BIOL 2200 Module 5: Cardiovascular Disorders

Atherosclerosis

Fibrous fatty “plaques” forming in medium and large sized arteries, blocking flow and causing ischemia

Which layer of arteries does atherosclerosis typically affect?

It typically affects the tunica intima, the innermost layer of an artery

How does endothelial cell damage contribute to atherosclerosis?

Endothelial cell damage increases permeability to lipids and plasma proteins, leading to migration of leukocytes which release growth factors that proliferate smooth muscle

Foam cells

Monocytes that have differentiated to macrophages and ingested lipids

Low density lipoproteins (LDL)

Transport form of lipids in the blood. Typically oxidized by ROS and ingested by macrophages (forming foam cells). Increases risk of coronary artery disease/atherosclerosis

Coronary artery disease (CAD)

Atherosclerosis of the coronary arteries. Is the cause of ischemic heart disease

Ischemic heart disease (IHD)

Ischemia to heart muscle, typically due to coronary artery disease

Which regions of the heart does the right coronary artery supply?

Mostly the right ventricle and posterior regions of the heart

Which regions of the heart does the left coronary artery supply?

Mostly the left ventricle and interventricular septum

Myocardial blood flow

Volume of blood supplying the heart muscle specifically. Controlled by either vasodilation or constriction of coronary blood vessels

Is myocardial blood flow highest during diastole or systole?

It is highest during diastole, since the relaxing of heart muscle allows blood to freely perfuse into tissue

How does high blood pressure increase risk of athosclerosis?

Through causing endothelial cell damage, which allows foam cells to form, driving athosclerosis

In Coronary Artery Disease (CAD), which muscle region is usually damaged first?

The subendocardial regions, since they have most difficulty obtaining adequate blood flow

Collateral circulation

Body’s network of backup blood vessels that reroute blood flow in the case of vessel blockage or damage

Anastomoses

Connections between blood vessels, enabling collateral circulation

Angina pectoris

Chest pain or discomfort when the heart muscle does not receive enough oxygen-rich blood

Myocardial infarction

Blockage of blood flow to a part of the heart.

Stable angina

Chest pain caused by constant myocardial ischemia. Not enough blockage to cause necrosis, but enough to cause pain

Unstable angina

Where vessel plaque may “flake off” and lead to development of small thromboses, causing occlusion. Spontaneous, no necrosis, may lead to myocardial infarction

Glycerol trinitrate

Relieves symptoms of stable angina through vasodilation

Acute Coronary Syndrome (ACS)

Spectrum of ischemic heart diseases. Includes angina and myocardial infarction

Are symptoms of unstable angina relieved by glycerol trinitrate?

No, the symptoms are not releieved by glycerol trinitrate

Myocardial infarction

Result of complete coronary occlusion, producing acute ischemia and ischemic injury and necrosis

STEMI (SegmenT Elevation Myocardial Infarction)

Myocardial infarction where the clot permanently lodges in the vessel, make the entire thickness of myocardium ischemic

Non-STEMI

Myocardial infarction where the thrombus disintegrates before complete tissue necrosis. Only affects subendocardium

Subendocardium

Innermost layer of heart wall, affected by Non-STEMI

General manifestations of acute coronary syndrome

Abrupt onset, tachycardia, pale skin, feeling of impending doom “silent MI”

“Silent MI”

Silent myocardial infarction, where a person does not experience any symptoms are has atypical symptoms

Cardiogenic shock

Where the blood suddenly cannot pump enough oxygen-rich blood to meet your body’s needs

Systolic stretch

Lengthening or bulging of a heart segment (not contracting) while the rest of the heart is contracting.

Ventricular fibrilation

Irregular, often rapid heart rhythm caused by irregular electrical signals. Ventricles “quiver” and have zero cardiac output

P wave

Atria depolarize

QRS complex

Ventricles depolarize, atria repolarize

T wave

Ventricles repolarize

Dysrhythmia (arrythmia)

“Missed” or rapid beats that impair the heart’s pumping ability. May be caused by abnormal impulses from the SA node

Atrial conduction abnormalities

Most common arrythmia, causes disorganized atrial rhythm followed by irregular ventricular rhythm. Leads to blood pooling in atria

Atrioventricular node abnormalities

Excessive delay or stopping of conduction at the AV node. Signal has trouble reaching ventricles

Asystole

No electrical activity, leading to absence of a heartbeat

Pericarditis

Acute pericardium inflammation, can lead to pain and fever

Cardiomyopathy

Group of diseases that affect the myocardium

Dilated cardiomyopathy

Leads to increased ventricular volume, impairing systolic function. 1/3 cases are inherited. Commonly causes heart failure

Hypertrophic cardiomyopathy

Septum thickening, decreasing left ventricular size and obstructing blood outflow. Quite common, mostly asymptomatic

Valvular dysfunction

When one of the four valves do not open or close properly. Commonly caused by rheumatic heart disease (Streptococcus pyogenes, acquired)

Stenosis

Narrowing of valve opening which enlarges emptying chamber and turbulent (chaotic) flow

Incompetent (regurgitant) valve

A dysfunctional valve that permits backward flow

Heart murmurs

Swooshing or blowing sounds produced by turbulent blood flow through the heart

Heart failure

Where the heart cannot generate an adequate cardiac output. Commonly caused by coronary artery disease

Which three factors affect stroke volume?

Preload, Afterload, Intropy (contractility)

Preload

Volume of blood in ventricle at the end of diastole. Determined by blood entering ventricle duringg diastole, and blood left in ventricle after systole

Frank-Starling law of the heart

States that more blood in the ventricles leads to more stretching, leading to stronger contraction

Afterload

The force that ventricles must overcome to push blood out

Intropy (contractility)

The force of cardiac muscle contraction. Increased by ventricular hypertrophy, decreased by myocardial infarction

Systolic heart failure

Occurs when the left ventricle cannot contract properly

How does systolic heart failure increase heart pre-load?

It increases pre-load by leading to more blood in the ventricle after contraction

Diastolic heart failure

Occurs when the heart muscle is stiff and cannot relax and fill heart chambers with enough blood

How does diastolic heart failure lead to pulmonary edema?

It can lead to pulmonary edema by causing blood to back up into pulmonary circulation, increasing pulmonary pressure

Left/congestive heart failure (LHF)

Occurs due to decreased cardiac output to systemic circulation (left ventricle → body)

How does blood backing up into pulmonary circulation cause pulmonary edema?

It forces fluids out of the blood vessels

Right heart failure (RHF)

Occurs when right ventricle cannot move blood from systemic to pulmonary circulation. Pressure thus rises in systemic venous circulation

Peripheral edema

Excess fluid buildup in the body’s tissues, primarily in the lower limbs due to gravity

How can the external jugular vein become visible due to right heart failure?

Excess systemic venous pressure leads to external jugular vein distension, making it visible

What is the most common cause of left heart failure?

RHF, leading to back up of blood into the right ventricle which cannot compensate

Cor pulmonale

RHF due to pulmonary disease, such as COPD or ARDS

Cardiomyopathy

Disease of the heart muscle that makes it harder to pump blood to the rest of the body

Role of sympathetic nervous system in heart failure compensation

Increases blood pressure and cardiac output → but also strains an already weakened heart

Role of Renin-Angiotensin Aldosterone System (RAAS) in heart failure compensation

Releases ADH to increase blood volume and angiotensin to vasoconstrict, in an ATTEMPT to deliver blood (won’t work!)

How does the Renin-Angiotensin Aldosterone System (RAAS) affect pre-load and afterload?

Increases pre-load through vasoconstriction and after-load through increased blood volume, straining the heart

Role of hypertrophy in heart failure compensation

Can either thicken ventricle walls (increase ischemia) or thin ventricle walls (dilation and impairment of contraction)

How can hypertrophy thin ventricle walls?

Muscle fiber stretching from constant excess blood volume leads to addition of new sarcomeres in series

Orthopnea

Shortness of breath from lying down, relieved by sitting up

How does heart failure reduce urine output?

Through decreasing kidney blood flow, making the kidney think the body is dehydrated

What does heart failure treatment focus on?

It focuses on decreasing preload and afterload, e.g. salt restriction and weight management

Treatment for heart failure

Digitalis (improves stroke volume), beta blockers, O2 therapy

Circulatory failure (shock)

Failure of the circulatory system to supply adequate blood, causing cellular hypoxia and even organ failure

Clinical manifestations of shock

Hypotension (mean arterial pressure under 60 mm Hg), increased respiration, weak, cold, hot, thirsty

Cellular effects of shock

Shock leads to cellular anaerobic respiration → less ATP → Na⁺/K⁺ pump failure→ weird ion concentrations → interference with nervous and muscular systems

How does shock worsen tissue perfusion? (positive feedback)

Shock → Na⁺/K⁺ pump failure → fluid leaves vessels → lower bP → lower tissue perfusion → worsens shock

Tissue perfusion

Process of delivering oxygenated blood to body cells and tissues while removing metabolic waste

How does shock worsen tissue damage? (positive feedback loop)

Shock → cell membrane disruption (Na⁺/K⁺ pump failure) → lysosomal enzyme release → inflammatory response → further tissue damage and cellular metabolism impairment

How does shock worsen tissue hypoxia? (positive feedback loop)

Anaerobic respiration → increased acidity → decreases hemoglobin O₂ affinity → further increases tissue hypoxia and anaerobic respiration

Cardiogenic shock

Shock from decreased contractility and cardiac output, increasing preload and/or afterload. Often follows MI and is unresponsive to treatment

Hypovolemic shock

Shock from insufficient blood volume. Caused by hemorrhage, treated with rapid fluid replacement

Obstructive shock

Shock from mechanical obstruction of blood flow through central circulation. Often caused by pulmonary embolism, often classified under cardiogenic shock

Distributive shock

Shock from massive vasodilation, reducing BP below what is necessary to drive nutrients across capillary membranes to cells

Neurogenic shock

Distributive shock (massive vasodilation) from overstimulation of parasympathetic NS and under-stimulation of sympathetic NS

Neurogenic shock cause and treatment

Cause: Spinal cord or medulla trauma, anesthetic agents

Treatment: Spinal immobiization

Anaphylactic shock

Distributive shock (massive vasodilation) from anaphylaxis (Type I hypersensitivity), leading to tissue edema

Anaphylactic shock cause and treatment

Cause: Severe allergic reaction

Treatment: Intramuscular epinephrine

Septic shock

Common distributive shock (massive vasodilation) from severe infection with a microorganism

How does severe microorganism infection lead to an overwhelming inflammatory response?

The microorganism releases toxins which stimulates an overwhelming inflammatory response

Treatment of shock

IV fluid to expand blood volume, vasopressors (vasoconstriction), supplemental oxygen

Why are effects of shock often irreversible?

Because it often enters a self-worsening cycle (positive loop), quickly escalating to irreversible tissue and cell damage

Hypertension

Constantly elevated blood pressure >140/90. Increases MI risk. Includes primary or secondary hypertension

Primary hypertension

Idiopathic hypertension from a combination of genetics and the environment (diet, obesity, gender)

Clinical manifestations of hypertension

Signs/symptoms are often invisible, and only become evident when damage occurs (CAD, stroke)

Pre-existing pregnancy hypertension

Hypertension present before pregnancy, or appears before 20 weeks of pregnancy

Gestational pregnancy hypertension

Hypertension at or after 20 weeks of preganncy

Why might hypertension develop during pregnancy?

Due to a decrease in placental blood flow, increasing toxic compound release that may affect many vessels throughout the body

Preeclampsia

Spike in blood pressure and stress to other organs (proteinuria or adverse conditions). Deprives fetus of blood, oxygen, and nutrients

Eclampsia

Seizures and possible coma in women with preeclampsia, due to clots in cerebral vessels