Cardiovascular Pathophysiology Review

• Sit in a different part of the room with a new seatmate
• Lora Packel PT, PhD, presents on Evaluation & Treatment of the Client with Cardiovascular Pathology: Part I – Ischemic Conditions, DPT 611 - Spring 2025

Learning Objectives

• Perform a brief subjective history of a mock patient with a primary cardiac disorder and provide a self-reflection on performance
• State the signs/symptoms, pathophysiology, medical/surgical intervention, and diagnostic tests for common cardiovascular conditions
• Identify risk factors for cardiovascular disease from a mock or real case study and determine implications for PT treatment including exercise
• State how physical therapy interventions can improve a patient or clients cardiovascular risk profile; this includes prevention as well as secondary intervention
• Synthesize information from a medical chart to determine if physical therapy is indicated and/or if referrals to other healthcare professionals are needed
• Perform a PT evaluation of a mock client with primary cardiovascular disease
• Synthesize information from a mock or real patient or case study evaluation to determine a PT diagnosis, prognosis, plan of care and discharge planning from acute care
• Create accurate and appropriate interventions for a patient or client with cardiovascular disease including exercise prescription
• Evaluate a patient's response to mobility and also be able to recognize common side effects of cardiovascular medications that may impact a patient's response to PT treatment
• Determine when a patient presents with signs and symptoms of a cardiovascular emergency and take appropriate next steps

Ischemic Cardiovascular Conditions

• Atherosclerosis refers to diseases that cause progressive hardening and narrowing of coronary, cerebral, and peripheral arteries
• Coronary artery disease (CAD) involves an obstruction that limits coronary blood flow without significantly impacting myocardial function
• Coronary heart disease (CHD) is defined by the presence of an obstruction that permanently damages heart muscle function
• Clinical presentation of patients with CHD may occur in sudden cardiac death (SCD)
• Clinical presentation of patients with CHD may occur in chronic stable angina
• Clinical presentation of patients with CHD may occur in acute coronary syndrome (ACS)
  • ACS includes unstable angina, STEMI, and Non-STEMI
• Clinical presentation of patients with CHD may occur in cardiac muscle dysfunction (heart failure)
• Sudden cardiac death (SCD) is the first presenting symptom for 40-50% of patients, with death occurring within 1 hour of symptom onset, usually due to a rhythm disturbance

Coronary Artery Anatomy & Physiology

• Coronary arteries are perfused during diastole or systole
• Determinants of blood flow include diastolic blood pressure
• Determinants of blood flow include vasomotor tone (vasoconstriction or dilatation)
• Determinants of blood flow include resistance to flow
• Determinants of blood flow include left ventricular end diastolic volume
• Flow = DBP + VMT – R - LVEDP

Plaque Formation

• The first sign of plaque is called a fatty streak
• Plaque formation consists of lipids, connective tissue, smooth muscle cells, platelets, and macrophages
• Some plaques calcify and are stable
• Some plaques do not calcify and covered with a thin fibrous cap and are more likely to rupture and called unstable

Atherosclerosis Mechanisms

• Nitric oxide (NO) in the endothelium is affected causing endothelial dysfunction and an immune response
• Lipid filled macrophages grow, causing the endothelium to stretch and separate
• Platelets aggregate
• Collagen levels increase and destroy the elastic media layer, which responsible for dilation
• A fibrous cap of thrombi forms over the plaque

Stable Angina

• Known level of "work" or activity brings on symptoms
• Supply of oxygen to myocardium does not meet demands
• Symptoms get relieved by reduction in intensity of work and Nitroglycerin
• Angina means "strangling" and indicates Ischemia
• Sensory impulse travels in unmyelinated sympathetic nerves to upper thoracic ganglia, through dorsal horn, to spinothalamic tract of thalamus

Warning Signs in Angina

• Ischemia can cause sensory impulse to land in the cortex
• The cortex has sensory input from cutaneous nerves that pass through spinal levels
• The brain can't determine the specific location of the pain

Common Warning Signs of Heart Attack:

• Includes uncomfortable pressure, fullness, squeezing or pain in the center of the chest (prolonged).
• Pain that spreads to the throat, neck, back, jaw, shoulders, or arms
• Chest discomfort with lightheadedness, dizziness, sweating, pallor, nausea, or shortness of breath
• Prolonged symptoms unrelieved by antacids, nitroglycerin, or rest

Atypical, less common warning signs (especially women)

• Unusual chest pain (quality, location, e.g., burning, heaviness; left chest), stomach or abdominal pain
• Continuous midthoracic or interscapular pain and continuous neck or shoulder pain
• Isolated right biceps pain and pain relieved by antacids; pain unrelieved by rest or nitroglycerin
• Nausea and vomiting; flu-like manifestation without chest pain/discomfort and unexplained intense anxiety, weakness, or fatigue
• Breathlessness or dizziness
• Level of discomfort does not correlate to severity of the issue
• Some people have a “silent MI"

Acute Coronary Syndrome

• Unstable angina involves any change from stable angina and has increased morbidity and mortality rates compared to those with stable angina
• Unstable angina consists of increased frequency and angina that occurs at rest
• Unstable angina consists of angina that feels more severe and angina lasting longer 20 min or longer
• Emergency referral is often needed
• Ischemia means an imbalance between oxygen demand and ability to supply oxygen, depriving the myocardium of oxygen (hypoxia) and seen in both stable and unstable angina
• Infarction means the oxygen deprivation lasted long enough to cause the myocardium to die in the distribution of the affected coronary artery

Acute Coronary Syndrome: Myocardial Infarction (MI):

• Oxygen demand outstrips supply in a narrowed artery
• Plaque grows to a point in which it occludes flow
• Plaque ruptures and travels down the coronary artery and occludes flow

ECG Results in Acute Coronary Syndrome

• NSTEMI (non-ST segment elevation myocardial infarction) occurs when blood tests indicate ischemia/infarction, there is ST depression or T wave inversion, but the ST segment doesnt elevate
• Blockage leading to NSTEMI is often partial or temporary, the damage is typically less than with STEMI
• STEMI (ST segment elevation myocardial infarction) involves prolonged blockage, often a “typical MI"

Myocardial Injury Remodeling

• Mycardial injury include zone of hypoxic that may function zone in 2-3 weeks
• Z. Infarct is a necrotic of heart tissue
  • Weak vulnerable scare form in the 10-14 days
  • Fibrous scare form in the 6-8 weeks

Complications with MI

• Presents as abnormal heart activity due to Akinesis/Dyskinesis
• Decreased ejection fraction (normal is 55-70%; 50-55% considered borderline)
  • % of blood ejected from the left ventricle with each contraction
• Increased end-systolic volume
• Reduced cardiac output
  • normal is 5-6 L/min at rest

Chart Review: Lab Values for cardiac function

• Complete Blood Cell Count
• WBC indicates of infection
• RBC indicates Hydration status (influences blood pressure and tolerance to upright positions)
• HgB Ability to fuel work
• Anemia will cause higher HR at rest and increase workload of a heart
• Expect reductions in exercise tolerance and modify intervention intensity
• Plt indicates Risk for bleeding/ consider fall risk
• Electrolytes are related to rhythm disturbances, especially postassium

Diagnosing and MI: Cardiac Enzymes

• Troponin I is the most specific and sensitive elevated if MI is suspected
  • Levels increase within 3-12 hours of angina, peak 24-48 hours, and return to baseline 5-14 days
• Creatinine Phosphokinase or CPK-MB indicates muscle disease, DM, muscle trauma, PE, alcohol toxicity
• Labs offers information into the degree of the MI & treatment.

Case Study

• 68yr old Male patient with following test value taken:
• Hgb 13 g/dL
  • normal range 13.8-17.2 g/dL
• WBC 5 k
  • normal range 4-11k
• Plt 200k
  • normal range 150-300k
• Troponin I 0.8 ng/ml
  • normal range 0.00 to 0.14 ng/ml
• CK-MB/CK 3.5
  • normal range < 2.5
• PT — TO TREAT OR NOT TO TREAT : Look for enzyme stabilization or decline, Consider hemodynamic stability, and Monitor

Relevant Tests/Results

• A physical therapy student is performing a chart review. They need to know normal HgB levels for males and females.
• Patient has myocardial damage
• To Decide PT treatment Look for enzyme stabilization or decline, consider hemodynamic stability, and monitor patient.

Echocardiography (“Echo")

• Non-invasive technique that gives information about structure
• Chamber size and wall thickness, Valve function, and Estimation of ejection fraction (55-70% is normal)
• EF is poorly associated with exercise tolerance
• Look for Ejection Fraction
• Comments about valve function – increased myocardial workload and comments about wall function

Chart Review

• Cardiac catheterization can identify the extent and location of coronary plaque with the use of a hollow tube inserted into an artery (femoral or other) and threaded up to the coronary arteries
• Dye is injected to light up the path and results are recorded
• Most common diagnostic usage to identify the extent and location of plaque in the coronary arteries

Review questions covering common causes of sudden cardiac death, characteristics of unstable plaques, factors affecting coronary artery blood flow and the role of endothelial dysfunction in atherosclerosis. Also covers the impact of collagen levels during atherosclerosis.