Pathology of the Lungs E-Book: Expert Consult: Online and Print
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Positive end-expiratory pressure is generally recommended to increase alveolar patency and to enhance oxygen delivery and carbon dioxide exchange. Nitroglycerin NTG is the most effective, predictable, and rapidly-acting medication available for preload reduction.
Several studies demonstrated greater efficacy and safety and a faster onset of action with NTG than with furosemide or morphine sulfate. The use of sublingual NTG is associated with preload reduction within 5 minutes and with some afterload reduction. Topical NTG may be as effective as sublingual NTG in most patients with CPE, but it should be avoided in patients with severe LV failure, because of poor skin perfusion manifesting as skin pallor or mottling and resultant poor absorption.
Intravenous IV NTG at high dosages provides rapid and titratable preload and afterload reduction and is excellent monotherapy for patients with severe CPE. The antianginal dose of NTG of 0. Considering the short half-life of nitrates, physicians should be comfortable with the high dosage for CPE, especially in most patients with CPE, who present with a hyperadrenergic state and moderately elevated blood pressure.
However, nitrates should not be used in hypotensive patients, and they should be used with extreme caution in patients with aortic stenosis and pulmonary hypertension.
Loop diuretics have been considered the cornerstone of CPE treatment for many years. Furosemide is used most commonly. Loop diuretics are presumed to decrease preload through 2 mechanisms: In most patients, diuresis does not occur for at least minutes; therefore, the effect is delayed.
Loop diuretics affect the ascending loop of Henle; therefore, the diminished renal perfusion in CPE may delay the onset of effects of loop diuretics. Many patients with CPE do not have fluid overload.
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Continued use of diuretics in these patients after their acute symptoms have resolved may be associated with adverse outcomes, including electrolyte derangements, hypotension, and worsening renal function GFR as a result of tubuloglomerular feedback. The presumption that these medications have a direct vasoactive venodilating effect has been questioned. Some studies demonstrated initial adverse hemodynamic consequences eg, elevations of PCWP, LV filling pressure, heart rate, and systemic vascular resistance after the administration of IV furosemide, perhaps due to direct neurohormonal stimulation.
Premedication with drugs that decrease preload eg, NTG and afterload eg, angiotensin-converting enzyme [ACE] inhibitors before the administration of loop diuretics can prevent potential adverse hemodynamic changes. The use of morphine sulfate in CPE for preload reduction has been commonplace for many years, but good evidence supporting a beneficial hemodynamic effect is lacking.
Data suggest that morphine sulfate may contribute to a decrease in cardiac output and that it may be associated with an increased need for ICU admission and endotracheal intubation. Adverse effects eg, nausea and vomiting, local or systemic allergic reactions, respiratory depression may outweigh any potential benefit, especially given the availability of medications that are more effective than morphine in reducing preload eg, NTG.
Any beneficial hemodynamic effect from morphine is probably due to anxiolysis, with a resulting decrease in catecholamine production and a decrease in systemic vascular resistance. An alternative can be low-dose benzodiazepines eg, lorazepam 0. This alternative reduces the risk of respiratory depression in patients whose condition responded to initial therapy. Nesiritide is recombinant human BNP that decreases PCWP, pulmonary artery pressure, RA pressure, and systemic vascular resistance while increasing the cardiac index and stroke volume index.
Therapy with nesiritide has decreased plasma renin, aldosterone, norepinephrine, and endothelin-1 levels and has reduced ventricular ectopy and ventricular tachycardia. Heart-rate variability also improves with nesiritide. IV nesiritide was associated with some hypotension but was otherwise well tolerated. A later meta-analysis of 3 randomized trials of patients receiving nesiritide and patients not receiving nesiritide showed a 7. In most large clinical trials nesiritide has not had a significant effect on renal function.
In one of the largest studies of nesiritide to date, the Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure ASCEND HF , nesiritide had a neutral effect on survival and rehospitalization and a small effect on dyspnea when used in combination with other treatments. The investigators recommended against the routine use of nesiritide in the broad population of patients with acute heart failure.
The hemodynamic effects of ACE inhibitors include reduced afterload, improved stroke volume and cardiac output, and a slight reduction in preload. The last effects happen when renal perfusion improves after cardiac output improves and diuresis occurs. Improvements occur much more slowly with the oral route.
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Studies have proposed a role for ACE inhibitors and ARBs in preventing structural and electrical remodeling of the heart, resulting in a reduced incidence of arrhythmias. BNP level and advanced age were the strongest independent predictors for AF occurrence. Assessment in Reduction of Mortality and Morbidity CHARM trial showed a reduction in the onset of AF in patients who were treated with Candesartan compared with placebo, with a median follow-up period of Nitroprusside results in simultaneous preload and afterload reduction by causing direct smooth-muscle relaxation, with an increased effect on afterload.
Afterload reduction is associated with increased cardiac output. The potency and rapidity of onset and offset of effect make this an ideal medication for patients who are critically ill.
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It may induce precipitous falls and labile fluctuations in blood pressure; intra-arterial blood pressure monitoring is often recommended. Nitroprusside should generally be avoided in the setting of acute MI. Its use is associated with the shunting of blood away from ischemic myocardium toward healthy myocardium ie, coronary steal syndrome , which potentiates ischemia. If nitroprusside is used, convert therapy to oral or alternative IV vasodilator therapy as soon as possible, because prolonged high-dose use is associated with thiocyanate and cyanide toxicity, particularly in patients with significant hepatic or renal dysfunction.
Use in pregnancy is associated with fetal thiocyanate toxicity. Prolonged infusion can induce tolerance, and reflex tachycardia may occur. Inotropic support is usually used when preload- and afterload-reduction strategies are not successful or when hypotension precludes the use of these strategies.
Two main classes of inotropic agents are available: Calcium-sensitizer agents are a new class of medications that have notably beneficial effects in acute decompensated heart failure; these drugs are under investigation. Dobutamine, a catecholamine agent, mainly serves as a beta1-receptor agonist, though it has some beta2-receptor and minimal alpha-receptor activity.
IV dobutamine induces significant positive inotropic effects, with mild chronotropic effects. It also induces mild peripheral vasodilation decrease in afterload. The combination effect of increased inotropy with decreased afterload significantly increases cardiac output. The vascular and myocardial receptor effects of dopamine, a catecholamine agent, are dose dependent. Low dosages of 0. Moderate and high dosages are arrhythmogenic and increase myocardial oxygen demand with the potential for myocardial ischemia.
Therefore, use these dosages only in patients with CPE who cannot tolerate dobutamine because of severe hypotension eg, systolic blood pressure mm Hg. Norepinephrine, a catecholamine agent, primarily stimulates alpha receptors, significantly increasing afterload and the potential for myocardial ischemia and reducing cardiac output. After blood pressure is restored, add other medications to maintain cardiac output. This results in a positive inotropic effect on the myocardium, in peripheral vasodilation decreased afterload , and in a reduction in pulmonary vascular resistance decreased preload.
Unlike the catecholamine inotropes, PDIs do not depend on adrenoreceptor activity. Therefore, patients are less likely to develop tolerance to PDIs than they are to other medications. Tolerance to catecholamine inotropes can rapidly develop by means of a down-regulation of adrenoreceptors. PDIs are less likely than catecholamine inotropes to cause the adverse effects that are typically associated with adrenoreceptor activity eg, increased myocardial oxygen demand, myocardial ischemia.
Several direct comparisons of PDIs milrinone to dobutamine in patients with CPE demonstrated that milrinone produced equal or greater improvements in stroke volume, cardiac output, PCWPs preload , and systemic vascular resistance afterload. However, milrinone was associated with the same or more tachycardia and with an increased incidence of tachyarrhythmias. All known IV inotropic agents are associated with an increased long-term mortality compared with placebo and therefore should be reserved for patients with heart failure and a markedly depressed cardiac index and stroke volume.
Levosimendan is a calcium sensitizer that is used in several European countries to manage moderate to severe heart failure. It has inotropic, metabolic, and vasodilatory effects. Levosimendan increases contractility by binding to troponin C.
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It does not increase myocardial oxygen demand, and it is not a proarrhythmogenic agent. Levosimendan opens potassium channels sensitive to adenosine triphosphate ATP , causing peripheral arterial and venous dilatation. It also increases coronary flow reserve. Moreover, studies have shown levosimendan to have an anti-inflammatory effect. Overall, levosimendan has been an effective and safe alternative to dobutamine.
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The most common adverse effects of levosimendan treatment are hypotension and headache. Tolvaptan is an oral vasopressin V2-receptor antagonist that was evaluated in a large patients , randomized, double-blind, placebo-controlled trial in patients with acute clinically decompensated CHF. Provides the user with all of the necessary diagnostic tools to make a complete and accurate pathologic report. Provides the trainee and general surgical pathologist with time saving diagnostic clues when dealing with difficult specimens.
Consistent and uniform approach incorporated for each disease and disorder Etiology, pathogenesis, clinical features, pathologic features, differential diagnosis User-friendly format enables quick and easy navigation to the key information required. Extensive use of summary tables, charts and graphs throughout the text. Extensive reference list highlights landmark articles as well as including most up-to-date citations. Directs the trainee and practitioner to the most recent and authoritative sources for further reading and investigation.
Acute alveolar injury and repair. Diffuse parenchymal disease of the lung.