Cardiovascular Emergencies PDF

Nursing Care of Clients with Altered Tissue Perfusion SHERHATA T. ADJID-SANAANI, RN, MAN, MD, MPH  Overview of the Cardiovascular System The CARDIOVASCULAR SYSTEM is a closed system of the heart and blood vessels the heart pumps blood into blood vessels blood vessels...

Nursing Care of Clients with Altered Tissue Perfusion SHERHATA T. ADJID-SANAANI, RN, MAN, MD, MPH  Overview of the Cardiovascular System The CARDIOVASCULAR SYSTEM is a closed system of the heart and blood vessels the heart pumps blood into blood vessels blood vessels circulate the blood to all parts of the body, to ALL cells Functions: To deliver oxygen and nutrients to all body cells, transport enzymes and hormones, and to remove carbon dioxide and other waste products from the cells  Can you describe the location of the heart? The heart is ________ to the lungs, ________ to the sternum, ________ to the vertebral column, and ________ to the diaphragm. Its ________ end, the apex, points to the left, terminating at the level of the 5th intercostal space.  Anatomy of the Heart Ø Location thoracic cavity in the mediastinum, between the lungs Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings External Heart Anatomy External Heart Anatomy Blood Flow Through the Heart  Major Blood Vessels of the Heart aorta carries _________________ blood from the left ventricle to upper & lower body pulmonary arteries (L & R): carries _________________ blood from right ventricle to lungs vena cava (superior & inferior): carries _________________ blood from upper & lower body into right atria pulmonary veins (2 pairs, L & R): carry _________________ blood from lungs into left atria Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Systemic circuit Pulmonary circuit Coronary Arteries Blood Flow DR Ngo Electrical System of the Heart  Normal Electrical Pathway SA node AV node SA Bundle of His Bundle Branches AV  ASSESSMENT OF THE CLIENTS WITH CARDIOVASCULAR DISORDER Nursing History: -The risk factors to cardiovascular disorders may be classified as follows: a. Non-modifiable Risk Factors (unavoidable risk factors) ü Age, Gender, Race, Hereditary b. Modifiable Risk Factors (avoidable risk factors) ü Stress, Lifestyle (Diet, Exercise), Smoking, Alcohol intake, Hypertension, Dyslipidemia, Diabetes Mellitus, Obesity, Contraceptive pills)  Common Signs and Symptoms of CVD CHEST PAIN OR DISCOMFORT (angina pectoris, ACS, dysrhythmias, valvular heart disease) SHORTNESS OF BREATH OR DYSPNEA (Dyspnea on exertion (DOE), Orthopnea) (ACS, cardiogenic shock, HF, valvular heart disease) PERIPHERAL EDEMA, WEIGHT GAIN, ABDOMINAL DISTENTION due to enlarged spleen and liver or ascites (HF) PALPITATIONS (tachycardia from a variety of causes, including ACS, caffeine or other stimulants, electrolyte imbalances, stress, valvular heart disease, ventricular aneurysms)  Common Signs and Symptoms of CVD Vital fatigue, sometimes referred to as vital exhaustion (an early warning symptom of ACS, HF, or valvular heart disease, characterized by feeling unusu- ally tired or fatigued, irritable, and dejected) Dizziness, syncope, or changes in level of consciousness (cardiogenic shock, cerebrovascular disorders, dysrhythmias, hypotension, postural hypotension, vasovagal episode)  PHYSICAL EXAMINATION: I. INSPECTION: ü SKIN COLOR. Pallor, cyanosis, cold & clammy, (inadequate oxygenation) jaundice (hemolysis of RBC) – the bilirubin component of RBC is released into the systemic circulation causing yellowish discoloration of the skin & sclerae. ü NECK VEIN DISTENTION (JUGULAR VEIN DISTENTION). This is due to venous congestion. ü RESPIRATION. Note for signs of dyspnea. This indicates inadequate oxygenation. ü POINT OF MAXIMAL IMPULSE (PMI). It is located in the left, mid-clavicular, fifth intercostal space (ICS). ü PERIPHERAL EDEMA. This is due venous insufficiency, heart failure. Varicosities or thrombophlebitis. ü GENERALIZED EDEMA, ASCITES (right-sided heart failure) II. PALPATION. ü PERIPHERAL PULSES. Weak or bounding & irregular pulses may indicate presence of cardiovascular disorder. Ø Pulses are graded: 4 (bounding), 3 (increases), 2 (normal), 1 (weak). 0 (absent) ü APICAL PULSE. is assessed at the point of maximum impulse. ü PULSATION in sternoclavicular area & epigastric area may be normal to thin aeg or aneurysm ü CHECK CAPILLARY REFILL (2mm or an arrhythmia  ST- segment depression q Management Þ Education, Tx RF & comorbidities, adaptation of activity, drug therapy, consider revascularization q Drug therapy ü Nitrates ® systemic venodilators which ¯ myocardial wall tension & O2 demand ü Beta-blockers ® ¯ O2 demand by inhibiting the ­ in HR, BP, & myocardial contractility ü CCB ® vasodilators producing ü Antiplatelet drugs ® ASA or Clopidogrel ü Ranolazine ® sodium channel blocker used with a BB or as a substitute for a BB q Coronary revascularization Þ performed in pts with severe symptoms despite medical therapy & pts with severe ischemia on stress testing ü PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA) ® balloon dilatation w/ stent deployment; usually reserved for pts with 1-2 vessel involvement with normal LV function ü CORONARY ARTERY BYPASS GRAFTING (CABG) ® surgical vessel anastomosis using IMA, SV, or RA; indicated in pts with: left main coronary artery stenosis, 3 vessel disease + EF75% stenosis in LAD, or vessel blockages that cannot be reached by catheters  SILENT MYOCARDIAL ISCHEMIA q Definition Þ Ischemia without anginal pain q Etiology Þ atherosclerosis or vasospasm q 3 populations 1) asymptomatic patients w/o CHD evidence 2) MI survivors that continue to have myocardial ischemia 3) Patients w/ angina who also have episodes of silent ischemia q Explanation for painless episodes is unclear q Can lead to Ischemic Cardiomyopathy q Tx Þ depends on extent of ischemia, comorbidities, age, occupation, & Risk Factor  PRINZMETALʼS ANGINA q Caused by vasospasm of coronary arteries, however in most instances, vasospasms occur in the presence of nearby plaques q Pathogenesis of vasospasm is uncertain q Chest pain usually occurs during rest or may awaken the patient from sleep; Serious arrhythmias can occur during anginal episodes q Patients are typically younger with fewer CV Risk factors q ECG demonstrates ST-segment elevation q Mainstay of treatment is SL nitroglycerin & CCBs  ACUTE CORONARY SYNDROMES (ACS) q Is an emergent situation characterized by an acute on- set of myocardial ischemia that results in myocardial death (ie, MI) if definitive interventions do not occur promptly. q ACS includes: v Unstable Angina - The patient has clinical manifestations of coronary ischemia, but ECG and cardiac bio- markers show no evidence of acute MI. v Non-ST-Segment Elevation (Non-q-wave) Myocardial Infarction (NSTEMI) - The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI. (ST segment depression or T-wave inversion) v ST-Segment (Q-wave) Myocardial Infarction (STEMI) - The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. (ST-segment in 2 contiguous leads or abnormal Q-wave) UNSTABLE ANGINA & NON-ST-ELEVATION MI q UA defined as chest pain or angina equivalents with at least 1 of 3 features: 1) occurs at rest 2) severe & new onset 3) more severe, prolonged, or frequent than previously q UA referred to as “pre-infarction syndrome” q NSTEMI is established if a patient with clinical features of UA develops evidence of myocardial necrosis as reflected in elevated cardiac biomarkers UNSTABLE ANGINA & NON-ST-ELEVATION MI q Pathophysiology Þ Decrease in O2 supply or increase in myocardial O2 demand q 4 contributing pathophysiologic processes for UA: 1) plaque rupture or erosion w/ superimposed nonocclusive thrombosis 2) dynamic obstruction due to vasospasm 3) progressive & rapidly advancing atherosclerosis 4) ­ myocardial O2 demand and/or ¯ supply UNSTABLE ANGINA & NON-ST-ELEVATION MI q Clinical manifestations Þ substernal Chest pain w/ radiation to neck, left shoulder or left arm; or anginal “equivalents”; q Physical examination similar to stable angina & may be unremarkable; with large area of ischemia or NSTEMI, the physical findings can include diaphoresis, pale cool skin, sinus tachycardia, S3, S4, rales, & sometimes hypotension UNSTABLE ANGINA & NON-ST-ELEVATION MI q ECG Þ ST-segment depression and/or T-wave inversion q Cardiac biomarkers Þ NSTEMI patients have Ý CK- MB and Troponin I q Diagnostic pathways Þ clinical history, ECG, cardiac markers, & stress testing q Goals 1) recognize or rule out MI 2) evaluate for rest ischemia 3) evaluate for significant CAD  HIGH OR CHEST PAIN, LOW LIKELIHOOD ATYPICAL INTERMEDIATE ISCHEMIA PAIN LIKELIHOOD RECURRENT OBSERVE PAIN +ECG/ CARDIAC MARKER MARKERS & ECG NO RECURRENT PAIN -EKG/ MARKER + STRESS EXERCISE OR - STRESS TEST PHARMACOLOGIC TEST STRESS TESTING (+/- IMAGING) ADMIT TO DISCHARGE UA/STEMI TX HOME & FOLLOW PATHWAY UP WITH PMD UNSTABLE ANGINA & NON-ST-ELEVATION MI Medical Treatment Þ anti-ischemic & antithrombotic q Anti-Ischemic Treatment ü Nitrates Þ Sublingual 1st, if pain persists after 3 doses given q5 minutes, then IV Nitroglycerine should be given ü Beta-blockers Þ IV Metoprolol followed by PO with a targeted HR of 50-60 bpm ü Calcium Channel Blockers (CCBs) Þ (Verapamil or Diltiazem) recommended in patients who have persistent or recurrent symptoms after full dose nitrates & Beta- Blockers or any C/I to B-Bs ü If pain persists, then administer Morphine sulfate ü ARBs or ACE-I & Statins for long-term prevention UNSTABLE ANGINA & NON-ST-ELEVATION MI q Antithrombotic Tx q Aspirin (ASA) Þ chewable aspirin should be initial treatment q Clopidogrel (Plavix) Þ ADP inhibitor; combination of ASA & Plavix is recommended for patients who are not at excessive risk for bleeding q Heparin Þ UFH or LMWH should be added to ASA & Plavix: LMWH appear to be superior q GP IIb/IIIa inhibitors Þ used for high-risk pts when an invasive management is intended (PCI); includes Abciximab, Eptifibatide, & Tirofiban UNSTABLE ANGINA & NON-ST-ELEVATION MI INVASIVE VS. CONSERVATIVE STRATEGY q Benefit of early invasive treatment in high-risk patients with multiple Risk factors q Invasive Þ Pre-treat 1st , then coronary angiography is done w/in 48 hours of admission, followed by PCI or CABG q Conservative Þ Anti-ischemic & antithrombotic therapy followed by “watchful waiting”  UNSTABLE ANGINA & NON-ST-ELEVATION MI LONG TERM MANAGEMENT q Risk factor modification ü Stop smoking ü TLC ü BP control ü Tight glycemic control q Beta-blockers q Statins & ACE-I (Plaque stabilization) q ASA & Plavix for 9-12 months, followed by ASA thereafter  ST-SEGMENT ELEVATION MI q Acute MI is one of the most common diagnosis in hospitalized patients q It is a critical emergency q 650,000 new & 450,000 recurrent AMIs annually q 30% early (30 day) mortality rate; more than ½ of deaths occur before patient reaches hospital; q 1 of every 25 surviving patients die in the 1st year after AMI q 30-40% AMIs affect RCA, 40-50% affect LAD & the remainder affect the LCX  ST-SEGMENT ELEVATION MI (STEMI) q Pathophysiology Þ vessel injury & plaque rupture followed by thrombotic occlusion q Occurs when plaque fissures or ruptures & when conditions favor thrombosis, so that a mural thrombus forms at rupture site & leads to coronary artery occlusion q STEMI may also be caused by coronary emboli or spasm & a wide variety of systemic inflammatory diseases  ST-SEGMENT ELEVATION MI q Clinical presentation Þ deep, visceral, heavy, squeezing, or crushing substernal chest pain w/ or w/o radiation; diaphoresis, nausea and vomiting, anxiety, palpitations, sense of impending doom q Proportion of painless STEMIs is greater in patients with DM & it increases with age q Elderly patients may present with sudden onset of SOB which may progress to pulmonary edema  ST-SEGMENT ELEVATION MI q Physical Examination Ø Anxiety, pallor, diaphoresis & cool extremities; Ø Tachy or bradycardia, Ø Hypo or hypertension Ø PMI may be difficult to palpate, +S3 or S4, ¯ intensity of S1, a mid or late systolic murmur or pericardial friction rub may be present; Ø Patients with large infarcts may have rales or signs of shock  ST-SEGMENT ELEVATION MI q ECG Þ Total occlusion produces ST-segment elevation; most patients with ST-segment elevation develop Q waves q When a thrombus is not totally occlusive or there is a rich collateral network, no ST-segment elevation is seen  ST-SEGMENT ELEVATION MI q Where is the infarct ?? q Lateral wall ® leads I, aVL, V5, V6 (LCX artery) q Inferior wall ® leads II, III, aVF (RCA or PDA) q Anterior ® leads V2, V3 (LCA or LAD diagonal branch) q Septal ® leads V1 & V2 (LCA and/or LAD septal branch) q Anteroseptal ® leads V1 – V4; (LCA & LAD or left main) q Posterior ® ST-segment depression in leads V1, V2, V3 or V4; involves RCA or LCX artery  ST-SEGMENT ELEVATION MI q Serum cardiac markers Þ proteins released in large quantities from necrotic heart muscle q Troponin I & Troponin T Þ Gold standard cardiac markers for MI; rises w/in 4-8 hours q Total CK or CPK Þ rises w/in 4-8 hours & generally returns to normal by 48-72 hours; lacks specificity q CK-MB Þ more specific over total CK in that it is not present in significant extracardiac tissue q Myoglobin Þ 1st marker released during AMI, lacks specificity & is rapidly excreted in the urine  ST-SEGMENT ELEVATION MI q Cardiac imaging q 2D-echo Þ wall motion defects, EF, pericardial effusions, aneurysms; cannot distinguish between old & new infarcts q Doppler echo Þ VSDs & mitral regurgitation (2 complications of STEMI) q Myocardial Perfusion Scans Þ used less than echo because its is more difficult to obtain acutely; infarcted tissue displays irreversible ischemic deficits; cannot distinguish between old & new infarcts; not specific for dx of AMI M O N A B A C H  ST-SEGMENT ELEVATION MI MANAGEMENT q ASA Þ chewable; other anti-thrombotic agents are Heparin & GP IIB/IIIA inhibitors q Oxygen Þ give 2-4L/min of O2 via nasal canula q Nitroglycerin Þ SL X 3 doses; if chest pain continues or there is ongoing ischemia on ECG, then IV Nitroglycerin q Morphine Þ 2-4 mg IV Q5 minutes q Beta-Blockers Þ Metoprolol 5mg Q5 min X 3; 15 min after last dose 50mg PO QID X 48 hours, then 100mg BID q ACE-Inhibitor Þ given w/in 24 hours to all patients who are hemodynamically stable w/ STEMI q All pts with AMI get MONA BACH BBs ¯ HR which prolongs diastole and increases myocardial perfusion  ST-SEGMENT ELEVATION MI MANAGEMENT STRATEGIES q Primary tool for screening pts & making triage decisions is initial ECG; with ST-segment elevation of at least 2 mm in 2 contiguous precordial leads or 1 mm in 2 limb leads, strongly consider reperfusion therapy q Deciding between PCI & fibrinolysis depends on capabilities of the facility  ST-SEGMENT ELEVATION MI q Limitation of infarct Þ central necrosis area occurs w/ AMI; fate of surrounding ischemic tissue improved by restoration of perfusion, ¯ O2 demand, preventing accumulation of noxious metabolites & reperfusion injury q Timely reperfusion prevents ischemic & injured zones from becoming infarct zones q Maintain balance between O2 supply & demand w/ pain control, ¯ tachycardia & HTN extends time “window” for myocardial salvage  ST-SEGMENT ELEVATION MI q Primary PCI Þ restores perfusion when carried out in 1st few hours; more effective than fibrinolysis when performed by experienced operators & associated w/ better short & long- term clinical outcomes q Compared w/ fibrinolysis, primary PCI is preferred when available especially if diagnosis is in doubt, cardiogenic shock is present, symptoms present for >2-3 hours  ST-SEGMENT ELEVATION MI q Fibrinolysis Þ fibrinolytics should ideally be initiated w/in 30 min of presentation (door-to- needle time < 30 min); includes tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK) & reteplase q ¯ infarct size, limits LV dysfunction & ¯ incidence of serious AMI complications q Pts treated w/in 1-3 hours of onset of symptoms benefit most, modest benefits are seen w/in 3-6 hours & mild benefit appears possible up to 12 hours  ST-SEGMENT ELEVATION MI q Absolute contraindications to fibrinolysis q History of cerebrovascular hemorrhage at any time q Nonhemorrhagic CVA w/in the last year q Marked Hypertension (SBP >180 and/or DBP >110) q Suspicion of aortic dissection q Active internal bleeding (excluding menses) q Relative contraindications q Anticoagulants, recent (40% infarction of LV or MV dysfunction q RV infarction Þ inferoposterior AMI can progress to RV infarction causing signs/symptoms of right Heart Failure  ST-SEGMENT ELEVATION MI q AMI complications q Acute MRÞ ischemia or papillary muscle rupture q Arrhythmias Þ most deaths due to fatal arrhythmia occur in the 1st few hours after AMI; other arrhythmias include PVCs, idioventricular rhythms, SVTs, sinus bradycardia q Hypovolemia Þ results from ¯ fluid intake during acute illness, vomiting due to AMI or narcotic medications, fluid loss due to prior diuretics q Myocardial rupture Þ LV free wall rupture occurs in