Pulmonary capillary wedge pressure

Crystalloid/colloid to achieve a pulmonary capillary wedge pressure (PCWP) between 15 and 18 mmHg... 

Use fluids and/or vasopressors to elevate MAP if necessary ° Maintain euvolemia (pulmonary capillary wedge pressure between 10 and 14 mmHg)... 

BP, blood pressure CO, cardiac output HR, heart rate PCWP, pulmonary capillary wedge pressure SVR, systemic vascular resistance T, increase 4, decrease 0, no or little change. 

Monitor changes in hemodynamic variables if available. Cardiac index should increase, with a goal to maintain it above 2.2 L/minute per square meter. Pulmonary capillary wedge pressure should decrease in volume overloaded patients to a goal of less than 18 mm Hg. 

The clinical scenario and the severity of the volume abnormality dictate monitoring parameters during fluid replacement therapy. These may include a subjective sense of thirst, mental status, skin turgor, orthostatic vital signs, pulse rate, weight changes, blood chemistries, fluid input and output, central venous pressure, pulmonary capillary wedge pressure, and cardiac output. Fluid replacement requires particular caution in patient populations at risk of fluid overload, such as those with renal failure, cardiac failure, hepatic failure, or the elderly. Other complications of IV fluid therapy include infiltration, infection, phlebitis, thrombophlebitis, and extravasation. 

PCWP Pulmonary capillary wedge pressure qid Four times daily (quater in die)... 

Preload The stretched condition of the heart muscle at the end of diastole just before contraction volume in the left ventricle at the end of diastole estimated by the pulmonary artery occlusion pressure (also known as the pulmonary artery wedge pressure or pulmonary capillary wedge pressure). 

Hemodynamic effects - Digoxin produces hemodynamic improvement in patients with heart failure. Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure, and systemic vascular resistance. 

Pharmacology The principal pharmacological action of nitrates is relaxation of the vascular smooth muscle and consequent dilation of peripheral arteries and especially the veins. Dilation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload). Dilation of the coronary arteries also occurs. The relative importance of preload reduction, afterload reduction, and coronary dilation remains undefined. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

Animal studies with the Impella pump have demonstrated a decrease in myocardial oxygen demand during ischemia and reperfusion, resulting in a smaller infarct size [23]. Initial experience in patients with cardiogenic shock treated with the Impella pump system showed improvements in cardiac output and mean blood pressure and a reduction in pulmonary capillary wedge pressure [24]. 

Ibutilide has no significant effects on cardiac output, mean pulmonary arterial pressure, or pulmonary capillary wedge pressure in patients with or without compromised ventricular function. 

B. Intravenous furosemide causes a significant decrease in pulmonary capillary wedge pressure and right atrial pressure, concomitantly decreasing stroke volume and increasing vascular resistance. This effect in many cases occurs before diuresis begins. 

Mechanism of Action AnACE inhibitor that suppresses the renin-angiotensin-aldos-terone system and prevents conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance, pulmonary capillary wedge pressure improves cardiac output and exercise tolerance. Pharmacokinetics ... 

Cardiac output and pulmonary capillary wedge pressure... 

Mectianism of Action A cardiac inotropic agent that inhibits phosphodiesterase, which increases cyclic adenosine monophosphate and potentiates the delivery of calcium to myocardial contractile systems. Therapeutic Effect Relaxes vascular muscle, causing vasodilation. Increases cardiac output decreases pulmonary capillary wedge pressure and vascular resistance. 

Measurements of arterial pressure, cardiac output, stroke work index, and pulmonary capillary wedge pressure are particularly useful in patients with acute myocardial infarction and acute heart failure. Such patients can be usefully characterized on the basis of three hemodynamic measurements arterial pressure, left ventricular filling pressure, and cardiac index. One such classification and therapies that have proved most effective are set forth in Table 13-4. When filling pressure is greater than 15 mm Hg and stroke work index is less than 20 g-m/m2, the mortality rate is high. Intermediate levels of these two variables imply a much better prognosis. 

In 142 patients with symptomatic heart failure (New York Heart Association classes III and IV) randomized to double-blind, placebo-controlled short-term treatment with a single intravenous dose of conivaptan 10, 20, or 40 mg, conivaptan significantly reduced pulmonary capillary wedge pressure and right atrial pressure and increased urine output (1). 

Hemodynamic effects During treatment with ACE inhibitors, systemic vascular resistance is decreased along with the pulmonary capillary wedge pressure and right atrial pressure (4). End-diastolic and end-systolic dimensions are reduced. Long-term ACE inhibition decreases echocardiographic left ventricle (LV) dimensions and increases the shortening fraction (5). 

Definition Characteristic criteria of PPH include (I.) elevated pulmonary artery pressure (> 25 mm Hg), (2.) increased pulmonary vascular resistance (> 120 dyne/ sec/cm ), and (i.) normal pulmonary capillary wedge pressure (<15 mm Hg). An elevated transpulmonary gradient (mean pulmonary artery pressure/pulmonary capillary wedge pressure = > 10 mm Hg) is likewise used as a diagnostic criterion. (62, 70) The presence of portal hypertension is considered as a prerequisite for the development of PPH. 

On the premise that phosphodiesterase inhibitors also inhibit the production of cytokines, milrinone has been used in the treatment of nine patients with the systemic inflammatory response sjmdrome and compared with seven patients with congestive heart failure (4). In both groups mikinone significantly altered cardiac index, pulmonary capillary wedge pressure, and left ventricular stroke work index. In the patients with cardiac failure it also reduced systemic vascular resistance index, and the dose of adrenaline had to be increased substantially during milrinone infusion to counteract vasodilatation. 

In a retrospective view of 63 patients who received intravenous milrinone for more than 24 hours for advanced cardiac failure, the mean dose was 0.43 micro-gram/kg/minute and the mean duration of therapy 12 (range 1-70) days (14). After 24 hours of therapy there was significant improvement in pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac index. Because of the nature of the study, which was not placebo-controlled, it is impossible to be sure what events could have been attributed to the milrinone. However, the authors reported five cases of asymptomatic, non-sustained ventricular tachycardia, six of symptomatic ventricular tachycardia, and three deaths, one in ventricular tachycardia and two in heart failure. There was no difference in the incidence of these adverse events in patients who received milrinone for more than 7 days compared with the others. 

There have been several case reports that high doses of nitric oxide (40-80 ppm) reduce pulmonary vascular resistance and increase pulmonary capillary wedge pressure in some patients with left ventricular dysfunction. The acute increase in left ventricular filling pressure that ensues can cause or exacerbate pulmonary edema. The author concluded that in patients with severe left ventricular dysfunction (pulmonary capillary wedge pressure over 25 mmHg) it would be prudent to avoid the use of inhaled nitric oxide. 

In CHF, increases cardiac output, decreases peripheral vascular resistance, B/P, pulmonary capillary wedge pressure, and heart rate. 

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