327 Exam 1 Cardiovascular Disease and Atherosclerosis

Primary Prevention

Treatment of conditions such as diabetes and inactivity that predispose patients to developing CVD

Secondary Prevention

Treatment of patients who have CVD while also attempting to decrease further damage, morbidity, and mortality

Blood flow through the heart

Superior and Inferior Vena Cava, right atrium, tricuspid, right ventricle, pulmonary SL valve, pulmonary arteries, lungs, pulmonary veins, left atrium, bicuspid (mitral) valve, left ventricle, aortic valve, aorta

LV

Left Ventricle

SV

Stroke Volume

EDV

Volume of the left ventricle at the end of diastole (relaxation)

ESV

Volume of left ventricle at the end of systole (contraction)

MAP

Mean arterial pressure

CO

Cardiac Output

CI

Cardiac Index

SVR

Systemic vascular resistance, contributor to afterload 

HR

Heart Rate

EF

Ejection fraction of the left ventricle

Blood Pressure

Perfusion to the organs of the body. Dependent upon the output of blood from the heart and the resistance of the arteries and arterioles

Cardiac Output

Amount of blood ejected from the heart. Dependent upon heart rate and volume of blood ejected from the heart with each beat

Formula for Cardiac Output

CO = HR x SV

Formula for MAP

MAP = CO x SVR

Equation for SV

SV = EDV-ESV

Equation for EF

EF = SV/EDV

Components of Stroke Volume

Preload, Inotrope, Afterload

Preload

Dependent upon venous return to the heart and is equal to the stretch of myocardial fibers from volume during diastole

Inotrope

Force of systolic contraction at any given end diastolic volume

Afterload

Ventricular wall stress/tension that develops during systole which equals the resistance that the ventricle must overcome to empty its blood content

Frank Startling Mechanism

States the force of ventricular contraction is a function of the initial muscle fiber length (longer is stronger), related to EDV and EDP. SV also increases in relation to increase in preload.

Tension formula

Tension = ventricular pressure x radius/ventricular wall thickness x2

Ischemic Heart Disease

Is represented by an imbalance of oxygen supply and demand, usually caused by atherosclerotic CAD. An imbalance can also occur because of a reduction in oxygen supply caused by vasoconstriction in the coronary arteries.

Acute coronary syndrome

Occurs when there is a sudden significant imbalance of oxygen supply and demand. Usually caused by rupture of an atherosclerotic plaque in the epicardial artery. Less commonly it is caused by excessive oxygen demand in the setting of CAD.

Normal Artery

Consists of the Adventitia, Media, Intima. Made up of epithelial cells

Response to Injury Hypothesis

Different risk factors like cholesterol, hypertension, tobacco, and diabetes can injure the lining of epithelial cells. That injury will elicit a series of cellular interactions (inflammatory Response) forming the lesions in atherosclerosis

Oxidized LDL and Monocyte Recruitment

LDL enters the blood vessel and oxidizes, stimulates adhesion in endothelial cells, impairs vasodilation, monocytes turn into macrophages ingest oxLDL forming foam cells, which collectively form a fatty streak

Fibroproliferative plaque

Made up of fibrous collagen connective tissue. Makes up the fibrous cap.

Fibrous Cap

Usually more voluminous in a stable, 70% of an average plaque, prevents disruption

Lipid Core Component

Usually less voluminous in stable plaque, dangerous component, destabilizes plaque, more vulnerable to rupture. If exposed to flowing blood, thrombus formation

General progression of Atherosclerosis

Injury to the blood vessel provokes inflammatory response, early fatty streak starts to form, late fibrous plaque formation, encroachment of the lumen of the vessel impairing blood flow- chronic stage angina, plaque ruptures, with exposure of lipid core to coronary blood circulation, thrombus development resulting in unstable angina and myocardial infarction

Oxygen Carrying Capacity

Is dependent on hemoglobin content and systemic oxygenation

When is maximum flow

During Diastole (relaxation) and perfusion pressure is approximated by the aortic diastolic pressure

What causes resistance to flow

atherosclerosis, coronary tone of epicardial arteries (constriction/dilation), and intrinsic tone of small resistance arteries

3 determinants of myocardial demand

Ventricular wall stress/tension, heart rate, and contractility 

How does heart rate determine myocardial oxygen demand

Also known as chronotropy. As HR accelerates the number of contractions and the amount of ATP consumed per minute ins creases, and oxygen requirements rise. Conversely a slowing heart rate decreases ATP utilization and oxygen demand.

How does contractility impact myocardial oxygen demand

Positive inotropy Increases the force of contraction and increases oxygen demand. Negative inotropic drugs decrease myocardial oxygen demand. 

Myocardial Ischemia

Refers to a lack of oxygen due to inadequate perfusion, which results from an imbalance between oxygen supply and demand. Most common cause is atherosclerotic disease of the coronary vessels.

Stable Angina

Chronic predictable pattern of intermittent angina

Evaluation of Patient with stable ischemic heart disease 

History of Symptoms, Physical Examination, Electrocardiogram, Testing Procedures

Characteristics of Stable Angina

Quality of chest discomfort: tightness, squeezing, pressure, burning, heartburn, heaviness, ache

Location and Radiation: discomfort is diffuse rather than localized, in the chest, upper abdomen, back, neck, and lower jaw. Can radiate to shoulders, arms.

Triggered by activities that increase myocardial oxygen demand

Duration and associated symptoms: more than 1-2 seconds, usually lasts 5-10 minutes. Does not last more than 20-30. Associated with SOB, nausea, indigestion, lightheadedness, sweating, fatigue.

Relieved by factors that either reduce oxygen demand or increase oxygen supply to the myocardium

Class I CV Classification System

Ordinary activity does not cause angina, such as walking or climbing stairs. Angina occurs with strenuous, rapid or prolonged exertion at work or recreation

Class II CV Classification System

Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, stairs, emotional stress, etc. 

Class III CV Classification System

Marked limitations of ordinary physical activity. Angina occurs on walking one to two blocks on the level and climbing on flight of stairs in normal conditions and at a normal pace.

Class IV CV Classification

Inability to carry on any physical activity without discomfort, anginal symptoms may be present at rest.

ECG for myocardial Ischemia and injury patterns

Lead localizes the area of the ventricle involved. ST Depression represents ischemia. ST elevation represents acute injury or MI

Exercise Stress Testing

Induced ST depression

Stress testing with nuclear imaging

Allows better estimation of the extent of myocardium that becomes ischemic. Reversible spots suggest ischemia. Irreversible spots support infarction.

Plaque Vulnerability Considerations

Size of the atheromatous core, thickness and collagen content of the fibrous cap, inflammation within the cap, cap fatigue

Atheromatous Core

Disrupted plaques tend to have a large soft lipid core, which redistributes stress to plaque shoulder and increases plaque vulnerability to disruption 

Fibrous Cap Breakdown

A disrupted fibrous cap has fewer smooth muscles cells, lower collagen content, and a greater degree of inflammation. It results from a thinning and weakening of the fibrous cap either from matrix breakdown or deceased synthesis

Results of Plaque Rupture

Thrombosis within the plaque causing rapid plaque growth or thrombosis within the lumen leading to partial or complete obstruction. 

Complications of Plaque Disruption

Formation of occlusive mural thrombi resulting in acute MI with tissue destruction and cell death due to lack of blood flow

Steps of thrombosis formation

Platelet attachment and spreading over the injured epithelium, platelet aggregation, activation of clotting cascade, thrombin generation, fibrin formation, thrombus

What happens in ST-segment Elevation MI

Acute thrombus obstructs blood flow, decrease oxygen, shift from aerobic to anaerobic metabolism, decrease glycogen granules and ATP stores, lactic acid production, decrease pH, decrease myocardial relaxation, decrease contractility, ECG changes, chest pain

Timeline of ST-Segment Elevation MI

10-mins: 50% depletion in ATP stores as well as cellular edema and decreased membrane potential which made lead to lethal arrhythmias

20-60 mins: Mitochondrial swelling, glycogen depletion, impaired sodium potassium pump, accumulation of intracellular calcium which leads to irreversible cell damage

Unstable Angina and Non ST segment Elevation MI

Plaque rupture leading to less obstructive thrombi typically produce the syndromes of unstable angina and non-ST segment myocardial infarction

Non-ST segment elevation MI

Episodes of plaque rupture are more prolonged and more severe than those producing unstable angina. Positive pathologic finding, results in release of serum markers of necrosis. 

Serum marker of cardiac necrosis

Troponins, cTn. Rises 1-6 hours post MI, levels will fall but will remain above the URL for several days. MI requires a rise of fall of cardiac troponin values with at least 1 value above the 99th percentile

Mechanical Dysfunction of the Heart

Sign of lower left Ventricular ejection fraction SOB, pulmonary edema, rejected BP

Electrical dysfunction of the Heart

Ventricular tachycardia or fibrillation, due to non-uniform oxygenation of ventricle, A-fib due to heart failure and stretch of atria, reduced oxygen supply to SA node or AV node causes sinus bradycardia or AV nodal blockage which results in conduction delays in the HIS-Purkinje system. Increased sympathetic tone can cause sinus tachycardia

Ventricular remodeling

Changes in left ventricular size, shape, and thickness involving both the infracted and Non infracted segments of the ventricle that occur as a consequence of an MI

Myocardial Wall Rupture

This period of tissue resorption combined with thinning and dilation of the infarcted zone, results in structural weakness of the ventricular wall and the possibility of myocardial wall rupture at this stage

Heart Failure from MI

Acute MI results in impaired LV function, LV EF is reduced and end diastolic pressure and volume increase. Cardiogenic shock can present and is often fatal.

Peripheral Artery Disease

Systemic Arterial Atherosclerosis most commonly in arteries of the lower extremities producing a reduction in blood flow, causing pain with activity and potentially at rest

Stroke

Sudden onset of a focal neurological deficit that persists for least 24 hours and is due to an abnormality in cerebral blood circulation. Deficits are dependent upon location of the stroke in the brain. May cause multiple mechanisms, including atherosclerosis

Ischemic Stroke causes

Thrombotic occlusion, embolic occlusion, atherosclerosis, hypertensive arterial changes, embolism