WEEK 3: Ischemic heart disease Flashcards

1
Q

Review physiologic anatomy of coronary blood flow.

A

The entire body must be supplied with nutrients and oxygen via the circulatory system and the heart is no exception.

The coronary circulation refers to the vessels that supply and drain the heart. Coronary arteries are named as such due to the way they encircle the heart, much like a crown.

Coronary Arteries
There are two main coronary arteries which branch to supply the entire heart.

They are named the left and right coronary arteries and arise from the left and right aortic sinuses within the aorta.

The aortic sinuses are small openings found within the aorta behind the left and right flaps of the aortic valve.

When the heart is relaxed, the backflow of blood fills these valve pockets, therefore allowing blood to enter the coronary arteries.

Branch from the aorta, above two cusps of the aortic.

Fill during diastole, when not occluded by valve cusps and when not squeezed by myocardial contraction.

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2
Q

Discuss the branches of the left coronary artery.

A

*The left coronary artery (LCA) initially branches to yield the left anterior descending (LAD), also called the anterior interventricular artery. The LCA also gives off the left marginal artery (LMA) and the left circumflex artery (Cx). In ~20-25% of individuals, the left circumflex artery contributes to the posterior interventricular artery (PIv).

  1. The left anterior descending artery
    -Runs in the anterior inter-ventricular groove
    -Supplies the anterior septum
    -Supplies the anterior left ventricular wall
  2. The left circumflex artery
    -Travels along the the left AV groove
    -Supplies the left atrium and the left ventricle
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3
Q

Discuss the branches of the Right coronary artery..

A

The right coronary artery (RCA) branches to form the right marginal artery (RMA) anteriorly. In 80-85% of individuals, it also branches into the posterior interventricular artery (PIv) posteriorly.

-Courses through the right side of the AV groove
-Supply the right atrium and the right ventricle.
-Continues as the posterior descending coronary artery,
*Runs in the posterior interventricular groove
*Supplies the posterior part of the interventricular septum
*Supplies the posterior left ventricular wall

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4
Q

Discuss blood supply to the Sinus node and the AV node.

A

Sinus node: Right coronary artery
60% of people
10% left circumflex artery or both.

AV node: Right coronary artery
90% of people
10% left circumflex artery.

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5
Q

Discuss venous drainage of the heart.

A

The venous drainage of the heart is mostly through the coronary sinus – a large venous structure located on the posterior aspect of the heart.

The cardiac veins drain into the coronary sinus, which in turn, empties into the right atrium. There are also smaller cardiac veins which pass directly into the right atrium.

The main tributaries of the coronary sinus are:

*Great cardiac vein (anterior interventricular vein) – the largest tributary of the coronary sinus. It originates at the apex of the heart and ascends in the anterior interventricular groove. It then curves to the left and continues onto the posterior surface of the heart. Here, it gradually enlarges to form the coronary sinus.

*Small cardiac vein – located on the anterior surface of the heart, in a groove between the right atrium and right ventricle. It travels within this groove onto the posterior surface of the heart, where it empties into the coronary sinus.

*Middle cardiac vein (posterior interventricular vein) – begins at the apex of the heart and ascends in the posterior interventricular groove to empty into the coronary sinus.

*Posterior cardiac vein – located on the posterior surface of the left ventricle. It lies to the left of the middle cardiac vein and empties into the coronary sinus.

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6
Q

Discuss lymphatic drainage of the heart.

A

The lymphatic vessels of the heart primarily drain into the cardiac lymphatic plexus, which is located in the epicardium (outer layer of the heart).
From the cardiac lymphatic plexus, lymphatic vessels converge to form larger lymphatic trunks.

The lymphatic trunks from the heart ultimately drain into the thoracic duct or right lymphatic duct, which return lymph to the bloodstream.

The lymphatic drainage territories of the heart correspond to the regions supplied by the coronary arteries.

The drainage territories typically include the left and right ventricles, atria, interventricular septum, and the conducting system of the heart (e.g., the sinoatrial and atrioventricular nodes).

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7
Q

Describe how fluid from the lymphatic system reach the venous system.

A

Lymphatic Capillaries and Collecting Vessels:
Lymphatic capillaries are blind-ended vessels with specialized endothelial cells that overlap, forming one-way valves.

Interstitial fluid, proteins, and cellular debris enter the lymphatic capillaries due to pressure differentials and the contraction of surrounding muscles.

Lymphatic capillaries merge to form larger collecting vessels, which have thicker walls and smooth muscle cells.

Lymphatic Trunks:
The collecting vessels converge to form larger lymphatic trunks, which are categorized based on their drainage territories.

The major lymphatic trunks include the jugular trunks, subclavian trunks, broncho mediastinal trunks, intestinal trunks, and lumbar trunks.

Thoracic Duct:
The thoracic duct is the largest lymphatic vessel in the body and receives lymph from the lower half of the body (below the diaphragm), left upper limb, and left side of the head and neck.

The thoracic duct ascends through the thoracic cavity alongside the vertebral column and drains into the venous system at the junction of the left subclavian vein and left internal jugular vein.

Right Lymphatic Duct:
The right lymphatic duct is smaller than the thoracic duct and receives lymph from the right upper limb, right side of the head and neck, and the right half of the thorax.

The right lymphatic duct drains into the venous system at the junction of the right subclavian vein and right internal jugular vein.

Venous Connection:
Both the thoracic duct and the right lymphatic duct empty their lymphatic contents into the venous system near the base of the neck.

Lymphatic fluid flows into the venous circulation through the subclavian veins, where it mixes with venous blood and returns to the heart.

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7
Q

Describe the blood vessel control.

A
  1. Central control of blood vessels
    achieved via the neuroendocrine system
    Sympathetic- vasoconstrictor
    Parasympathetic - vasodilator
  2. At a local level
    maintained automatically and by the effect of various factors synthesized and/or released in the immediate vicinity
    Blood flow to an organ remains constant over a wide range of perfusion pressures (autoregulation)
    blood vessels constrict independent of nervous input when blood pressure drops and vice versa.
  3. Autoregulation is a consequence of

-Bayliss myogenic response – the ability of blood vessels to constrict when distended.

-Vasodilator washout effect – the vasoconstriction triggered by a decrease in the concentration of tissue metabolites

-Local metabolites in the organ cause vasodilation
Heart-O2, adenosine, NO
Brain-CO2 (pH)

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8
Q

Myocardial oxygen extraction is near-maximal at rest, ≈75 % of arterial oxygen content
increases in myocardial oxygen consumption are primarily met by increases in coronary flow and oxygen delivery.

Outline the major determinants of myocardial oxygen consumption.

A

Major determinants of myocardial oxygen consumption are.

*Heart rate, systolic pressure, and left ventricular (LV) contractility

An increase in any of these individual determinants of oxygen consumption requires an ↑ in coronary flow.

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9
Q

What is Coronary Atherosclerosis?

What triggers it?

A

is a complex inflammatory process characterized by the accumulation of lipid, macrophages and smooth muscle cells in intimal plaques in the large and medium-sized.

Triggered by endothelial ‘injury’ or dysfunction

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10
Q

State Coronary Atherosclerosis: Causes of endothelial dysfunction.

A

Mechanical shear stresses (e.g. from morbid hypertension)

Biochemical abnormalities (e.g. elevated LDL, diabetes mellitus)

Immunological factors (e.g. free radicals from smoking)

Inflammation (e.g. infection such as Chlamydophila pneumoniae)

Genetic alteration

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11
Q

Describe the pathogenesis of Coronary Atherosclerosis.

A
  1. Endothelial dysfunction lead to increased permeability to and accumulation of oxidized lipoproteins
  2. Oxidized lipoproteins are taken up by macrophages at focal sites within the endothelium to produce lipid-laden foam cells. ‘fatty streaks’.
  3. Extracellular lipid within the endothelium
    Release of cytokines by monocytes, macrophages or the damaged endothelium platelet derived growth factor and transforming growth factor-β (TGF-β)
  4. Cytokines promotes further accumulation of macrophages as well as smooth muscle cell migration and proliferation.
  5. The proliferation of smooth muscle with the formation of a layer of cells covering the extracellular lipid
  6. Smooth muscles produce collagen in larger and larger the whole sequence of events cumulates as an ‘advanced or raised fibrolipid plaque’.
    may grow slowly and encroach on the lumen
    May become unstable, undergo thrombosis and produce an obstruction (‘complicated plaque’).

Endothelial cell dysfunction → → macrophage and LDL accumulation → → foam cell formation → → fatty streaks → → smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition → → fibrous plaque → → complex atheromas

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12
Q

Discuss what happens in an advanced atherosclerosis.

A

In an established atherosclerotic plaque, macrophages mediate inflammation and smooth muscle cells promote repair.

if inflammation predominates, the plaque becomes active or unstable and may be complicated by ulceration and superadded thrombosis.

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13
Q

Describe ‘Vulnerable plaques’.

A

Have lipid-rich cores, thin fibro cellular caps, increased inflammatory cells, and the release of specific enzymes that degrade matrix proteins.

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14
Q

Describe Stable plaques.

A

Have small lipid pools, a thick fibrous caps, calcification and plentiful collagenous cross-struts

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15
Q

Discuss the fate of a vulnerable or unstable plaque.

A
  1. Plaque disruption
  2. Exposure of subendothelial collagen
  3. Platelet aggregation and activation
  4. Vasospasm due to several mediators released
  5. Formation of microthrombi
  6. Aggregation of all microthrombi
  7. Coronary Artery Occlusion
16
Q

Describe the Manifestation of Atherosclerosis.

A
  1. Atheroma’s are often silent until they
    enlarge enough to impair arterial perfusion or
    ulcerate to results in thrombotic occlusion or embolization of the affected vessel.
  2. coronary heart disease
  3. cerebrovascular disease
  4. Peripheral vascular disease
    These entities often coexist and the pathogenesis of the diseases is similar
17
Q

Discuss the complications of atherosclerosis.

A
  1. Mechanical obstruction.
  2. Rupture leading to vessel thrombosis.
  3. May weaken the underlying media causing aneurysms
18
Q

What is Ischemic heart disease?

A

A condition caused by an inadequate supply of blood and O2 to a portion of the myocardium.

Caused by increased myocardial demand, reduced myocardial oxygen supply or both an imbalance btn myocardial oxygen supply and demand.

19
Q

Discuss Stable Angina Pectoris.

A

Stable Angina Pectoris:

Definition: Stable angina pectoris is chest discomfort or pain that typically occurs with exertion or emotional stress and is relieved by rest or nitroglycerin. It is considered stable when the symptoms are consistent in frequency, duration, and intensity over time.

Symptoms: Chest pain or discomfort typically described as pressure, squeezing, heaviness, or tightness. Pain may also radiate to the arms, neck, jaw, shoulders, or back. Other symptoms may include shortness of breath, fatigue, nausea, or sweating.

Causes: Stable angina is often caused by coronary artery disease (CAD), which occurs due to atherosclerosis (plaque buildup) in the coronary arteries, leading to reduced blood flow to the heart muscle during exertion.

Treatment: Treatment may involve lifestyle changes (such as quitting smoking, adopting a healthy diet, and exercising regularly), medications (such as nitroglycerin, beta-blockers, calcium channel blockers, and aspirin), and possibly invasive procedures like angioplasty or coronary artery bypass surgery in severe cases.

20
Q

Discuss Unstable angina pectoris.

A

Unstable Angina Pectoris:

Definition: Unstable angina pectoris is chest pain or discomfort that occurs suddenly, even at rest, or with minimal exertion. It represents a more serious and unpredictable form of angina compared to stable angina.

Symptoms: The symptoms are similar to stable angina but are typically more severe, occur at rest, or have a sudden onset. Unstable angina may also last longer and may not respond as well to nitroglycerin.

Causes: Unstable angina is often caused by the rupture of atherosclerotic plaque in a coronary artery, leading to the formation of a blood clot (thrombus) that partially or completely blocks blood flow to the heart muscle.

Treatment: Treatment of unstable angina involves immediate medical attention, often in a hospital setting. It may include medications to relieve symptoms (such as nitroglycerin and morphine), antiplatelet therapy (such as aspirin and clopidogrel), anticoagulants, and possible invasive procedures like angioplasty or coronary stent placement.

21
Q

Discuss Myocardial infarction.

A

Myocardial Infarction (STEMI):

Definition: Myocardial infarction, commonly known as a heart attack, occurs when blood flow to a part of the heart muscle is blocked for an extended period, leading to the death of heart muscle cells.

Symptoms: Symptoms of a heart attack can be similar to those of angina but are typically more severe and prolonged. Chest pain or discomfort may be accompanied by sweating, shortness of breath, nausea, vomiting, dizziness, or lightheadedness.

Causes: STEMI is usually caused by the sudden complete blockage of a coronary artery, often due to the rupture of a plaque and the formation of a thrombus. This results in a lack of oxygen and nutrients to the affected part of the heart muscle.

Treatment: Immediate medical attention is crucial for a heart attack. Treatment may involve administering oxygen, aspirin, nitroglycerin, and pain relievers. Additionally, prompt reperfusion therapy, such as thrombolytic therapy or percutaneous coronary intervention (PCI, also known as angioplasty with stenting), is necessary to restore blood flow to the blocked artery and minimize heart muscle damage.

22
Q

Outline the modifiable risk factors of IHD.

A
  1. Elevated Cholesterol
    ↑low density lipoprotein (LDL)
    Hypertriglyceridemia
    Low High-density Lipoprotein (HDL)
  2. Tobacco
    Smoking has a twice increase in IHD risk
    Risk reduced to nonsmoker level after two years of quitting.
  3. Hypertension
    ↑ risk of MI, stroke, kidney disease and heart failure
    Systolic BP is as important as diastolic BP in IHD risk.
  4. Physical inactivity
    Exercise are protective to IHD
    Exercise help to increase HDL cholesterol, control Diabetes, obesity and hypertension.
  5. Obesity
    Increased body fat, esp waist area, is risky- also for stroke
    Also increase risk for type 2 DM
  6. Diabetes mellitus
    Elevated blood glucose as well as insulin resistance increases risk for IHD
    Associated with mortality comparable to prior MI
    Hence referred to as IHD equivalent
23
Q

Outline the Non-modifiable Risk Factors of IHD.

A
  1. Age
    > 45 years for men
    > 55 years for women
  2. Sex
    Men > Women ( till menopause)
    Men develop IHD earlier in life
  3. Heredity
    Family history, esp if there is a family history of premature disease