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5 Cardiovascular Diseases |
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Coronary Artery Disease (CAD, CVD) Ischemic Heart Disease (IHD, CHD) Hypertension (HTN) Peripheral Vascular Disease (PVD) Stroke (generally ischemic) |
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obstruction but doesnt affect heart function |
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L coronary a R coronary a L circumflex a |
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Myocardial Blood Flow Determinants |
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Diastolic BP Resistance Vasomotor Tone LV End-diastolic pressure |
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Atheroslcerosis (process) |
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active process involving molecular signals that produce altered cellular behavior and endothelial dysfunction with subsequent inflammation. (starts with an injury, shearing of the arterial wall, tearing, inflammation, intima and media get LDLs deposited between the layers) |
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Fatty Streak (lipid deposits) *aorta and coronary arteries |
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fibrotic (fibrous plaque: increase collagen level, medial elastin destruction, change in fibrous protein composition) *stable vs. unstable, progression based on risk factors |
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Atherogensis Chain of Effect |
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Endothelial injury with increased infiltration of atherogenic lipoprotein(LDL, VLDL) Sub endothelial retention and modification of LDL,VLDL leads to intimal entry of monocytes and T lymphocytes Subintimal diffusion of monocytes to macrophage which internalize LDL ,transform into foam cells (First stage of fatty streak development) Haemodynamic stress or inflammatory process activate PDGF which will stimulate SMCs ending by having atherosclerotic plaque separated from blood by fibrous cap Death of foam cells by necrosis or apoptosis lead to necrotic core formation Rupture of fibrous cap, exposure of thrombogenic substrate, subsequent arterial thrombosis |
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smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteglycans, neovascularization |
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cell debris, cholesterol crystals, foam cells, calcium |
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Mechanism of Vascular Response to Injury |
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blockage of signaling build of gunky yellow necrosis higher shear of blood flow gross necrotic tissue can rupture and spill out into vessel |
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Progression of Atherosclerosis |
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normal artery fatty streak fibrofatty plaque advanced/vulnerable plaque clinical phases:aneurysm and rupture, occlusion by thrombosis, critical stenosis |
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gooey is bad hard fibrous cap = contained and able to be stinted |
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What is the most powerful contributor to cardiovascular disease? |
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Classification of Hypertension: Normal |
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Classification of Hypertension: Pre-hypertension |
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Classification of Hypertension: Stage 1 |
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Classification of Hypertension: Stage 2 |
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Classification of Hypertension: Stage 3 |
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Classification of Hypertension: Stage 4 |
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With activity drop in BP 20 mmHg SBP or 10 SBP and 10 DBP chronotrophic incompetence |
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Hypertension: PT Intervention |
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avoid valsalva movements aerobic ex 4-7x's a week 30-45 min 60-85% HR max RPE |
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Ischemic Heart Disease: Clinical Presentations |
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Chronic stable angina Unstable angina (STOP EX's!) Myocardial infarction Silent ischemia Arrythmia Sudden death |
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Typical Signs and Symptoms of a Heart Attack |
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pain radiating down left arm females: unusual fatigue, disturbed sleep, shortness of breath, indigestion, anxiety, chest discomfort |
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isoelectric line dropping |
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characterized by chest pain transient hypoxia relieved with activity change or SLNG |
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Circadian variation (4 hours) in catecholamine levels Increases HR and BP Increased platelet activation Pathologic changes in atherosclerotic plaques |
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Unstable Angina: notify physician if... |
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Angina at rest Typical angina occurs at lower exertion Deterioration of previously stable pattern Physiological changes Drop in HR or BP with usual exercise |
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Only at rest ST segment elevation on EKG increased coronary vasomotor tone or spasm |
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Prinsmetal Angina: Treatment |
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nitrates+calcium channel blockers usually avoid beta blockers(alpha adrenergic activity and worsening vasoconstriction) |
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MI: pathological diagnosis |
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requires evidence of myocyte death as a consequence of prolonged ischemia. |
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requires an integrated assessment of history and combination of indirect evidence of myocardial necrosis using biochemical, EKG, and imaging modalities |
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in at least 2 consecutive leads >2mm in leads V1, V2, V3 >1mm in all other leads indicates an occlusion in a large vessel and therefor a large area is at risk *cardiac emergency* |
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findings of MI, without ST elevation on EKG. Not always, but may represent smaller area, or high grade lesion, without total occlusion. *better outcome: smaller vessel* |
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Onset: 3-4 hours Peak: 33 hours Return to normal: 3 days |
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Cardiac Markers: Troponins |
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Onset: 3-12 hours Peak: 18-24 hours Return to norm: up to 10 days |
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Cardiac Markers: Myoglobin |
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Onset: 1-4 hours Peak: 18-24 hours Return to normal:- |
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Onset: 12-24 hours Peak: 72 hours Return to normal: 5-14 days |
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EKG: II, III aVF Artery: R Coronary |
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EKG: I, aVL, V5, V6 Artery: LAD or circumflex |
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EKG: V1-V2, tall broad initial R wave, ST depression, Tall upright T wave Artery: Posterior Descending |
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Largest most damaging infacrtion |
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What effect does inactivity have? |
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Oxygen- increase oxygen saturation, and delivery Nitroglycerin- decrease myocardial oxygen demand, vasodilator. Aspirin/Clopidrigrel- anti-platelet Heparin/enoxaparin- anticoagulation Pain relief Revascularization |
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Treatment: Coronary Artery Bypass |
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internal mammary artery bypass saphenous vein bypass |
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inhibit sympathetic stimulation |
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Treatment: calcium channel blockers |
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if beta blockers are not effective |
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decrease production of cholesterol in liver, anti-inflammatory |
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Disease Specific Effects on Physiological responses and Fitness: Chronotropic Incompetence |
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Failure to reach 85% of APMHR in the absence of β-blockers or other medications with similar effects |
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Disease Specific Effects on Physiological responses and Fitness: Abnormal heart rate recovery |
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A decrease in HR of <12 bpm at 1 minute of ACTIVE RECOVERY or <22 bpm at 2 minutes of supine recovery |
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Disease Specific Effects on Physiological responses and Fitness: BP |
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In the absence of β-blockers or ACE inhibitors, a failure of systolic BP to rise in proportion to exercise intensity |
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Disease Specific Effects on Physiological responses and Fitness: cardiac output and oxygen uptake |
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The reduction in VO2 is SELDOM the result of decreased oxygen extraction but rather is the result of decreased oxygen delivery |
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The Fick Equation: compromised cardiac functioning |
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a-vO2 allows resting VO2 to be maintained |
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The Fick Equation: if cardiac output cannot increase |
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oxygen extraction can achieve a small increase in VO2 at the onset of exercise, but not enough to sustain exercise for an increased duration |
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incidence of cardiac arrest survival to discharge |
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causes of post-cardiac arrest damage |
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Free Radical formation (increase in ROS) Activation of apoptotic pathways Activation of inflammatory pathways |
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most common cause of cardiac arrest |
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60-70% of cardiac arrest occurs in individuals with coronary artery disease |
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sustainable cardioprotection |
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exercise vs. ischemic preconditioning |
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Definition
IPC: Regulated by iNOS and COX-2 EPC: Regulated by ? HSP72 ? |
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