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ABSITE - Critical Care Exam With Questions And 100% Correct Answers
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ABSITE - Critical Care Exam With Questions And100% Correct Answers
Pathophysiologic diffusion states - what is the mechanism of re-expansion pulmonary
edema - ANSWER Ischemic-reperfusion injury.
Although fluid overload is potentially an exacerbating component of
postpneumonectomy pulmonary edema, the inciting cause for this and other similar
pathologic situations such as re-expansion pulmonary edema, is likely
ischemic-reperfusion injury possibly as a result of hypoxic pulmonary vasoconstriction.
Chronic tobacco abuse results in the destruction of septae within acini with the
subsequent coalescence of alveoli into air sacs that are without perfusion and result in
physiologic dead space. This removal of large numbers of alveoli from respiratory units
eliminates area for diffusion resulting in diffusion block. A significant component of
pulmonary contusion is disruption of the integrity of the alveolar-capillary barrier such
that administered albumin relocates to the interstitium or alveoli with adverse
consequences on the Starling equation for capillary fluid exchange. Exercise decreases
transit time through the respiratory unit thereby exposing more hemoglobin to the
alveolus per unit time, thereby increasing oxygen delivery. It has no effect on the rate of
diffusion of oxygen through the alveolar-capillary barrier.)
Mechanism of mechanical ventilation at which tidal volume is variably determined by the
amount of inspiratory effort. ANSWER Pressure-support ventilation (PSV).
(With PSV, tidal volume is pressure limited where inspiratory effort acts as a trigger to
deliver variable tidal volume as determined by the amount of preset support, airway
resistance, and patient effort. With assist-control ventilation, mandatory minute
ventilation and synchronized intermittent mandatory ventilation, predetermined rate
and tidal volume are programmed so that set minute ventilation is mandated whether
determined solely by the machine or in part by the patient. CPAP is not a means of
delivering tidal volume but rather of decreasing functional residual capacity.)
Curve of pressure-volume of the pericardium states that: - ANSWER Removal of a small
amount of pericardial fluid may dramatically increase cardiac output.
(As little as 10 mL of pericardial fluid removed may dramatically increase cardiac
output.)
,The risk of endocarditis is significantly enhanced with - ANSWER Disruption of
endocardium.
(This is a necessary condition for the development of endocarditis, but bacteremia is
also required of course, and bacteremia is a common condition, whereas endocarditis is
not.)
You are managing a postsurgical patient with a history of congestive heart failure. The
patient is hypotensive despite fluid resuscitation with an elevated SVR. Management
considerations should include: - ANSWER - β-1 agonist infusion.
Phosphodiesterase inhibitor infusion.
Nitroprusside infusion.
Fluid infusion following afterload reduction.
The following are the causes of sudden postoperative hypotension in a patient shortly
after undergoing a pneumonectomy and partial resection of the pericardium except:
Massive tear of the pulmonary vein
Cardiac herniation through the pericardium
Massive leak of the pulmonary artery stump
Acute myocardial infarction
Cardiac tamponade - ANSWER Cardiac tamponade.
This would not result in tamponade if bleeding were to occur around the heart because
it would decompress into the pleural space at the site of pericardial resection.
factors that determine cardiac output-ANSWER- Stroke work index.
Afterload.
Preload.
Compliance.
All these factors, preload, afterload, stroke volume, compliance, heart rate, and
inotropic state of the heart, are causing an impact on the cardiac output.
,Which of the following formulas best describes the relationship of the content of oxygen
in arterial blood [CaO], in hemoglobin [Hgb], partial pressure of oxygen [PaO2,], and
arterial oxygen saturation [SaO2]? ANSWER CaO= (1.34 × Hgb × SaO2) + (0.003 ×
PaO2).
(The first part of the equation represents oxygen transported by hemoglobin. The
constant 1.34 represents the volume in milliliter of oxygen that each gram of hemoglobin
is capable of carrying when fully saturated. This is multiplied by the grams of
hemoglobin available [Hgb] and the percentage of hemoglobin saturation [SaO].). The
other fraction of equation refers to the quantity of oxygen that may be transported
dissolved in plasma. The solubility coefficient of oxygen in plasma is extremely small
0.003, and the partial pressure of dissolved oxygen should be multiplied by this
constant. This makes it obvious that dissolved oxygen's share in blood oxygen content is
very negligible.)
Acute life-threatening complications of myocardial infarction- ANSWER-
Total AV nodal block.
Ventricular septal rupture.
Myocardial rupture
(Left ventricular aneurysm formation is a chronic condition and does not occur acutely
following myocardial infarction. Moreover, it is usually not life threatening except
possibly due to some of its complications. )
respiratory effects of epinephrine- ANSWER >Note due to β-2 stimulation are
bronchodilation and prevention of mast cell degranulation.
ARDS - ANSWER - ARDS is part of the SIRS response to certain inciting factors.
ARDS involves a change in the filtration coefficient of the Starling equation for fluid
exchange.
Is due to toxic cytokines, free radicals, and other inflammatory mediators.
ARDS includes disseminated intravascular coagulopathy as part of the pathology.
Though volume overload may be exacerbating the developed process, it does not
precipitate ARDS. It appears that ARDS is part of SIRS-a systemic inflammatory
response to certain factors like sepsis, trauma, extracorporeal perfusion, and so on.
, ARDS is a permeability pulmonary edema, as opposed to hydrostatic pulmonary edema,
wherein the release of toxic mediators affect not only the alveolar-capillary membrane
permeability but also causes C-reactive protein mediated platelet aggregation of the
microvasculature leading to DIC and multisystem organ failure. )
A noncompliant dialysis patient presents with a 3-day history of lethargy and fatigue.
The general physical examination notes that he has cold clammy skin, a thready pulse of
125 and respiratory variation in the blood pressure from 110/85 mm Hg on expiration to
90/70 mm Hg on inspiration with an audible systolic murmur but no diastolic murmur.
Which of the following is true about this patient: - ANSWER An echocardiogram will most
likely reveal diastolic collapse of the right ventricle and respiratory variation of flow in
the ascending aorta.
(The patient probably has dialysis noncompliance and has developed uremic
pericarditis with cardiac tamponade; the "murmur" is probably a pericardial friction rub
and not a valvular abnormality. ACE-inhibitor therapy and ultrafiltration of volume by
hemodialysis are contraindicated in tamponade and may be used to treat a low cardiac
output state. A pulmonary embolism could be responsible for many of the physical
examination findings mimicking tamponade except the murmur or friction rub, and the
history of dialysis noncompliance would cause one to have a high suspicion of
pericarditis over embolism. Acute aortic valve endocarditis is associated with a
diastolic murmur and low diastolic blood pressure. Diastolic collapse of the right
ventricle and respiratory variation of blood flow in the aorta are common findings in
tamponade.)
A patient with an anatomic dead space of 150 ml has a tidal volume of 500 ml, a
respiratory rate of 20/min, and an arterial PCO of 45 mm Hg. Postoperatively, total
physiologic dead space increases to 250 ml and tidal volume decreases to 450 ml/kg. To
maintain the same arterial PCO, the patient`s respiratory rate must be - ANSWER 35/min
(?)
How does anaerobic glycolysis damage cellular function? - ANSWER - Accumulation of
lactic acid.
- Inhibited production of ATP.
- Accumulation of hydrogen ions.
A blood clot in the left iliac vein may reach the brain by way of a patent - ANSWER
foramen ovale
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