COMMON CARDIOVASCULAR CONDITIONS Ischemia loss of O2 and nutrients to heart muscles d/t poor coronary blood flow; commonly

y caused by atherosclerosis Risk Factors: Non-modifiable Hereditary Age(above 40) Sex/gender more in men and women w/ contraceptives Race Modifiable Diet Habits DM, Obesity, Stress response Lipid profile (LDL, HDL) Coronary Artery Spasm associated with atherosclerosis How to control CAD 1. Aspirin and anti-anginal therapy 2. Beta-blocker therapy and BP control 3. Cigarettes and cholesterol 4. Diet and Diabetes 5. Education and exercise Angina Pectoris (TIA) Precipitating Factors: Temp change Exercise Heavy meals Emotions Sexual intercourse Valsalva maneuver Smoking Stimulants PTCA, CABG, Stress test Characteristics -Pain or chest discomfort burning, suffocating, squeezing or crushing tightness -Radiates left arm, neck, jaw or shoulder blade -Clenching fist or rubbing left arm Nausea, vomiting, fainting, sweating, and cool extremities are noted. 1. Stable (chronic) Angina - Physical exertion, emotional stress, or cold weather - Stable pattern of onset, duration, and severity and relieving factors Pain - Mild to severe and lasts for 1-5minutes - ST segment depression; T wave inversions - Relieved with rest and sublingual NTG, or both 2. Unstable Angina - Unpredictable degree of exertions or emotion that occur at night. - Medical Emergency - Progressive, prolonged, or frequent angina with increasing severity

Pain - Up to 30 minutes awakens pt from sleep - Not completely relieved with NTG - Morphine SO4 - No ECG changes - Dx is based on Hx 3. Prinzmetals Angina - Chest pain longer duration may occur at rest - Happen bet midnight and 8 am - Occlusions in coronary artery associated w/ elevation of ST segment - NTG - Calcium channel blockers are most effective - Goal: vasodilation and reduction of myocardial O2 demand. Category Stable Unstable Prinzmetals Onset Exertion, Unpredictable Bet stress degree of midnight exertion or and 8am emotion, at night Duration 1-15min >30min ECG ST May or may Elevated ST changes depression, not have ECG segment T wave changes inversion Tx Rest, NTG Unrelieved NTG, with NTG Calcium morphine channel blockers Administering NTG - Vital Signs (BP,PR/HR) - Sublingually 3x every 5min - VS after each dosage - HOLD if BP is <90-100mmHg - Activity of NTG burning sensation (indicates potency of medication) - Common S/E headache (d/t central vasodilation), dizziness (d/t dec. BP) - Pain relieved 45s to 5mins SL Nitrates (Short-acting) Guidelines: - Stop any activity right away - Retain saliva - Note burning sensation - Potency: 3-6 months - Inactivated by light, heat, and time Patches (Long-lasting) Guidelines: - Use gloves - Use in non-hairy areas - Rotate - Avoid heat/ defibrillation Acute MI -

Necrosis of the myocardial cells Loss of functional myocardium affects heart ability to maintain effective cardiac output - Life-threatening event Pathophysiologic changes:

Ulceration or rupture of complicated atherosclerotic lesion - Clot occludes vessel in myocardium distal to obstruction - Prolonged ischemia (>20-45 mins): irreversible hypoxemic damage - Anaerobic Metabolism: H+ ions and lactic acid - Pain and discomfort; Heart failure - Common site: Anterior wall of the left ventricle ECG changes 1. Zone of ischemia (3) outer region of the myocardium; composed of viable cells: ECG (T wave invertion) 2. Zone if injury (2) IZ is surrounded by injured but still potentially viable cells: ECG (elevated ST segment) 3. Zone of infarction (1) area of cellular death and muscle necrosis in the myocardium: ECG (pathologic Q waves) Depth of Infarction Subendocardial or non-Q-wave infarction 1. Subendocardial tissue 2. Within 20mins of injury 3. S-T segment depression with small infarction 4. Ischemia- T wave inversion possible 5. Reversible Intramural infarction 1. Myocardium 2. Associated with frequent angina pectoris 3. Injury 30-45mins 4. Reparable Transmural infarction or Q-wave infarction 1. All layers of myocardium to epicardium 2. Within 1-6 hours 3. S-T segment elevation with large infarction 4. Prominent Q-wave 5. Irreversible Pain: Classic Manifestation - >15-20mins - Rest and NTG ineffective - Sudden and not associated w/ activities - Crushing and severe, heavy or squeezing sensation - Location: center of chest and may radiating atypical chest pain: CC: indigestion, heartburn, nausea, vomiting - No chest discomfort in 25% of clients with acute MI Laboratory Exams: 1. Cardiac Serum Markers 2. CBC, ESR (inflammation) 3. ABGs - T wave inversion - Elevation of S-T segment - Formation of Q wave 4. Electrocardiography (Anatomical assessment) - Transesophageal Echocardiography [C.A.S.E (Cardiography, ABGs, Serum Markers, Elecrocardiogram)]

Nursing Diagnoses 1. Acute Pain 2. Ineffective Tissue Perfusion: 12-lead ECG 3. Ineffective Coping: overuse of denial Nursing Interventions 1. Relief of pain- MONA (Morphine sulfate, O2 therapy, Nitrates, Aspirin) is the guide of Tx of clients with chest pain 2. Measures to maintain cardiac parameters - Cardiac monitoring (lead 2) - Report changes in LOC, Heart/Lung sounds - Pulses and CRT <3 seconds - JVD assessment - PAWP if less that 18mmHg volume depletion; if more than 18mmHg pulmonary congestion or cardiogenic shock - MIO - Dec. ADL (provide rest periods) - Stool softeners 3. Promote measures for oxygenation - O2 administration; caution in COPD - Pulse oximetry - ABG results - Monitor secretions: coughing and suctioning - Intubation PRN Fibrinolytics Guidelines: - w/in 3-6hours from onset of symptoms - SE: bleeding, allergic reaction, fever, N/V, Hypotension - Precs: reperfusion dysrhythmias - Antidote: Aminocaproic acids Anticoagulants Guidelines: A. Heparin Avoid: massage, aspirin, same site, alcohol, pressure B. Warfarin Avoid: aspirin, green leafy vegies - Watch for signs of bleeding Heparin Warfarin Onset Rapid Delayed Route IV & SC Oral (abdomen) Route PTT: No=20-35s PT: No=12-15s (2xNo=40-70s) (2xNo)=24-30s APTT: No=30-40s (2xNo=60-80s Antidote Protamine Vitamin K Surgical Interventions: A. Percutaneous Transluminal Angioplasty (PTCA) B. Laser Revascularization C. Intracoronary stents placement of a tubular mesh or coil spring device D. Intra-aortic Balloon Pump inflation of a balloon in the coronary artery during diastole and deflated systole E. Coronary Artery Bypass Graft Complications 1. Dysrhythmias fibrillation is the most common 2. HF 3. Cardiogenic Shock d/t massice LVfailure

4. Ventricular Aneurysm a healing necrotic tissue can cause weakening of the ventricular wall 5. Pericarditis inflammatory response to MI 6. Dresslers syndrome Aka. Post-MI syndrome - Late pericarditis, precordial pain, friction rub or pleuritis and/or pleural effusion. 7. Pulmonary embolism 8. Ventricular septal rupture 9. Papillary muscle rupture ARDS 1. Hypoxemia - PO2, below 50mmHg 2. Hypercapnia - Occurs in a person with no previous pulmonary problems - PCO, above 45 mmHg 3. Mortality rate is high (50%) - Acute failure: pH falls below 7.30 - Lungs with bilateral infiltrates Common Causes of RF 1. COPD 2. Pneumonia 3. Tb 4. Contusion 5. Aspiration 6. Inhaled chemicals 7. Pulmonary embolism 8. Sepsis, Uremia, Anaphylaxis, Hypervolemia, DIC, Shock, Massive Blood Trans, Drug overdose Phases of ARDS 1. Exudative Leakage of fluid from capillaries w/in 24hours due to capillary damage from inflammation; leads to alveolar damage (Type 2) 2. Proliferative 7-10days (destruction of Type 1 & 2 pneumocytes by leukocytosis of macrophages, proteases); decreases surfactant production, atelectasis, intrapulmonary shunting; V/Q mismatch decreased lung compliance 3. Fibrinolytic 2-3 weeks; irreversible deposition of fibrin in the lung with hyaline membrane formation; decreased FRC Nursing Interventions 1. Maintain client on a ventilator with the correct settings 2. Provide care for either an oral airway of a tracheostomy 3. Monitor breath sounds for pneumothorax especially when positive and expiratory pressure (PEEP) is used (5-10cc of water) 4. Provide emotional support Medical Management - Artificial Surfactant (Survanta/Beractant) - Nitric Oxide Pulmonary vasodilator - Dobutamine/Dopamine for fluid instability - Steroids (prevent fibrin production; stabilize capillary and membrane stability) - Antibiotics - Ventilatory support with PEEP

SHOCK Hypovolemic Shock Decreased Blood volume Decreased Venous Return Decreased Filling Pressures Decreased Stroke Volume Decreased Cardiac Output Decreased Tissue Perfusion

Cardiogenic Shock Ineffective Pump Dec. Ventricular Emptying Dec. End Diastolic Vol. Inc. Filling Pressures Dec. Stroke Vol. Dec. Cardiac output Dec. BP

Neurogenic Shock Massive Vasodilation Venodilation Dec. Venous Return Dec. Filling Pressures Arteriolar Dilation Dec. Peripheral Resistance

Dec. Stroke Volume Dec Cardiac output Dec. BP Dec. Tissue Perfusion SHOCK will SNACH your life away S-Septic N-Neurogenic A-Anaphylactic C-Cardiogenic H-Hypovolemic Nursing assessment Skin Changes: 1. Cool, clammy 2. Diaphoresis 3. Pale Fluid Status (acute tubular necrosis) 1. Urine output decreases 2. Abnormal CVP (<4cm of H2O) 3. Urine specific gravity >1.020 (indicates hypovolemia) Nursing Interventions 1. Monitor CVP 2. VS and arrhythmias every 15mins 3. Urine every hour 4. MAST, IABP, External Pulsation Device 5. Aminister fluids as prescribed

6. Place client in modified Trendelenbrgs position 7. Administer medications IV (not IM) Medical Interventions: - Digitalis - BT (whole blood, Packed RBC) - Autotransfusion (trauma) Hct rises 4% and Hgb rises about 1mcg% for each unit for packed RBC

~God Bless~