By David R Dantzker; Steven M Scharf

content material: Pathogenesis of acute lung harm --
Pulmonary gasoline alternate --
Pathohysiology of the pulmonary vascular mattress --
Mechanical cardiopulmonary interactions in serious care --
Peripheral regulate of venous go back in severe sickness : position of the splanchnic vascular compartment --
The muscle groups of breathing --
Cardiac functionality --
Oxygen delivery and usage --
The microcirculation and tissue oxygenation --
Pulmonary mechanics in severe care --
ideas of mechanical air flow and weaning --
Ventilatory keep watch over within the serious care atmosphere --
severe care radiology --
Cardiopulmonary resuscitation --
Pharmacologic and ventilatory aid of the move in significantly unwell sufferers --
Acute myocardial infarction --
Cardiac rhythm problems within the serious care environment : pathophysiology, prognosis, and administration --
Acute respiration misery syndrome --
Heart-lung interactions in sepsis --
Community-acquired pneumonia --
Hospital-acquired pneumonia and pneumonia within the immunosuppressed host --
Deep venous thrombosis and pulmonary embolism --
prestige asthmaticus --
power obstructive pulmonary ailment --
Smoke inhalation damage --
Hyperbaric medication --
Pulmonary failure brought on by excessive altitude.

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71:620–629.  86:623–632.  25:786–794.  Care 155:473–480.  Blackwell, Oxford.  55–64.  295–302. 1 Cardiac function Cardiac performance is regulated by the integration of four major determinants: • preload: an estimate of ventricular end­diastolic volume, highly predictive of systolic function; • afterload: the degree of ventricular wall tension; • inotropy: the contractility of the ventricular muscle; • heart rate.  Indexing cardiac output permits us to compare values between large and small patients.

Acute myocardial infarction A. New right bundle branch block B. Pre­existing bundle branch block C. Asymptomatic type I second­degree AV block or first­degree AV block D. 4 Pulmonary edema may develop whether left ventriculir (LV) compliance is decreased, normal or increased—as indicated by the pressure­volume curves depicted here With decreased LV compliance, even a normal LV volume may increase diastolic pressure enough to cause pulmonary ede ma (A); when the volume is low, pressure also increases, but to a lesser extent (B).

Heart rate <30 beats min–1 persisting for ≥10 min 2. Acute myocardial infarction: A. Asystole B. Complete heart block C. Right bundle branch block with left anterior or left posterior hemiblock with acute anterior myocardial infarction D. Type II second­degree AV block with acute anterior myocardial infarction E. Symptomatic bradycardia unresponsive to atropine 3. Procedures that may be associated with significant bradycardia A. 4. Overdrive suppression of tachyarrhythmias A. Symptomatic recurrent ventricular tachycardia refractory to drug therapy B.

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