Page 612 - Cardiac Nursing

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588 PA R T I V / Pathophysiology and Management of Heart Disease
are hypoperfused and have pulmonary congestion (cold and wet). hemodynamically directed pharmacologic protocol for acute HF
For patients with adequate intravascular volume, inotropic agents and cardiogenic shock therapy.
should be initiated. Inotropic agents are used to increase systemic
and coronary artery perfusion pressure. Dobutamine can im- Goal 3: Reduce Myocardial Work
prove myocardial contractility and increase cardiac output and is The efficacy of vasodilators has been shown in the treatment of
usually the agent of choice in patients with systolic pressures cardiogenic shock. The major physiologic effect of vasodilators is
greater than 80 mm Hg. Dobutamine can precipitate tach- a reduction in LV end-diastolic pressure and SVR, with a subse-
yarrhythmias and exacerbate hypotension. Dopamine is prefer- quent increase in stroke volume and improved LV function. In-
able in patients with systolic pressures less than 80 mm Hg. travenous nitroprusside remains the drug of choice in cardiogenic
Tachycardia and increased peripheral resistance is dose depend- shock, because it acts rapidly and has a balanced effect, dilating
1
ent, and can exacerbate myocardial ischemia. In some situations, both veins and arterioles, thereby reducing both preload and af-
a combination of dopamine and dobutamine can be more effec- terload. Nitroglycerin can also be used, but it is predominantly a
tive than one agent alone. When hypotension remains refractory, venous vasodilator, and large doses are sometimes required to re-
NE may be necessary. Other agents used for positive inotropic ef- duce SVR (afterload). Intravenous nitroglycerin may be preferred
fect include phosphodiesterase inhibitors, such as milrinone. in patients with acute MI because of its favorable effect on coro-
Afterload reduction by peripheral vasodilators appears particu- nary blood flow. 1
larly well suited to reducing PAWP and SVR and improving CI. Mechanical support of circulation may be used in the reduc-
Inotropic agents are also used to increase systemic and coronary tion of LV workload in cardiogenic shock. The IABP is used to re-
artery perfusion pressure. Intra-aortic balloon pump (IABP) duce afterload and improve cardiac output at the time of systolic
1
counterpulsation may also be indicated. Display 24-3 reviews the contraction and to increase myocardial perfusion during
DISPLAY 24-3 Hemodynamically Directed Protocol for Acute Heart Failure/Cardiogenic Shock Therapy
I. General hemodynamic goals
RAP 7 mm Hg
PAWP 14–16 mm Hg
SVR 1,000 to 1,200 dyne/s/cm 5
CI 2.5 L/min/m 2
“Optimum” systolic or mean BP is the lowest pressure that adequately supports renal function and central nervous sys-
tem activity without significant orthostatic symptoms (systolic BP usually 80 to 90 mm Hg)
II. Patient-specific hemodynamic goals
“Optimum filling pressure” (PAWP): lowest PAWP that can be maintained without preload-related decline in systolic BP or
CI. A higher PAWP (18 to 20 mm Hg) is usually required in acute myocardial injury
“Optimum afterload” (SVR): lowest SVR that leads to reasonable cardiac index while maintaining adequate systolic BP
(usually 80 mm Hg) and renal perfusion (urine output 0.5 mL/kg/h)
III. Specific intravenous pharmacologic therapy
Nitroprusside: begin when combined preload and afterload reduction is most important hemodynamic goal
Start at 0.1 to 0.2 g/kg/min
Titrate upward by 0.2 g/kg/min at 3- to 5-minute intervals
Target hemodynamics (Section I of this display)
Hemodynamic effects resolve rapidly when infusion stopped
Nitroglycerin: begin when preload reduction is primarily desired
Start at 0.2 to 0.3 g/kg/min
Titrate at 3- to 5-minute intervals
Be aware of tolerance
Target hemodynamics (Section I of this display)
Effects resolve rapidly when infusion stopped
Dobutamine: begin when both inotropic and vasodilating effects desired but inotropic effects most important
Start at 2.5 g/kg/min
Attempt to keep dose 15 g/kg/min; avoid significant tachycardia
Consider adding low-dose dopamine to assist with augmenting renal perfusion or milrinon to achieve hemodynamic
endpoints
Hemodynamic effects resolve over minutes to hours when infusion stopped
Milrinone: begin when both vasodilating and inotropic effects desired
Dose range is 0.375 to 0.75 g/kg/min (usual is 0.5 g/kg/min)
Target hemodynamics (Section I of this display)
Prolonged hemodynamic effects after drug is stopped
BP, blood pressure; CI, cardiac index; PAWP, pulmonary artery wedge pressure; RAP, right atrial pressure; SVR, systemic vascular resistance.
Adapted from text Lyengar, S., Hass, G., & Young, J. (2006). Acute heart failure. In E. J. Topol (3rd ed.), Textbook of cardiovascular medicine (pp. 1845–1898).
Philadelphia: Lippincott-Williams & Wilkins.