2013 Flashcards
- Oscillate trial
a. 3 reasons (that the authors listed in their paper) explaining why the mortality in the treatment arm was higher than the control
- HFOV protocol mean airway pressure was set too high leading to hemodynamic effects (venous return, RV function)
- HFOV had higher rates of sedatives potentially leading to hemodynamic effects
- HFOV with ?increased rates of barotrauma
- 2 papers
a. Crash-2 trial
i. List the intervention that was used
b. Hypolyte Trial
i. List the intervention and the primary outcome
Crash-2 trial:
-bolus of tranexemic acid 1 g then 1g over 8 hours
Hypolyte Trial:
- Continuous IV infusion of either hydrocortisone or placebo within 36 hour of trauma onset immediately after the completion of a short corticotropin test
- hydrocortisone 200 mg/d for 5 days, followed by 100 mg on day 6 and 50 mg on day 7
-Primary outcome: Hospital acquired pneumonia within 28 days
- End stage liver disease now with new renal failure (question describes hepatorenal syndrome)
a. 2 treatments to consider
UTD:
In patients with hepatorenal syndrome who are critically ill, we suggest initial treatment with norepinephrine in combination with albumin. Norepinephrine is given intravenously as a continuous infusion (0.5 to 3 mg/hr) with the goal of raising the mean arterial pressure by 10 mmHg, and albumin is given for at least two days as an intravenous bolus (1 g/kg per day [100 g maximum]). Intravenous vasopressin may also be effective, starting at 0.01 units/min and titrating upward as needed to raise the mean arterial pressure as noted below.
In patients with hepatorenal syndrome who are not critically ill, our suggestions depend upon the availability of certain drugs:
•terlipressin in combination with albumin
•Where terlipressin therapy is not available…midodrine, octreotide, and albumin.
In highly selected patients who fail to respond to medical therapy with the above regimens and who are considered well enough to undergo the procedure, transjugular intrahepatic portosystemic shunt (TIPS) is sometimes successful. However, this procedure is associated with numerous complications and, because of the need for intravenous contrast, it may cause acute kidney injury. For this reason, some experts prefer dialysis as a first option (continuous renal replacement therapy) in most cases, particularly for patients whose serum creatinine remains above 1.5 mg/dL despite medical therapy.
In patients who fail to respond to the above therapies, develop severely impaired renal function, and either are candidates for liver transplantation or have a reversible form of liver injury and are expected to survive, we recommend dialysis as a bridge to liver transplantation or liver recovery.
- Graph of antibiotic level vs time with points described – peak:MIC, area under curve:MIC, Time:MIC.
a. Describe the principle of each strategy
b. how you would dose your drug to achieve this
c. List 1 antibiotic class that demonstrates each strategy
http://www.rxkinetics.com/antibiotic_pk_pd.html
The primary measure of antibiotic activity is the minimum inhibitory concentration (MIC). The MIC is the lowest concentration of an antibiotic that completely inhibits the growth of a microorganism in vitro. While the MIC is a good indicator of the potency of an antibiotic, it indicates nothing about the time course of antimicrobial activity.
PK parameters quantify the serum level time course of an antibiotic. The three pharmacokinetic parameters that are most important for evaluating antibiotic efficacy are the peak serum level (Cmax), the trough level (Cmin), and the Area Under the serum concentration time Curve (AUC). While these parameters quantify the serum level time course, they do not describe the killing activity of an antibiotic.
Integrating the PK parameters with the MIC gives us three PK/PD parameters which quantify the activity of an antibiotic: the Peak/MIC ratio, the T>MIC, and the 24h-AUC/MIC ratio. The Peak/MIC ratio is simply the Cpmax divided by the MIC. The T>MIC (time above MIC) is the percentage of a dosage interval in which the serum level exceeds the MIC. The 24h-AUC/MIC ratio is determined by dividing the 24-hour-AUC by the MIC.
Concentration-dep killing and prolonged persistent effects
-These antibiotics (AG’s, fluoroquinolones, daptomycin and the ketolides), the ideal dosing regimen would maximize concentration, because the higher the concentration, the more extensive and the faster is the degree of killing. Therefore, the Peak/MIC ratio is the important predictors of antibiotic efficacy. For aminoglycosides, it is best to have a Peak/MIC ratio of at least 8-10 to prevent resistence.
Time-dep killing and minimal persistent effects
-These antibiotics (beta-lactams, clindamycin, erythromcyin, and linezolid) demonstrate the complete opposite properties. The ideal dosing regimen for these antibiotics maximizes the duration of exposure. The T>MIC is the parameter that best correlates with efficacy. For beta-lactams and erythromycin, maximum killing is seen when the time above MIC is at least 70% of the dosing interval.
Time-dep killing and moderate to prolonged persistent effects
-These antibiotics (vancomycin, tetracyclines, azithromycin, and the dalfopristin-quinupristin combination) have mixed properties, they have time-dependent killing and moderate persistent effects. The ideal dosing regimen for these antibiotics maximizes the amount of drug received. Therefore, the 24h-AUC/MIC ratio is the parameter that correlates with efficacy. For vancomycin, a 24h-AUC/MIC ratio of at least 400 is necessary for MRSA.
old answer
Peak:MIC; or Cmax:MIC Peak MIC
One time dose drug administrations
Aminoglyocsides
T:MIC Drug concentration that remain above MIC
Bacterial eradication is time dependent concentration dependent
Increase frequency of dosage due to short half-life Beta-lactams
AUC:MIC Hybrid of time and concentration
The true dose is more important than the amount of time Fluoroquinolones
Vancomycine
Azithromycine
- Pheochromocytoma
a. List 4 classic symptoms of Pheo
b. Which drug class should not be given as initial treatment
classic symptoms:
- episodic headache
- sweating
- tachycardia
- Other symptoms include:
- forceful palpitations
- tremor
- pallor
- dyspnea
- generalized weakness
- panic attack-type symptoms
All patients with pheochromocytoma need to undergo preoperative alpha-adrenergic blockade; we suggest phenoxybenzamine as the first-line drug (Grade 2C).
After adequate alpha-adrenergic blockade has been achieved, beta-adrenergic blockade is begun. For beta-adrenergic blockade, we suggest cautious, low-dose administration. As an example, a patient is usually given 10 mg of propranolol every six hours to start.
Because of the reduction in postoperative morbidity, hospital stay, and expense compared with open laparotomy, we suggest laparoscopic adrenalectomy by an experienced endocrine surgeon for adrenal pheochromocytomas (Grade 2C).
- Long stem, suspicious for hereditary angioedema
a. List 4 features that support a diagnosis of hereditary angiodedema.
b. What is the pathophysiology of hereditary angioedema?
c. What are 2 treatment options other than epi, steroids, Benadryl, ranitidine?
a) HAE should be considered in patients who demonstrate one or more of the following:
●Recurrent episodes of angioedema without urticaria or pruritus, lasting two to five days (without treatment).
●Unexplained recurrent episodes of self-limited, colicky, abdominal pain (typically lasting one to three days), especially in patients who also have had cutaneous angioedema.
●Unexplained laryngeal edema (even a single episode).
●Angioedema episodes in the absence of angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), or history to suggest an allergic cause.
●A family history of angioedema.
●A low complement component 4 (C4) level in a patient with angioedema.
b) The swelling (ie, angioedema, sometimes called “giant” swelling) that occurs in HAE results from excessive production of bradykinin, a potent vasodilatory mediator. Bradykinin also has important vascular permeability-enhancing effects. The best characterized forms of HAE arise from deficiency or dysfunction of C1 inhibitor (C1INH).
c) …Of note – none of those would be helpful (this treatment is mostly for mast-cell stimulated histamine release
-human plasma-derived C1 inhibitor concentrate
Hereditary angioedema (HAE) is a condition characterized by recurrent episodes of angioedema affecting the upper airway, bowel wall, or skin, which typically last two to four days. The angioedema of HAE is mediated by bradykinin and does not respond to epinephrine, antihistamines, or glucocorticoids. Instead, first-line therapies for HAE act by replacing the C1 inhibitor (C1INH) that is deficient or dysfunctional in this disease or by inhibiting the production or function of bradykinin.
- One intervention for brain dead donors that has been shown to improve success of lung transplant
high-dose steroids, recommended dose of methylprednisolone is 15mg/kg IV daily (to a maximum of 1000mg IV daily)
according to:
file:///C:/Users/mr683636/AppData/Local/Temp/TGL_eBook_English_Android_v25.pdf
but UTD also seems to suggest thyroxine and vasopressin
- Post cardiopulmonary bypass for MVR, initially ok, valve is perfect on initial ECHO, on volume A/C, FiO2 0.4, Peep 5. Then 6 hours later, on Pressure support, peep 12, FiO2 0.4, now hypoxemic, PCO2 36 PaO2 50 sats 90%. Chest xray is exactly the same as 6 hours earlier.
a. What is the most likely cause of his hypoxemia?
b. Which one test would you perform?
a) -Iatrogenic ASD from a transeptal approach with R to L shunt (due to pulmonary HTN)
b) -TEE with bubble study
- Research Ethics
- Industry sponsored research trial, you are considering running this trial at your centre.
a. Which 4 criteria must be met for you to participate
b. What 4 things need to be completed before enrolling patients
c. What 4 things need to be told to the patient when consenting in this setting
test
sfg
?????
- An important ethical component or research is respect for persons.
a. What are 4 key features
b. Another question we don’t remember…
a) autonomy
?from Belmont report: protecting the autonomy of all people and treating them with courtesy and respect and allowing for informed consent. Researchers must be truthful and conduct no deception.
so would you say:
- autonomy
- courtesy/respect
- informed consent
- truthful, no deception
- A recent paper (unsure when) which employed the “VALUE” mnemonic and used a family handout
a. List the 4 ways this intervention improved psychologic outcomes in family members
b. Another question we can’t remember about this paper
VALUE Value family statements Acknowledge family emotions Listen to family Understand patient as a person Elicit family questions
?decreased rates of depression, anxiety and PTSD in family members?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628462/
- IABP normal tracing showing
a. What is the timing?
b. Mark the point of inflation and deflation
c. What is the most important indicator of balloon deflation (or maybe it was inflation….can’t remember)
c) ?lowering of pts supported DBP 10-15mm Hg lower than their unsupported DBP?
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.
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
- Patient with inferior STEMI, giving fibrinolytics, doing well, ST’s normal, pain free, intermittently has a rhythm that is abnormal. Showed a wide complex rhythm at a rate of 60 (just the rhythm strip)
a. What is the rhythm?
b. What are 2 management options
Accelerated idioventricular rhythm:
Slow ventricular tachycardia is also known as an “accelerated idioventricular rhythm” or “AIVR” and is a common rhythm after an MI. An idioventricular rhythm — not accelerated — has a heart rate of < 60 beats per minute.
AIVR is hemodynamically stable, and thus no specific treatment is needed. This rhythm meets all of the ACC/AHA and Brugada Criteria for ventricular tachycardia except the heart rate is < 100 beats per minute, hence the term “slow ventricular tachycardia” is commonly used. AV dissociation may be seen similar to ventricular tachycardia.
Clinically, AIVR has been best studied in patients with acute ST-elevation myocardial infarction (STEMI). In the thrombolysis era, AIVR was noted to be a marker of reperfusion. [11] However, not all patients with reopened coronary artery have AIVR. In patients with acute myocardial infarction treated with primary percutaneous coronary intervention, the reported incidence of AIVR varied significantly, raging from 15-50%, depending on methods of monitoring.
no specific treatment needed…
old answers: Management options: Atropine Manage electrolyte abnormalities TVP
- Sudden drop in ETCO2 in an intubated patient. The vent, circuit, and ETT are all in good position with no problems.
a. List 4 causes of the drop in ETCO2
- Pulmonary embolism
- Cardiac arrest
- Pneumothorax
- Decreased production – hypothermia or intoxication
- What are 2 causes of a false positive ETCO2 when the ETT is actually in the esophagus?
Causes of a false positive EtCO2 when ETT is in esophagous
- Production of CO2 in stomach due to previous ingestion of CO2
- Gastric pH can cause change in the indicator
- CO2 being “blown” down to stomach
- List 4 ways to manage bleeding from a pelvic fracture
- massive transfusion protocol
- pelvic binder
- unstable + FAST pos —> emergency laparotomy with preperitoneal packing
- pelvic angiography and embolization/coiling
- resuscitative endovascular balloon occlusion of the aorta (REBOA)
- internal/external fixation
old answers:
- Apply binder to close pelvic ring
- Manage hypothermia and acidosis
- Give tranexemic acid bolus and infusion
- Go for embolization
- External or internal fixation
- 3 medications to give to a brain dead donor
- Vasopressin 1U IV bolus then 0.04 U/min
- T4 20 mcg bolus followed by infusion of 10 mcg/hr
- Methylprednisolone 15 mg/kg q24h
- list the 4 types of tissue hypoxia and briefly describe the mechanism of each
hypoxemia - low oxygen content in arterial blood
anemia - amount of functional Hgb is too small and hence capacity to carry oxygen is too low
stagnant type - blood flow is reduced or unevenly distributed
histotoxic type - cells are unable to use the oxygen, characteristically produced by cyanide but can be done by any agent that decreases cellular respiration including narcotics, alcohol, formaldehyde, acetone, and certain anesthetic agents
- define the following
a. inotropy
b. chronotropy
c. lusitropy
d. dromotropy
e. List 3 medications that increase lusitropy
f. Inotropy - A reflection of contractility
g. Chronotropy - Heart rate
h. Lusitropy - rate of myocardial relaxation
i. Dromotropy - AV velocity conduction
o List 3 medications that increase lusitropy
Milrinone (phosphodiesterase inhibitor)
Dobutamine
Epinephrine
-isoproterenol
?Digoxin
—I also found that ACEi and angiotensin subtype type I blockers increase myocardial relaxation in experimental studies
- Long stem, diabetic patient, multiple meds, recently started on enalapril, glyburide, metformin, nifedipine. Now presents with nausea, vomiting, abdom pain, resp rate of 40, blood pressure stable, labs showed elevated Cr (140), pH = 6.96, HCO3 = 7, PCO2 = 12
a. What is the most likely diagnosis?
b. What one treatment will you do?
Metformin overdose
IHD – multiple rounds required
*use of bicarb is controversial and UTD suggests only in severe acidosis
UTD:
dialysis recommended if
-severely elevated serum lactate concentration (>20 mmol/L)
-severe metabolic acidosis (pH ≤7.0)
-failure to improve (as determined by pH, lactate concentration, or clinical status) with supportive care and bicarbonate therapy within two to four hours.
dialysis suggested if:
-Elevated serum lactate concentration between 15 to 20 mmol/L
-Metabolic acidosis (pH of 7.0 to 7.1)
-Comorbidities:
•Shock or persistent hemodynamic instability requiring vasopressor therapy despite acute administration of IV boluses of isotonic crystalloid totalling 30 mL/kg
•Kidney injury – Creatine >2 mg/dL (adults), or >1.5 mg/dL (elderly), or 2 times upper limit of normal (children), or chronic kidney disease (stage 3b or higher with eGFR <45 mL/min/1.73 m2, oliguria, or anuria)
•Liver failure – liver injury with coagulopathy (INR >1.5) and any degree of encephalopathy
•Decreased level of consciousness
- Using data from the “Trauma coma databank”
a. What are 4 predictors of poor outcome clinically on exam?
b. What are CT findings that predict a poor outcome (list 2).
???couldn’t find answer
old ones o What are 4 predictors of poor outcome clinically on exam? Hypoxia Hypotension Low GCS Absence of brainstem reflexes o What are CT findings that predict a poor outcome (list 2) Herniation Midline shift Hydrocephalus ICH Depressed skull fracture
- Patient presents post head injury with a decreased LOC
a. Calculate the GCS and show each component
b. Other than brainstem reflexes, list 4 clinical exam findings of elevated ICP
c. What are 4 types of cerebral edema
d. List 4 interventions to manage elevated ICP
Eyes 4 - spontaneously open 3 - opens to voice 2 - opens to pain 1 - closed
Motor
6 - follows commands
5 - localizes to pain
4 - withdraws from pain
3 - decorticate posturing (abnormal flexion)
2 - decerebrate posturing (extension to painful stimuli)
1 - no response
Verbal 5 - oriented 4 - disoriented 3 - words 2 - incomprehensible sounds 1 - no response
o Other than brainstem reflexes, list 4 clinical exam findings of elevated ICP Decreased LOC -spontaneous periorbital bruising Hypertension Bradycardia respiratory depression
Vasogenic
Cytotoxic
Osmotic
Interstitial
- normocapneia
- head of bed elevation
- hyperosmolar therapy (hypertonic saline, mannitol)
- sedation
- paralysis
- cooling
- EVD for CSF drainage
- barbiturates
- ensure no neck ties or trach ties
- don’t over PEEP pt
-Decompressive craniectomy
Level IIA
Bifrontal DC is not recommended to improve outcomes as measured by the GOS-E score at 6 mo post-injury in severeTBIpatients with diffuseinjury(without mass lesions),andwith ICP elevationtovalues.20 mmHg for more than 15 min within a 1-h period that are refractory to first-tier therapies. However, this procedure has been demonstrated to reduce ICP and to minimize days in the ICU.
A large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended over a small frontotemporoparietal DC for reduced mortality and improved neurologic outcomes in patients with severe TBI.
*The committee is aware that the results of the RESCUEicp trial2 were released soon after the completion of these Guidelines. The results of this trial may affect these recommendations and may need to be considered by treating physicians and other users of these Guidelines. We intend to update these recommendations if needed. Updates will be available at https://braintrauma.org/coma/guidelines.
Prophylactic hypothermia
Level IIB
Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury.
Hyperosmolar therapy
Recommendations from the prior (Third) Edition not supported by evidence meeting current standards. Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body weight. Arterial hypotension (systolic blood pressure ,90 mm Hg) should be avoided. Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes.
Cerebrospinal fluid drainage
Level III
An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use.
Use of CSF drainage to lower ICP in patients with an initial GCS ,6 during the first 12 h after injury may be considered.
Ventilation therapies
Level IIB
Prolonged prophylactic hyperventilation with PaCO2 of #25 mm Hg is not recommended. Recommendations from the prior (Third) Edition not supported by evidence meeting current standards. Hyperventilation is recommended as a temporizing measure for the reduction of elevated ICP. Hyperventilation should be avoided during the first 24 h after injury when CBF often is reduced critically. If hyperventilation is used, SjO2 or BtpO2 measurements are recommended to monitor oxygen delivery.
Anesthetics, analgesics, and sedatives
Level IIB
Administration of barbiturates to induce burst suppression measured by EEG as prophylaxis against the development of intracranial hypertension is not recommended.
High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy.
Although propofol is recommended for the control of ICP, it is not recommended for improvement in mortality or 6-month outcomes. Caution is required as high-dose propofol can produce significant morbidity.
Steroids
Level I
The use of steroids is not recommended for improving outcome or reducing ICP. In patients with severe TBI, highdose methylprednisolone was associated with increased mortality and is contraindicated.
Nutrition
Level IIA
Feeding patientsto attain basal caloric replacement at least by the fifth day and at most by the seventh day post-injury is recommended to decrease mortality.
Level IIB
Transgastric jejunal feeding is recommended to reduce the incidence of ventilator-associated pneumonia.
Infection prophylaxis
Level IIA
Early tracheostomy is recommended to reduce mechanical ventilation days when the overall benefit is thought to outweigh the complications associated with such a procedure. However, there is no evidence that early tracheostomy reduces mortality or the rate of nosocomial pneumonia.
The use of PI oral care is not recommended to reduce ventilator-associated pneumonia and may cause an increased risk of acute respiratory distress syndrome.
Level III
Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during external ventricular drainage.
Deep vein thrombosis Prophylaxis
Level III
LMWH or low-dose unfractioned heparin may be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage.
In addition to compression stockings, pharmacologic prophylaxis may be considered if the brain injury is stable and the benefit is considered to outweigh the risk of increased intracranial hemorrhage.
There is insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic prophylaxis for deep vein thrombosis.
Seizure prophylaxis
Level IIA
Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS.
Phenytoin is recommended to decrease the incidence of early PTS (within 7 d of injury), when the overall benefit is thought to outweigh the complications associated with such treatment. However, early PTS have not been associated with worse outcomes.
At the present time there is insufficient evidence to recommend levetiracetam compared with phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity.
- Patient of CVVHDF (blood flow = 125, dialysate = 1l/hour), unhappy with metabolic picture
a. List 2 strategies to improve clearance
- increase dialysate flow rate
- ensure fluid replacement is post filter
- can also increase blood flow rate?
- CXR and CT scan of a trauma patient
a. List 4 findings on either CT or CXR (basically subQ emphysema, bilat pneumos, rib fractures, left hemo, pneumomediatinum)
b. What is the most likely pulmonary cause for this
?traumatic injury to lung parenchyma…?BPF with PPV
- CXR shown with 2 devices – PPM and ICD (maybe cardiac resynch), huge heart
a. What is the underlying disease process in this patient
b. Now post cardiac surgery CXR of same patient – basically frankenstein’s CXR – more devices than I have ever seen!!!
i. What is the anatomical course that the impella takes
ii. What is the device labeled (pointed to 2 large tubes, one at the apex, the other about 6 inches beside the first one, to the patient’s right and at the same level)
iii. What is the marker pointing at – maybe something in the tricuspid or mitral valve region?
Dilated cardiomyopathy
- Sits across the aortic valve in – drawing blood from the LV into the aorta
- LVAD device?
- Patient with ARDS, bunch of info about vent, (with suboptimal vent settings – Vt = 6mL/kg, Pplat = 26, Peep = 5, Fio2 = 0.60, sats 85-88%, and a PCO2 of 36)
a. What 4 changes can you make to the vent to improve this patient’s condition while maintaining a lung protective strategy
Increase PEEP to 10
Allow for permissive hypercapnea
Increase Vt by 1 to 2 mL/kg to 8 mL/kg
Target oxygenation goal to SpO2 88-95%
ARDSnet ventilator setup
1. calculate PBW
men = 50+2.3[ht inches-60]
women = 45.5+2.3[ht inches-60]
2. select any ventilator mode
3. set ventilator settings to 4. achieve initial Vt 8mL/kg PBW
4. reduce Vt by 1mL/kg until 6mL/kg
5. set initial rate to approximate baseline MV (not >35bpm)
6. adjust Vt and RR to achieve pH and plateau pressure goals
oxygenation goal PaO2 55-80 or SpO2 88-95%
plateau pressure goal =30cm H2O
- check plateau pressure
- if Pplat >30 decrease Vt by 1mL/kg
- if Pplat<25 and Vt <6 increase Vt by 1ml/kg until Pplat 25 of Vt 6
- if Pplat <30 and breath stacking or dys-synchrony occurs may increase Vt in 1mL/kg increments to 7-8 if Pplat remains <30
- Severe asthmatic, presents with resp failure, intubated, has cardiac arrest post intubation
a. List 3 etiologies for the cardiac arrest in this patient
b. Now, patient has ROSC and is doing well, what are 2 risk factors (specific to the treatment of her condition) for critical illness weakness
- dynamic hyperinflation
- breath-stacking
- hypovolemia from presentation
- ?tension pneumothorax
- tube migration and mainstem vs esophageal intubation
old answers High RVSP Hypoxia Hypercarbia Life threatening bronchospasm Auto PEEP High risk pneumothorax
?steroids
paralysis
- List 2 mechanisms for auto peep
mechanistically I think the answers should be:
- breath stacking (which can occur in someone with normal lungs)
- obstructive lung disease (asthma, COPD)
old answers:
o Breath stacking
o High RR
o High Ti (i.e. high I:E ratio)