HEXS 420 Exam 2

HEXS 420: Exam 2 Study Guide

Cardiovascular Diseases:

1. List and describe the steps of atherosclerotic plaque development

a. An injury happened to the ENDOTHELIUM

i. Due to shear stress and this is BAD bc it’s the innermost layer that protects the integrity of the heart and deals with metabolic properties (nitric oxide))

b. LDL-C moves into the TUNICA INTIMA

c. LDL-C oxidizes and starts causing damage to the surrounding tissue, creating an immune response

i. Inflammation and free radical mutation

d. White Blood Cells (Monocytes) respond and collect the oxidized LDL-C

i. These monocytes overtime turn into macrophages

ii. These macrophages can cluster and then turn into a FATTY STREAK

e. The FATTY STREAK continues to grow, attracting COLLEGEN, SMOOTH MUSCLE CELLS, and other materials that will create ATHEROSCLERATIC PLAQUE

f. The plaque is contained by a FIBEROUS CAP to contain the growth of it

i. The continued growth of the plaque NARROWS the artery

g. If/when the plaque is disrupted, the plaque can burst

i. Platelets respond to the combustion/injury and form a CLOT (Thrombus)

ii. The CLOT can fully OR partially occlude blood flow

iii. OR will break off and travel to other parts of the body

2. Discuss how atherosclerosis progresses over the lifespan

a. This develops over a person’s lifetime starting at childhood.

b. Fatty streaks are formed in the arteries and are made of foam cells and will probably not cause any symptoms. If a poor diet, lack of exercise, obesity, and genetic predisposition persist, this early stage of Fatty Streak formation will get a foundation for problems later.

c. Into young adulthood, the fatty streaks can progress to be fibrous plaques and progress into LDL-C oxidizing to cause inflammation. The arteries begin to lose their elasticity and increase BP and decrease BF. They can still be asymptomatic but having a poor diet, lack of exercise, smoking, etc. can exacerbate the disease.

d. Into older adulthood, advanced plaques may rupture and blood clots will form and may cause a heart attack. The arteries can have severe calcification and harden the arteries, reducing its capability to vasoconstrict and vasodilate to push blood out into the body. This can lead to chronic heart failure, and at this stage, interventions of angioplasty’s, stents, and bypass surgery may be required to restore blood flow.

Angina, Ischemia, Infarct, and PAD:

1. Identify the major coronary arteries

a. Right CAà supplies the right atria/ventricle and SA and AV Nodes

b. Left Main CAà supplies the left atria/ventricle

c. Left Circumflex CAà supplies the left atria and lateral wall of the left ventricle

d. Left Anterior Descending CAà supplies the front of the heart and the left ventricle

i. Describe mechanisms of coronary blood flow (CBF) and cardiac oxygen consumption

1. Coronary blood flow (CBF)

a. regulated by multiple factors, including metabolic demands, vascular resistance, and autonomic nervous system control.

2. Renin/Angiotensin

a. Regulating blood pressure and fluid balance. When blood flow is reduced, renin is released, leading to angiotensin II production, which causes vasoconstriction and increases BP.

3. Cardiac Oxygen Consumption

a. Depends on factors such as heart rate, contractility, and wall stress. Myocardial oxygen demand increases with increased workload, while coronary arteries must supply sufficient oxygenated blood

i. Oxygen supply and demand ratio:

1. If O2 consumption is NOT meeting the demand, a decrease in ratio causes symptoms of CHF starting w/ angina

About 100% of O2 is taken from hemoglobin in CBF; if we cannot provide that during exercise or rest, there will be issues in the body due to the oxidative nature of the cardiac cells. Our blood flow is altered and no being able to INCREASE the percentage of O2 from hemoglobin that we’re taking causes the body to INCREASE the rate oat which we deliver RBC to the cardiac cells and atherosclerosis can deeply occlude blood flow in this.

2. Describe relationship between atherosclerosis and acute coronary syndrome (ACS)

a. Acute Coronary Syndrome (ACS) includes conditions such as unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

b. Atherosclerosis can lead to ACS when a plaque ruptures, triggering thrombus formation that may partially or fully block coronary arteries.

c. Angina

i. results from temporary ischemia due to narrowed arteries but no permanent damage; first indication of this occurs during exerciseà increased HR and BP and O2 Demand and Cardiac Cells are stressed

d. Ischemia

i. occurs when oxygen supply to the heart is insufficient due to decrease in Blood Flow; silent and cannot feel it; can start immediately from a decrease in Blood Flow

ii. critical stenosisà threshold is large (75% of luminal closing)

e. Myocardial infarction (MI)

i. occurs when prolonged ischemia leads to cardiac muscle cell death; 16 mins to restore blood flow to cardiac tissues

ii. Classification:

1. Type 1à caused by pathology of walls of the Coronary Artery

2. Type 2à caused by imbalance of O2 supply and myocardial demand

3. Type 3à sudden, unexpected cardiac death

4. Type 4aà PCI=

5. Type 4bà associated with stent thrombosis

6. Type 4cà caused by stent restenosis

7. Type 5à CABG=

3. Describe the impact of atherosclerotic plaque development on peripheral arteries

a. Peripheral Artery Disease (PAD) is caused by atherosclerosis in non-coronary arteries, often affecting the legs and lower extremities.

b. Reduced blood flow leads to claudication (pain with exertion), poor wound healing, and in severe cases, critical limb ischemia or gangrene.

Heart Failure:

1. Describe chronic heart failure (CHF) and identify underlying causes

a. A chronic and progressive condition where the heart muscle is unable to pump enough blood through the body due to a thinner LEFT VENTRICULAR WALL

b. Causes:

i. Ischemia

ii. Myocardial Infarction

iii. Genetic pre-disposition

iv. Lifestyle (diet, drugs, etc)

v. Idiopathic

vi. Hypertension

vii. coronary artery disease

viii. valvular disease

ix. cardiomyopathy

x. myocarditis

xi. long-term diabetes

2. Differentiate between systolic and diastolic CHF

a. Systolic (HFrEF)

i. Heart failure with REDUCED Ejection Fraction

ii. Left ventricle has a reduced capacity to contract (Frank Sterling)

1. Ischemia/MI

2. Chronic Volume Overload

a. Mitral Valve + aortic regurgitation

3. Dilated Cardiomyopathy

iii. Reduction is SV and Q

b. Diastolic (HFpEF)

i. Heart failure with PERSERVED Ejection Fraction

ii. Left ventricle is stiff and inadequately fills

1. LV Hypertrophy

2. Restrictive Cardiomyopathy

3. Transient Ischemia

3. Explain the significance of ejection fraction as it relates to CHF

a. Ejection Fraction (EF)à measures the percentage of blood pumped out of the left ventricle per beat.

b. Helps diagnose CHF type and guide treatment (medications, lifestyle modifications, or interventions).

c. Lower EF = Worse prognosis and higher risk of hospitalization or mortality.

d. Used to monitor disease progression and response to therapy (e.g., ACE inhibitors, beta-blockers).

4. Explain how CHF impacts SV and Q

a. SV decreases due to weakened contraction or poor filling.

b. Q (Cardiac Output = HR × SV) declines, leading to fatigue, fluid retention, and poor circulation.

i. Describe the compensatory mechanisms implemented to preserve Q

1. Frank-Starling Mechanism: The heart increases preload to maintain output.

2. Sympathetic Nervous System Activation: Increases HR and contractility with epi and norepi- activation from the adrenal medulla.

3. Renin-Angiotensin-Aldosterone System (RAAS): Causes vasoconstriction and fluid retention to maintain/increase BP and perfusion.

Valvular Diseases:

1. Describe the role and function of heart valves.

a. Ensure one-way blood flow through the heart by opening and closing in response to pressure changes.

b. Mitral and tricuspid valves: Control blood flow between atria and ventricles.

c. Aortic and pulmonary valves: Control blood flow from ventricles to systemic/pulmonary circulation

d. Main focus is on the Mitral and Aortic valves as these most directly impact blood flow delivery

2. Identify the primary underlying causes of valvular dysfunction.

a. Congenital Defects

i. Most common

ii. Born w/ defective/incomplete/incomplete valves

iii. Can be fixed w/ surgery dependent on location of impaired valve

b. Connective Tissue Disorders

i. Effects development and function of the valve itself

c. Ineffective Endocarditis

i. Inflammation of the ENDOCARDIUM muscle

ii. Impacts the pressure inside the chambers of the heart

d. Rheumatic Heart Disease

i. Untreated or undiagnosed strep or scarlet fever results in Rheumatic Fever causing RHD

ii. Detrimental to MITRAL Valve, 60% of cases prove this

e. Calcific Disease of Aging

i. Increase in age, Increase in Calcium

ii. Causes ridges in the valves

3. Describe the impact of valvular stenosis vs. regurgitation.

a. Stenosis: Narrowing the valve opening, increasing resistance to blood flow.

b. Regurgitation: Incomplete closure, causing backward blood leakage.

i. Describe the mechanisms of mitral and aortic valvular diseases.

1. Mitral Regurgitationà valves improperly shut and are stretchy; backflow in LEFT ATRIA

2. Mitral Stenosisà narrower opening of valves, increases/builds more pressure; Increased resistance in LEFT VENTRICLE filling, reducing Q

3. Aortic Regurgitationà backflow into LEFT VENTRICLE from the AORTA; insufficient closing of the aorta

4. Aortic Stenosisà increased ventricular pressure and reduction in Q; can cause LVH; narrower opening and more pressure on LV

Revascularization and Transplant:

Discuss and compare the following:

1. Percutaneous interventions

a. Percutaneous transluminal coronary angioplasty

i. A procedure was carried out on the coronary arteries itself to restore blood flow by removing plaque. The groin area is numbed and a guidewire is brought into the heart with a catheter will go to the coronary artery. Dye is used to see the blockages and the guidewire is used if the blockage is significant enough with a balloon at the tip of the catheter. The balloon will then be inflated, expanding the artery and a stent may be placed to increase Blood Flow.

b. Stent placement

i. A stent is a mesh tube inserted in the CA’s to keep it open to increase blood flow.

ii. Four types of stents:

1. Revolution of the sheet

2. Coil

3. Braided Wires

4. Slotted Tubes

c. Comparison

2. Coronary artery bypass surgery

a. Uses grafted veins/arteries to bypass blockages that remain open for 5-10 years maximum; requires general anesthesia w/ major surgery; criteriaà restenosis, missed window for angioplasty, multi-vessel blockage, vessel lesions

3. Heart transplant

a. Used in end-stage heart failure if all other preventive measures do not work

Pacemakers:

1. Trace the history of the modern-day pacemakers.

a. First one made in 1958

2. Describe the purpose of a pacemaker and:

i. Restores normal rhythm in patients with arrhythmias or conduction block

b. How it presents in ECG tracings,

i. Sharp vertical spike before paced beats

c. How it paces the heart,

i. Sends electrical impulses to stimulate contraction.

d. How it is coded

i. Five-letter system indicating chamber(s) paced, sensed, and response type.

3. Describe advancements in the modern-day pacemaker.

a. Leadless pacemakers, dual-chamber pacing, and wireless monitoring

SCAD and Aneurysm

1. Describe SCAD and aneurysm

a. SCAD: A tear in the coronary artery, leading to spontaneous occlusion.

b. Aneurysm: Abnormal dilation of a blood vessel, which may rupture

2. Understand assessment and treatment options

a. SCAD: Managed with beta-blockers, stents, or bypass surgery if needed.

b. Aneurysm: Monitored via imaging; large or symptomatic aneurysms may require surgical repair.