14. Hemodynamic Monitoring and Shock.docx

14. Hemodynamic Monitoring and Shock.docx - Hemodynamic...

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Hemodynamic Monitoring & Shock All content in red is a review from previous courses. Review the content prior to coming to class since this material will not be covered in detail during class. --Readings: Lewis, et al., pp. 1685-1695; 1717-1743 (8 th ed.) ch66, 67 Student Learning Outcomes: 1. Define and identify normal values for measurements from arterial, CVP, and PAP catheters in an adult. 2. Discuss nursing responsibilities when caring for an individual who is receiving hemodynamic monitoring. 3. Describe hemodynamic responses in selected situations. 4. Relate the pathophysiology to the clinical manifestations of the different types of shock: cardiogenic, hypovolemic, distributive, and obstructive. 5. Compare and contrast the effects of shock, systemic inflammatory response, and multiple organ dysfunction on the major body systems. 6. Compare the collaborative care, drug therapy, and nursing management of patients experiencing different types of shock. 7. Describe the nursing management of a patient experiencing multiple organ dysfunction syndrome. Outline: I. Hemodynamics is: A. Measure of pressure, flow and oxygenation within the cardiovascular system. B. Used to identify the response to therapies C. Indicators of organ perfusion D. Must be accurate readings 1. Non-invasive – What are some ways to determine CO? Cardiac output- blood through heart per minute, Cardiac index- based on Body surface area- BSA, Preload- volume within ventricle at end of diastole, Afterload-forces opposing ventricular ejection, vascular resistance, pulse ox, B/p, pulses, urine output, LOC, numbers can be deceiving 2. Invasive –CVP monitoring, catheredor that sits in SVCava measures pressures in right atrium, Swans gans- pulm artery, PWAP, arterial pressure monitoring II. Hemodynamic Terminology – Review Table 66-1 A. Contractility 1. Frank Starling’s Law - the more the myocardial fiber is stretched during filling, the more it shortens during systole and the greater the force of the contraction- increased force of contraction 2. Affected by: -- Sympathetic activity – increase HR, vasoconstrict vessels -- Electrolyte imbalance –decrease Ca, K, contractility is lessened -- Myocardial oxygen status - -- Pathologic conditions –cardiomyopathy, previous MI wont contract as well --Hypothermia – heart won’t contract as well in low temperatures -- Pharmacological effects a. Positive inotropes increase contractility- dig, dop, epi, dobutamine b. Negative inotropes decrease contractility-alcohol, ca channel blockers, beta blockers, acidotic states B. Preload 1. Volume within a ventricle at the end of diastole 2. Measurements RV preload CVP/RAP (central venous pressure/right atrial pressure & preload 2-8 mmHg) LV preload PAWP or LVEDP (pulmonary artery wedge pressure normal 6-12 mmHg) or (left ventricular end diastolic pressure) 2. Affected by: -- Blood volume- more volume, more stretch, more CVP/ preload -- Distribution of blood volume –vascular (preload higher) v extracellular
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-- Atrial function –a-fib- ineffective pump, increased preload
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