CAD 2025 - Evaluation & Treatment of Cardiovascular Pathology PDF

Sit in a different part of the room with a new seatmate  EVALUATION & TREATMENT OF THE CLIENT WITH CARDIOVASCULAR PATHOLOGY: PART I – ISCHEMIC CONDITIONS Lora Packel PT, PhD DPT 611 - Spring 2025  LEARNING OBJECTIVES At...

Sit in a different part of the room with a new seatmate  EVALUATION & TREATMENT OF THE CLIENT WITH CARDIOVASCULAR PATHOLOGY: PART I – ISCHEMIC CONDITIONS Lora Packel PT, PhD DPT 611 - Spring 2025  LEARNING OBJECTIVES At the end of the cardiac module, students should be able to: 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. LEARNING OBJECTIVES, CONTINUED 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 determine whether the treatment should continue, be progressed, regressed, or terminated. Students should 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 Hillegass, 4 th ed Atherosclerosis: Diseases that causes progressive hardening and narrowing of the coronary, cerebral, and peripheral arteries Coronary artery disease (CAD): presence of an obstruction that limits coronary blood flow but doesn’t significantly impact myocardial function Coronary heart disease (CHD): presence of an obstruction that causes permanent damage to heart muscle function CLINICAL PRESENTATION OF PATIENTS WITH CHD OCCURS IN ONE OF FOUR WAYS 1. Sudden cardiac death or SCD 2. Chronic stable angina 3. Acute coronary syndrome (ACS) a. Unstable angina b. STEMI c. Non-STEMI 4. Cardiac muscle dysfunction (heart failure) 1. SUDDEN CARDIAC DEATH (SCD) FIRST presenting symptoms in 40-50% of patients Death within 1 hour of symptom onset Usually caused by a rhythm disturbance CLINICAL PRESENTATION OF PATIENTS WITH CHD OCCURS IN ONE OF FOUR WAYS 1. Sudden cardiac death or SCD 2. Chronic stable angina 3. Acute coronary syndrome (ACS) a. Unstable angina b. STEMI c. Non-STEMI 4. Cardiac muscle dysfunction (heart failure) 2. CHRONIC STABLE ANGINA & ACUTE CORONARY SYNDROME CORONARY ARTERY ANATOMY & PHYSIOLOGY Coronary arteries are perfused during diastole or systole? Determinants of blood flow are: Diastolic blood pressure Vasomotor tone (vasoconstriction or dilation) Resistance to flow Left ventricular end diastolic volume Flow = DBP + VMT – R - LVEDP  PLAQUE FORMATION First sign of plaque called FATTY STREAK Plaque consists of lipids, connective tissue, smooth muscle cells, platelets, macrophages https://www.cdc.gov/heartdisease/f Some plaques calcify and are “stable” acts.htm Some plaque do not calcify and are rich in lipids and inflammatory cells. Covered with a thin fibrous cap and are more likely to rupture - “unstable”  ATHEROSCLEROSIS MECHANISMS 1 WINZER, E., WOITEK F., LINKE, A. (2018). PHYSICAL ACTIVITY IN THE PREVENTION AND TREATMENT OF CORONARY ARTERY DISEASE. JOURNAL OF THE AMERICAN HEART ASSOCIATION 7. ACCESSED ONLINE. 1. **Nitric oxide (NO) in the endothelium is affected causing endothelial dysfunction and an immune response 1. Lipid filled macrophages grow causing the endothelium to stretch and separate 1. Platelets aggregate 1. Collagen levels increase and destroy elastic layer of the media*Media is responsible for dilation 1. A fibrous cap of thrombi forms over plaque  VIDEO: MCGRAW HILL (FREE ON ACCESS PHYSIOTHERAPY 🡪 MULTIMEDIA🡪 ANATOMY AND PHYSIOLOGY REVEALED🡪 LAUNCH🡪 MODULE 9 CARDIOVASCULAR🡪 ANIMATION🡪 CLINICAL APPLICATION🡪 CAD) http://anatomy.mheducation.com/html/apr.html?animal=human&id=17023 (Watch until minute 3) **Not working – stay tuned. Watch this video from minute 2:30 to 7:45 https://youtu.be/EATkbpqlxvc?feature=shared Take notes on: Role of damaged endothelium Role of LDL, monocytes/macrophages Foam cells Rupture Ischemia vs infarction 2. STABLE ANGINA Known level of “work” or activity brings on symptoms Supply of oxygen to myocardium doesn’t meet demands REST* Symptoms are relieved by one Reduction in intensity of work or all of the following: Nitroglycerin  ANGINA OR ANGINA PECTORIS Angina means “strangling” and indicates Ischemia Ischemia - sensory impulse travels in unmyelinated sympathetic nerves to upper thoracic ganglia, through dorsal horn, to spinothalamic tract of thalamus and lands in the cortex The brain also receives input from the cutaneous nerves that pass through those spinal levels as well. Brain can’t determine the specific location of the pain. Végh AMD, Duim SN, Smits AM, Poelmann RE, Ten Harkel ADJ, DeRuiter MC, Goumans MJ, Jongbloed MRM. Part and Parcel of the Cardiac Autonomic Nerve System: Unravelling Its Cellular Building Blocks during Development. Journal of Cardiovascular Development and Disease. 2016; 3(3):28. https://doi.org/10.3390/jcdd3030028  Pay Close Attention to: Common warning signs and Atypical Angina Level of discomfort DOES NOT correlate to severity of the issue Some people have a “silent MI” Hillegass, 3rd ed  CLINICAL PRESENTATION OF PATIENTS WITH CHD OCCURS IN ONE OF FOUR WAYS 1. Sudden cardiac death or SCD 2. Chronic stable angina 3. Acute coronary syndrome (ACS) a. Unstable angina b. Acute Myocardial Infarction (“heart attack”): STEMI c. Acute Myocardial Infarction (“heart attack”): Non-STEMI 4. Cardiac muscle dysfunction (heart failure) 3. ACUTE CORONARY SYNDROME Unstableangina Any change from stable angina increased frequency of angina Angina that occurs at rest Angina that feels more severe Angina lasting longer 20 min or longer Emergency referral* Increased morbidity and mortality rates compared to those with stable angina Ischemia vs Infarction Ischemia means an imbalance between oxygen demand and ability to supply oxygen. The myocardium is deprived of oxygen (hypoxia) See this in both stable and unstable angina. Infarction means the oxygen deprivation lasted long enough to cause the myocardium in to die in the distribution of the affected coronary artery. ACUTE CORONARY SYNDROME: MYOCARDIAL INFARCTION (MI) Three main mechanisms for an MI: 1. Oxygen demand outstrips supply in a narrowed artery 2. Plaque grows to a point in which it occludes flow 3. Plaque ruptures and travels down the coronary artery and occludes flow  ACUTE CORONARY SYNDROME NSTEMI – non-ST segment elevation myocardial infarction. Blood tests indicate ischemia/infarction, but ST segment doesn’t elevate. May see ST depression or T wave inversion Blockage is partial or temporary, so typically the damage is less than STEMI STEMI – ST segment elevation myocardial infarction Blockage is prolonged – “typical MI”  MYOCARDIAL INJURY & REMODELING Zone of Hypoxic Injury: may function in 2-3 weeks  COMPLICATIONS WITH MI ABNORMAL CONTRACTION PATTERNS IN MYOCARDIUM Akinesis Dyskinesis or abnormal movement 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 CARDIAC FOCUS Complete Blood Cell Count WBC: Infection RBC: Hydration status; implications for blood pressure and tolerance to upright HgB: Ability to fuel work; Anemia will cause higher HR at rest, limiting HR reserve for exercise Anemia will increase workload of a heart that already has difficulty with providing adequate blood flow Expect reductions in exercise tolerance and modify intervention intensity Plt: Risk for bleeding; consider fall risk Electrolytes – rhythm disturbances, especially potassium Cardiac Enzymes DIAGNOSING AND MI: CARDIAC ENZYMES AHA GUIDELINES 2007 (LATEST UPDATE FOR MI DX), ACADEMY OF ACUTE CARE PHYSICAL THERAPY – 2017 LABORATORY VALUES INTERPRETATION RESOURCE. Troponin I is the most specific and sensitive marker for a MI Levels increase within 3-12 hours of angina, peak 24-48 hours, and return to baseline 5-14 days Creatinine Phosphokinase or CPK-MB *false (+): muscle disease, DM, muscle trauma, PE, alcohol toxicity PT Implications: Labs give you insight into the extent of the MI & whether the person’s MI is still evolving. Treat or defer? Level of intensity once cleared for treatment?  CASE STUDY A physical therapy student is performing a chart review. They notice the following lab values for a 68-year-old male: Hgb 13 g/dL [13.8-17.2 g/dL] WBC 5 k [4-11k] Plt 200k [150-300k] Troponin I.8 ng/ml [0.00 to 0.14 ng/ml] CK-MB/CK 3.5 [< 2.5] *You do need to know normal HgB levels for males and females. PT – TO TREAT OR NOT TO TREAT? 1 2 3 Look for enzyme Consider Monitor, monitor, stabilization or hemodynamic monitor decline stability CHART REVIEW: RELEVANT MEDICAL TESTS  ECHOCARDIOGRAPHY (“Echo”) Non-invasive technique that gives information about structure: Chamber size and wall thickness Valve function 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 Comments about wall function  CARDIAC CATHETERIZATION or Angiogram Hillgass & Sadowski 2017 Elsevier Hollow tube is inserted into an artery (femoral or other) and threaded up to the coronary arteries. Dye is injected and coronaries are illuminated Identify: – Most common use: identify the extent and location of coronary plaque