2009 Flashcards
Given patient in HFO ventilation and asked:
a. Of the three parameters (I:E ratio, Amplitude, and Frequency) which has the greatest effect on Tidal volume? Which has the least effect on tidal volume.
b. If the bias flow is decreased to 20L/min from 40L/min does this affect CO2 clearance? Explain your answer.
a)
greatest effect on tidal volume: amplitude
least effect on tidal volume: ? I:E ratio
b)
??? yes because bias flow washes out CO2 from the vent circuit and if it’s too low rebreathing will occur (reference)
Unlike mechanical ventilation at physiological breathing rates where changes in ventilator settings on contemporary ventilators inevitably affect both oxygenation and ventilation, traditional teaching of HFOV promoted changes in mean airway pressure as the means of influencing arterial oxygen tension and alterations to proximal pressure amplitude (ΔP) and frequency (f) of the oscillatory waveform as the determinants of arterial carbon dioxide tension (Pa,CO2).
from kemh website:
Clinically, when HFOV is used without volume guarantee, tidal volume is altered in response to blood gas/TcpCO2 trends by adjusting:
- Amplitude or Delta-P (most important) Primary manipulations in PaCO2 are achieved by altering the oscillatory pressure amplitude (or power). Increasing the amplitude increases the displacement of the diaphragm/piston, increasing the VT delivered to the patient, lowering the PaCO2.
- Frequency (Hz) Lowering the frequency in HFOV increases the tidal volume (when there is a fixed I:E ratio), thereby lowering the PaCO2. However, as frequency decreases, the percentage of the oscillatory amplitude transmitted to the proximal airways increases. The frequency, at which this amplitude increases significantly, is influenced by the mechanical properties of the lung. The appropriate frequency is dependent on the disease being treated. As a general rule for the SM3100A, higher frequencies (12-15 Hz) are used for low compliance (e.g. HMD), whilst lower frequencies (8-10 Hz) are used in the presence of high resistance (e.g. early phase meconium aspiration, CLD). Smaller babies with poorly compliant lungs require higher frequencies than more mature infants. Hybrid ventilators may have limited capacity to achieve required tidal volumes at high frequencies, in the absence of spontaneous breathing. It may be necessary to use lower frequencies in hybrid ventilators than previously selected when using the SM3100A. In general, the highest frequency achievable should be used, to reduce the risk of barotrauma when using HFOV mode in hybrid ventilators.
- % I-Time I:E ratio is generally set at 1:2 for the Fabian and VN500, or 33 % (% inspiratory time) on the SM3100A. Increasing the I:E ratio to 1:1 (Fabian, VN500) or 50 % inspiratory time (SM3100A) may improve CO2 elimination at any given frequency. Increasing the absolute inspiratory time in this manner, permits more tidal volume to be delivered.
Given pt with asthma attack on B-agonist therapy q1h for last 24 hours. Increased WOB for last 24 hours….Long stem to the question. End of the stem says patient develops lactate of 6. List 2 causes for lactic acidosis in this patient.
- medication-induced from B agonist
- direct effect of endogenous catocholamines
- hypoxia/hypoperfusion
- high demand of respiratory muscles
Given patient admitted to ICU with severe pneumonia, ARDS, pneumothorax and chest tubes. Physiotherapist is concerned that there is ongoing leak in chest tubes. CT thorax is done and one slice is shown. List 3 abnormalities on the CT (there was s.c. emphysema, undrained pneumo, bilateral consolidation.
?anything to add?
Given with COPD who has been tried on NIV for 12 hours and now failing. You proceed to intubate the patient. CO2 is detected when you connect up the detector. The patient is bagged at rate of 25b/m. Immediately after intubation BP is 65/30. List 4 possible causes for hypotension.
- dynamic hyperinflation
- pneumothorax/tension pneumothorax
- distributive shock component from induction meds
- pre-existing hypovolemia
- ?tube migration/incorrect placement (esophagela intubation?)
Given COPD patient who is intubated. Question was: Aside from respiratory arrest and cardiac arrest, list 4 adverse effects of dynamic hyperinflation.
- increases mean airway pressure increasing risk of barotrauma/pneumothorax
- increases pt-ventilator dyssynchrony, in form of inadequate triggering since patient must achieve a higher negative presure or flow to reach atmospheric pressure then further negative pressure or flow to trigger breath
- flattens diaphragm which puts it into a less ideal position for force generation
- decreases cardiac output by decreasing venous return
Dynamic hyperinflation (DHI) is characterized by increased levels of intrinsic positive end-expiratory pressure (PEEPi or “auto-PEEP”). The hyperinflation is progressive (dynamic) because air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath. In patients with COPD who are intubated for respiratory failure, DHI can occur as a consequence of airflow obstruction due to bronchoconstriction, combined with a higher than normal minute ventilation (respiratory rate multiplied by tidal volume) delivered by the ventilator. DHI (spontaneous or ventilator-induced) creates elevated levels of auto-PEEP, which can lead to patient-ventilator dyssynchrony and increased work of breathing, barotrauma, cardiovascular collapse, and potentially even death.
Auto-PEEP is common in patients with COPD. In a prospective cohort study of 13 patients with COPD who were being mechanically ventilated, all of the patients had measurable auto-PEEP (mean 9.4 cm H2O), and seven had an auto-PEEP greater than 10 cm H2O. Auto-PEEP is responsible for up to one-third of the total work of breathing in patients mechanically ventilated with COPD [39].
Auto-PEEP can be detected in a number of ways. One practical and reliable method in patients with COPD is the demonstration on ventilator graphics of a progressive rise in peak airway pressures during mandatory tidal volume ventilation [40-43]. Alternatively, ventilator time-flow graphics may demonstrate the commencement of inspiratory flow before expiratory flow reaches zero (figure 7 and figure 4). These methods are not quantitative. While auto-PEEP can be quantitatively assessed by measuring airway opening pressure during an end-expiratory pause (Paw) (waveform 2) [44], this method is only accurate when the patient is paralyzed or exhibiting negligible abdominal and chest wall muscle engagement during exhalation, which is uncommon in COPD patients requiring mechanical ventilation.
Given a pt with ventilatory parameters. Asked to give formula for static compliance, and dynamic compliance.
static lung compliance = tidal volume/(plateau pressure - total PEEP)
dynamic lung compliance = tidal volume/(peak inspiratory pressure - total PEEP)
total PEEP = intrinsic PEEP + ventilator PEEP
Hypoxic patient on FiO2 1.0, PEEP 15. ph 7.24, PO2 48, PCO2 60. List four interventions that can assist with improving oxygenation of this patient.
- prone positioning
- NMB (now more controversial)
- decrease oxygen consumption (treat fever, agitation etc)
- ECMO?
- conservative fluid strategy
- inhaled pulmonary vasodilators
- high PEEP strategy
The use of etomidate has increased as a drug for intubation. List the one major
potential side effect of this drug.
Concerns with etomidate include adrenal suppression, myoclonus, and evidence of regional cerebral excitation (determined by electroencephalogram) after intubation [18,24,25]. Myoclonus has been misidentified as seizure activity, leading to incorrect recommendations that etomidate be avoided in patients with seizure disorders. Myoclonus during RSI is brief and minimal, because of the concomitant administration of a paralytic agent, and of no clinical significance. Etomidate decreases cerebral blood flow and cerebral metabolic oxygen demand, while preserving cerebral perfusion pressure [21]. Postintubation sedation with propofol or a benzodiazepine helps to prevent neuroexcitation.
Adrenocortical suppression — The major controversy surrounding etomidate stems from the reversible adrenocortical suppression associated with its use.
Although etomidate transiently inhibits cortisol biosynthesis, the preponderance of evidence suggests that this is not harmful in most clinical settings and does not preclude its use [46-50]. To avoid further suppression of cortisol, we do not administer multiple bolus doses or infusions of etomidate. In patients with suspected adrenal insufficiency, such as those on chronic glucocorticoid therapy, the clinician must weigh the risk of further cortisol suppression caused by etomidate against the risk of hemodynamic instability that may be caused by alternative induction agents.
Following a single induction dose of etomidate, reversible inhibition of 11-beta-hydroxylase (which converts 11-deoxycortisol to cortisol) causes adrenocortical suppression lasting <24 hours in both healthy and critically ill patients [46-55]. Although cortisol plasma concentrations may not appropriately rise in response to surgical stimulation after etomidate administration, concentrations do not necessarily fall below the normal range, and the clinical significance of this finding is uncertain.
In critically ill patients undergoing emergency tracheal intubation, a 2015 systematic review of eight randomized trials concluded that etomidate was not associated with increased mortality compared with any other induction agent (OR 1.17, 95% CI 0.86-1.60) [51]. Also, there is no definitive evidence that a single dose of etomidate increases mortality in critically ill patients diagnosed with sepsis [59]. However, use of etomidate in patients with frank septic shock may increase the likelihood of development of adrenal insufficiency [60]; thus, we usually select an alternative anesthetic induction agent in this circumstance.
List 4 strategies to decrease incidence of VAP.
- early mobilitiy
- change vent circuit only if visibly solied or malfunctioning
- elevate head of bed 30-45 degrees
- chlorhexidine oral wash
- minimize sedation
- minimize invasive mechanical ventilation (use NIPPV when possible)
- daily SBT and SAT
- use ETT with supraglottic secretion clearance for pts intubated >48-72h
- perform SBT with sedation turned off
Given balloon pump wave form:
a. What is the timing on the balloon?
b. Please mark with an “I” where balloon inflation occurs.
c. Please mark with a “D” where balloon deflation occurs.
d. Describe how balloon deflation assists cardiac function.
a) and b) and c)
Caption for the image: The timing of balloon inflation and deflation is adjusted in the 1:2 mode. The inflation point is moved rightward (later) until it occurs in late diastole, and the dicrotic notch is uncovered. The inflation timing is moved progressively earlier in the cardiac cycle until the dicrotic notch on the central aortic tracing just disappears. Examples of early, late, and correct inflation are shown in the top two tracings. Similarly, the deflation knob is moved leftward (earlier) and then slowly advanced toward the right (later in the cardiac cycle) until the end-diastolic pressure dips 10 to 15 mmHg below the patient’s unassisted diastolic pressure. This will produce a maximal lowering of the patient’s unassisted systolic pressure. Examples of early, late, and correct deflation timing are shown in the bottom two traces.
d)
diastolic augmentation (increases DBP)
- increases coronary perfusion pressure
- increases coronary blood flow
- increases myocardial oxygen supply
systolic unloading (decreases SBP, decreases HR, decreases mean pulm wedge pressure, increases CO)
- decreases LV wall tension
- decreases LVEDP
- increases cardiac output
- decreases myocardial oxygen demand
Given patient with long stem basically describing RV infarct.
a. List 4 principles in the management of this patient.
- optimize RV preload
- typically through volume loading, but consideration for gentle diuresis could also be made
- decrease RV afterload
- In patients with predominant RV dysfunction, RV afterload reducing therapy is not indicated and may worsen the hemodynamic profile. In patients with RVMI and significant left ventricular dysfunction, the use of an intraaortic balloon pump, and occasionally afterload reducing agents, may be effective in unloading the left ventricle and subsequently the right ventricle (I don’t get this…aside from the situation where pulmonary vasodilation increases LV preload and the LV can’t deal with it but why would this happen in isolated RV infarct???)
- optimize heart rate and AV syncrhony
- The ischemic right ventricle has a relatively fixed stroke volume and therefore right ventricular output is dependent upon heart rate and optimal transport of blood from the right atrium to the RV (referred to as atrioventricular [AV] transport).
As a result, bradyarrhythmias can significantly worsen the hemodynamic status. Atropine may be beneficial to increase heart rate, but right ventricular or atrioventricular sequential pacing (to provide an atrial contribution and AV synchrony) may be necessary
- optimize inotropy and RV perfusion (MAP)
- When fluid resuscitation is insufficient, hypotension should be rapidly corrected with an inotropic agent that also exerts vasoconstrictor effects. Uptodate says to use dopamine then maybe dobutamine, and if that fails consider mechanical support (IABP)…I’m not sure I agree and would suggest milrinone +/- vasopressin…
- mechanical support
- IABP (if also have cardiogenic shock from poor LV). Although there are little data on its benefits in shock due to RVMI, we have found it helpful in stabilizing aortic pressure and improving systemic perfusion in some patients and thus may be temporizing in refractory hypotension while performing emergency percutaneous revascularization and subsequently awaiting recovery of RV function
- RVAD
- anti-ischemic drug therapy
- Beta blockers and calcium channel blockers, which might be considered as tools to improve ischemia (and in particular, angina), can reduce heart rate and contractility and slow AV conduction.
These drugs should be avoided in patients with RVMI, and in particular, those who are hemodynamically unstable. They can be tried with careful monitoring in those who are stable and have a clear indication.
List 4 echocardiographic findings suggesting a patient has a Pulmonary embolus.
- RV dilation
- RV dysfunction with normal or slightly elevated RVSP (<60mm Hg, i.e. if it’s really high suggests chronicity)
- short pulmonary artery acceleration time (<60ms)
- dilated IVC
- clot in transit (or in pulmonary arteries)
- McConnell’s sign (RV free wall akinesia with apical sparing)
- TR
Post Heart Transplant patient with RV failure or something like that. iNO started and ordered at 20ppm. You find out that 30 mins later the iNO was accidentally set to 2000 ppm.
a. what is your next immediate step with the iNO.
b. The patients sats begin to fall to 85% and CO level 3%. What is the cause of this?
c. What is the treatment for this?
a) stop it or decrease to 20ppm and monitor for rebound pulmonary hypertension…not sure which I’d do though (stop vs decrease to typical dose)
b)
methemoglobinemia
Clinical clues to the diagnosis of acute toxic methemoglobinemia include the following:
- Sudden onset of cyanosis with symptoms of hypoxia and/or clinical symptoms of reduced oxygen availability after administration or ingestion of an agent with oxidative potential (table 1). (See ‘Signs and symptoms’ above.)
- Hypoxia that does not improve with an increased administration of oxygen.
- Abnormal coloration of the blood observed during phlebotomy. The blood in methemoglobinemia has been variously described as dark red, chocolate, or brownish to blue in color, and, unlike deoxyhemoglobin, the color does not change when the blood is exposed to oxygen
- Methemoglobinemia is strongly suggested when there is clinical cyanosis in the presence of a normal arterial pO2 (PaO2). Thus, arterial blood gas analysis may be deceptive because the PaO2 is generally normal in individuals with excessive levels of methemoglobin.
Routine pulse oximetry is generally inaccurate for monitoring oxygen saturation in the presence of methemoglobinemia and should not be used to make the diagnosis of this disorder. The reason is that methemoglobin absorbs light at the pulse oximeter’s two wavelengths, and this leads to error in estimating the percentages of reduced and oxyhemoglobins. A high concentration of methemoglobin causes the oxygen saturation to display as approximately 85 percent, regardless of the true hemoglobin oxygen saturation.
- Blood gas analysis measures arterial oxygen partial pressure and estimates oxygen saturation by comparison with a standard curve. Since arterial oxygen partial pressure is normal in patients with methemoglobinemia, blood gas analysis will give falsely high levels of oxygen saturation in the presence of methemoglobin.
As noted above, suspected methemoglobinemia should be confirmed by co-oximetry and, when available, re-confirmed via the Evelyn-Malloy method.
Pathogenesis:
Methemoglobin is an altered state of hemoglobin in which the ferrous (Fe++) irons of heme are oxidized to the ferric (Fe+++) state. The ferric hemes of methemoglobin are unable to reversibly bind oxygen. In addition, the oxygen affinity of any remaining globins’ ferrous hemes in the hemoglobin tetramer are increased. As a result, the oxygen dissociation curve is “left-shifted”.
The net effect is that patients with acutely increased concentrations of methemoglobin have a functional anemia (ie, the amount of functional hemoglobin is less than the measured level of total hemoglobin). The circulating methemoglobin-containing hemoglobin molecules are unable to deliver oxygen and the remaining oxyhemoglobin has increased oxygen affinity, resulting in impaired oxygen delivery to the tissues. Those with chronically increased methemoglobinemia and functional anemia may develop compensatory polycythemia/erythrocytosis.
c)
Treatment of methemoglobinemia:
-
stop offending medication/chemicals (see list below)
- In lesser degrees of methemoglobinemia (ie, an asymptomatic patient with a methemoglobin level <20 percent), no therapy other than discontinuation of the offending agent(s) may be required
- Patients with symptomatic and severe degrees of methemoglobinemia should be managed in the intensive care unit for stabilization of their airway, breathing, and circulation. This may require the use of oxygen supplementation, inotropic agents, and mechanical ventilation
- Blood transfusion, especially in anemic subjects, or exchange transfusion may be helpful in patients who are in shock; hyperbaric oxygen has been used with anecdotal success in severe cases
-
methylene blue or vitamin C
- While there have been no randomized trials comparing these two agents, the general experience has been that the action of a single dose of MB in this setting rapidly reduces toxic levels of methemoglobin to non-toxic levels (eg, <10 percent) within 10 to 60 minutes, whereas treatment with ascorbic acid requires multiple doses and may take 24 or more hours to reach similarly low levels and is therefore a poor alternative in emergency situations.
- Accordingly, since high levels of methemoglobin constitute a medical emergency requiring urgent intervention, the more rapid and more dramatic action of MB in reducing methemoglobin levels has made MB the treatment of choice. When MB is not available or when its use is contraindicated (eg, as in glucose-6-phosphate dehydrogenase [G6PD] deficiency), ascorbic acid, and, in life-threatening situations, red cell blood exchange transfusions, are the only reasonable alternatives, although responses to these therapies are less marked and dramatic than they are to MB.
- red blood cell transfusions
List of meds/chemicals that can cause methemoglobinemia
Medications
- Amino salicylic acid (also called p-aminosalicylic acid or 4-aminosalicylic acid)
- Clofazimine
- Chloroquine
- Dapsone
- Local anesthetics, topical sprays and creams including benzocaine (in teething rings and ointments), lidocaine, and prilocaine
- Menadione
- Metoclopramide
- Methylene blue*
- Nitroglycerin
- Phenacetin
- Phenazopyridine
- Primaquine
- Rasburicase
- Quinones
- Sulfonamides
Chemicals and environmental substances
- Acetanilide (used in varnishes, rubber, and dyes)
- Anilines and aniline dyes (eg, diaper and laundry marking inks, leather dyes, red wax crayons)
- Antifreeze
- Benzene derivatives (used as solvents)
- Chlorates and chromates (used in chemical and industrial synthesis)
- Hydrogen peroxide (used as a disinfectant and cleaner)
- Naphthalene (used in mothballs)
- Naphthoquinone (used in chemical synthesis)
- Nitrates and nitrites (eg, amyl nitrite, farryl nitrite, sodium nitrite, nitrate- and nitrite-containing foods, nitric oxide, well water)
- Nitrobenzene (used as a solvent)
- Paraquat (used in herbicides)
- Resorcinol (used in resin melting and wood extraction)
- Inherited disorders (extremely rare)
- Cytochrome b5-reductase deficiency
- Hemoglobin M disease
Patient presents with Aortic dissection and BP of 180/100.
a. Over what time period would you proceed to lower his blood pressure?
b. Nitroprusside is one the drugs that can be used to lower BP in this
situation. What is a side effect of nitroprusside?
a) ?immediate
guidelines seem to differ whether to target SBP <140 or SBP <120 but I think most argue for a little more aggresive targets in the acute setting. Canadian guidelines seem to suggest target <140/90 in stable pts (but <130/80 in those with cardiovascular disease or major risk factors)
b)
cyanide toxicity (although I don’t think I’d call it a “side effect”)
Sodium nitroprusside, when administered by intravenous infusion, begins to act within one minute or less, and once discontinued, its effects disappear within 10 minutes or less. Frequent monitoring is required since this drug can produce a sudden and drastic drop in blood pressure.
Nitroprusside is metabolized to cyanide, possibly leading to the development of cyanide (or, rarely, thiocyanate) toxicity that may be fatal [10]. This problem, which can manifest in as little as four hours, presents with altered mental status and lactic acidosis. Risk factors for nitroprusside-induced cyanide poisoning include a prolonged treatment period (>24 to 48 hours), underlying renal impairment, and the use of doses that exceed the capacity of the body to detoxify cyanide (ie, more than 2 mcg/kg per minute).
Nitroprusside can result in dose-related declines in coronary, renal, and cerebral perfusion.
- Nitroprusside should not be given to pregnant women, patients with Leber optic atrophy, or patients with tobacco amblyopia. In addition, nitroprusside should be avoided, if possible, in patients with impaired renal function.
Nitroglycerin is also administered by intravenous infusion and is similar in action and pharmacokinetics to nitroprusside except that it produces relatively greater venodilation than arteriolar dilation. It has less antihypertensive efficacy compared with other drugs used to treat hypertensive emergencies, and its effects on blood pressure are variable from person to person and, potentially, from minute to minute. However, it may be useful in patients with symptomatic coronary disease and in those with hypertension following coronary bypass.
List three hormonal therapies recommended for a donor with EF found to be <40%.
- thyroid hormone replacement
- methylprednisolone
- vasopressin
I couldn’t find the effect of inotropes on this question (previously question said aside from inotropes but one heart donation criteria on uptodate said “inotropic support less than 10mcg/kg/min of dopamine or dobutamine”
In a retrospective analysis of data on 66,629 donors, thyroid hormone therapy was associated with increased procurement of hearts, lungs, kidneys, pancreases, and intestines, but not livers.
from 2006 Canadian guidelines: Weight of currently available evidence in a large retrospective cohort study by the United Network for Organ Sharing (UNOS)10 in the United States suggests a substantial benefit of triple hormone therapy with minimal risk. A multivariate logistic regression analysis of 18 726 brain-dead donors showed significant increases in kidney, liver and heart utilization from donors receiving 3 hormonal therapies. Significant improvements in 1-year kidney graft survival and heart transplant patient survival were also demonstrated. A prospective randomized trial has not been performed.
Post op cardiac surgery patient with pacer wires. What is the rhythm? List 2 non-pharmacological therapies to address this rhythm.
- vagal maneuvers (on ventilator kind of like a recruitment maneuver, or carotid sinus massage)
- synchronized cardioversion
- overdrive pacing (aka pace termination)
Nonpharmacologic therapy to convert back to normal sinus rhythm including direct current cardioversion, pace termination, or catheter ablation are reasonable treatments if the patient is having adverse hemodynamic consequences from the arrhythmia, if pharmacologic therapies are unsuccessful or not tolerated, or if the patient has pre-excitation syndrome.
List 2 tools used to assess patient for delirium.
Confusion Assessment Method ICU (CAM-ICU)
- Acute onset and fluctuating course
- Usually obtained from a family member or nurse and shown by positive responses to the following questions:
- “Is there evidence of an acute change in mental status from the patient’s baseline?”;
- “Did the abnormal behavior fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?”
- inattention
- Shown by a positive response to the following:
“Did the patient have difficulty focusing attention, for example, being easily distractible or having difficulty keeping track of what was being said?”
- disorganized thinking
- Shown by a positive response to the following:
“Was the patient’s thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?”
- altered level of consciousness
- Shown by any answer other than “alert” to the following:
“Overall, how would you rate this patient’s level ofconsciousness?”
* Normal = alert
* Hyperalert = vigilant
* Drowsy, easily aroused = lethargic
* Difficult to arouse = stupor
* Unarousable = coma
Intensive Care Delirium Screening Checklist (ICDSC)
see image
List 4 adverse outcomes/complications that delirium can lead to in the ICU patient.
- cognitive impairment at 3 months
- cognitive impairment at 12 months
- longer hospital LoS
- mortality
- +/-costs although not really pt centered (uptodate)
Woah, interesting statement from the PADIS guidelines:
Questions: What are the short- and long-term outcomes of delirium in critically ill adults and are these causally related?
Ungraded Statements: Positive delirium screening in critically ill adults is strongly associated with cognitive impairment at 3 and 12 months after ICU discharge (316–319) and may be associated with a longer hospital stay (257, 279, 316, 320–327).
Delirium in critically ill adults has consistently been shown NOT to be associated with PTSD (328–333) or post-ICU distress (316, 333–336).
Delirium in critically ill adults has NOT been consistently shown to be associated with ICU LOS (257, 258, 272, 279, 318, 320–326, 334, 337–352), discharge disposition to a place other than home (257, 342, 344, 353, 354), depression (330, 356), functionality/dependence (330, 334, 350, 353, 354, 357–360), or mortality.
uptodate, not specifically on ICU pts, but pts with delirium in general:
Delirium has an enormous impact upon the health of older persons. Patients with delirium experience prolonged hospitalizations, functional and cognitive decline, higher mortality, and higher risk for institutionalization, even after adjusting for baseline differences in age, comorbid illness, or dementia.
Delirium can be disturbing for affected patients and relatives and is associated with worse outcome, and much higher ICU and hospital LOS and costs.
Describe one difference that distinguishes a donor after neurological determination of death and donor after cardiac death.
not sure exactly what they are getting at here…
Donation after neurologic determination of death (DNDD) — Most (80 to 90 percent) organs from deceased donors are procured after declaration of death by neurologic criteria, also known as “brain death.” Brain death is the complete and irreversible cessation of cerebral and brainstem function; in most countries and situations, this is considered to be equivalent to cardiopulmonary death. Brain death is a relatively uncommon event, occurring in approximately 1 percent of all deaths [2]. The three most common causes of brain death are trauma, cerebrovascular accident, and anoxia, with the incidence of anoxic brain death increasing, in part due to nonmedical drug overdose.
Donation after circulatory determination of death (DCDD) — Because of the severe shortage of donated organs and the limited number of brain-dead donors, another option for organ donation is donation after circulatory determination of death.
If the patient expires in the allotted time, usually 60 minutes from withdrawal of ventilatory support, and is declared dead by cardiorespiratory criteria (permanent absence of respiration, circulation, and responsiveness) by the attending clinician, a mandatory waiting period of at least two minutes and not more than five minutes is observed for autoresuscitation.
Although kidneys are procured most frequently after DCDD, liver, pancreas, and lungs may also be procured. Cardiac transplantation after DCDD occurs in Australia and the United Kingdom and is being contemplated in the United States
List 5 physical signs required for neurological determination of death.
do you agree all of the bolded ones would count as physical signs?
We recommend use of the following minimum clinical criteria
as a Canadian medical standard for NDD:
- Established etiology capable of causing neurological death in the absence of reversible conditions capable of mimicking neurological death
- Deep unresponsive coma with bilateral absence of motor responses, excluding spinal reflexes
- Absent brain stem reflexes as defined by:
- absent gag
- absent cough reflexes
- bilateral absent corneal responses
- bilateral absent pupillary responses to light, with pupils at mid-size or greater
- bilateral absent vestibulo-ocular responses
- Absent respiratory effort based on the apnea test
- Absent confounding factors
List 4 factors that would preclude you from performing neurological determination of death by physical exam only.
We recommend that, at the time of assessment for NDD, the
following confounding factors preclude the clinical diagnosis:
- Unresuscitated shock
- Hypothermia (core temperature < 34°C)
- Severe metabolic disorders capable of causing a potentially reversible coma
- Severe metabolic abnormalities, including glucose, electrolytes (including phosphate, calcium and magnesium), inborn errors of metabolism, and liver and renal dysfunction may play a role in clinical presentation. If the primary etiology does not fully explain the clinical picture, and if in the treating physician’s judgement the metabolic abnormality may play a role, it should be corrected.
- Peripheral nerve or muscle dysfunction or neuromuscular blockade potentially accounting for unresponsiveness
- Clinically significant drug intoxications (e.g., alcohol, barbiturates, sedatives, hypnotics); however, therapeutic levels or therapeutic dosing of anticonvulsants, sedatives and analgesics do not preclude the diagnosis.
List one ancillary test to determine neurological determination of death.
The demonstration of the absence of intracerebral blood flow is considered the standard as an ancillary test for NDD. Currently validated imaging techniques are cerebral angiography and radionuclide angiography (aka …CT perfusion….Mo says is different from nuclear scan, or perfusion scintography).
CT angiography (according to Mo)
We recommend that an ancillary test be performed when it is impossible to complete the minimum clinical criteria as defined in Recommendation A.1. At a minimum, 2 particular clinical criteria must be met before ancillary tests are performed:
- An established etiology capable of causing neurological death in the absence of reversible conditions capable of mimicking neurological death
- Deep unresponsive coma
We recommend that demonstration of the global absence of intracerebral blood flow be considered as the standard for NDD by ancillary testing.
Patient who had ventricular drain placed few weeks back for head trauma. He was discharged from ICU and now returns a week later with ↓ LOC and diagnosis of ventriculitis is made.
a) what are the diagnostic criteria for healthcare-associated ventriculitis or meningitis?
b) what is the treatment for it?
a)
The United States Centers for Disease Control and Prevention’s National Healthcare Safety Network has described healthcare-associated ventriculitis or meningitis as being present in patients who meet at least one of the following criteria:
- An organism cultured from the CSF
- At least two of the following signs or symptoms with no other recognized cause in patients aged >1 year of age: fever >38°C or headache, meningeal signs, or cranial nerve signs, or at least two of the following signs or symptoms with no other recognized cause in patients aged ≤1 year of age: fever >38°C or hypothermia <36°C, apnea, bradycardia, or irritability and at least one of the following:
- Increased CSF white blood cell count, elevated CSF protein, and decreased CSF glucose
- Organisms seen on a CSF Gram stain
- Organisms cultured from the blood
- Positive nonculture diagnostic test from the CSF, blood, or urine
- Diagnostic single-antibody titer (immunoglobulin M) or fourfold increase in paired sera (immunoglobulin G) for organism
b) treatment
There are no randomized trials addressing optimal treatment of CSF shunt infections. Management of CSF shunt infection should include:
- removal of the device
- external drainage
- parenteral antibiotics
- Parenteral antibiotic selection should be guided by the results of CSF Gram stain and culture. Pending these results, for adults, we recommend empiric therapy, taking into account local in vitro susceptibility results and bacteria previously isolated from the patient [4]. For most patients, we give vancomycin (15 to 20 mg/kg intravenously [IV] per dose every 8 to 12 hours, adjusted to a trough level of 15 to 20 mcg/mL; not to exceed 2 g per dose) and an agent to cover gram-negative bacilli, including P. aeruginosa. For adults, an agent to cover healthcare-associated gram-negative bacilli (ceftazidime [2 g IV every 8 hours], cefepime [2 g IV every 8 hours], or meropenem [2 g IV every 8 hours]) is appropriate. For adults with severe beta-lactam allergies (eg, anaphylaxis) and for whom meropenem is contraindicated, aztreonam (2 g IV every 6 to 8 hours) or ciprofloxacin (400 mg IV every 8 to 12 hours) should replace the cephalosporin or carbapenem.
- and shunt replacement once the CSF is sterile. If device removal is not feasible, intraventricular antibiotics may be useful.
Patient with crush injury develops rhabdomyolysis with dark urine.
a. List two lab tests that you could perform to confirm diagnosis of rhabdomyolysis.
b. List 2 therapies to minimize the risk of renal injury.
a) these answers seem too easy…am I missing something?
- serum creatine kinase
- serum myoglobin
- urine myoglobin
urine findings and myoglobinuria - Myoglobin, a heme-containing respiratory protein, is released from damaged muscle in parallel with CK. Myoglobin is a monomer that is not significantly protein-bound and is therefore rapidly excreted in the urine, often resulting in the production of red to brown urine. Visible changes in the urine only occur once urine levels exceed from about 100 to 300 mg/dL, although it can be detected by the urine (orthotolidine) dipstick at concentrations of only 0.5 to 1 mg/dL. Myoglobin has a half-life of only two to three hours, much shorter than that of CK. Because of its rapid excretion and metabolism to bilirubin, serum levels may return to normal within six to eight hours.
Thus, it is not unusual for CK levels to remain elevated in the absence of myoglobinuria. In rhabdomyolysis, myoglobin appears in the plasma before CK elevation occurs and disappears while CK is still elevated or rising. Therefore, there is no CK threshold for when myoglobin appears. As above, rhabdomyolysis does not occur unless CK is elevated five times or more above the upper limit of normal.
b)
- volume administration
- bicarb administration
In addition to treating the underlying rhabdomyolysis or hemolysis, the general goals for prevention of AKI in all patients at risk for heme pigment-induced AKI are twofold:
●Correction of volume depletion if present
●Prevention of intratubular cast formation
The underlying conditions and factors that have led to rhabdomyolysis or hemolysis must also be addressed to avoid continued heme pigment release.
Volume administration — The prevention of AKI requires early and aggressive fluid resuscitation. The goals of volume repletion are to maintain or enhance renal perfusion, thereby minimizing ischemic injury, and to increase the urine flow rate, which will limit intratubular cast formation by diluting the concentration of heme pigment within the tubular fluid, wash out partially obstructing intratubular casts, and increase urinary potassium excretion.
Intravenous isotonic saline should be administered as soon as possible after the onset of injury (even while the patient is being rescued) or detection of hemolysis and continued until the muscle injury or hemolysis has resolved.
For patients who are at risk for heme-associated AKI due to rhabdomyolysis from any cause, we suggest initial fluid resuscitation with isotonic saline at a rate of 1 to 2 L/hour. The plasma creatine kinase (CK) concentration correlates with the severity of muscle injury, and concentrations >5000 unit/L identify patients who are at risk for the development of AKI. However, it may be difficult to identify patients who are at high risk for AKI based upon the initial plasma CK value since the CK level may still be rising from ongoing muscle injury. Thus, sequential CK measurements are critical in tailoring therapeutic interventions.
All patients should be initially treated with vigorous fluid repletion until it is clear from sequential laboratory values that the plasma CK level is stable and not increasing. Patients who have a stable plasma CK level <5000 unit/L do not require intravenous fluid, since studies have shown that the risk of AKI is low among such patients.
Bicarbonate — Patients with rhabdomyolysis who are appropriately monitored may benefit from bicarbonate therapy. We generally administer a bicarbonate infusion to patients who have severe rhabdomyolysis, such as those with a serum CK above 5000 unit/L or clinical evidence of severe muscle injury (eg, crush injury) and a rising serum CK, regardless of the initial value. In such patients, bicarbonate may be given, providing the following conditions are met:
- Hypocalcemia is not present
- Arterial pH is less than 7.5
- Serum bicarbonate is less 30 mEq/L
We generally do not administer bicarbonate to patients with hemolysis, unless another indication is present (such as concurrent rhabdomyolysis, which may occur in the settings of envenomation and poisonings).
Among patients with rhabdomyolysis, we infuse approximately 130 mEq/L of sodium bicarbonate (150 mL [3 amps] of 8.4 percent sodium bicarbonate mixed with 1 L of 5 percent dextrose or water) via an intravenous line separate from that used for the isotonic saline infusion. The initial rate of infusion is 200 mL/hour; the rate is adjusted to achieve a urine pH of >6.5.
If bicarbonate is given, the arterial pH and serum calcium should be monitored every two hours during the infusion. The bicarbonate infusion should be discontinued if the urine pH does not rise above 6.5 after three to four hours, if the patient develops symptomatic hypocalcemia, if the arterial pH exceeds 7.5, or if the serum bicarbonate exceeds 30 mEq/L. If the bicarbonate solution is discontinued, volume repletion should be continued with isotonic saline.
