Cloned from:

Bookmark and Share

Front Back
Coronary Artery Disease (aka coronary heart disease)
-impairs pumping ability of heart by depriving heart of O2 and nutrients -diminishes myocardial blood supply until deprivation impairs myocardial metabolism-atherosclerosis-artheriosclerosis.
age -gender >male b/c center weight closer to heart >post menopausal women b/c estrogen is protective to heart -family history –tobacco. HTN. Hyperlipidemia. Diabetes. Obesity. physical inactivity. ETOH.
CAD or Heart Disease Prevention
antiplatelet/anticoagulant therapy (ASA/plavix and coumadin). -Ace inhibitor (lisinopril and captopril) -ARBs (cozaar and diovan and benicar – BP meds) -blood pressure beta blockers –cholesterol -diet/weight loss -exercise
-growing mass of plaque and platelets and fibrin and cellular debris eventually narrows coronary artery lumen enough to impede blood flow. -a type of arteriosclerosis in large vessels. -causes increased rigidity and decreased lumen size.
-thickening and hardening of arterial wall -causes increased rigidity and decreased lumen size.
-arteries/arterioles thicken to withstand stress leading to hypertrophy and hyperplasia of smooth muscle -ultimately leads to lumen narrowing. -BP numbers. dx by> -2 or more readings taken at 2 or more visits -seated for 10 minutes. feet on floor. arm at rest –rested. relaxed as possible -if v high BP w/ assoc symptoms. rapid tx necessary!lifestyle changes first! (DASH diet) -stage 1: start with thiazide diuretic or beta blocker. or ACE inhibitor alone -stage 2:start with combination therapy
Complicated Hypertension
- sustained primary that alters stricture and fx of small vessels: eye. Brain. Kidney. aorta -increase CO and increase vasoconstricton -LV hypertrophy -CAD
Malignant Hypertension
-rapid and progressive ->140 diastolic-cerebral edema related to hydrostatic pressure> increased intracranial pressure leads to worsening compliance -increased membrane permeability -monroe-kellie hypothesis –headache -FATAL IS UNTREATED!;
Ischemic Heart Disease
-decreaed pumping ability of heart which results in decreased cardiac output -cardiac output=amt of blood pumped per minute (SV X HR) CAUSES-decrease 02 -mechanical (motion and decreased contractability) -biochemical (anaerobic. Acidosis) -cardiac cells viable for 20 min under ischemic conditions -electrical (changes in EKG are seen within 30-60 seconds of hypoxia) -infarct=death and irreversible.
4 factors affecting heart output
1.preload (CVP ventricular filling) 2.afterload (BP resistance of ejection of blood from heart) 3.cardiac contractability (actin/myosin and ionotropic influence) 4.heart rate (diastolic filling)
Heart Failure (right and left sided) CAUSES and TX
-CAD –HTN -MI –DM –Cardiomyopathy -Valvular Disease -Congenital Heart Disease –Arrythmias -Endocarditis -Anemia -Lung Disease. TREATMENT -goal=relieve symptoms and improve QOL. treat reversible causes -pharmacological treatment=diuretics. ACE inhibitors. BB. Digitalis. nesiritide -resynchronization-AF -correcting reversible causes=thyrotoxicosis. valve replacement. AF. CABG -transplant
Systolic Heart Dysfunction
-impaired ejection of blood from heart during systole -decrease in cardiac contractability -decrease in ejection fraction (normal is 65%) -decrease in EF causes increase in ventricular dilation and ventricular wall tension
Diastolic Dysfunction
-impaired filling of ventricles during diastole -ventricular hypertrophy -poor ventricular compliance (ability to stretch during filling) -persons with diastolic dysfunction often becoming symptomatic during activities that increase HR
Left Sided Heart Failure
-LV pumping is impaired and blood backed up into LA. -LA has reduced filling capacity to accept blood from pulmonary veins -blod backs up into pulmonary vascular bed -increased hydrostatic pressure in pulmonary vascular bed causes acculmulation of fluid in interstitial and alveolar spaces. -pulmonary veins which empty blood into LA have no valves so blood can easily back up into lungs -pulmonary venous system becomes congested when outflow from LA is impeded
Left sided heart failure S/S
-exertional/noctural dyspnea -blood tinged sputum –orthopnea –cough –cyanosis -decreased urinary output -rales/crackles -fatique -s3 gallop –PND -DOE - FACES –Fatigue- Activities Impaired -Chest Congestions –Edema -ankle swelling -Shortness of Breath
Left Sided Heart Failure DX
Left Sided Heart Failure =DIAGNOSIS -history and physical –lab –EKG –CXR –echocardiography ASSESSMENT-FACES –Fatigue- Activities Impaired -Chest Congestions –Edema -ankle swelling -Shortness of Breath
Right Sided Heart Failure
-left sided failure caused by increase in LV filling pressure that’s reflected back into pulmonary circulation -pulmonary hypoxia resulting from COPD or sleep apnea -stenosis or regurgitation of tricuspid or pulmonic valves -RV infarction -acute or chronic pulmonary disease-jugular veins become prominent in severe right sided heart failure -superior vena cava which empties blood into right atrium has no valves
Right Side Heart Failure S/S
-fatique –ascites -liver and sleen enlargement -elevated venous pressure
Right Sight Heart Failure DIAGNOSIS and ASSESS
-history and physical –lab –EKG –CXR –echocardiography. ASSESSMENT –FACES- Fatigue- Activities Impaired -Chest Congestions -Edema or ankle swelling -Shortness of Breath –PND -DOE
Normal Sinus Ryhthm
-normal heart rythmn
Atrial Fibrillation
-atria quivers. An electrical problem -stagnant bloodflow
Ventricular Fibrillation
Premature Ventricular Contraction (PVC)
-regularly irregular -could be due to excess K+ due to too much Lasix
Chronic Ischemic Heart Disease
-Chronic stable angina -Silent Myocardial ischemia -variant or vasospasctic angina
Acute Coronary Syndromes
-unstable agina -myocardial infarction
Stable Angina
-symptomatic chest pain -transient myocardial ischemia- associated with exertion and relieved by rest -TEMPORARY -assc with fixed coronary obstruction –reversible -goes away with rest!!
-medications –02 -SL nitro NGT (vasodilates to increase blood flow) -ASA aspirin *calcium channel blockers * (because Ca+ goes into muscle to cause contraction. Bloack Ca+ decreases contractability).
Unstable Angina
-clinical syndrome of ischemia ranging between stable angina and myocardial infarction -more frequent episodes of chest pain. Can occur at any time. -episodes last longer than 20 minutes -plain not totally relieved with SL NGT Nitro –REVERSIBLE
Variant Angina
-caused by coronary artery spasm -spasms often occur is presence of coronary artery stenosis -pain occurs at rest and with minimal exertion and or nocturnally -may be secondary to hyperactive SNS responses -arrythmias may occur with severe pain -v rare but v dangerous. Unpredictable when it does occur.
Acute Myocardial Infarction
-endpoint of CAD -prolonged lack of myocardial oxygenation leads to necrosis (death) of a portion of heart muscle -irrerversible cellular death. S/S=SOB –nausea. emesis –diaphoresis –PND –fatigue -levines sign (patient localizes chest pain by placing first over sternum). ASSESSING must first rule out: GERD. thyroid problems. anemia
-detailed history and presence of risk factors -rule out non cardiac pain (GI. MS) -cardiac enzymes: troponin. CPK-MB and myoglobin –echocadriogram -stress test -cardiac catheterization and angiopathy
x of y cards