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
There were three different diagrams of renal replacment circuits. You had to figure out what time (?type) of renal replacement each was based on the diagram. One diagram had pre and post filter fluid replacement, another had dialysate and fluid replacement and the last just had dialysate.
This is how I would reason this question:
- pre and post fluid replacement - CVVH
- dialysate and fluid replacement - CVVHD
- dialysate - CVVD
- no dialysate and no replacement - SCUF
aims of RRT are achieved through diffusion or convection, which are respectively referred to as hemodialysis or hemofiltration. Middle molecules are preferentially cleared by convective methods, rather than smaller molecules that are more reliably cleared by diffusion.
- Diffusion = hemodialysis
- Convection = hemofiltration
- CVVH = continuous veno-venous hemofiltration
- CVVHD = continuous veno-venous hemodialysis
- CVVHDF = continuous veno-venous hemodiafiltration
- majority of ICU RRT is CVVHF or CVVHDF
HEMOFILTRATION
Haemofiltration is a convective process whereby a hydrostatic pressure gradient is used to filter plasma, water, and solute across a membrane. This is analogous to the process within the renal corpuscle. The underlying mechanism is that of ‘solute drag’ where appropriately sized molecules are pulled along with the mass movement of solvent, traditionally termed ultrafiltration (UF). The convective transport is independent of solute concentration but determined by the direction and magnitude of the transmembrane pressure (TMP). Measures that result in a higher flow rate will increase UF production and in turn increase solute clearance. Equally, measures that increase the negative pressure across the membrane, including the pump on the effluent line, can have a marked effect. This fluid, known as effluent, is discarded. Owing to the high volumes produced, the circulating volume of the patient is replaced with a balanced crystalloid buffer solution.
HEMODIALYSIS
In haemodialysis, solute clearance is achieved by diffusion across the membrane. The space outside the blood-containing fibres within the ‘filter’ is filled with dialysate, which is pumped in a counter-current fashion to the flow of blood. Dialysate is reconstituted to include a buffer (which may be either acetic acid or bicarbonate) and essential electrolytes dissolved in ultrapure water rendered devoid of toxins and impurities. Diffusion occurs down concentration gradients allowing rapid equilibration of solutes across the membrane. The purpose of this counter-current flow system is to maintain a waste-solute concentration gradient (i.e. always lower on the dialysate side of the membrane, similar to solute movement within the Loop of Henle).
RRT Membrane
Two types of RRT membrane exist: cellulose based or synthetic. Exposure to an extracorporeal circuit and the interaction between blood and the membrane is known as biocompatibility. Less biocompatible membranes increase the likelihood of harmful side-effects associated with RRT.
Cellulose-based membranes trigger activation of inflammatory pathways, which may increase the longevity of AKI. Studies suggest that the use of more biocompatible membranes may lead to faster restoration of renal function and improved patient outcomes.3 In short, it can be assumed that the most biocompatible membrane available should be used for RRT.
Filter Fluid
During haemofiltration, bicarbonate ions are freely filtered and therefore need to be replaced. Previously, standard lactate-based fluids were used as buffers, with the lactate subsequently being metabolized in the liver. In the context of critical illness, impaired hepatic function can lead to lactic acid accumulation. To compensate for this, bicarbonate-based buffer solutions have become commercially available. These fluids may be added to the circuit before the haemofilter (pre-dilution) or mixed with the blood in the venous drip chamber (post-dilution). Pre-dilution replacement reduces the incidence of filter clotting but reduces the effective clearance of solutes. Post-dilution replacement is, therefore, the ideal, but a compromise is often made to maintain the integrity and lifespan of the filter. Although there is no mortality benefit associated with the use of bicarbonate-based fluids, there is evidence for improved control of acidosis and cardiovascular instability.
RRT Dosing
For continuous techniques, dose is the sum of all effluent fluids expressed as millilitres per kilogram body weight per hour. It is important to note that the addition of dialysate and the targeting of negative fluid balance both add to the summative dose. Dosing of intermittent techniques is difficult because of urea kinetics and fluid shifts in the critically ill: because of this, most studies assessing IHD measure dose in relationship to frequency and duration of sessions.
Adult patient who has PMH of streptococcal glomerulonephrits as a child. Patient now post op or something like that and they give you a bunch of physical findings (lowish BP, tachycardic, oliguric, urine Na 5mmol, Cr 500. There was more information.
a. Give formula for FeNa.
b. List lab values that would suggest patient is hypovolemic.
a) see images
FeNA = fractional excretion of sodium
The FENa can be measured in patients suspected of having AKI due to either prerenal disease or acute tubular necrosis (ATN). A variety of studies have confirmed that the FENa more clearly differentiates between these two conditions than other laboratory tests.
In general, a FENa below 1 percent suggests prerenal disease, where the reabsorption of almost all of the filtered sodium represents an appropriate response to decreased renal perfusion. In comparison, a value between 1 and 2 percent may be seen with either disorder, while a value above 2 percent usually indicates ATN. However, a FENa below 1 percent is not diagnostic of prerenal disease, since it can be seen in a variety of other causes of AKI.
The above cut-off values apply only in patients with advanced AKI. The FENa values that define prerenal disease are lower in patients with less severe disease since the filtered sodium load is much higher, being as low as 0.1 percent in patients with normal kidney function. Another potential problem is that the glomerular filtration rate (GFR) cannot be estimated from a single serum creatinine measurement, since the serum creatinine is not stable.
The relatively high FENa in ATN can be due to one or both of the following factors: inappropriate sodium wasting due to tubular damage and/or an appropriate response of the remaining, well-preserved nephrons to volume expansion.
Limitations of fractional excretion of sodium — There are at least four important limitations to the use of FENa in establishing the cause of AKI:
- The FENa criterion of less than 1 percent to diagnose prerenal disease applies only to patients with a marked reduction in GFR.
- Single measurements of serum creatinine may not provide an accurate estimate of the GFR.
- There are a number of causes of AKI other than prerenal disease in which the FENa can be less than 1 percent.
- The FENa may be above 1 percent when prerenal disease occurs in patients with chronic kidney disease or any cause of sodium wasting, such as diuretic therapy while the diuretic is still acting.
b)
- Urine sodium concentration — A low urine sodium concentration (or low urine chloride concentration in patients who have metabolic alkalosis) is strongly suggestive of reduced tissue perfusion, and it is usually present in hypovolemic patients unless there is a salt-wasting state (eg, diuretics, underlying renal disease), selective renal ischemia (eg, acute glomerulonephritis or bilateral renal artery stenosis), or a very low-sodium diet.
However, the presence of a low urine sodium does not necessarily mean that the patient has true volume depletion, since edematous patients with heart failure, cirrhosis with ascites, and the nephrotic syndrome also avidly conserve sodium. These disorders are characterized by reduced effective arterial blood volume due to a primary reduction in cardiac output (heart failure), to splanchnic vasodilatation and sequestration of fluid in the peritoneal cavity and arterial shunts (cirrhosis), and to a low plasma oncotic pressure (in some patients with severe or acute nephrotic syndrome).
The response of the kidney to true volume depletion and reduced effective arterial blood volume is to conserve sodium and water in an attempt to expand the extracellular volume. With the exception of those disorders in which sodium reabsorption is impaired, the urine sodium concentration in hypovolemic states should be less than 20 mEq/L and may be as low as 1 mEq/L. There are two additional exceptions in which the urine sodium concentration may be higher than 20 mEq/L despite the presence of hypovolemia:
- When there is also a high rate of water reabsorption; in this setting, the rate of sodium excretion and urine volume are low, but the urine sodium concentration is higher than expected due to concentration of the urine.
- When sodium is excreted with another anion [10]. This most often occurs in metabolic alkalosis due to vomiting or nasogastric suction. In such disorders, the metabolic alkalosis is associated with a high filtered bicarbonate load. The stimuli that increase renal sodium and bicarbonate reabsorption (volume depletion and hypokalemia) may sometimes be inadequate to remove all of the filtered sodium and bicarbonate from the urine. Under these conditions, urinary bicarbonate excretion occurs (with sodium as the accompanying cation). This occurs early in the disorder and also intermittently during established alkalosis, usually when transient further increases in serum bicarbonate occur (disequilibration phases of metabolic alkalosis). In such settings, the urine chloride concentration remains low (ie, below 20 mEq/L) and is a better index of extracellular fluid volume.
-
elevated BUN
- (However, an elevation in the BUN can also be produced by an increase in the rate of urea production or tubular reabsorption. As a result, the serum creatinine concentration is a more reliable estimate of the GFR since it is produced at a relatively constant rate by skeletal muscle and is not reabsorbed by the renal tubules)
- elevated Cr
- Hypernatremia and hyponatremia — A variety of factors can influence the serum sodium concentration in hypovolemic states, and it is the interplay between them that determines the level observed in a given patient. Primary water loss, as in insensible losses or diabetes insipidus, results in hypernatremia. On the other hand, salt and water loss may be associated with hyponatremia. Volume depletion stimulates the release of antidiuretic hormone (ADH), which will tend to cause retention of ingested water.
- Hypokalemia and hyperkalemia — Either hypokalemia or hyperkalemia can occur in hypovolemic patients. The former is much more common because of potassium loss from the gastrointestinal tract or in the urine. However, there may be an inability to excrete the dietary potassium load in the urine because of renal failure, hypoaldosteronism, or volume depletion itself since the delivery of sodium and water to the potassium secretory site in the cortical collecting tubule will be reduced.
- Metabolic alkalosis and acidosis — The effect of fluid loss on acid-base balance also is variable. Although many patients maintain a normal extracellular pH, either metabolic alkalosis or metabolic acidosis can occur. Patients with vomiting or nasogastric suction or those given diuretics tend to develop metabolic alkalosis because of hydrogen ion loss and volume contraction. On the other hand, bicarbonate loss (due to diarrhea or intestinal fistulas) can lead to metabolic acidosis. In addition, lactic acidosis can occur in shock and ketoacidosis in uncontrolled diabetes mellitus.
- Hematocrit and serum albumin concentration — Since red blood cells and albumin are essentially limited to the vascular space, a reduction in the plasma volume due to volume depletion tends to elevate both the hematocrit (ie, relative polycythemia) and serum albumin concentration. However, these changes are frequently absent because of underlying hypoalbuminemia and/or anemia, due, for example, to bleeding.
?Helpful
- Urine osmolality — In hypovolemic states, the urine is relatively concentrated with an osmolality often exceeding 450 mosmol/kg [11-13]. This response may not be seen, however, if concentrating ability is impaired by renal disease, an osmotic diuresis, the administration of diuretics, or central or nephrogenic diabetes insipidus. As an example, both severe volume depletion (which impairs urea accumulation in the renal medulla) [14] and hypokalemia (which induces antidiuretic hormone [ADH] resistance) can limit the increase in the urine osmolality in some patients. Thus, a high urine osmolality is consistent with hypovolemia, but a relatively isosmotic value does not exclude the disorder. Urinary concentration can also be assessed by measuring the specific gravity. The results are less reliable than the urine osmolality because specific gravity is determined by the mass rather than number of solute particles in the urine. A value above 1.015 is suggestive, but not diagnostic, of a concentrated urine, as is usually seen with hypovolemia. The urine specific gravity is misleadingly high with proteinuria or after administration of radiocontrast agents.
Not that helpful
- Urinalysis — Examination of the urine is an important diagnostic tool in patients with elevations in the BUN and plasma creatinine concentration. The urinalysis is generally normal in hypovolemic states since the kidney is not diseased. This is in contrast to most, but not all, of the other causes of renal insufficiency in which the urinalysis reveals protein, cells, and/orcasts.
List 2 other factors in FFP other than vitamin K dependent factors.
factor VIII
factor V
…factor XIII, factor XII, factor XI,
fibrinogen (would this count as a “factor”?…I think so cause it’s also called factor I)
FFP contains all coagulation factors except platelets.
Fresh Frozen Plasma (FFP) is prepared from single units of whole blood or from plasma collected by apheresis techniques. It is frozen at -18 to -30°C within eight hours of collection and, when appropriately stored, is usable for one year from the date of collection. Standard FFP units derived from a single unit of whole blood have a volume of approximately 200 to 250 mL. FFP contains all of the coagulation factors and other proteins present in the original unit of blood, slightly diluted by the citrate-containing anticoagulant solution used to collect the blood.
Vitamin K dependent factors (think 1972)
II
VII
IX
X
…and protein C and S which are Vitamin K dependent proteins that are ANTI COAGULANT
Given 85 y.o. female 48 hr post hip Sx and now oliguric, febrile, tachycardic, hypotensive (BP 90/50). It was clear that she was septic.
a. Give 2 clinical indicators that this pt is mounting SIRS response.
b. List 3 clinical goals in the management of this patient from the surviving sepsis guidelines (MVO2 >70, U/O >0.5ml/kg/hr, MAP>65, CVP>12)…this must be too old now…maybe change to list components of the 1 hour bundle?
a) SIRS criteria (must have >/=2)
HR >90bpm
temp >38, <36
RR >20 or PaCO2 <32
WBC >12 or <4 or >10% immature bands
b)
A. INITIAL RESUSCITATION
- Sepsis and septic shock are medical emergencies, and we recommend that treatment and resuscitation begin immediately (BPS).
- We recommend that, in the resuscitation from sepsis-induced hypoperfusion, at least 30 mL/kg of IV crystalloid fluid be given within the first 3 h (strong recommendation, low quality of evidence).
- We recommend that, following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hemodynamic status (BPS).
Remarks
Reassessment should include a thorough clinical examination and evaluation of available physiologic variables (heart rate, blood pressure, arterial oxygen saturation, respiratory rate, temperature, urine output, and others, as available) as well as other noninvasive or invasive monitoring, as available.
- We recommend further hemodynamic assessment (such as assessing cardiac function) to determine the type of shock if the clinical examination does not lead to a clear diagnosis (BPS).
- We suggest that dynamic over static variables be used to predict fluid responsiveness, where available (weak recommendation, low quality of evidence).
- We recommend an initial target mean arterial pressure (MAP) of 65 mm Hg in patients with septic shock requiring vasopressors (strong recommendation, moderate quality of evidence).
- We suggest guiding resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion (weak recommendation, low quality of evidence).
D. ANTIMICROBIAL THERAPY
- We recommend that administration of IV antimicrobials be initiated as soon as possible after recognition and within 1 h for both sepsis and septic shock (strong recommendation, moderate quality of evidence; grade applies to both conditions).
1 hour bundle
- measure lactate level, remeasure if initial lactate is >2mmol/L
- obtain blood cultures prior to antibiotic administration
- administer broad-spectrum antibiotics
- begin rapid administration of 30mL/kg crystalloid for hypotension or lactate >/=4mmol/L
- apply vasopressors if patient is hypotensive during or after fluid resuscitation to maintain MAP >/= 65mm Hg
There was another question on influenza pandemic and the question listed some CMAJ 2006 article on influenza pandemic.
List the drug or drug class, or receptors associated with the following presentations: There were 5 of them. I can remember 3.
a. bronchospasm, bradycardia, diarrhea etc.
b. metabolic acidosis, abdominal pain and hypocalcemia
c. muscle rigidity, diminished LOC…..can’t remember the rest.
a) cholinergic meds (?organophosphates)
- muscarinic signs:
- SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
- It should be noted that these mnemonics do NOT take into account the critical CNS and nicotinic effects of these toxins. The nicotinic effects include fasciculations, muscle weakness, and paralysis via acetylcholine stimulation of receptors at the neuromuscular junction. This mechanism is analogous to the depolarizing effects of succinylcholine in producing neuromuscular blockade. Nicotinic and muscarinic receptors also have been identified in the brain, and may contribute to central respiratory depression, lethargy, seizures, and coma
- Medication Causes: Organophosphates have been used as insecticides worldwide for more than 50 years. The use of these agents has declined in the last 10 to 20 years, in part due to the development of carbamate insecticides, which are associated with similar toxicities [1]. Medical applications of organophosphates and carbamates include reversal of neuromuscular blockade (neostigmine, pyridostigmine, edrophonium) and treatment of glaucoma, myasthenia gravis, and Alzheimer disease (echothiophate, pyridostigmine, tacrine, and donepezil).
b) ?ethylene glycol or maybe propylene glycol toxicity (maybe from benzo preservative)
Propylene glycol is the diluent used in the parenteral formulations for these 2 benzodiazepines, and prolonged use can cause propylene glycol toxicity which includes skin and soft tissue necrosis, hemolysis, cardiac dysrhythmias, hypotension, significant lactic acidosis, seizure, and multisystem organ failure. While propylene glycol toxicity is rare, it must be considered when patients are receiving large or continuous infusions of parenteral benzodiazepines, for example when treating severe sedative or ethanol withdrawal syndromes such as delirium tremens. but I couldn’t find that it causes hypocalcemia or abdo pain
c) ?NMS
