ABSITE CRITICAL CARE EXAM 2024-
2025 WITH ACTUAL CORRECT
QUESTIONS AND VERIFIED
DETAILED RATIONALES ANSWERS
|FREQUENTLY TESTED QUESTIONS
AND SOLUTIONS |ALREADY GRADED
A+|NEWEST|GUARANTEED PASS
|LATEST UPDATE
All of the following are potent cardiac inotrope except
- Digoxin.
- Dopamine.
- Amrinone.
- Norepinephrine.
Digoxin.
(Digoxin is only a minimally effective cardiac inotrope. In fact, its usefulness in congestive heart failure
may be due to factors other than its very mild inotropic effect. It certainly has no role as an inotrope
in the acutely failing heart. )
Hypoxic pulmonary vasoconstriction is worsened by
acidosis
Three days following completion debridement for Fournier's gangrene, a patient remains septic,
requiring vasopressor therapy. Corticosteroid therapy should be considered because:
Relative adrenal insufficiency is suspected.
(A high index of suspicion should be maintained for relative adrenal insufficiency in septic patients
who are vasopressor dependent.)
increased oxygen delivery with exercise
- Improved ventilation-perfusion matching.
- Increased extraction ratio.
1|Page
,- Decreased functional residual capacity.
- Rightward shift of the oxyhemoglobin dissociation curve.
(With exercise, metabolically active tissues result in increased temperature, 2-3 DPG levels and Pco,
shifting the oxyhemoglobin dissociation curve to the right thereby facilitating off-loading of oxygen.
Cardiac output rather than ventilation is the limiting factor in oxygen delivery to tissues. Increased
oxygen extraction from hemoglobin therefore occurs until anaerobic threshold occurs. Transit time
through the alveolar-capillary unit is decreased with exercise, thereby increasing the amount of blood
(hemoglobin) exposed to the alveolus for gas exchange. Chemoreceptor stimulation affects
sympathetic output to increase cardiac output and arterial pressure, which by minimizing zone one
improves V̇ /Q̇ matching. With exercise, afferents from joints, tendons, and peripheral chemoreceptors
influence the respiratory center increasing minute ventilation by increasing both the rate and depth of
breathing. This latter occurrence minimizes FRC, thereby making more alveoli available for
respiration.)
pulmonary blood flow
- Pulmonary vascular resistance is lowest at end-tidal volume .
- Hypoxia causes pulmonary vasoconstriction.
- Hypercapnia causes pulmonary vasoconstriction.
- Pulmonary vascular resistance is equally distributed among the arteries, capillaries, and veins.
- Passive dispensability and recruitment of the pulmonary capillary bed is responsible for constant, low
pressures with increasing cardiac output.
(Hypercapnia and hypoxia, as well as other humoral factors, cause pulmonary vasoconstriction. Unlike
the systemic vascular bed where varying organ demands require different degrees of perfusion, which
is accomplished by variably regulating resistances, the pulmonary vascular resistance is evenly
distributed. This is accomplished through a highly compliant circuit with relatively meager smooth
muscle resistance that is passively responsive to changes in pressure and flow, distending open
vessels and recruiting closed ones. Distended alveoli compress and stretch surrounding pulmonary
capillaries thereby increasing resistance in accordance with Poiseuille Law; therefore, the least such
distension of alveoli occurs at functional residual capacity or end-tidal volume.)
irreversible shock
In the setting of "damage control" laparotomy, not only should ostomies not be matured, but it is even
acceptable to leave packing inside the abdomen if it has effectively obtained hemostasis.
(In the setting of "damage control" surgery, patients are dangerously close to the threshold of
irreversible shock. They are coagulopathic, hypothermic, and acidotic. Consequently, surgery should
be terminated as soon as active sources of exsanguination are controlled. The patient should be
returned to the intensive care unit for rewarming and correction of their other metabolic
derangements. Should they survive long enough to complete resuscitation, they are then returned to
the operating room for definitive treatment of their injuries. )
Chronic anticoagulation is required for patients with
Mechanical valves.
(All mechanical valves require full anticoagulation with warfarin. Some have tried to utilize
2|Page
,mechanical valves without full anticoagulation, but with an unacceptably high embolization and
thrombosis risk. )
polymorphonuclear cells (PMNs)
- PMNs are nonspecific in their host defense functions.
- Experimental evidence has demonstrated that blocking the interaction of PMN and endothelial
adhesion molecules reduces organ injury.
- They migrate through the endothelial barrier by a process called diapedesis.
Anaerobic glycolysis occurs as a result of
Inadequate oxygen delivery to the cell
Which of the following mediators are likely to dominate the anti-inflammatory late stages of injury?
Interleukin-10 (IL-10).
(IL-10 is an anti-inflammatory mediator produced by the host in an attempt to bring the organism
back to homeostasis after surviving the early stages of injury. It acts to inhibit the release of a host of
proinflammatory mediators, and infusion of IL-10 has been shown to improve survival in septic
animals. Its potential role in causing late incidents of MOF and sepsis through relative
immunosuppression by overproduction is being investigated. )
Class I hemorrhage
loss of 0-15%
- In the absence of complications, only minimal tachycardia is seen.
- Usually, no changes in BP, pulse pressure, or respiratory rate occur.
- A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately
10%.
Class II hemorrhage
loss of 15-30%
- Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse
pressure, cool clammy skin, delayed capillary refill, and slight anxiety.
- The decrease in pulse pressure is a result of increased catecholamine levels, which causes an
increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.
Class III hemorrhage
loss of 30-40%
- By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP,
oliguria, and significant changes in mental status, such as confusion or agitation.
- In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that
consistently causes a decrease in systolic BP.
- Most of these patients require blood transfusions, but the decision to administer blood should be
based on the initial response to fluids.
Class IV hemorrhage
3|Page
, loss of >40%
- Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse
pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed
mental status (or loss of consciousness), and cold and pale skin.
- This amount of hemorrhage is immediately life threatening.
lung volumes and pulmonary function testing
- Quantitative perfusion scans utilize radiolabeled albumin to act as a surrogate for functioning
(ventilated) lung. Insofar as its relative distribution relies on perfusion, this presupposes that ventilation
matches perfusion and that hypoxic, nonventilated lung restricts perfusion by means of HPV.
- The ratio FEV:FVC is usually normal in restrictive disease, although the individual lung volumes are
reduced and compliance curves are shifted to the right.
- MMFR reflects the volume of flow within the second and third quarters of the first second of forced
expiration when the effects of transpleural pressure and obstructive flow dynamics are maximal within
compromised airways. It is the most sensitive indicator of obstructive parenchymal disease.
- The RER is the proportion of oxygen consumption to the production of carbon dioxide at the cellular
level during aerobic respiration. At anaerobic threshold during stress testing, oxygen consumption is
maximized and carbon dioxide production continues to increase via the anaerobic glycolytic pathway
such that the RER markedly increases.
mandatory minute volume-controlled ventilation
It requires greater than calculated tidal volume delivery.
(Because volume delivery is preset, excess volume above that calculated as necessary for the
individual must be delivered to account for the circuitry dead space. Also because the volume is
preset, it is not dependent on thoracic or pulmonary compliance or airway pressures for complete
delivery. Pressure controlled ventilation uses airway pressure limits to cease delivery of tidal volume
when certain peak airway pressures are met as a means of minimizing barotrauma. Because volume-
controlled ventilation has no such limits, high tidal volumes may persistently raise mean airway
pressures contributing to barotrauma. Other permutations of volume-controlled ventilation rely on
patient effort and participation, therefore are usually associated with the development of lower
airway pressures than MMV. )
regarding lateral decubitus, one-lung ventilation during anesthesia for thoracotomy
- Compliance is decreased.
- Physiologic shunting is increased.
- Intravenous anesthetics are preferred to inhalation anesthetics.
- Functional residual capacity is decreased.
(With upside lung collapse, no increase in dead-space ventilation occurs but there is a substantial
increase in physiological shunting of nonventilated, perfused lung. This is partially offset by hypoxic
pulmonary vasoconstriction which is nullified with inhalation anesthetics. With anesthesia and lateral
decubitus positioning paralysis of the diaphragm and its subsequent upward displacement,
mediastinal shifting downward by gravity and restriction of chest wall movement of the downside
lung result in marked decrease in FRC and downside lung and chest wall compliance. )
4|Page
