Question 11#

Using pulse pressure variability (PPV) to determine pre-load responsiveness:

A. Is reliable for a patient in rate-controlled atrial fibrillation, but not for a patient in atrial flutter

When intrathoracic pressure increases during the application of positive airway pressure in mechanically ventilated patients, venous return decreases and, as a consequence, left ventricular stroke volume also decreases. Therefore, pulse pressure variation (PPV) during a positive pressure episode can be used to predict the responsiveness of cardiac output to changes in preload. PPV is defined as the difference between the maximal pulse pressure and the minimal pulse pressure divided by the average of these two pressures. This approach has been validated by comparing PPV, CVP, PAOP, and systolic pressure variation as predictors of preload responsiveness in a cohort of critically ill patients. Receiver-operating characteristic curves demonstrated that PPV was the best predictor of preload responsiveness. Although atrial arrhythmias can interfere with the usefulness of this technique, PPV remains a useful approach for assessing preload responsiveness in most patients because of its simplicity and reliability. 

Question 12#

Strategies for increasing oxygen delivery in mechanically ventilated, critically ill patients include:

A. Increasing Sao₂ by increasing inspiratory time

Sao₂ in mechanically ventilated patients depends on the mean airway pressure, the fraction of inspired oxygen (Fio₂), and SVO₂• Thus, when Sao₂ is low, the clinician has only a limited number of ways to improve this parameter. The clinician can increase mean airway pressure by increasing positive-end expiratory pressure (PEEP) or inspiratory time. Fio₂ can be increased to a maximum of 1.0 by decreasing the amount of room air mixed with the oxygen supplied to the ventilator. SVO₂ can be increased by increasing Hgb or Q_T or decreasing oxygen utilization ( eg, by administering a muscle relaxant and sedation).

Question 13#

All of the following are true regarding airway pressures EXCEPT:

A. Bronchospasm will cause increased peak pressure with a relatively normal plateau pressure

The peak airway pressure measured at the end of inspiration (P_peak) is a function of the tidal volume, the resistance of the airways, lung/chest wall compliance, and peak inspiratory flow. The airway pressure measured at the end of inspiration when the inhaled volume is held in the lungs by briefly closing the expiratory valve is termed the plateau airway pressure (P_plateau ) • As a static parameter, plateau airway pressure is inder ateau pendent of the airway resistance and peak airway flow, and is related to the lung/chest wall compliance and delivered tidal volume. If both P_peak and P_plateau are increased (and tidal volume pea p ateau is not excessive), then the underlying problem is a decrease in the compliance in the lung/chest wall unit. Common causes of this problem include pneumothorax, hemothorax, lobar atelectasis, pulmonary edema, pneumonia, acute respiratory distress syndrome (ARDS), active contraction of the chest wall or diaphragmatic muscles, abdominal distention, and intrinsic PEEP, such as occurs in patients with bronchospasm and insufficient expiratory times. When P_peak is increased but P_plateau is relatively normal, the primary problem is an increase in airway resistance, such as occurs with bronchospasm, use of a small-caliber endotracheal tube, or kinking or obstruction of the endotracheal tube.

Question 14#

Causes of an increase in end-tidal-CO₂ include:

A. Massive pulmonary embolism

Causes of an increase in Petco₂ include reduced minute ventilation or increased metabolic rate. Sudden reduction in end-tidal-CO₂ (Petco₂) suggests either obstruction of the sampiing tubing or a catastrophic event such as loss of the airway, airway disconnection or obstruction, ventilator malfunction, or a marked decrease in Q_T. If the airway is connected and patient and the ventilator is functioning properly, then a sudden decrease in Petco₂ should prompt efforts to rule out cardiac arrest, massive pulmonary embolism, or cardiogenic shock. Petco₂ can be persistently low during hyperventilation or with an increase in dead space such as occurs with pulmonary embolization (even in the absence of a change in Q_T).

Question 15#

Which of the following is NOT an indication for intracranial pressure (ICP) monitorin

A. Glasgow Coma Scale (GCS) less than or equal to 8 with an abnormal computed tomography (CT) scan

Monitoring of intracranial pressure (ICP) currently is recommended in patients with severe TBI, defined as a Glasgow Coma Scale (GCS) score less than or equal to 8 with an abnormal CT scan, and in patients with severe TBI and a normal CT scan if two or more of the following are present: age older than 40 years, unilateral or bilateral motor posturing, or systolic blood pressure less than 90 mm Hg. ICP monitoring is indicated in patients with acute subarachnoid hemorrhage with coma or neurologic deterioration, intracranial hemorrhage with intraventricular blood, ischemic middle cerebral artery stroke, fulminant hepatic failure with coma and cerebral edema on CT scan, and global cerebral ischemia or anoxia with cerebral edema on CT scan. The goal of ICP monitoring is to ensure that cerebral perfusion pressure (CPP) is adequate to support perfusion of the brain.