Cardiopulmonary critical care by David R Dantzker; Steven M Scharf
By David R Dantzker; Steven M Scharf
content material: Pathogenesis of acute lung damage --
Pulmonary gasoline alternate --
Pathohysiology of the pulmonary vascular mattress --
Mechanical cardiopulmonary interactions in serious care --
Peripheral regulate of venous go back in serious ailment : 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 --
rules of mechanical air flow and weaning --
Ventilatory regulate within the severe care atmosphere --
severe care radiology --
Cardiopulmonary resuscitation --
Pharmacologic and ventilatory help of the circulate in significantly in poor health sufferers --
Acute myocardial infarction --
Cardiac rhythm issues within the serious care atmosphere : pathophysiology, prognosis, and administration --
Acute breathing 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 --
persistent obstructive pulmonary illness --
Smoke inhalation harm --
Hyperbaric drugs --
Pulmonary failure attributable to excessive altitude.
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Additional resources for Cardiopulmonary critical care
When the patient is dependent on pacing to maintain an appropriate heart rate or when it is anticipated that temporary pacing will be needed for greater than 24 h, insertion of a transvenous pacemaker is usually preferred. Transcutaneous ventricular pacing can be useful in acute settings such as cardiac arrest to avoid delays and complications from central venous cannulation. This will allow accommodation of large volumes of blood, normally with minimal changes in diastolic pressure. Volume overload states can cause pulmonary edema even with normal LV compliance (C).
Inhaled nitric oxide in COPD patients has been shown to increase hypoxemia, as have other systemic vasodilators (nitroprusside). If the size of the alveoli continually decreases and nitrogen is absent, closing volume will eventually be reached and atelectasis develops. In critically ill patients, low areas are generally considered the primary cause of hypoxemia. As a result, little O2 is available to increase O2 content in blood from shunted areas. As discussed in Chapter 15, PEEP keeps unstable lung units open and improves oxygenation.
Bradycardia owing to conduction system disease (permanent pacing not immediately available) A. Asymptomatic complete heart block B. Asymptomatic type II seconddegree AV block 2. Acute myocardial infarction A. Bradycardia with acute inferior infarction responding to atropine B. Left bundle branch block with firstdegree heart block of unknown duration C. Bifascicular block of unknown duration 3. Procedures associated with important bradycardia A. General anesthesia with right bundle branch block with left anterior or left posterior hemiblock B.