section.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the isoelectric line represent?

A

There is no difference in electrical activity between the two sections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the endocardium made of?

A

Endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the seven subphases of the cardiac cycle?

A

Atrial systole, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid ventricular filling, diastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The S4 heart sound occurs in which phase of the cardiac cycle?

A

Atrial systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where does rapid ejection happen on the ECG?

A

During the ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does ventricular systole begin on the ECG?

A

At the peak of the R wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where does reduced ejection happen on the ECG?

A

During the T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What phase of the cardiac cycle happens during the T wave of one complex and the p wave of the next?

A

Rapid ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which phase of the cardiac cycle can the S3 heart sound be heard?

A

Rapid ventricular filling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Usually, how much is cardiac output at rest?

A

5L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the equation for cardiac output?

A

Stroke volume x HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the equation for MAP from cardiac output?

A

MAP = CO x total peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Poiseuille’s Law - explain it’s significance to the cardiac system.

A

A small change in the radius of blood vessels can greatly affect the resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What two mechanisms are used to maintain homeostasis of MAP?

A

Baroceptor reflex and endocrine system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does aldosterone work?

A

Increases salt and water retention by the kidneys, therefore increasing cardiac output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does ADH do?

A

Constricts blood vessels and increases water retention in kidneys, therefore increasing cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where is erythropoietin released from?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is aldosterone released from?

A

Adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is ADH released from?

A

Posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does atrial natriuretic peptide work?

A

Released from the atria when they are stretched from high MAP, increases salt and water excretion in the kidneys, therefore decreasing CO

27
Q

Where is renin released from and when?

A

glomeruli in kidneys when there is low perfusion to the kidneys

28
Q

Angiotensin has two forms, which is the active form?

A

Angiotensin II

29
Q

What converts angiotensin I into II?

A

angiotensin converting enzyme (ACE)

30
Q

What are the main actions of angiotensin II?

A

Constricts blood vessels,
and promotes the release of ADH and aldosterone, all to maintain blood volume and increase MAP

31
Q

What is the significance of BNP?

A

Released from ventricles when they are stretched, has a longer half life than ANP and can be detected in a blood sample to indicate HF

32
Q

Which receptors are used for immediate BP regulation?

A

Baroreceptors

33
Q

What part of the ANS is the cardiac accelerator nerve part of?

A

Sympathetic

34
Q

How do calcium channel blockers work?

A

Blocking calcium channels, less calcium = less constriction of vessels = decreased resistance = decreased MAP

35
Q

What does adrenergic B1 receptor activation by noradrenaline do in the heart?

A

Increase heart rate and force

36
Q

What is the general mechanism of action of diuretics?

A

Inhibit sodium ion transporters which decreases sodium reabsorption = decreases water reabsorption = increased urine output

37
Q

What are the main classes of diuretics?

A

Thiazide, potassium sparing and loop

38
Q

Why is a negative side effect of loop diuretics gout?

A

Compete for transporter proteins with uric acid = decreased excretion of uric acid = gout

39
Q

Which diuretic can cause gynaecomastia and why?

A

Spironolactone, have an action on progesterone androgen receptors

40
Q

What are the two types of calcium-channel blockers and how do they differ?

A

Cardiac selective (used in arrhythmias) and vascular selective (used in hypertension)

41
Q

What type of protein is AT1 receptor linked to and what is it’s mechanism?

A

Gq protein, activates phospholipase C which activates IP2 and DAG which releases calcium from sarcoplasmic reticulum. Causing smooth muscle contraction.

42
Q

Where are ACE inhibitors excreted?

A

Kidneys

43
Q

Where are ARBs metabolised?

A

Liver

44
Q

What other action does angiotensin converting enzyme have that cause a side effect of ACE inhibitors?

A

breaks down bradykinin, so ACE inhibitors = more bradykinin = irritated cough receptors = dry cough

45
Q

What is the action of alpha-1 antagonists?

A

Block adrenergic alpha-1 receptors = vasodilation = decreased resistance = lower MAP

46
Q

Why is it important to use selective alpha-1 drugs?

A

Non-selective drugs can block alpha-2 receptors = interfere with the baroreceptor reflex and cause tachycardia

47
Q

What is the role of beta-1 receptors and where are they found?

A

Found in the cardiac muscle, Gs coupled, activates adenylyl cyclase which synthesises cAMP. Increases calcium influx = increased force of contraction.

48
Q

What is the role of beta-2 receptors and where are they found?

A

Found in smooth muscle of airways, Gs coupled. cAMP phosphorylates MLCK, inactivating it = smooth muscle relaxation

49
Q

What is active hyperaemia?

A

Release of chemicals and activation of SNS cause vasodilation in peripheral tissues which improves blood flow, this is as a consequence of increased metabolic rate.

50
Q

What is metabolic rate?

A

The energy expended in a given time frame, measured by the use of oxygen, carbon dioxide and the release of heat.

51
Q

What is the equation for MAP?

A

DBP + 1/3(SBP-DBP) OR cardiac output x total peripheral resistance

52
Q

What is pre-load and how can it be measured?

A

The stretch of the ventricles at the end of diastole, directly related to ventricular filling.

Can be measured as end-diastolic volume (the volume of blood in the ventricles before contraction) on an echocardiogram.

53
Q

What three main factors affect stroke volume?

A

Preload, contractility and afterload

54
Q

How could you estimate stroke volume from an echocardiogram?

A

end-diastolic volume minus end-systolic volume

55
Q

An increase in preload would result in what effect on stroke volume?

A

Increase

56
Q

What affect would angiotensin II have on pre-load?

A

Stimulate aldosterone release = salt and water retention = increased pre-load

57
Q

Sympathetic stimulation of alpha receptors has what effect on pre-load?

A

Vasoconstriction = forces more blood into veins = increased pre-load

58
Q

How can sepsis cause a reduced pre-load?

A

Capillary leakage causes hypovolaemia which decreases pre-load

59
Q

cfvtgbyhujWhat are the features of pathological ventricular remodelling and why does it occur?

A

Thickening of the ventricular wall, cardiac myocyte growth, enlargement of the ventricular chamber or dilation and thinning/fibrosis of the ventricular wall.

Occurs as a response to wall stress from hypertension, ischemic cell death, arrhythmias, valve disease, structural abnormalities etc

The body is trying to ensure perfusion remains adequate, by increasing chamber size and muscle it can increase pre-load and stroke volume to maintain perfusion.

60
Q

What are the three features of cardiac tamponade?

A

Beck’s Triad: low BP, JVD and muffled heart sounds.

61
Q

When looking at the Frank-Starling curve, preload is proportional to what?

A

Length of the sarcomeres (stretch of the muscle)

62
Q

What value can you use to estimate afterload?

A

Systemic vascular resistance (or total peripheral resistance)

63
Q

What is afterload?

A

The pressure the ventricle must overcome to eject blood

64
Q
A

Module Three (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions