Rehab Medicine- Exam 2

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32 Cards. Created by Danielle Toohey ().


-Chronic increase of luminal stenosis and decreased compliance of arterial walls from buildup of plaque -caused by lipoproteins and immune cells -immuno- inflammatory process

Progression of Atherosclerosis

-injury to endothelium of arterial walls -injured endothelial cells are inflamed, do not produce normal amounts of antithrombotic and vasodilating cytokines are released -growth factors are released -stimulates smooth muscle proliferation -macrophages adhere to injured endothelium -macrophages create oxidative stress causing more injury to vessel wall LDL is oxidized in the blood stream -Oxidized LDL is toxic to the endothelial cells -LDL is engulfed by macrophages which then become foam cells (come together)

Fatty Streaks

-Foam cells accumulate and create a fatty streak in the arterial walls -Fatty streaks are in most people, including children -fatty streaks produce oxygen radicles, cause immune and inflammatory changes, continuing to damage arterial wall

Progression of plaque

-smooth mm. cells proliferate, produce collagen, and migrate over fatty streak creating a fibrous plaque -the plaque can calcify and become a stable plaque -stable plaques are characterized by smooth mm. cells and a matrix of collagen I & II -this can be large enough to obstruct blood flow

Signs/ symptoms of CAD

angina sweating nausea/vomiting activity intolerance palpitations

Diagnosis of CAD

Exercise stress test drug stress test

Exercise stress test

-perform exercise protocol on treadmill -NOT a VO2 max test -resting ECG -Heart rate, blood pressure, respiratory rate, ECG monitored during activity -Look at ECG for abnormal readings indicating ischemia to the heart

Adenosine stress test

-pharmaceutical stress test (adenosine) -patient unable to tolerate walking on treadmill for exam -monitor ECG, BP, HR -Give patient medication-- a vasodilator

Cardiac Catheterization

  • Invasive procedure in which MD can observe coronary arteries
  • coronary arteries accessed with a catheter usual via femoral artery -Dye is injected to help visualize arteries using external X-ray (angiography) -Results will guide further treatment

Treatment for CAD

-pharmacology -angioplasty -stents -coronary artery bypass graft (open heart, graft vessels around the heart to help blood flow)

Pharmacology for CAD- Statins

  • Lipitor (atorvastatin), Zocor (simvastatin)

-inhibits enzymes for cholesterol synthesis, lowering blood LDL -Side effects- dizziness, fainting myopathy

Pharmacology for CAD- Aspirin

Salicylate--antiplatelet effect -block cox enzyme, prevents prostaglandins -GI upset

Pharmacology for CAD- Nitroglyn

Nitroglycerine -cGMP production, vasodilation smooth mm.

Side effects- headaches, dizzy, nausea, orthostasis

Pharm. for CAD- Beta Blockers

-Tenormin (atenolol), Inderal (propranolol) -B adrenergic receptor antagonist, decreases in heart rate, contractility, vasodilation of coronary arteries -Bradycardia, dizziness

Pharm for CAD- Calcium channel blockers

-Norvasc (amlodipine) -Procardia (nifedipine)

-inhibits Ca influx in vascular smooth mm. Vasodilator, decreased HR and inotropy -hypotension, edema, fatigue, dizzy


-Catheter inserted into coronary artery has balloon that can be inflated -procedure increases diameter by compressing plaque against artery walls -a stent can be inserted to help preserve the artery diameter

Cardiac precautions

-blood pressure changed that are abnormal for activity. SBP > 20 mmHg change -HR increase inappropriate to activity. Pt may be on meds to control HR -Dyspnea or SaO2


-Sustained elevation of systemic arterial blood pressure >120 -1 in 3 adults has been diagnosed with HTN -increased risk of MI, kidney disease, stroke -Caused by increased CO, peripheral vascular resistance or both -primary hypertension- no known cause, 90-95% of diagnosis

primary hypertension

no known cause, 90-95% of diagnosis

secondary hypertension

caused by another disease, such as renal disease