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MS1 > Week 1: Cardiology > Flashcards

Week 1: Cardiology Flashcards

1
Q

Base Surface of the heart (Position and Chambers)

A

Posterior
Left atrium; Right atrium

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2
Q

Diaphragmatic Surface of the heart (Position and Chambers)

A

Inferior
Right ventricle; Left Ventricle
PS: it connects to the diaphragm

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3
Q

Left Pulmonary Surface of the heart (Position and Chambers)

A

Left lateral
Left ventricle
PS: Adjacent to the lungs

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4
Q

Right Pulmonary Surface of the heart (Position and Chambers)

A

Right Lateral
Right Atrium
PS: Adjacent to the lungs

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5
Q

Anterior Surface of the heart (Position and Chambers)

A

Anterior
Right Ventricle; Left Ventricle; Right Atrium

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6
Q

Surfaces of the Heart

A

Base
Diaphragmatic
Left and Right Pulmonary
Anterior

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7
Q

Borders of the Heart

A

Right, Left, Inferior, and Superior

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8
Q

The Right Border of the Heart

A

Formed primarily by the right atrium, which extends between the superior and inferior Vena Cava

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9
Q

The Left Border of the Heart

A

Is predominantly formed by the left ventricle, ad a minority of the left atrium

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10
Q

The inferior border of the heart

A

Created mainly by the right ventricle, though the left ventricle is also part of it slighlty

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11
Q

Superior Border of the Heart

A

Is formed by the right and left atria, including the auricles, and is marked by the emergence of the superior vena cava and pulmonary trunk

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12
Q
A

Brachiocephalic Trunk

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13
Q
A

Top to bottom:
Left Common Carotid
Left Subclavian
Aortic Arch

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14
Q
A

Ligamentum arteriosum

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15
Q
A

Top to Bottom:
Left Pulmonary Artery
Pulmonary Trunk
Pulmonary Veins

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16
Q
A

Top to Bottom:
Left Atrium
Auricle of Left Atrium

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17
Q
A

Branch of Left coronary artery

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18
Q
A

Top to Bottom:
Left Ventricle
Anterior interventricular sulcus (deep to the fat)

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19
Q
A

Descending Aorta

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20
Q
A

Inferior and superior Vena cava

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21
Q
A

Right Ventricle

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22
Q
A

Coronary Sulcus (deep to fat)

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23
Q
A

Top to Bottom
Auricle of the right atrium
right coronary artery
right atrium

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24
Q
A

Top to Bottom:
Ascending aorta
Right Pulmonary Artery
Fibrous pericardium
Right pulmonary veins

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25
Q

Cardiac Skeleton

A

Aka annulus fibrosis
Dense fibrous tissues surrounding the four cardiac valves

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26
Q

Functions of the Cardiac Skeleton

A

Anchorage: maintains proper alignment
Insulation: eleticually insulated atria from ventricles
Attachment: serves as the myocardial attachment point
Structure: maintains structural integrity

27
Q

Venous Drainage of the heart

A

Occurs mostly through the coronary sinus which collects boood from the myocardium and empties into the right atrium

28
Q

Dominance patterns of regional supply in myocardium

A

Refers to which coronary artery (left main or right main) that supplies the posterior descending artery
In right dominant circulation the RCA supplies the PEA and the majority of the inferior portion of the heart! Making it the primary source of blood for posterior inter-ventricular septum and the left ventricles inferior wall. This pattern is seen in about 70-80% of people

29
Q

Coronary arteries

A

The Left Coronary: splits in it the left anterior descending and the left circumflex

The left Anterior decesnding: supplies anterior wall of the septum of the left ventricle Anterior Spetal Leads V1-V4

The left circumflex: supplies the lateral and posterior walls of the left atrium and left ventricle (also spilts into the left marginal artery)
Lateral Leads I, aVL, V5, V6

The right coronary: supplies the SA node, and dived into the right marginal and the Posterior descending artery
Inferior Leads II, III, aVF

30
Q
A

Posterior Intercostal artery

31
Q
A

descending aorta

32
Q
A

Internal thoracic

33
Q
A

Left subclavian

34
Q

a

A

Brachiocephalic trunk (splits into the right common carotid and right subclavian)

35
Q
A

right subclavian artery

36
Q
A

Anterior Intercostal artery

37
Q
A

Musculophrenic artery

38
Q
A

Hemi-azygos vein

39
Q
A

accessory hemi azygos vein

40
Q
A

subclavian vein

41
Q
A

internal jugular

42
Q
A

azygos

43
Q
A

superior vena cava

44
Q
A

brachiocephalic

45
Q

Coronary sinus

A

The main collecting vein for cardiac venous blood; receives blood from the great cardiac vein, middle cardiac vein, and small cardiac vein, and it empties into the
right atrium.

46
Q

Small cardiac vein

A

Drains the right atrium and ventricle.

47
Q

Middle cardiac vein

A

Located on the posterior surface of the heart; collects blood from the posterior portion of the left ventricle.

48
Q

Great cardiac vein

A

This vein runs alongside the anterior interventricular artery and collects deoxygenated blood from the left ventricle.

49
Q

Sympathetic Innervation of coronary arteries

A

Sympathetic innervation involves preganglionic fibres from the spinal cord (Th1-5) and postganglionic fibres
from the cervical ganglia, targeting the SA/AV node, coronary arteries, and cardiomyocytes.

50
Q

Parasympathetic Innervation of coronary arteries

A

Parasympathetic innervation consists of preganglionic fibres from the brainstem’s vagal nuclei traveling with the vagus nerve, and postganglionic fibres from neurons in the cardiac plexus, targeting the SA and AV nodes
and coronary arteries.

51
Q

Role of Endothelium in Cardiac Physiology

A

-Regulate vascular tone and blood flow
-ie: by releasing factors such as nitric oxide (increase vasodilation)
-can also release endothelin (causing vasoconstriction)

52
Q

Ohms law

A

Pressure (gradient)= Flow x Resistance

53
Q

Determinants of coronary blood flow

A

-Availability of oxygen (delivered from the lungs through the bloodstream)
-Blood vessel diameter (dictated through vasomotor tone)
-Cardiac output, stroke volume, and blood pressure.

54
Q

Vasomotor tone

A

the intrinsic level of contraction and relaxation of vascular smooth muscle, which maintains the baseline diameter of blood vessels

55
Q
A
56
Q

Atherosclerosis Mechanism

A
  1. Injury to endothelium of the artery —> membrane permeability
  2. This causes LDLs enter the tunic intima and inflammation
  3. Endothelial cells express adhesion molecules
  4. Leukocytes to squeeze between endothelial and enter the tunica intima (aka diapedesis)
  5. Monocytes differentiate into macrophages
  6. Inflammatory cells release free radicals that oxide LDLs
  7. Macrophages engulf the oxLDLs causing them to produce more free radicals
  8. The positive feedback loop results in an accumulation of oxLDLs ad Macrophages
  9. Macrophages accumulates multiple oxLDLS ,turning them into foam cells
  10. Foam cells: Undergo apoptosis, release inflammatory factors, and stimulate the smooth muscle cells to move from the tunica media to the intima, and take up more free radicals
  11. Accumulated debris forms a lipid core, AKA fatty streak (1st stage of atherosclerosis)
  12. Endothelial cells form a layer over the plaque
  13. Plaque accumulates Calcium salts and more cell debris, leading to hardening
  14. A fibrous cap is formed from college that has been synthesised by the smooth muscles cells that migrated from the tunica media
  15. The Plaque grows outwards, encroaching on the lumen and reducing blood flow
  16. If the endothelial cells over the plaque is comprised, plaque rupture can occur
  17. A thrombosis (AKA a blood clot) forms around the ruptured plaque, if this comes loose it is now called an embolus
57
Q

Atherosclerosis Mechanism

A
  1. Injury to endothelium of the artery —> membrane permeability
  2. This causes LDLs enter the tunic intima and inflammation
  3. Endothelial cells express adhesion molecules
  4. Leukocytes to squeeze between endothelial and enter the tunica intima (aka diapedesis)
  5. Monocytes differentiate into macrophages
  6. Inflammatory cells release free radicals that oxide LDLs
  7. Macrophages engulf the oxLDLs causing them to produce more free radicals
  8. The positive feedback loop results in an accumulation of oxLDLs ad Macrophages
  9. Macrophages accumulates multiple oxLDLS ,turning them into foam cells
  10. Foam cells: Undergo apoptosis, release inflammatory factors, and stimulate the smooth muscle cells to move from the tunica media to the intima, and take up more free radicals
  11. Accumulated debris forms a lipid core, AKA fatty streak (1st stage of atherosclerosis)
  12. Endothelial cells form a layer over the plaque
  13. Plaque accumulates Calcium salts and more cell debris, leading to hardening
  14. A fibrous cap is formed from college that has been synthesised by the smooth muscles cells that migrated from the tunica media
  15. The Plaque grows outwards, encroaching on the lumen and reducing blood flow
  16. If the endothelial cells over the plaque is comprised, plaque rupture can occur
  17. A thrombosis (AKA a blood clot) forms around the ruptured plaque, if this comes loose it is now called an embolus
58
Q

Histopathological features of atherosclerosis

A
  1. Neovessel Formation of visible branching arteries around blood vessels
  2. Apoptotic macrophages are visbale in flow cytometry
  3. Plaque crystal around edges of lumen and blood vessel wall
59
Q

Primary Hypertension vs secondary

A

Primary: no identifiable cause, but due to genetic, lifestyle and/or environmental factors
Secondary: arises from an identifiable underlying condition, which directly contributes to elevated blood pressure.

60
Q
A
61
Q

How does cardiovascular disease cause dyspnoea

A

• Dyspnoea in acute coronary syndrome (ACS) or stable angina often results from impaired myocardial oxygen delivery and subsequent heart failure.
• Myocardial ischemia leads to decreased cardiac output (due to reduced heart contractility and elevated end- diastolic pressure), which increases pulmonary venous pressure.
• This elevated pressure causes pulmonary congestion and interstitial oedema, which impairs gas exchange in the lungs; patients experience dyspnoea due to decreased oxygenation and increased fluid in the pulmonary interstitium and alveoli.

62
Q

How does Cardiovascular disease cause chest pain

A

• The mechanisms behind chest pain in infarction/ischaemia were defined in the previous module and relate to referred pain arising from the build-up of anaerobic metabolites.
• Anaerobic metabolites can directly interfere with pain pathways, or can cause tissue damage, resulting in inflammatory processes which produce mediators that irritate the nerves innervating the cardiac plexus.
• In both instances, disruption to pain pathways results in the characteristic crushing pain that begins in the chest and often radiates to the left jaw/shoulder.

63
Q

How does cardiovascular disease cause intermittent claudation (calf pain during walking)

A

• The primary mechanism involves atherosclerotic plaques in the peripheral arteries, which cause stenosis and reduce blood flow to the muscles during physical activity.
• As muscles work harder and oxygen demand increases, the impaired blood supply cannot meet the metabolic needs, leading to ischemia.
• This ischemia triggers the release of metabolic by-products, such as lactic acid, which stimulate sensory nerves and cause pain.
• The intermittent nature of claudication results from the temporary relief of symptoms during rest when oxygen demand decreases and blood flow partially restores.

64
Q

How does Reffered pain cause reffered pain

A

• During acute coronary syndrome (ACS), myocardial ischemia activates nociceptors in the heart, sending pain signals via the sympathetic nerves to the spinal cord.
• These pain signals synapse with neurons that also receive input from somatic structures, such as the skin and muscles, particularly in the thoracic region.
• As a result, the brain may misinterpret the source of the pain, leading to referred pain in areas like the left arm, jaw, or back.

MS1 (12 decks)

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