- Measures electrical activity of the heart

(detects damage to cardiac tissue)

- Useful in the inital diagnosis and monitoring of arrhythmias, myocardial infarction, infection and paericarditis

-valvular abnormalities

-- abnormal shunting of blood

-uses sound waves

-image provides functional info. about the heart

- doppler studies assess blood flow and pressure in peripheral vessels

-measure pressure and assess valve and heart function

-determination of central venous pressure and pulmonary capillary wedge pressure

-radio-opaque dye injected into coronary arteries

- visualization of blood flow in the coronary arteries

- 3 forms (isoenzymes)

-- CK-MM (skeletal muscle), CK-BB (brain tissue), CK-MB (heart)

-used to detect damage to tissues

-rises 3-12 hours after onset

- peaks in 24 hours

- returns to normal in 24-48 hours

-detects damage to myocardium

-current gold standard or MI

-rise within 2-12 hours

- peak in 24-48 hours

- returns to normal 7-14 days

-decrease total fat intake (sat. fat and trans fat)

-general weight reduction

-reduce salt intake

-increaes high-density lipoprotiens

-lowers serum lipid levels

-reduces stress levels

-reduction of peripheral resistance

- increase coronary blood flow

ex. Nitroglycerin

What do beta-blockers do for cardiac disorders 

and

examples

-treatment of hypertension and dysrhythmias (block beta 1 receptors in heart and prevent action of SNS on cardiac tissue)

-reduction of angina attacks

ex. atenolo, metoprolol

-prevent movement of calcium into cardiac and smooth muscle 

- decrease cardiac contractility

-antihypertensive and vasodilator

-prophylactic against angina

ex. Diltiazem, Verapamil, Nifedepine

-decrease conduction and contractility

(it is selective for myocardium)

-slows conduction of impulses

-antidysrhythmic drug for atrial dysrhythmias

-block conversion of angiotensin I to angeiotensin II

-decrease peripheral resistance and lower water retention

-decrease preload and afterload

ex. Enalapril, Ramipril, Captopril (the pril's)

-remove excess sodium and/or water

- may require K+ supplementation unless Spironolactone is used which is a potassium sparing diuretic

ex. of non-potassium sparing is Lasix

- used in treatment of high BP and congestive heart failure

-reduce risk of blood clot formation

- used in people with Hx. of thrombus or prostehtic heart valves

ex. Warfarin - coumadin (measure the PT and PTT), or 81 mg of ASA

-reduction of low-density lipoproteins and cholesterol content

ex. Simvastatin (Zocor) and Atorvastatin (Lipitor)

Coronary Artery Disease

-any vascular disorder that narrows or occludes the coronary arteries

Ischemic Heart Disease

-occurs when CAD diminishes coronary blood supply to the point that ischemia results 

-cells are temp. deprived of blood flow

-cells remain alive but cannot function normally

Acute Coronary Syndrome

-due to persistent ischemia or complete occlustion of a coronary artery (thrombus formatin over a ruptured or ulcerated plaque)

-results in: unstable angina, MI or heart attack

-strikes 65+ age group

-males develop it earlier than females

-females typically have worse outcome due to delayed diagnosis 

-arteriosclerosis

-atherosclerosis

-hardening of the arteries 

-general term for all types of degenerative changes in arteries and arterioles (loss of elasticity, lumen gradually narrows and may become obstructed, causes of increased BP)

-specific type of arteriosclerosis

-refers to presence of atheroma in wall of artery 

-"lump of gruel"

-plaques consisting of lipids, calcium, fibrin, cell debris and possible clots

-common in large arteries at sites of bifurcation

-r/t diet, exercise and stress

-major risk factor is elevated LDL and low HDL

Low density lipoprotein

-transport of cholesterol from liver to cells

-mostly composed of cholesterol

-major factor contributing to atheroma formation

high density lipoprotein

-mostly phospholipid with little cholesterol

-transport of cholesterol away from the peripheral cells to liver 

-the "good" lipoprotein

-catabolism in liver and excretion

-multifactorial

-many factors are synergistic

-two groups of risk factors: non-modifiable and modifiable

-age

-gender

-genetics or familial factors (hyperlipidemia, familial hypercholesterolemia)

-obesity

-sedentary lifestyle

-cigarette smoking

-DM

-poorly controlled hypertension

-combinatino of oral contraceptives and smoking

-serum lipid levels

-CRP (C-reactive protein as a marker of inflammatin)

-angiography

-nuclear medicine scans

-weight loss

-increase exercise

-lower total cholesterol and LDL levels

-reduced sodium intake

-control hypertension

-cessation of smoking

-anti-lipidemic drugs

-surgical intervention 

-coronary artery bypass graft

-balloon angioplasty

-stent placement

-form of reversible IHD without permanent damage

-occurs when there is a deficit of O2 to meet myocardial needs

-attacks vary in severity and duratin, but usually become more frequent and longer as disease progresses

-recurrent, intermittent brief episodes of substernal chest pain

-tightness or pressure in chest

-may have radiatino of pain to neck and left arm 

-pallor

-diaphoresis

-nausea

"stable angina"

-develops with exertion and improves with rest

-usually less than 10-15 min. duration

-responds well to nitro

"prinzmetal agina"

-due to vasospasm of coronary arteries (may or may not have atherosclerosis)

-occurs at rest, often during sleep

-responds well to calcium channel blockers

-angina that chnages or worses

-prolonged and more severe than other anginas

-occurs at rest or minimal exertion

-considered a form of ACS

-transient ischemia

-do not see release of cardiac enzymes or serum markers

-may precede myocardial infarction

-no chest pain

- feels like indigestion

- more common in women and those with DM due to neuropathy

-rest, stop activity

-sit in upright position

-give nitro

-check pulse and respirations

-administer O2 if necessary

-if pt. has hx. of angina give 2nd dose of nitro

-if pt. does not have hx. of angina they need emergencey medical aid

-acute coronary syndrome

-atherosclerosis is most common cause

-occurs when coronary artery is totally obstructed 

-thrombus from atheroma builds up to obstruct artery

-embolus from thrombus breaks free

-vasospasm combined with partial occlusion of coronary artery by atheroma (not as common)

collateral circulation

(less well developed if infarction is due to emboli)

-feeling of pressure, heaviness, or burning in cehst

-sudden SOB, weakness, fatigue

-nausea, indigestion

-anxiety and fear

-pain (substernal, crushing, raidating)

-pain typically not relieved by nitro

-hypotension due to drop in CO

-weak, rapid pulse

-NSTEMI

-STEMI

-non-ST elevation

-ST segment depression

-T wave inversion

-pt. usually has hx. of unstable angina

-partial occlusion (see subendocardial infarction)

-benefit not as great from thrombolytics

ST elevation MI

-elevation of ST segment

-acute occlusive thrombus (see transmural infarction)

-greatest benefit from thrombolytics

-cardiac enzymes and isoenzymes are elevated

-serum levels of myosin and cardiac troponin are elevated (myoglobin in urine)

-leukocytosis, elevated CRP and ESR common

ABG may be altered in severe cases (acidosis)

-sudden death

-cardiogenic shock (due to damage to LV)

-CHF

-rupture of necrotic heart tissue/cardiac tamponade

-thrmboembolism causing CVA (with LV MI)

-pulmonary embolus with RV MI

-reduce cardiac demand (rest)

-anticoagulants (if alert and oriented give one 325mg ASA)

-O2 if available

-analgesics (morphine)

-thrombolytic agents (tissue plasminogen activator, streptokinase)

-medication to treat dysrhythmias, HTN, CHF)

-PTCA

Percutaneous transluminal coronary angioplasty

-re-opneing of occluded vessels 

(improved outcomes over thrombolytics for STEMI)

Arrhythmias

-deviations from normal cardiac rate or rhythm

-reduction of the efficiency of the heart's pumping cycle

-caused by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity

-inadequate filling in diastole

-inadequate pumping in systole

-SA node

-bradycardia

-tachycardia

-sick sinus syndrome

-pacemaker of the heart

-rate can be altered by SNS or PNS

-marked by altering bradycardia and tachycardia

-often requires mechanical pacemaker

-most common of all dysrhythmias

 -premature atrial contractions or beats

-extra contraction or ectopic beats

-"palpitations"

-irritable atrial muscle cells outside conduction pathway

-re-entry of signal that passes through damaged myocardium and is delayed then re-enters and stimulates same tissue before next normal beat and may be caused by drugs, caffeine, smoking and stress

-atrial flutter

- atrial fibrillation

atrial flutter

-atrial heart rate of 160-350 bpm

-AV node delays conduction

-ventricular rate is slower

-can see pulse deficit

-atrial heart rate over 350 bpm

-causes pooling of blood in the atria

-thrombus formation is a risk (CVA) and treated with coumadin

-ventricular rate is slower

Heart blocks 

and 

s/s

-conduction is excessively delayed or stopped at AV node or bundle of His

- EKG changes

-lighheadedness, fainting and palpitations

-first degree (partial block)

-second degree (partial block)

-third degree (total block)

-partial block

-conduction delay between atrial and ventricular contractions

-see prolonged PR interval

-total block

- no transmission from atria to ventricles

-AV pacemaker controls ventricular contraction and HR is 30-45 bpm

-see reduced CO which produces syncope and Stokes-Adams attacks (sudden syncope and possible seizures)

-bundle branch block

-ventricular tachycardia

-ventricular fibrillation

-premature ventricular contractions

For bundle block, VT and Vfib - ischemia, MI and damaged myocardium

for PVC's - ischemia, electrolyte imbalances, stress

-interference with conduction in one of the bundle branches

-on EKG - widened QRS

-doesn'y typically interfere with CO

-see decreased cardiac output due to reduced diastolic filling

-may progress to vfib

ventricular fibrillation

-muscle fibers contract indenpendently and rapidly

-"quivering" ventricle (doesn't pump blood)

-cardiac standsill occurs if not treated immediately 

-additional beats from ventricular muscle cell or ectopic pacemaker

-may lead to vfib if from mulitple sites or occur in pairs

-cause needs to be determined and treated

-antidysrhythmic drugs 

-SA nodal problems or total heart block require pacemaker

-defibrillator may be implanted for conversion of ventricular fibrillation

-cessation of all heart activity (Asystole)

-no conduction of impulses

-Flat EKG

-LOC, no pulse, no respirations

-excessive vagal nerve stimulation

-potassium imbalance

-cardiogenic shock

-drug toxicity

-insufficient oxygen

-respiratory arrest

-blow to heart

-usually a complication of another cardiopulmonary condition

MI

valvular disease

HTN

lung disease (Cor Pulmonale)

may involve a combination of the above factors

-cardiac output or stroke volume decreases "forward effect"

-"backup" and congestion develops behind the affected ventricle

-cardiac output or stroke volume decreases

-less blood reaches the various organs

-decreased cell function

-fatigue and lethargy

-mild acidosis

-output from ventricle is less than the inflow of blood

-congestion in venous circulation draining into the affected side of the heart

-decreased blood supply to tissues, general hypoxia

-fatigue and weakness

-dyspnea and SOB

-tachycardia

-cutaneous and visceral vasoconstriction

-daytime oliguria

-r/t pulmonary congestion

-dyspnea and orthopnea

(develops as fluid accumulates in the lungs)

-cough (associated with fluid irritating the respiratory passages)

-paroxysmal nocturnal dyspnea (usually develops during sleep, excess fluid in lungs frequently leads to infections)

-dependent edema in feet, legs or buttocks

-increased pressure in jugular veins > distention

-hepatomegaly and spenomegaly (digestive disturbances)

-ascites

-acute right-sided failure (pressure buidls up in SVC)

-flushed face, distended neck veins, headache, visual disturbances 

-often secondary to congenital heart disease

-feeding difficulties often first sign (failure to gain weight or meet developmental guidelines)

-short sleep periods 

-tripod position to play

-cough, rapid, grunting respirations, flared nostrils, wheezing

-radiographs show cardiomegaly

-gallop rhythm (S3 and S4)

-ABG used to measure hypoxia