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255 exam 1
225 exam 1
| Question | Answer |
|---|---|
| pericardium | normal range of fluid-10-15mL, outer layer, reduces friction |
| layers of the heart | the endocardium (innermost lining), the myocardium (thick, muscular middle layer), and the epicardium (outer layer, also the visceral pericardium) |
| blockages impact | pumping of the heart |
| heart gives out blood through the | coronary arteries |
| direction of blood flow in heart | Blood flows into the right atrium, then right ventricle, to the lungs for oxygen, and returns to the left atrium, then left ventricle, before being pumped out the aorta to the body |
| cardiac output | amount of blood pumped by each ventricle in one minute, measure with echocardiogram |
| CO= | SV x HR |
| ejection fraction | percent of blood pumped out of filled ventricle with each beat. normal is 60%. worry when number gets low |
| SV | volume of blood that ejects over period of time |
| factors influencing CO | HR-rapid HR= low CO. SV- preload(into heart), afterload (out of heart), contractility (how much heart squeezes and electrifies) |
| heart age related changes | thick valves, thick arterial blood vessels, less elastic myocardium , number of pacemaker cells decrease, incr bp, kyphosis, different landmarks for auscultation |
| dysrhythmias | increases vagal tone=bradydysrhythmias. afib=HF, premature beats. pulse deficit of 23 beats? |
| murmers | aortic mitral valves are most affected |
| enlarged heart | 2nd to htn, valve disorders, fluid overload |
| cardiac patients are usually | confused |
| BNP | natriuretic peptide that determines heart failure |
| BMP | a blood test checking blood sugar, electrolytes, and kidney function |
| CRP | indicates inflammation in the body |
| troponin | a protein complex essential for heart and skeletal muscle contraction |
| diet examples for heart failure | mediterranean bc its anti inflammatory and healthy fats. low cholesterol and high fiber |
| locations of each heart valve | RSB 2nd IC=aortic LSB 2nd IC=pulmonic LSB 3rd ICS-erbs LSB 4th ICS=tricuspid MCL, 5th ICS=mitral |
| BP= | CO x SVR |
| factors influencing BP | HR, contractility, conduction, renal fluid volume, angiotensin, vasoconstrictors, sympathetic nervous system, vasodilators |
| what is BP | force exerted by blood against walls of blood vessel. maintains tissue perfusion |
| SVR | force opposing movement of blood within blood vessels. radius of small arteries is determining factor of SVR |
| as arteries dilate | resistance to blood flow decreases |
| as arteries narrow | resistance to blood flow increases |
| sympathetic nervous system | fight or flight, increased SNS activity=incr HR and contractility. incr BP by incr CO and SVR. |
| baroreceptors | senses change in BP and sends signals to brainstem. affects cardiac and vascular smooth muscle cells. inhibits sns and enchances pns lowering hr |
| norepinephrine | causes peripheral vasoconstriction, incr HR, low BP, incr force of contraction, incr conduction speed |
| SNS vasomotor center | regulates during postural changes to prevent orthostatic hypotension |
| vascular endothelium | vasodilation and vasoconstriction, the single-cell layer lining the interior of all blood vessels |
| dilation- | low bp |
| renal system | controls sodium excretion and extracellular fluid volume. kidneys secrete renin in response to sns stimulation or decr renal perfusion. vasoconstriction and incr SVR, high bp |
| endocrine system | adrenal cortex releases aldosterone=incr blood volume and cardiac output |
| what bp needs to be treated | > or = 140/90 |
| HTN blacks | highest prevalence, more resistant, younger age, women more, nocturnal non dipping bp, more severe, dont respond well to renin inhibiting drugs |
| HTN manifestations | silent killer, fatigue, dizziness, palpation, angina, dyspnea |
| HTN complications | heart, brain-stroke, peripheral vessels, kidney, eye damage |
| DASH diet | rich in fruits, vegetables, fat-free or low-fat milk products, whole grains, fish, poultry, beans, seeds, and nuts.limit: Salt, sweets, fats, red meat. prioritize: Nutrients lowering blood pressure, potassium, magnesium, calcium, protein, and fiber |
| DASH emphasizes two levels of sodium intake | 2,300 mg (about 1 teaspoon of salt) or 1,500 mg. • Read Labels: Aim for foods with 5% or less of the Daily Value for sodium. Avoid foods with 20% or more. Use herbs, spices, lemon, lime, or vinegar instead of salt |
| thiazide diuretics | lowers water which lowers bp. excretes Na and water by blocking reabsorption in diluting tube in kidney. vasodilation. uses- edema and htn. not immediate. admin IV or PO. 2-4 weeks to work |
| thiazide diuretics ex | chlorothiazide, hydrochlorothiazide, metolazone |
| what to monitor for thiazide diuretics | hypotension, tachycardia, electrolytes, i&O, eat high K foods, restrict sodium, change positions slow |
| loop diuretics | action=blocks Na and H2O reabsorption at loop of henle, excretes na, H20, and K. renal vasodilation and incr GFR and decr PVR. |
| loop diuretics uses | htn emergencies, edema, pulm edema, CHF, cirrhosis. admin PO or IV |
| loop diuretics ex | bumetanide, furosemide, torsemide. admin slowly |
| pushing loop diuretics fast can cause | hypotension and hearing loss |
| what to assess for loop diuretics | assess VS, electrolytes (K, Na, Ca, Mg), weight, eat high K foods, restrict Na, avoid dehydration, report tinnitus. don't give if low BP |
| K Sparing diuretics | action- inhibits aldosterone, na excreted in exchange for K. acts directly on distal convoluted tubule. uses-HTN, edema w HF, admin PO with food, avoid K and salty foods, admin PO |
| k sparing diuretics ex | spironolactone, amiloride, triamterene |
| k sparing diuretics monitor | VS, stop k supplements, dehydration, K Na and BUN, take with food, avoid K, avoid sunlight, may take up to 3 days to reach max and continue 2-3 days once stopped |
| coronary artery angioplasty aka | percutaneous coronary intervention, done on coronary arteries, goal is to restore blood flow if plaque narrows the vessels, needle first placed in radial artery |
| coronary arteries supply heart muscle with | oxygen |
| coronary artery angioplasty gets checked with a | fluoroscope |
| coronary artery bypass graft | performed to improve circulation to heart muscle, healthy vein/artery is grafted to blocked artery. carries oxygen blood to heart, general anesthesia, 3-6 hrs |
| valves keep blood flowing | FORWARD |
| mitral/tricuspid valves | connect to chordae tendineae, prevents eversion of valve leaflets into the atria |
| pulmonic/aortic | prevent blood from regurgitating back into ventricles |
| what veins are oxygenated | pulmonary |
| arterioles | a small branch of an artery leading into capillaries., maintaining mean arterial pressure and tissue perfusion |
| The heart perfuses itself primarily during | primarily during diastole (heart relaxation), not systole (contraction), through the coronary arteries that branch off the aorta, delivering oxygen and nutrients to the heart muscle |
| ventricles | pumping chambers |
| s1 | closure of mitral and tricuspid valves. heard best with diaphragm |
| s2 | closure of aortic and pulmonic. heard best with diaphragm |
| heart sounds are made by | movement of blood through valves |
| s3 | listen wt bell, |
| s4 | listen wt bell. |
| preload | pressure from volume of blood in ventricles at end of diastole. incr in hypervolemia and regurgitation in cardaiac valves |
| afterload | resistance left ventricle must overcome to circulate blood. incr in hypertension and vasoconstriction |
| The tricuspid valve brings deoxygenated blood from the | right atrium to the right ventricle, while the mitral valve brings oxygenated blood from the left atrium to the left ventricle |
| aortic valve | Connects the left ventricle to the aorta, supplying the heart, brain, and body with oxygenated blood.pumps oxygen-rich blood from the left ventricle into the aorta to the rest of the body |
| pulmonic valve | Connects the right ventricle to the pulmonary artery, directing blood to the lungs to pick up oxygen. |
| A patient has a severe blockage in the right coronary artery. Which heart structures would the nurse expect to be affected by this blockage | atrioventricular (AV) node b. left ventricle d. right ventricle |
| Which part of the vascular system prevents hemostatis? | endothelial layer of arteries |
| left sided vs right sided heart failure | Left-sided heart failure causes pulmonary congestion due to reduced blood output from the left ventricle, shortness of breath, while right-sided heart failure causes systemic venous backup, resulting in peripheral edema (swelling) in legs and abdomen |
| right sided vs left sided heart failure symptoms | Left-sided- fluid backup in the lungs, shortness of breath, cough , wheezing,(orthopnea). Right-sided failure causes fluid to back up into the body, resulting in swelling (edema) in the legs, ankles, abdomen, weight gain, and jugular vein distention |
| Left-Sided Heart Failure Causes (The Pumper Fails) | (CAD): Heart Attack (Hypertension): The heart works harder, thickening the muscle. Valve Diseases: Aortic or mitral valve issues. Cardiomyopathy/Arrhythmias |
| Right-Sided Heart Failure Causes (The Back-up in the Body) | Left-Sided Heart Failure: The #1 cause; pulmonary hypertension COPD Pulmonary Hypertension: High blood pressure specifically in the pulmonary arteries. Pulmonary Embolism Congenital Heart Defects/Valve Issues |
| hypertensive urgency | no evidence of target organ damage, can be treated in clinic, associated with stable angina, chronic HF, prior MI |
| hypertensive emergency | organ damage, incr BUN, GFR, creatinine. do not lower bp too fast, hospitalization |
| heart failure patho | Complex clinical syndrome resulting from myocardial insult The inability of the heart to provide sufficient blood to meet O2 demands |
| heart failure risk factors | HTN & CAD Long term tx of HTN reduces risk of HF by 50% Diabetes, metabolic syndrome, advanced age, tobacco use, vascular disease, congenital, cardiomyopathies, infections, dysrhythmias, toxins, alcohol use, chemotherapy Any interference with CO |
| Left sided heart failure | most common form of heart failure Heart failure with reduced EF (Systolic failure) Inability of heart to pump blood effectively Heart failure with preserved EF (Diastolic failure) Inability of ventricles to relax and fill during diastole |
| Right sided heart failure | RV does not pump effectively. Cause: Left sided heart failure (most common), RV infarction, PE, cor pulmonale, peripheral edema, ascites, hepatomegaly, JVD |
| Biventricular failure | Both LV and RV pump dysfunction |
| Left sided heart failure with reduced reduced ejection fraction. SYSTOLIC failure | Inability of the heart to pump effectively Reduction of LVEF <40% Causes: impaired contractile function, increased afterload, cardiomyopathy, mechanical abnormalities LV becomes dilated & hypertrophied Blood will back up into the LA and lungs |
| Left sided heart failure with preserved EF. DIASTOLIC FAILURE | inability of the ventricle to relax and fill during diastole About 50% of pts with HF, fluid congestion |
| cardiomyopathy | restructure of heart |
| hypertrophic cardiomyopathy | Asymmetric left ventricular hypertrophy common genetic heart disease characterized by abnormally thick, stiffened heart muscle, typically in the left ventricle. It impairs blood pumping and is the leading cause of sudden cardiac death in young people |
| right sided heart failure usually caused by | lungs or right ventricle damage |
| Renin-angiotensin-aldosterone system (RAAS) | Increase preload and ventricular contraction Promotes retention of Na and fluid when decreased renal perfusion is sensed Kidneys release renin angiotensin I to II vasoconstriction water and Na retention, hyponatremia |
| Sympathetic nervous system | Baroreceptors sense low pressure SNS release epinephrine/norepinephrine stimulate beta receptors = Incr HR and contractility |
| Ventricular dilation | Elevated ventricular pressure cause muscle fibers to stretch increases preload excessive preload overstretched |
| Ventricular hypertrophy | Slow increase in muscle mass increased contraction= incr cardiac muscle O2 demand and prone to dysrhythmias |
| Ventricular remodeling | Change in the structure of the heart over time, shape becomes more spherical= incr ventricular mass, incr wall tension, incr O2 consumption, impaired contractility |
| frank starling | within physiological limits, the force of ventricular contraction increases as the cardiac muscle fibers are stretched by higher end-diastolic volume (increased preload), resulting in a greater stroke volume |
| what medicines can make HF worse | NSAIDS |
| Natriuretic peptides | Released in response to increased blood volume and ventricular wall stretching Increased GFR and diuresis Excretion of sodium Inhibition of aldosterone and renin Interference with ADH release |
| Atrial natriuretic peptide | released from atria |
| Brain (b-type) natriuretic peptide | Released from ventricles **this level is often monitored in hospitalized cardiac patients |
| Nitric oxide and prostaglandins | Relax arterial smooth muscles |
| Compensated HF | when compensatory mechanisms work to keep adequate CO |
| decompensated HF | a sudden, severe worsening of heart failure, where the heart can't pump enough blood, causing fluid buildup (congestion) and poor oxygen delivery, requiring immediate medical help. |
| decompensated HF manifestations | mild tachypnea and dec. PaO2, Interstitial edema: tachypnea, aveolar edema: decreasing PaO2, incr. PaCO2, acidosis Pulmonary edema, dyspnea, orthopnea, PND, JVD, coughing, anxious, pale, cyanotic, tachypnea, pink, frothy sputum, |
| Right-sided heart failure signs | achycardia Anasarca Ascites Edema Hepatomegaly JVD Murmurs Weight gain |
| Left-sided heart failure signs | Tachycardia S3 & S4 sounds Cough Crackles Pleural effusion Frothy pink sputum (late sign) |
| acute decompensated HF treatment | telemetry or ICU VS, I&O, daily weights Supplemental O2 Biventricular pacemaker Balloon pump, ventricular assist devices IV diuretics, vasodilators, positive inotropes |
| chronic hf treatment | Supplemental O2 Physical and emotional rest Structured exercise (cardiac rehab) Device Therapy: pacemaker/defibrillator Nutrition Therapy: 2g sodium diet |
| HF management diuretics | Loop diuretics Blocks Na and water reabsorption causing excretion of Na, water, Cl, and K Bumetamide (Bumex), furosemide (Lasix), torsemide (Demadex) Given PO, IV Potassium sparing Inhibits aldosterone, Na excreted in exchange for K |
| HF management Vasodilators | Used when pt does not have hypotension Decreases afterload and improves coronary blood flow Given PO, SL, IV Isosorbide dinitrate, Nitroglycerin (NTG), nitroprusside |
| HF management Positive inotropes | Beta agonists Increase myocardial contractility Used in cardiogenic shock or low CO Dopamine, dobutamine, norepinephrine (Levophed), phosphodiesterase inhibitors (milrinone) Given IV only Assess for improved CO, BP |
| HF management Cardiac glycosides | Positive inotropic and negative chronotropic effects Given PO, IV; Never give IM (tissue irritation) digoxin Monitor for Digoxin toxicity Many drug interactions |
| HF management digoxin | Risk increases w hypokalemia Fatigue, muscle weakness, headache, confusion, dysrhythmias, Assess BP, HR, EKG, high k foods apical pulse for 1 full minute prior to admin, hold if <60 Assess serum digoxin level |
| management hf with reduced ef | ACE inhibitors: first line drug; reduce ventricular remodeling Angiotensin II receptor blockers (ARBs): pts who cannot tolerate ACE, reduce afterload Neprilysin-angiotensin receptor inhibitors: decreases SVR, afterload |
| Beta blockers: directly block | SNS effects and decrease HR |
| Hydralazine/isosorbide dinitrate combo | (Bidil): vasodilator and reduces afterload |
| further treatment for reduced EF | implantable cardiac devices ICD (defibrillator with or without a pacemaker) Rec for pts with EF < 35% - risk for sudden cardiac death CRT (cardiac resynchronization therapy – pacemaker) will help to coordinate RV and LV contraction |
| HF assessment | implantable cardiac devices ICD (defibrillator with or without a pacemaker) Rec for pts with EF < 35% - risk for sudden cardiac death CRT (cardiac resynchronization therapy – pacemaker) will help to coordinate RV and LV contractions |
| HF nursing care | implementation ID and treat risk factors & slow progression Teach that HF is a chronic & progressive condition needing lifelong therapy Establish Home Health Teach medications, how to take BP & pulse Eat small frequent meals |
| LVAD | Cardiac pump device that is inserted through the chest and abdominal wall Runs externally on a battery that the patient wear |
| TRANSPLANTS Contraindications | Absolute: 70, Life threatening illness, Advanced cerebral disease, Active infection (like HIV), Severe pulmonary disease Relative: severe obesity, psychologic impairment, substance use, uncontrolled diabetes, irreversible kidney dysfunction |
| TRANSPLANTATION PROTOCOL IMMUNOSUPPRESSIVE THERAPY Calcineurin inhibitors - ta | Calcineurin inhibitors - tacrolimus Antiproliferative – mycophenolate mofetil Corticosteroids – Prednisone Infection is primary concern |
| Endomyocardial biopsies are done | weekly for first month, monthly for 6 mo., then yearly to detect rejection |
| ventricular contractions | purkinje fibers |
| CAD = | Progressive disease Atherosclerosis: soft fat deposits that harden with age. starts with chronic endothelial injury |
| If progression of CAD is slow… | collateral circulation may form 2 factors contribute to the development: Inherited predisposition to develop new blood vessels (angiogenesis) The presence of chronic ischemia With rapid onset CAD or spasm, there is NO TIME to develop collateral |
| cad risk factors | white, male, old age, family history,elevated lipids, Elevated homocysteine, metabolic syndrome |
| CAD MAJOR MODIFIABLE RISK FACTORS | Elevated serum lipids Cholesterol > 200mg/dl Fasting triglyceride > 150mg/dl LDL > 160 mg/dl HDL < 40mg/dl (men), <50mg/dl (women) Hypertension (>/= 140/90mmHg), tobacco |
| Lipid lowering agents | HMG-CoA Reductase Inhibitors –Statins Niacin (B vitamin; causes flushing) Fibric Acid Derivatives (Gemfibrozil, fenofibrate) Omega-3 fatty acid Bile-acid sequestrants Cholesterol absorption inhibitor (Ezetimibe) Antiplatelets ASA |
| CAD IS PROGRESSIVE Can lead to | Angina Myocardial Infarction (MI) Sudden Cardiac Death Heart Failure Arrhythmias Conduction Problems |
| CHRONIC STABLE ANGINA | Chest pain that occurs intermittently over a long period of time, with a similar pattern of onset, duration and intensity Often caused by physical exertion, stress or emotional upset Due to: › Inc. demand for oxygen or dec. supply of oxygen |
| Factors for Myocardial O2 needs | Decreased O2 supply: spasm, thrombosis, Valve disorders, heart failure, anemia, dysrhythmias, hypovolemia, drug abuse › Increased O2 demand: tachycardia, dysrhythmias, drug abuse, anxiety, HTN |
| CAD PRECIPITATING FACTORS | Activity, physical exertion Strong Emotions = SNS, stress response Heavy Meal = blood diversion Temperature Extremes Tobacco use Sexual Activity Stimulants (cocaine, amphetamines) Circadian Rhythms (early morning) |
| Chronic Stable Angina characteristics | predictable, consistent, occurs on exertion and is relieved by rest & NTG (Nitroglycerin) Pain lasts a few minutes Intermittent, similar pattern Pressure, heaviness or discomfort Controlled with med |
| ASSESSMENT OF ANGINA | Precipitating events Q Quality of pain R Radiation of pain S Severity of pain T Timing |
| DIAGNOSTIC STUDIES: CHRONIC STABLE ANGINA | Diagnostic Studies History, Physical, CXR, EKG Lab – Lipids & Cardiac Enzymes (CPK-MB & Troponin) Echocardiogram Stress test Nuclear Med - perfusion studies Coronary catheterization/angiogram |
| TREATMENT OF CAD | Antiplatelet/anticoagulants, antianginals (NTG), ACE & ARBs Beta-blocker & BP control Cholesterol meds, cigarette smoking cessation, Ca- channel blockers, Cardiac rehab Diet & diabetes management Education & exercise Flu vaccination |
| Coronary catheterization & revascularization/percutaneous coronary intervention (PCI) | Gold standard to identify and localize CAD, for pts with increasing symptoms Involves angioplasty and/or stenting of artery |
| Coronary Surgical Revascularization (CABG) (recommended if…) | Failed medical management Have left main CAD or disease in 3 coronary vessels not a candidate for PCI Failed PCI with continued chest pain Rec for diabetics, LV dysfunction, and CKD pts |
| ACUTE CORONARY SYNDROME (ACS) | Myocardial Cells become ischemic in 10 seconds of occlusion After several minutes, heart pumping function decreases IRREVERSIBLE DAMAGE starts in 20 minutes When ischemia is prolonged and not immediately reversible, ACS develops |
| PROGRESSION OF ACS | Stable plaque ruptures… Leading to unstable plaque…& platelet rich thrombus formation Partial occlusion = UA or NSTEMI Total occlusion = STEMI (Tombstones) |
| UNSTABLE ANGINA (UA) | New onset or progressive increase in frequency, intensity, and duration of attack, Occurs at rest, Pain even after NTG Pain lasts 10 mins or more UNPREDICTABLE Occurs with minimal exertion or during sleep |
| Women more commonly experience | dyspnea, unusual fatigue, and sleep disturbances |
| MYOCARDIAL INFARCTION (MI) | Abrupt cessation of blood flow through a coronary artery Irreversible myocardial cell death to muscle beyond blockage NSTEMI or STEMI Most affect the left ventricle Presence of collateral circulation determines the severity of the MI |
| NSTEMI (NON-ST ELEVATION MI) | Cause: nonocclusive thrombus Does not cause ST segment elevation May show ST depression or T wave inversion on ECG Do NOT go to Cardiac Cath Lab emergently, may go 12-72 hours later Thrombolytic therapy is NOT INDICATED |
| STEMI (ST-ELEVATION MI) | Cause: Occlusive thrombus EMERGENCY SITUATION!!! Artery must be opened within 90 minutes of presentation By PCI or thrombolytic tx “Door to Balloon Time” PCI is first-line tx if hospital is capable of performing PCI |
| LOCATION OF BLOCKAGE | Majority of MIs affect the left ventricle Damage can occur in more than one location MIs are described based on the location of the damage Anterior, inferior, lateral, septal, or posterior wall infarction |
| CLINICAL MANIFESTATIONS- MI | Pain – severe chest pain, not relieved by rest Heavy, crushing, burning, tight, pressure : substernal or epigastric Radiate to neck, jaw, arms, back Ashen, cool , clammy skin & diaphoresis, increased HR & BP (early- SNS Stimulation) BP drop |
| COMPLICATIONS | #1 is dysrhythmias (80-90% of patients) VT and VF most common cause of death pre-hospital arrival Bradycardias & PVC’s VT and VF often within first 4 hours of pain Heart failure Cardiogenic Shock - Severe LV Failure, pericarditis |
| DIAGNOSTIC STUDIES: ECG | Viewing the ST segment gives the physician information about the type of MI Leads facing the area of infarction are abnormal ST depression and/or T wave inversion (NSTEMI = not an emergency) ST elevation Significant if 1mm or more |
| DIAGNOSTIC STUDIES: SERUM CARDIAC BIOMARKERS | Proteins released into the blood from necrotic heart muscle after MI CPK, CK-MB, Troponin drawn usually every 6-8 hours over a 24 hour period An elevation in Troponin or CK-MB can differentiate between UA |
| Troponin | highly specific for MI Levels increase 4-6 hours after MI Peak at 10-24 hours Return to baseline at 10-14 days Negative < 0.5 mcg/L |
| Creatine kinase MB (CK-MB) | Levels increase 6 hours after MI Peak at 18 hours Return to baseline at 24-36 hours |
| NURSING CARE – ACS/MI | Meds: nitroglycerin, morphine, ASA and/or antiplatelets, statin, oxygen, bedrest |
| TREATMENT – ACS/MI | Emergent Coronary catheterization & PCI (Percutaneous Coronary Intervention) First line tx for patients with STEMI Gold standard to identify and localize arterial blockages Involves angioplasty and/or stenting of artery |
| TREATMENT – STEMI | Thrombolytics Only indicated for STEMI Used in hospitals without access to Cardiac Cath Lab Give within 30 mins of arrival to ER |
| stemi thrombolytics condradictions | Hx Intracranial hemorrhage or neoplasm recent stroke (w/in 3 mo) head trauma (w/in 3 mo) uncontrolled HTN active bleeding prior thrombolytics (w/in 6 mo) |
| TREATMENT – ACS/MI | Coronary Surgical Revascularization: Coronary Artery Bypass Grafting (CABG) Requires sternotomy and Cardiopulmonary bypass Grafts: IMA (internal mammary, most common), radial artery, or saphenous vein |
| CARDIOPULMONARY BYPASS MACHINE | A cannula in the superior and inferior vena cava removes venous blood, which is then pumped through an oxygenator and heat exchanger. After filtering, oxygenated blood is returned to the ascending aorta. |
| PREOP CABG | Baseline surgery labs (CBC, BMP, PT/PTT/INR, UA, CXR, angiogram) Type and screen 4 or more units of blood |
| POST OP CABG | Monitor labs Hgb, Hct, Serum electrolytes [K, Mg, Ca, BUN, Cre] Strict, hourly I & O UOP < 30 ml for 2 hours, call MD Critical care 1st 24 hours Monitor chest tube output IV fluids and blood replacement Temporary pacemaker at bedside |
| IV nitroglycerin (NTG) (Tridil) | Reduces pain and improves coronary blood flow Monitor BP for hypotension |
| morphine | For CP unrelieved by NTG Vasodilator, decreases cardiac workload |
| Antidysrhythmic drugs | common after MI |
| Beta Blockers therapy | Decreases myocardial O2 demand by dec. HR, BP and contractility Reduces the risk for reinfarction and heart failure Given in 1st 24 hours |
| ACE Inhibitors therapy | ACE tx should begin in 1st 24 hours Prevents ventricular remodeling and slows progression of heart failure |
| Angiotensin Receptor Blockers (ARBs) | used for patients intolerant of ACE Inhibitors vasodilator |
| Lipid-Lowering Drugs | Pts with ACS or CAD should receive |
| Anticoagulants | Heparin SQ or IV , enoxaparin (Lovenox) SQ Used for UA and NSTEMI pts Prevents extension of clot & stop formation of new clots |
| Antiplatelet Agents | ASA, clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilenta) Inhibits platelet aggregation |
| NSTEMI/STEMI: Dual | antiplatelet therapy (ASA plus clopidogrel) {used for 1 year post MI} |
| ACS TEACHING | Warm up and cool down (stretching) › Perform most days of the week (30 mins) › Intensity is determined by heart rate › Check pulse before, during, & after exercise › Stop activity if pulse increases more than 20 bpm, dyspnea › Avoid straining |
| TEACHING - NITROGLYCERIN | take for chest pain May take one tablet q5min x 3 doses If pain is unrelieved after 3 doses, call 911 Sit down when taking Keep NTG nearby but not on body Keep in dark bottle Watch expiration date |
| SUDDEN CARDIAC DEATH | Unexpected; cardiac function is disrupted, resulting in loss of blood flow to the brain & death Almost 400,000 people yearly! Majority are ventricular dysrhythmias (VT or VF) |
| Strongest predictor of risk sudden cardiac death | LV dysfunction (EF less than 30%) Ventricular dysrhythmias after MI |
| SUDDEN CARDIAC DEATH (SCD) risk factors | Hx of hypertropic cardiomyopathy Conduction system distubances (prolonged QT syndrome or Wolff-Parkinson- White Syndrome) LV dysfunction (EF < 30%) Hx of syncope or ventricular dysrhythmias Aortic stenosis Male (African American highest) |
| CAUSES OF SUDDEN CARDIAC DEATH | CAD Reperfusion following ischemia Myocardial hypertrophy Cardiomyopathy Inflammatory Myocardial disorders Valve disorders Dissecting or ruptured aneurysm Cardiac drug toxicity |
| CAUSES OF SUDDEN CARDIAC DEATH non cardiac | Pulmonary embolism (PE) Cerebral hemorrhage Autonomic dysfunction Choking Electrical shock Electrolyte and acid-base imbalance |
| CLINICAL MANIFESTATIONS OF SCD | Angina, palpitations, dizziness, lightheadedness |
| MANAGEMENT OF SCD | ICD (implantable cardioverter-defibrillator) Most common approach; improves survival Anti-Arrhythmic Meds (amiodarone) Life vest- bridge to ICD or heart transplant Teach symptoms of impending cardiac arrest |
| low oxygen means heart | grows more blood vessels |
| HDL= | good cholesterol |
| lipid lowering agents can | decrease good cholesterol |
| fibric acid derivatives | decr triglycerides |
| statins | binds through cholesterol and works on the liver, lowers cholesterol |
| CABG recommended for | diabetes or CKD, LV dysfunction |
| what to monitor before cardiac catherization | K levels, BUN, GFR, creatinine, pulses |
| low urine outout= | not enough blood <30 ml hour notify doctor |
| antiplatelets cause high risk for | GI bleeds |
| 12-Lead EKG | Printout of the heart’s electrical activity viewed from 12 different angles as seen in 12 different leads. A lead is an electrocardiographic picture of the heart’s electrical activity. Rhythm Strip: Printout of only one or two leads at a time. |
| Isoelectric line | baseline where every wave starts and comes back |
| calculating hr 6 second strip method | count the number of complexes within 6 seconds and multiply by 10 -Estimated number of bpm per minute -Least accurate; use in conjunction with another method |
| calculating hr large block method | -Count the number of big blocks between QRS complexes then divide into 300 300 ÷ 3.5 = 86 hr -Fastest method |
| calculating hr little block method | Count the number of little blocks between QRS complexes and divide into 1,500 1500 ÷ 11 = 136 |
| normal hr intervals | PR Interval = 0.12-0.20 secs QRS Interval = <0.12 secs QT Interval = 0.34-0.43 secs |
| NSR | Rate: 60–100. Regularity: Regular. P waves: Upright, matching, one in front of each QRS PR: 0.12–0.20 secs, constant. QRS: <0.12 secs |
| sinus bradycardia | Rate: <60. Regularity: Regular. P waves: Upright, matching, married to QRS. PR: 0.12–0.20 secs, constant. QRS: <0.12 secs. |
| sinus bradycardia cause/treatment | Cause: Vagal stimulation, MI, hypoxia, digitalis toxicity, well-trained athlete. Manifestations: Dizziness, pallor, weakness, syncope, diaphoresis, hypotension. Treatment: Atropine (if symptoms), oxygen, pacemaker |
| anticholinergics hr | Atropine Form: IV (avail in other forms for other uses- for cardiac, it is IV) Action: bind with muscarinic receptors to block cholinergic effects on the heart and smooth muscles of the bronchi and int. bradycardia, cardiopulmonary resuscitation |
| anticholinergics considerations | tachycardia, restlessness, irritability, hallucination, delirium, urinary retention, dilated pupils, decreased salivation, decreased GI motility, 3-5 mins (3 doses) Contraindicated-closure glaucoma, renal and liver dysfunction and GI disorders |
| sinus tachycardia | Rate: 101–160. Regularity: Regular. P waves: Upright, matching, married to QRS. PR: 0.12–0.20 secs, constant. QRS: <0.12 secs. |
| sinus tachycardia cause/treatment | Atropine, emotions, pulmonary embolus, MI, CHF, fever, vagus nerve inhibition, thyrotoxicosis. Manifestations: Decreased cardiac output. Treatment: Treat cause if symptomatic or at risk for myocardial damage. Vagal maneuver |
| premature atrial contraction | Regularity: Regular with interruptions P waves: different shape from P wave originating from the SA node or it may be hidden in T wave. PR: may be shorter or longer than the P-R interval, but it is within normal limits. QRS: <0.12 secs. |
| premature atrial contraction causes/treatment | Cause: stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolyte Manifestations: palpitations, “skips a beat” Treatment: Monitoring, withhold stimulants, Beta blockers |
| SVT atrial tachycardia | Rate: 151–220. Regularity: Regular (but may interrupt a slower rhythm). P waves: Different from sinus Ps. PR: 0.12–0.20 secs. QRS: <0.12 secs |
| SVT atrial tachycardia cause/treatment | Cause: Same as PAC, digitalis toxicity, heart disease Clinical Significance: Decreased cardiac output, hypotension, dyspnea, angina Treatment: Vagal maneuvers, calcium channel blockers, beta- blockers, amiodarone, adenosine, ablation |
| adenosine | Form: IV Action: Slows electrical conduction time through AV node Uses: SVT Side effects: Bradycardia or cardiac arrest, tachycardia, PVCs, facial flushing |
| adenosine admin | Rapid IV push (1-2 seconds), followed by rapid normal saline flush, half life 10 secs Crash cart in room with ECG monitoring Expect SUDDEN slowing of HR, even asystole for a brief period |
| atrial flutter | Atrial—200–350, ventricular—varies depending on conduction. Regularity: Regular or irregular. P waves: None. Flutter waves instead. PR: Not applicable. QRS: <0.12 secs. |
| atrial flutter cause/treatment | Pulmonary embolus, valvular heart disease, lung disease, thyrotoxicosis, HF Decreased cardiac output, heart failure, clots Treat-calcium channel blockers and/or beta-blockers first, adenosine, antiarrhythmics cardioversion, ablation |
| A FIB | Paroxysmal or persistent Most common dysrhythmia Prevalence increases with age Usually occurs in patients with underlying heart disease Can also occur with other disease states |
| A FIB rates | Atrial—350–600, ventricular—varies depending on conduction. Regularity: Irregularly irregular. P waves: None. Wavy baseline between QRSs instead. PR: Not applicable. QRS: <0.12 secs. |
| A FIB cause | MI, lung disease, valvular heart disease, hyperthyroidism |
| A FIB duration | If duration <48 hours: Digoxin, calcium channel blockers, beta-blockers, amiodarone, cardioversion. If duration >48 hours: Anticoagulation , TEE, cardioversion (must anticoagulate 3-4 weeks before) |
| digoxin | Action: Positive inotropic and Negative chronotropic effects thereby increasing CO Use: CHF & Atrial Dysrhythmias (Atrial fibrillation, atrial flutter) Route: PO, IV Side Effects: Nausea Loss of “usual appetite” Headache |
| glycosides toxicity effects | Muscle weakness Headache Hallucinations Confusion Dysrhythmias AV heart block N/V/D Visual disturbances |
| potassium channel blocker | Amiodarone (Cordarone) Form: PO or IV Action: Blocks potassium from re-entering cell to repolarize causing a prolonged refractory period and decrease automaticity Uses: Vtach, Vfib, SVT, atrial fib, atrial flutter |
| ventricular dysrhythmias | Heart rate ranges from zero to 250 beats/min. The most lethal of all rhythms. Most will cause symptoms of decreased cardiac output, if not frank cardiac standstill. Impulse originates in one or more irritable foci and travels slowly,cell by cel |
| premature ventricular contractions | Rate: Can occur at any rate. Regularity: Regular but interrupted by premature beat. P waves: Usually not seen. PR: Not applicable. QRS: Wide and bizarre in shape; >0.12 secs wide. T wave: Opposite QRS |
| premature ventricular contractions cause and treatment | Heart disease, hypokalemia, hypoxia, hypomagnesemia, stimulants, caffeine, stress. Clinical Significance: reduced CO, angina Treatment: treat cause (supplemental potassium, oxygen), amiodarone, procainamide, beta blockers. |
| ventricular tachycardia | Rate: 150-250 Regularity: Usually regular but can be a bit irregular. P waves: Usually none; dissociated if present. PR: Variable if Ps present. QRS: Wide and bizarre; >0.12 secs wide, mono or polymorphic T wave: Opposite QRS. dont give bl |
| ventricular tachycardia cause/treat | Cause: MI, CAD, hypoxia, hypokalemia, hypomagnesemia, pulse or no pulse, Dec CO, Shock, unconsciousness, death. treat cause, VT with pulse: procainamide, amiodarone, lidocaine Polymorphic VT: IV magnesium, isoproterenol, cardioversion |
| cardioversion | Used for supraventricular dysrhythmias and VT with pulse Usually a small shock= less electricity (joules) Requires synchronization with cardiac cycle = must have a pulse |
| V FIB | Rate: not measurable Regularity: Not applicable. P waves: None PR: Not applicable. QRS: None; wavy or spiked baseline. T wave: None. |
| V FIB cause/treat | Cause: MI, hypoxia, hypokalemia, hyperkalemia, drowning, drug overdose, accidental electric shock. Clinical Significance: unresponsive, pulseless, and apneic. Death if untreated. Treatment: Immediate CPR, defibrillation, epinephrine, amiodarone |
| defibrillation | Larger shock = more electricity (joules) Treatment of choice for ventricular fibrillation and pulseless v-tach. Not synchronized! Three ways to deliver a shock: Monitor/defibrillator AICD (implanted) AED |
| asystole | nothing. Cause: Hypoxia, advanced cardiac disease, severe cardiac conduction problem, end stage heart failure Clinical Significance: pulseless, dead Treatment: CPR, epinephrine, oxygen. |
| pacemakers | Electronic devices implanted into or attached to a patient. Sends out electrical signal to cause the heart to depolarize. Generally used to maintain a reasonable heart rate in a patient whose own heart rate is too slow. |
| pacemaker indications | Symptomatic sinus bradycardia. Junctional rhythms. Slow ventricular rhythms. AV Blocks. Tachydysrhythmias. |
| temp pacemaker | Used when dysrhythmia is likely to last only a few days. Most common types Transvenous: Inserted into a large vein and threaded into the right atrium or ventricle. Transcutaneous: Attached to skin by way of large electrodes. |
| permanent pacemaker | Used when a dysrhythmia is thought to be permanent. Implanted surgically. Components Pulse generator (battery pack). Pacing catheter. Batteries last 5–10 years. |
| cardiac resynchronization therapy | Pacing technique that paces both ventricles to promote ventricular function in HF patients |
| implantable cardioverter defibrillator | Treatment for life-threatening ventricular arrhythmias Lead system placed via subclavian vein to endocardium Pulse generator is implanted over pectoral muscle Battery must be changed similar to pacemakers, every 5-10 years. only chocks when need |
| P wave | atrial depolarize |
| QRS wave | atria repolarize, ventricular depolarization (contraction) |
| T wave | ventricles repolarize |
| cant do what on atropine | see, spit, pee, poo |
| atrial dysrhythmias is a problem with | P wave |
| give what for ventricular tachycardia | Mg |
| nitroglycerin should be used cautiously or avoided in patients with | aortic stenosis bc it can cause low bp |
| The ST depression and T wave inversion on the ECG of a patient diagnosed with ACS indicate | myocardial ischemia from inadequate supply of blood and oxygen to the heart. |
| PR interval | The length of time for the electrical impulse to travel from the sinoatrial (SA) node to the Purkinje fibers. |
| VT | Rate 200 beats/min; P wave not visible |
| flat line on monitor | Epinephrine or vasopressin |
| infective endocarditis | Blood flow allows organisms to contact and infect previously damaged heart valves or other endothelial surfaces Staphylococcus aureus (50%), Streptococcus viridans, or coagulase- negative staphylococci Organisms make biofilms |
| infective endocarditis risk | Valve disease, cardiomyopathy, congenital heart disease, IV drug use, prosthetic heart valves, IV devices, renal dialysis, rheumatic heart disease |
| infective endocarditis symptoms | Fever Flu like symptoms Chills, malaise, fatigue, anorexia, arthralgias, myalgias, headache Heart murmur, heart failure |
| infective endocarditis signs | Petechiae Splinter Hemorrhages streaks under fingernails or toenails Osler’s Nodes Janeway’s Lesions small, nontender red lesions on palms and soles Roth’s spots |
| pericarditis | Inflammation of the pericardial sac with fluid accumulation Idiopathic (most) or infectious (bacterial or viral), myocardial infarctions, cancer, radiation, renal failure Influx of neutrophils fibrin deposition on epicardium |
| pericarditis manifestations | Chest Pain Abrupt onset, progressive & sharp, worsens with deep breathing & lying flat Sitting up and leaning forward usually relieves the pain, Pericardial Friction Rub , scratching, high-pitched produced by inflamed pericardial layers |
| pericarditis complications | Pericardial Effusion accumulation of fluid in the pericardial sac, get distant & muffled heart sounds, if not relieved, we get... Cardiac Tamponade (medical emergency) compression on the heart |
| cardiac tamponade signs and symptoms | confusion, anxious, restless,tachypnea, JVD, SOB, tachycardia, muffled heart tones, narrowed pulse pressure, pulses paradoxus (SBP decreased during inspiration) |
| pericarditis treatment | Bedrest Antibiotics for bacterial NSAIDS for pain & inflammation Corticosteroids for autoimmune conditions Pericardiocentesis (inserting a needle to remove fluid) Pericardial window |
| rheumatic fever | Acute inflammatory disease that involves all heart layers Usually ages 5-15 Abnormal immune response 2-3 weeks after a Strep pharyngitis Prevalence decreased s/t antibiotics |
| rheumatic fever criteria | Arthritis: (most common) joint redness, swelling, tenderness, limited ROM Carditis: Murmur (endocarditis) Cardiomegaly & HF (myocarditis) CP & Friction rub (pericarditis) Chorea, Subcutaneous nodules, erythema |
| rheumatic fever treatment | Eradicate strep infection with penicillin 10 day course Use Erythromycin or Clindamycin if allergy to PCN (cephalosporins) Use NSAIDS/ Corticosteroids to control fever & joint pain |
| penicillin | Check allergies GI upset (diarrhea) No juices, milk, or sodas Monitor renal, liver, and electrolytes (K) Deep IM |
| Cephalosporins | Monitor renal & liver Give separate of antacid, H2receptor blockers, & iron supplements (2hrs) Deep IM Cross-sensitivity with PCN May take with food GI, Inc PT/INR, lethargy |
| rheumatic fever assesment | strep infection, history of RF or RHD, malaise, anorexia, fatigue, chest pain, joint pain or tenderness, rash Objective: fever, subq nodules, erythema marginatum, tachycardia, pericardial friction rub, muffled heart tones, murmurs, chorea, arthritis |
| MITRAL VALVE STENOSIS | Most common cause is Rheumatic Heart Disease Thickening and shortening of the mitral valve Blocks blood flow increase atrial pressure & volume increase increased pulmonary pressures |
| MITRAL VALVE STENOSIS manifestations | Dyspnea due to reduced lung compliance with Hemoptysis (late) Fatigue, palpitations assoc with Afib Hoarseness Diastolic murmur |
| MITRAL REGURGITATION | caused by RHD, MI rupture of chordae, MVP, IE Blood able to flow backward from the LV to the LA s/t incomplete valve closure LA & LV working hard to maintain CO |
| MITRAL REGURGITATION manifestations | Acute – thready pulses, cool, clammy skin, pulmonary edema, & shock, systolic murmur Chronic – asymptomatic, fatigue, weakness, DOE, palpitations, orthopnea, peripheral edema, audible S3 heart sound |
| MITRAL VALVE PROLAPSE | abnormality of one/both MV leaflets prolapse or bulge into the Left atrium during systole benign Cause unknown; strong familial / hereditary factor |
| MITRAL VALVE PROLAPSE manifestations | Asymptomatic (most) 10% become symptomatic Regurgitation systolic murmur (louder during systole) Dysrhythmias: PVCs, SVT, palpitations, lightheaded, syncope |
| MITRAL VALVE PROLAPSE treat | Palpitations treated with beta blockers Avoid stimulants (caffeine) Watch for worsening symptoms |
| AORTIC VALVE STENOSIS | Causes: congenital, RF or degeneration 3% over 65 years old Blocks blood flow from LV to Aorta LVH & Inc. O2 consumption pulmonary HTN & HF |
| AORTIC VALVE STENOSIS manifestations | Angina, syncope, DOE Crescendo-decrescendo systolic murmur May be asymptomatic |
| AORTIC VALVE REGURGITATION | Causes: Rheumatic heart disease, acute aortic dissection, infective endocarditis, trauma Allows backward flow of blood from the aorta to the LV s/t incomplete valve closure volume overload |
| AORTIC VALVE REGURGITATION manifestations | Chronic High pitched diastolic murmur, gallop Asymptomatic for years DOE, orthopnea, paroxysmal nocturnal dyspnea Acute widened pulse pressures, weakness, hypotension, severe dyspnea |
| valvular heart disease treatment | Conservative Treat HF: vasodilators, + inotropes, BB, diuretics, low-sodium diet Treat atrial dysrhythmias: BB, CCB, antidysrhythmics Prevent thromboembolism: anticoagulants in Afib Prevent recurrent RF & IE: prophylactic Abx |
| Valve Repair | Suture torn leaflets, chordae, or papillary muscles Used for mitral or tricuspid regurgitation Less risky than replacement, but may not restore total function |
| Valve Replacement | Mechanical (durable and last longer, but incr risk of thromboembolism) Need long-term anticoagulants Biologic (less durable, but no thromboembolism risk) Do not need long-term anticoagulants unless pt has a.fib |
| dilated cardiomypathy | Most common type: 5-8 cases/100,000 20-45% HF Patho Diffuse inflammation & rapid degeneration of heart fibers Ventricle dilates…but no proportional increase in CO… overstretching occurs This affects systolic function dec CO & dec SV |
| dilated cardiomypathy causes | CAD, cardiotoxic agents (alcohol, cocaine), myocarditis, autoimmune, genetic, HTN, pregnancy, valve disease |
| DILATED CMO manifestations | Fatigue, dyspnea at rest, PND, orthopnea Dry cough, palpitations, bloating, N/V, anorexia Dysrhythmias, heart murmurs, crackles, edema, weak pulses, JVD, hepatomegaly, blood clots emboli |
| DILATED CMO nursing care | Keep the patient functional Control heart failure: improve contractility, dec afterload/preload Nitrates (NTG), Digoxin, Diuretics, ACE, beta blockers Antidysrhythmics IV dobutamine or milrinone Nutritional Therapy Cardiac Rehab |
| HYPERTROPHIC CMO manifestations | Asymptomatic DOE, fatigue, angina, syncope Dysrhythmias, v tach, v fib Apical impulse exaggerated or displaced to left Systolic murmur |
| HYPERTROPHIC CMO care | Improve ventricular filling by reducing ventricular contractility, plus we need to better get the blood out of the heart Meds: BBs & CCBs; Amiodarone or sotalol for dysrhythmias |
| RESTRICTIVE CMO | Least common Cardiac muscle is stiff & resists filling, so high pressure is mandated to fill the ventricle Causes is unknown; myocardial fibrosis and infiltrative processes such as amyloidosis, radiation involved in development |
| RESTRICTIVE CMO sign | S/S: Angina, dyspnea, & fatigue, exercise intolerance, syncope, palpitations |
| fungal infections at risk for | pericarditis |
| complication of endocarditis | regurgitant murmer |
Created by:
cwehner125