Exam 5 Study Guide - Hemodynamic Monitoring PDF

EXAM 5 STUDY GUIDE CH 35 - HEMODYNAMIC MONITORING - Hemodynamic Monitoring: the measurement of pressure, flow, and oxygenation in the CV system *Purpose = assess the heart function and fluid balance - Cardiac Output (CO): volume of blood in liter pumped by the heart in 1 min - Cardiac...

EXAM 5 STUDY GUIDE CH 35 - HEMODYNAMIC MONITORING - Hemodynamic Monitoring: the measurement of pressure, flow, and oxygenation in the CV system *Purpose = assess the heart function and fluid balance - Cardiac Output (CO): volume of blood in liter pumped by the heart in 1 min - Cardiac Index (CI): CO adjusted for body surface area *normal = 2.8-4.2 liters/min/meter^2 - Stroke Volume (SV): volume ejected with each heartbeat - Preload: volume in ventricle at the end of diastole *diuresis and vasodilation decreases preload *fluid administration increases preload - Afterload: forces opposing ventricular ejection of blood *vasodilation decreases afterload - Contractility: strength of contraction *positive inotropes increase contractility (epinephrine, norepinephrine, dopamine) *negative inotropes decrease contractility (calcium channel blockers and beta blockers) *increased afterload = decreased CO and increased O2 demand *increased contractility = increased SV and increased myocardial O2 needs *contractility is reduced with a failing heart - Non-Invasive Hemodynamic Monitoring: 1. Detect early s/s of pulmonary or cardiac problems 2. Detect cause of dyspnea 3. Evaluate cause and treat hypertension 4. removal/insertion of PA catheter 5. Evaluate effectiveness of drug therapy 6. Diagnose rejection after heart transplant *can be less accurate than invasive hemodynamic monitoring  - Invasive Lines: measure systemic and pulmonary BP’s - Dynamic Response Test (square wave test): every 8-12 hours, done when system is open to air or the accuracy is questioned - Phlebostatic Axis: 4th intercostal space (nipple line) *transducers higher than phlebostatic axis = false low BP *transducers lower than phlebostatic axis = false high BP - Arterial Blood Pressure: insertion of catheter into radial or femoral artery used to obtain diastolic, systolic, and mean arterial pressure (MAP) *perform Allen test before insertion of line to confirm circulation *keep zero reference stop cock level with phlebostatic axis Risk Factors: hemorrhage, infection, thrombus formation, neurovascular impairment, and loss of a limb Maintaining Line + Preventing Clot Formation: assess every 1-4 hours for: 1. Pressure bag inflated to 300 mmHG 2. Fluids in flush bag 3. Slow delivery of fluids (1-3 mL/hr) - Arterial Pressure Based CO (APCO): minimally invasive technique to determine continuous CO or continuous CI - Arterial Pressure: force generated by the ejection of blood from the left ventricle into arterial circulation - Pulmonary Artery Flow Directed Catheter: PA pressure monitoring guides the management of patients with select complicated heart and lung problems *PADP + PAWP increase heart failure and fluid overload + decrease volume depletion - PA Catheter: multiple lumen, distal lumen is within the PA - RA Port: CVP measurement, blood specimens, CO measurement - RV Port: infusing + blood samples - PA Pressure Monitoring: not common anymore - too many risks *PA insertion can be done at bedside - Monitor HR during insertion - Obtain x ray for correct placement - Occlusive sterile dressing  - Central Venous Pressure: measurement of right ventricular preload and fluid volume status *central venous catheter is placed in internal jugular or subclavian vein *High CVP = RV failure or volume overload *Low CVP = hypovolemia - Hemodynamic Monitoring Nurse Management: assess mental status, monitor urine output, monitor bowel sounds, monitor for bleeding, monitor HR/BP, monitor for neurovascular issues, monitor oxygen levels *single hemodynamic values are rarely helpful *many sources + time = good hemodynamic assessment - Goal: intervene before pt status declines CH 38 - HEART FAILURE *A PUMP PROBLEM - Etiology: anything that interferes with the normal mechanisms that regulate cardiac output Preload: stretch on ventricles before diastole Afterload: resistance the heart has to overcome to pump blood to the rest of the body Contractility: how forcefully and effectively the heart is contracting - Defect in ventricular ejection fraction = systolic dysfunction (reduced) - Defect in ventricular filling = diastolic dysfunction (preserved) *CAN BE BOTH = mixed systolic and diastolic *Primary Cause = direct damage to the heart - Causes: HTN, CAD, MI, Pulm HTN, rheumatic heart disease, congenital heart defects, cardiomyopathy, valvular disorders, myocarditis - Precipitating Factors: (conditions that increase the workload) thyroid issues, anemia, infections, sleep apnea, pulmonary emboli, nutritional deficiencies, paget’s disease, dysrhythmias - Associated with CVDs such as HTN, CAD, MI - Most common cause of hospital admission in adults over 65 *25% of pts discharged with HF are readmitted within 30 days !! - Risk Factors: Hypertension (most modifiable) & CAD - Comorbidities: diabetes, metabolic syndrome, advanced age, tobacco use, and vascular diseases Left Sided Heart Failure *most common form of HF - Results from inability of left ventricle to empty adequately systole and fill adequately during diastole - Blood backs up into left atrium and pulmonary veins *LEFT = LUNG - Manifestations: pulmonary congestion, dyspnea, cough, blood-tinged frothy sputum, restless, tachycardia, S3, orthopnea, nocturnal dyspnea, edema, wet lung sounds Right Sided Heart Failure - Right ventricle fails to pump effectively - Fluid backs up in venous system and moves into tissues and organs *left-sided heart failure is most common cause - Other Causes: RV infarction, PE, Cor pulmonale *RIGHT = REST OF BODY - S/S: enlarged organs, edema, weight gain, distended neck veins (JVD), ascites - Systolic HF: heart cannot contract & eject (HF with reduced ejection fraction) - Diastolic HF: ventricles cannot relax & fill (HF with preserved ejection fraction) *can affect the RV, LV, or BOTH *ejection fraction: amount of blood pumped out / amount of blood in the chamber Normal = 50-70% COMPENSATORY MECHANISMS - Renin-Angiotensin-Aldosterone-System (RAAS): Homeostatic Regulatory System: the goal is the change in preload and ventricular contractility to maintain CO Fluid & Sodium retained in response to stress *Neuro-Hormonal response - SNS: Baroreceptors sense low arterial pressure Catecholamines are released (epi and norepi) Stimulation of B-adrenergic receptors increase HR & ventricular contractility - Dilation: Enlargement of the heart chambers - Heart muscle fibers stretch in response to the volume of blood in the heart at the end of diastole - Increased contraction is initially effective and increases cardiac output and maintains BP and perfusion  - Hypertrophy: increase in muscle mass and cardiac wall thickness in response to overwork & strain COUNTERREGULATORY MECHANISMS - B-Type Natriuretic Peptides (BNP): released in response to increased blood volume in heart, causes diuresis, vasodilation, and lowered BP CLASSIFICATION SYSTEMS OF HF ACCF/AHA Stages NYHA Functional Classification A) High risk but no heart disease or NONE s/s B) Heart disease present but no s/s No limitation of physical activity C) Heart disease present with s/s I) Same as above II) Slight limitation of physical activity III) Marked limitation of physical activity D) Advanced heart disease requiring IV) Inability to carry out any physical specialized therapy activity without discomfort ACUTE DECOMPENSATED HEART FAILURE (ADHF) - Sudden increase in symptoms of HF with a decrease in functional status requires rapid escalation of therapy and hospitalization - S/S: pulmonary congestion + fluid overload *lungs are less compliant *most common presentation is wet-warm - Early Stage: slight increase in respiratory rate and decrease in PaO2 PULMONARY EDEMA CLINICAL MANIFESTATIONS - Anxious, pale, cyanotic, cool and clammy, dyspnea, orthopnea, tachypnea, cough with frothy blood-tinged sputum, crackles/wheezes, S3 or S4 CHRONIC HEART FAILURE - Has had heart failure for a while - Manifestations: “FACES” fatigue, limited activity, chest congestion, edema, shortness of breath, dyspnea, nocturia *fatigue is the earliest symptom *report weight gain of 3 lbs in 2 days or 3-5lbs in a week  - Complications: pleural effusion, dysrhythmias, LV thrombus, hepatomegaly, renal failure, anemia - Diagnostics: echo, ekg, chest x ray, BNP levels (elevated), 6-minute walk test, MUGA scan, heart cath, endomyocardial biopsy, swan ganz catheter, Allen test, 5 P’s - Drug therapy: digitalis (lanoxin + digoxin), diuretics (lasix + thiazides)- potassium-wasting & potassium-sparing, ACE inhibitors (-pril), BeatBlockers (-olol), ARBs DIGOXIN: use carefully with afib & usually given with another drug *before administration: assess apical pulse for 1 minute DIG TOXICITY: Early: anorexia, n/v Late: arrhythmias, vision changes - Nutritional Therapy: low sodium diet 2g/day, small frequent meals INTRA AORTIC BALLOON PUMP (IABP) - Most common cardiac assist device - Decreases ventricular workload, increases myocardial perfusion and circulation - Works by counterpulsation *temporary use only !! *confirm placement with x ray - Complications: balloon leak, thrombocytopenia, infection, nerve damage, thrombus or embolus formation, vascular injuries, mechanical malfunction *keep pt immobile & limited to side-lying or supine with HOB