Week 2 - Alterations to Blood Flow Pt. 1

Define blood pressure

The amount of force exerted onto arterial walls by the blood as its being pumped around the body

Differentiate between systolic and diastolic pressre

• Systolic - pressure exerted onto the arteries as the heart is contracting

• Diastolic - pressure exerted onto arteries as the heart is contracting

State the formula of blood pressure

BP = Cardiac output x peripheral resistance

Define peripheral resistance

The force opposing blood flow within the arteries

Define hypertension

Consistent increase in systemic arterial blood pressure

Explain the advice a GP would give to someone will prehypertension or hypertension stage 1

Lifestyles changes such as diet and exercise

Explain the advice a GP would give to someone with hypertension stage 2

Lifestyles changes as well as medication

Explain the advice a GP would give to someone with hypertension crisis

They require immediate medical attention (possibly emergency)

List the 2 types of hypertension and state how common they are

• Primary Hypertension - 95%

• Secondary Hypertension - 5%

Explain the cause of primary hypertension

There is no specific cause, instead a combination of factors including genetic, environmental and lifestyle factors

List the risk factors of primary hypertension

• Aging

• Obesity

• Anxiety and stress

• Increased sodium intake

• Increased alcohol consumption

• Being male

Explain the cause of secondary hypertension

Specific causes including kidney diseases, endocrine diseases such as hyper/hypothyroidism as well as drugs

State the 4 processes within the body that contribute to hypertension

• Reduced renal sodium excretion

• Overactive RAAS

• Overactive sympathetic nervous system

• Endothelium dysfunction

Explain how reduced renal sodium excretion can contribute to hypertension

Reduced sodium in urine results in sodium and water retention in the blood. Increasing blood volume and therefore BP.

Explain how the 3 ways an overactive RAAS system can contribute to hypertension

• Angiotensin ll increased vasoconstriction, increasing peripheral resistance and therefore BP

• Angiotensin ll stimulates aldosterone production, increasing sodium and therefore water retention. This increases blood volume and therefore BP

• Angiotensin ll activates sympathetic nervous system activity, increasing HR, vasoconstriction and therefore BP

List 2 causes for endothelium dysfunction

• Inflammation

• Insulin resistance

Explain how hypertension can lead to serious complications

• High blood pressure can damage endothelial cells

• Endothelium can no longer undergo normal functions eg, vasodilation/constriction, prevent blood clotting and play a role in inflammation

• Consequences are location-dependent

List some of the complications that arise from hypertension

• Myocardial infarction

• Stroke

• Renal failure

• Vision loss

• Sexual dysfunction

• Fractures

Name some of the symptoms of hypertension in later stages

• Headaches

• Chest pain

• SOB

• Cardiac arrhythmias

• Blurred vision

Differentiate between arteriosclerosis and atherosclerosis

• Arteriosclerosis is an overarching term for arterial disorders that result in decreased blood flow due to degeneration.

• Atherosclerosis is a form of arteriosclerosis in which lipid accumulation in the arteries leads to plaque formation and hypertension

Explain where the plaque forms in atherosclerosis

In the tunica intima, the innermost layer that is directly in contact with the blood.

State what 2 main diseases arise from atherosclerosis

• Coronary heart disease

• Cerebrovascular disease

Explain how a plaque is formed within the artery

1. Endothelium damages

2. LDL enters the tunica intima through damaged endothelium

3. LDL oxidises and inflammatory response is activated, triggering monocytes and T cells adhere to endothelium

4. Monocytes differentiate into macrophages as they enter the tunica intima

5. Macrophages phagocytose LDL, forming foam cells

6. Foam cells release cytokines that amplify immune response and attract more macrophages

7. Foam cells accumulate to form a fatty streak

8. Smooth muscle proliferates which migrates to cover the fatty streak, creating plaque

State the alternative name for plaque

Atheroma

Name and explain the 2 components of an atheroma

• Fibrous cap - top portion made of smooth muscle cells, extracellular matrix and collagen

• Necrotic core - progression of fatty streak containing debris, dead cells, foam cells and lipids.

Name and explain the 2 types of plaques

• Stable plaque - contain a thick fibrous cap and result in predictable decreased blood flow

• Unstable plaque - contain a thin fibrous cap that typically ruptures, resulting in the formation of a thrombus and can cause more serious consequences

Name the 4 outcomes of atherosclerosis

• Aneurysm and rupture of blood vessel

• Stenosis

• Thrombus occlusion

• Atheroembolism

Explain an aneurysm

The dilation of a vessel wall or cardiac chamber in which changes to collagen and elastin cause weakening. The vessel/chamber can no longer efficiently propel blood throughout the systemic circulation and are prone to rupture.

State the part of the body most susceptible to aneurysms and explain why

The aorta due to the constant stress to propel blood to the rest of the body

Define a thrombus

A blood clot that forms within a vessel

Explain why a thrombus forms

• Inflammatory response activates coagulation

• Stasis of blood flow

Explain the difference between a thrombus and an embolus

• Thrombus is a blood clot that lodges and occludes a blood vessel

• Embolus is a blockage that breaks off and travels to and lodges at a distal site

Define a thromboembolism

An embolus that forms by breaking off from a thrombus, travelling and lodging at a distal site

Explain DVT

Deep vein thrombosis occurs when a thrombus forms within a vein (typically the femoral vein) that is likely to cause a pulmonary embolism.

State what will occur if there is atherosclerosis to the internal carotid artery

Ischemia to the brain and a stroke

State what will occur if there is atherosclerosis to the anterior descending coronary artery

Ischemia to the myocardium and myocardial infarction

State what will occur if there is atherosclerosis to the renal artery

Ischemia to the kidneys and renal failure

Define acute coronary syndromes

Any condition that occurs due to a severe reduction in blood flow to the myocardium

List 2 examples of acute coronary syndromes

• Unstable angina

• Myocardial infarction

Define angina pectoris

Intermittent chest pain as a result of periodic myocardial ischemia

Name the 3 types of angina

• Stable

• Prinzmetal/variant

• Unstable

List symptoms of angina

• Chets pain

• Dyspnea (SOB)

• Pain radiating to the neck, jaw, shoulder and arm

Define stable angina

Predictable chest pain caused by the onset of stress

Explain how atherosclerosis can lead to stable angina

Those who have atherosclerosis with stable plaques will experience stable angina.

Explain why those will stable plaques have stable angina

This is because at rest, blood flow is normal and energy demands can be met. However during periods of stress such as exercise, energy demands increase and the narrowing of arteries due to stable plaque prevents the body from increasing blood flow in order to meet these demands.

Explain how symptoms of stable angina can be relieved

Symptoms are relieved by rest, ceasing stressful activities and certain medications.

Define prinzmetal/variant angina

Rare chest pain caused by coronary artery vasospasms.

Define unstable angina

Unpredictable chest pain caused by sudden myocardial ischemia

Explain how atherosclerosis leads to unstable angina

Those who have atherosclerosis with unstable plaques will rupture and form a thrombus. This thrombus occludes a blood vessel in which there is transient myocardial ischemia for 10-20 mins and blood flow returns before necrosis.

Explain how the symptoms of unstable and stable angina differ

Symptoms are the same however for unstable angina these symptoms occur at rest and are more severe and frequent.

List these features of an ECG that occur for patients with unstable angina during an episode

• A - ST depression

• B - T wave inversion

Define a myocardial infarction

Necrosis of the myocardium due to the lack of blood flow through the coronary arteries for a sustained period of time.

Name the 2 types of myocardial infarctions

• Subendocardial infarction

• Transmural

Differentiate between subendocardial and transmural infarctions

• Subendocardial occurs when there is damage only to the endocardium due to thrombus breaking off and travelling elsewhere before further damage occurs

• Whereas transmural occurs when there is damage to all layers of the cardiac wall due to a permanently lodges thrombus

Explain the different terms used when analysing an ECG for infarctions

• STEMI - ST elevation caused by a transmural infarction

• NSTEMI - no ST elevation caused by a subendocardial infarction

Explain how atherosclerosis can lead to a myocardial infarction

Those who have an atherosclerosis with unstable plaques that rupture and form a thrombus. This thrombus occludes a vessel that causes sustained myocardial ischemia, leading to a myocardial infarction.

State the percentage of unstable angina cases that progress to myocardial infarction

20%

Differentiate between transient and sustained ischemia

Transient ischemia is periodic and cell damage is reversible whereas sustained ischemia is for extended time periods in which cell damage is irreversible.

Explain how transient ischemia/partially ischemic cells can lead to reduced impulse conduction and contractile function

• Reduce blood flow and oxygen results in anaerobic respiration

• This causes accumulation of lactate that reduces pH

• Also causes reduction in ATP production

• These changes reduces pumping of ions and the integrity of cell membranes

• This decreases impulse conduction and contractions

Explain how transient ischemia/partially ischemic cells can lead to the activation of the SNS and RAAS

• Use of anaerobic respiration reduces ATP production

• This triggers SNS and RAAS to increase vasoconstriction and BP in attempt to increase cardiac output for aerobic respiration

Explain how sustained ischemia/totally ischemic cells leads to cell death

• Lack of blood flow means no oxygen reaching cells

• After 20 mins cells lose integrity of cell membrane

• Cell death

Explain how myocardial infarction can be diagnosed from blood tests

Certain intracellular enzymes are released into the blood after myocardial cell death.

List the 3 phases of cell repair after a myocardial infarction

• Inflammatory

• Proliferative

• Maturation/remodelling

Explain the inflammatory phase of myocardial repair including time-span

24 hours after, immune cells such as macrophages and neutrophils migrate to remove debris and dead cells.

Explain the proliferative phase of myocardial repair including time-span

10-14 days after, angiogenesis occurs and fibroblasts form scar tissue.

Explain the maturation/remodelling phase of myocardial repair including time-span

Myocyte hypertrophy occurs to compensate for inefficient function of scar tissue.

Explain how symptoms of myocardial infarction differ for men and women

The traditional symptoms including intense chest pain, dyspnea and nausea are not as common forr women who may experience dizziness, weakness and trouble sleeping.