2014 Flashcards
- Investigators have shown that the annual risk of stroke in elderly patients with untreated atrial fibrillation is 13%. Patients treated with coumadin however had an annual stroke risk of 3%. The annual risk of significant bleeding in the patients that where on coumadin was 6%, while those that where not on coumadin had an annual risk of bleeding of 0.5%. a. With your knowledge of statistical methods and equations (they actually say that in the exam), show us how an absolute risk reduction would be calculated and plug in the numbers without actually doing the calculation (1). b. How would you calculate the number needed to treat based on the information given in the stem? Please plug in the numbers without actually doing the calculation (1).
a. ARR = CER-EER = 13% - 3% = 10% (control and experimental event rate) b. NNT = 1/ARR NNT= 1/(EER-CER) = 1/(0.10) = 10
- They give you a long stem of a lady in her 60’s that presents with dysphagia, hematemesis and chest pain. She is admitted to the ICU with unstable vitals. They provide you with her saggital CT scan image, which we (the people who took the exam) largely disagreed on what it showed. In essence the image showed a bone window saggital cut CT image with an opacification extending all the way down to the diaphragm. Cephalad it extended up to the superior medastinum and encroached on the right lung apical region. Some of us thought it was a large ascending, transverse and descending thoracic aortic aneurysm (possibly a dissected aneurysm but you couldn’t really make out a dissection flap on the image). Some of my colleagues thought that it was an image of achalasia or an esophageal stricture with contrast dye filling up all her esophagus. Others thought it was a case of oesophageal rupture. They tell you she is now in distress and requires intubation. a) They ask you what the diagnosis is (1). b) During her intubation she has massive aspiration (Mendelson syndrome). In this patient specifically, how would this complicate things and worsen her outcome (3), yes they asked for 3 things! What steps would you take with intubation to minimize aspiration(3)?
a) ? achalasia vs. esophageal rupture b) -chemical pneumonitis (seems to be like Mendelson syndrome), can lead to ARDS -bacterial pneumonia -mechanical obstruction (airway obstruction or reflex airway closure) -difficult intubation The term chemical pneumonitis refers to the aspiration of substances that are toxic to the lower airways, independent of bacterial infection. The prototype and best studied clinical example is chemical pneumonitis associated with the aspiration of gastric acid first described by Mendelson in 1946 [25] and sometimes referred to as Mendelson’s syndrome. Classically occurs with aspiration of gastric contents followed by resp distress, cyanosis and infiltrates on CXR. Pts usually have rapid clinical recovery (24-36h) with radiographic resolution within 4-7d without the use of Abx. The following clinical features should raise the possibility of chemical pneumonitis [39]: ●Abrupt onset of symptoms with prominent dyspnea ●Fever, which is usually low grade ●Cyanosis and diffuse crackles on lung auscultation ●Severe hypoxemia and infiltrates on chest imaging involving dependent pulmonary segments. The dependent lobes in the upright position are the lower lobes. However, aspiration that occurs while patients are in the recumbent position may result in infection in the superior segments of the lower lobes and the posterior segments of the upper lobes. c) -Perform as a RSI (do not bag patients at high risk of aspiration - these were excluded from BVM-RSI study) -dedicated suction person -Perform intubation with head of bed elevated - +/-Decompress stomach prior to intubation (don’t put in NG if you think it’s ruptured) -+/-Cricoid pressure
- Bronchoscopy is an important skill for critical care physicians. Identify what the following images show. a. They show you an image with a circle around the RUL bronchus (1). b. They show you an image with a circle around the RML bronchus take-off from the bronchus intermedius (1). c. They show you an image with a circle around the LLL bronchus(1).
- https://www.youtube.com/watch?v=VLsXe5oB2W0&feature=player_embedded - https://www.youtube.com/watch?v=ThYHLG50pH0
- A younger gentleman was involved in an MVC and presents to the emergency department with polytrauma. They give you bunch of vitals and a bunch of CT images. His CT thorax transverse cut shows a left hemopneumothorax, his saggital CT chest shows sternal fractures and burst fracture in one of the thoracic vertebra and his pelvic CT scan shows a pelvic fracture. -Identify the injuries (4). o Hemopneumothorax o Sternal fracture o Thoracic vertebral fracture o Pelvic fracture -The patient is now in shock. Identify the different potential causes of shock in this gentleman and briefly describe their mechanism (4).
o Hemorrhagic - pelvis, chest o Obstructive - tension pneumothorax, cardiac tamponade o Neurogenic - high T-spine fracture above level of sympathetics o Cardiogenic - given sternal fracture patient at risk for cardiac contusion
- Your ICU is looking to implement a quality control system. -What steps would you take to implement a quality control system in the ICU (4)? -What components would you consider essential for any ICU quality control system (4)?
a) PDSA (plan, do, study, act) Plan - hypothesis and idea, questions and predictions Do - carry out the plan Study - analyze the data and compare to predictions Act - adapt, what changes can be made for next cycle? b) from previous answers…couldn’t find an official resource to support this o A system to flag issues o A comprehensive multidisciplinary team from all areas to develop new solutions o System to test the solution and transition into practice o System to assess the outcome of the new solution -?regular feedback to clinical teams?
- A middle aged lady has been receiving ovulation induction therapy to get pregnant. They are able to retrieve multiple ova for IVF. Later on she starts developing abdominal pain and respiratory distress. They show you a low cut in her pelvo-abdominal CT scan with multiple large follicles and some free fluid. They tell you she has developed ARDS and ask, what is the most likely cause of her ARDS (1)?
- Ovarian hyperstimulation syndrome Ovarian hyperstimulation syndrome (OHSS) occurs when the ovaries are hyperstimulated and enlarged due to fertility treatments (or rarely, mutations in the follicle-stimulating hormone [FSH] receptor), resulting in the shift of serum from the intravascular space to the third space, mainly to the abdominal cavity. In its severe form, OHSS is a life-threatening condition because it can cause venous or arterial thromboembolic events, including stroke and loss of perfusion of an extremity. Severe OHSS is characterized by an extraparenchymal restrictive type of pulmonary dysfunction, attributed to intraabdominal or pleural fluid accumulation, which limits descent of the diaphragm and expansion of the thoracic cage. This may induce uncoordinated lung ventilation and atelectasis with subsequent ventilation-perfusion mismatch and hypoxemia. The clinical picture may deteriorate further because of pulmonary infection, pulmonary thromboembolism, or ARDS, all of which have distinct clinical, radiographic, and blood gas characteristics.
- An elderly gentleman has had an aortic valve replacement and in the OR lead III is being monitored. He has a change in rhythm and they show you a rhythm strip showing sinus rhythm and then about 6 or 7 beats of wide complexes, which then goes back to normal sinus rhythm. They also show you underneath that rhythm strip, a print-out of the art. line trace. It shows that patient still has cardiac output throughout the wide complex rhythm but with a slightly lower pressure. - What is the rhythm change (1)? (some people thought it was a paced rhythm, others thought it was a non sustained VT, there were no clear pacing spikes) o Non-sustained VT What are 5 causes of WCT? Why did the pressure drop with that change (1)?
- What is the rhythm change (1)? (some people thought it was a paced rhythm, others thought it was a non sustained VT, there were no clear pacing spikes) o Non-sustained VT? A variety of definitions of NSVT have been published, but the most commonly used definition is [1]: ●Three or more consecutive ventricular beats ●Rate of >100 beats per minute ●Duration of less than 30 seconds 5 causes of WCT: 1) VT (look for AV dissociation, fusion beats, capture beats) 2) SVT with aberrhancy 3) SVT with pre-excitation 4) SVT with paced rhythm 5) artifact o Loss of atrial kick, given that the patient is having an aortic valve replaced likely has significant LVH and requires the atrial kick for optimal filling
- Non-invasive ventilation is a well established mode of treating respiratory failure of various etiologies. - How does non-invasive ventilation help patients with acute excarbations of COPD (2 mechanisms)? - How does NIV help patients with cardiogenic pulmonary edema (2 mechanisms)?
COPD -offloads respiratory muscles by providing inspiratory pressure augmentation to assist ventilation -applied PEEP can reduce work of breathing and assist in breath triggering/inspiratory initiation by reducing the pressure differential the pt’s diaphragm needs to generate in order to trigger a breath Cardiogenic pulm edema -increases intrathoracic pressure and thus decreases preload to heart causing less ventricular stretch and therefore in a more optimal position for force generation -increasing intrathoracic pressure decreases LV wall tension thereby decreasing myocardial workload -increases intrathoracic pressure which helps to move blood from aorta outside of thoracic cavity, thereby decreasing LV afterload -increases RV afterload decreasing RV output and leading to decreased LV preload -shift fluid from alveolar to interstitial tissue improving gas exchange and hypoxia
- List 5 pathogens associated with severe sepsis in patients 2 to 4 months after a solid organ transplant (5). BONUS: list common infections within the first month post transplant!
- Legionella - Mycoplasma In the period one to six months post-transplant, the nature of common infections changes. The effect of immunosuppression is often maximal, and patients are at greatest risk for the development of opportunistic infections. -PJP (pneumocystis jirovecii pneumonia) -aspergillus -viruses (CMV, EBV, HCV, HBV), including community acquired viruses (influenza, parainfluenza, RSV, adenovirus) -latent infections (strongyloidiasis, toxoplasmosis, Chagas) -geographic/endemic fungal infections: histoplasma capsulatum, coccidiodes -tuberculosis -NTB mycobatceria -GI parasites: cryptosporidium previous answers also listed: - Listeria - Norcardia - TB - CMV - HSV - Aspergillus - PJP - Cryptococcus - Influenza - Histoplasma - If still ventilated – MRSA, pseudomonas 1st month since transplant there are two major causes for infection: pre-existing infection from either the donor or recipient and infectious complication of the surgery/hospitalization…the major effects of exogenous immunosuppression are not yet evident! -VRE -MRSA -G neg bacteria -fluconazole resistant candida -HBV -HCV -colonizers that may cause infection (VRE) or organisms not covered by surgical prophylaxis
- Epiglottitis versus Ludwig’s angina. - What are the two most common pathogens that cause Epiglottitis (2)? - What are the two most common pathogens that cause Ludwig’s angina (2)? - What is the most important difference in management between the above conditions (1)?
Epiglottitis -Hemophilus influenza -B-hemolytic streptococci (ex. strep pyogenes) -+/-strep pneumoniae ***Mo says this one Ludwig’s angina (think oral flora) -Strep viridans (one of which is strep anginosus - formerly strep milleri -Polymicrobial (anaerobes: peptostreptococcus, fusobacterium, bacteroides, actinomyces) difference …after more thought I’m thinking Ludwig’s is different in that it is a deep neck space infection and can track down through fascial layers and into mediastinum/lungs…other option from prev answer was: o Ludwig’s angina more likely to need surgical or interventional drainage (look for infected teeth that can be extracted) o May need a trach -both however may need urgent and CAREFUL airway management/securing LUDWIGS Ludwig’s angina is a life-threatening cellulitis of the soft tissue involving the floor of the mouth and neck. It involves two compartments on the floor of the mouth namely sublingual and submaxillary space. It usually does not involve lymphatic system nor it forms abscess. Infection of the lower molars is the most common cause of Ludwig’s angina.[1] The infection is rapidly progressive leading to aspiration pneumonia and airway obstruction. The most common cause is dental disease in the lower molars mainly second and third which accounts for over 90% of cases.[2] Any recent infection or injury to the area may predispose the patient to develop Ludwig’s angina. Some common etiologies include injury or laceration to the floor of the mouth, mandible fracture, tongue injury, oral piercing, osteomyelitis, traumatic intubation, peritonsillar abscess, submandibular sialadenitis and infected thyroglossal cysts.[3] Predisposing factors include diabetes, oral malignancy, dental caries, alcoholism, malnutrition, and immunocompromised status. Since the infection does not spread via the lymphatic system, the infection is bilateral. The infection is usually polymicrobial involving the oral flora. The most common organisms are Staphylococcus, Streptococcus, Peptostreptococcus, Fusobacterium, Bacteroides and Actinomyces. The most common presenting symptoms include fever and chills with neck swelling, neck pain, odynophagia and dysphagia. People often describe the appearance as a “bull neck.” Less common symptoms include mouth pain, hoarse voice, drooling, tongue swelling, stiff neck and sore throat.[4] Stridor may indicate impending airway obstruction. Early airway management is critical to the treatment of Ludwig’s angina as the most common cause of death is sudden asphyxiation from airway obstruction. Flexible fiberoptic nasal intubation is clinician’s favored method of intubation. If the patient is not able to be intubated, the next step would be an emergency tracheotomy. Cricothyrotomy is very challenging because of the edema in the neck which can obscure the anatomy.
- A resident tried putting in a femoral central line in a 65 year old lady with septic shock and after poking the femoral artery a few times he/she was able to eventually cannulate the vein. The patient’s vitals stabilized with resuscitation but then her leg (with the line in place) started to become cold and mottled and showed signs of acute ischemia. Vascular surgery were consulted and they think the artery might have developed an intimal flap that caused the acute ischemia. They will operate and try to salvage that limb but an amputation is a strong possibility. -What are the 4 essential elements that need to be present in any disclosure of an adverse event (4)? -When do you disclose the adverse event (1)? -In general, who should be the one to disclose any adverse events to families(1)?
mine: attend to pt’s clinical care honesty documentation post analysis disclosure ?apology old answers: o Honest, open, and transparent disclosure of the facts o Empathetic expression of regret and apology o Comprehensive and timely investigation of the facts o The steps taken to manage the adverse patient safety event after providing care/stabilizing the patient and after preparing the known facts… o As soon as reasonably possible (as per CMPA) after ensuring the patient’s care needs have been met o The MRP Disclosure road map 1) attend to clinical care 2) plan the initial disclosure 3) attend disclosure meeting
- A patient with terminal COPD underwent a double lung transplant and the anesthesiologist inserted a pulmonary artery catheter in the OR that was confirmed to be in the right spot by the pressure waveform and by blood gases. The patient is now in the ICU and this is his chest X-Ray. They show you a left IJ line that doesn’t take the normal course. It comes down the left side of the heart before coursing medially half-way into the heart, then it goes back again and up pulmonary artery. Trace the pulmonary artery catheter course from it’s point of insertion in the IJ to the main pulmonary artery excluding the valves it passes through (i.e. no need to mention the valves it goes through) (4).
- Left internal jugular - Persistent left SVC - Coronary sinus - RA - RV - PA
- A post line insertion chest X-ray was done after insertion of a 7 Fr central line in the right internal jugular vein. They show you an image where the right “IJ” line courses down to the arch of the aorta (i.e. looks like a carotid line). - How would interpret this CXR (1)? - How would you deal with this situation (2)?
o Arterial cannulation o Leave the line insitu, labelled to ensure it is not used o Contract vascular surgery -later plan to disclose to patient/family
- A lady admitted to the medicine ward with an upper GI bleed, stated that she wanted nothing done and that if she were to worsen she wanted to be left to die in peace. After that she bleeds profusely and deteriorates. Her family arrive and want her intubated, and want her to get an upper GI scope and the works. - What ethical principle would be violated if you were to do as the family wants (1)? - What are 3 essential elements of any consent (3)?
o Autonomy -voluntary -pt must have mental capacity -pt must be properly informed
- Patient has a history of a single lung transplant 3 years ago. Now with a viral illness severe enough to require intubation in the ICU. They give you vent parameters that are relatively high from and airway pressure standpoint. They give you a CXR of a patient with a single lung (right) that is clearly quite big (likely due to compensatory emphysema plus the IPPV) and the medastinum is very slightly shifted to the left, with an empty (or fluid-filled) small left hemithorax. They tell you that the patient now is in obstructive shock (yes they actually say obstructive shock). Provided there is no pneumothorax, what single non-pharmacological maneuver could you do to help treat this hypotension (1)?
Decompress the trapped air
- What is the most important physiotherapy intervention in the ICU (1)? What are three benefits of this intervention?
-Early progressive mobilization my answers: -shorter duration of MV -more likely to walk without assistance at hospital discharge -improved muscle strength -improved physical function -more days alive and out of hospital to day 180 -prevents delirium ***LOOK AT PADIS guideline https://www.ncbi.nlm.nih.gov/pubmed/27864615?dopt=Abstract old answers: o Improved muscle strength o Improved physical function o Improved quality of life o Decreased ICU LOS o Decreased duration of mechanical ventilation
- Fat embolism syndrome (FES) is common with long bone fractures. - What is the pathognomic sign of fat embolism syndrome (1)? - Name 3 non-traumatic causes of fat embolism syndrome (3)?
o Petechial/purpural rash that appears on the upper portion of the body Fat embolism syndrome (FES) typically manifests 24 to 72 hours after the initial insult, but may rarely occur as early as 12 hours or as late as two weeks after the inciting event [37]. Affected patients develop a classic triad: hypoxemia, neurologic abnormalities, and a petechial rash. None of these features are specific for FES. The characteristic red-brown petechial rash may be the last component of the triad to develop and occurs in only 20 to 50 percent (on average one third) of cases. It is found most often on the nondependent regions of the body including the head, neck, anterior thorax, axillae, and sub-conjunctiva.
- o Acute pancreatitis
- o Liposuction
- -osteonecrosis
- -bone marrow necrosis
- -lipid based infusions or contrast agents
- -IM injection of oil for cosmetic purposes
- -sickle cell/thalassemia-related hemoglobinopathies (esp during crisis)
- Name 4 indications for hyperbaric oxygen therapy (4).
-Carbon monoxide poisoning -cyanide poisoning -Decompression sickness -Acute traumatic or thermal injury (compartment syndrome) -Necrotizing soft tissue skin infection -Non-healing ulcers -radiation injury
- A polytrauma patient with a closed head injury, rib fractures, pulmonary contusions, and some other injuries is intubated and has a right sided chest tube inserted before he is transferred by air ambulance. Before take off, his ETT cuff is filled with saline and his chest tube is clamped. He is put on board of a fixed wing aircraft and they mention that the ambient pressure on-board the aircraft is pressurized to 2500 metres high or 8000 feet altitude (as per the standards for pressurizing fixed-wing aircrafts, which usually fly much higher than that - they usually fly 10,000 metres altitude). The patient starts to desaturate and his oxygen requirement go up. The patient is now on an FiO2 of 0.8 with SpO2’s barely in the high 80’s. - What are 4 reasons for his desaturation (4)? - What would be the reason the ETT cuff was filled with saline (1)?
o Expansion of pneumothorax due to decreased ambient pressure o Decreased partial pressure of inspired oxygen o Progression of pulmonary contusion o Expansion of stomach gases compressing lungs -ETT displaced from position -?fat embolism o If air is used, as ambient pressure decreases the cuff would expand, this does not happen with saline
- You are trying to wean a patient off a ventilator but she keeps failing despite everything else heading in the right direction. You do a set of blood work to rule out metabolic causes of her failure and you find a very high TSH of 15 (normal is up to around 4), but her free T3, and free T4 are both normal. - What is the diagnosis (1)? - What lab test rules out non-thyroidal illness syndrome (1)?
recovering sick euthyroid (vs subclinical hypothyroidism) o Normal T3 and T4 o Elevated reverse T3 in sick euthyroid The most common hormone pattern in sick euthyroid syndrome is a low total T3 and free T3 levels with normal T4 and thyroid-stimulating hormone levels. The serum level of reverse T3 (rT3) is increased in euthyroid sick syndrome, except in renal failure. Low serum T3 is correlated with an increased length of hospital stay, intensive care unit admission, and the need for mechanical ventilation in patients with acute heart failure. The serum T4 value also correlates with outcome in critically ill patients; values under three microg/dL have been associated with mortality rates in excess of 85%. Two general guidelines are important in evaluating a critically ill patient. —First, measure TSH only if there is a high clinical suspicion of thyroid dysfunction. If TSH is abnormal, then further workup is done. If the TSH is greater than 20 microUnits/mL or is undetectable, euthyroid sick syndrome is less likely to be the cause, and overt thyroid dysfunction should be strongly considered. —When serum TSH is not elevated, euthyroid sick syndrome should be considered in patients with known thyroid disease and low serum-free T4. Thyroid function in non-thyroidal illness (UTD) TSH subnormal — Almost all patients who have a subnormal but detectable serum TSH concentration (greater than 0.05 mU/L and less than 0.3 mU/L) will be euthyroid when reassessed after recovery from their illness. In contrast, approximately 75 percent of patients whose TSH is undetectable (<0.01 mU/L) have thyrotoxicosis. ●In patients without a strong clinical suspicion of thyroid disease and minor TSH abnormalities (TSH between 0.05 and 0.3 mU/L with normal or low free T4), we reassess thyroid tests (TSH, free T4) after recovery. If true central hypothyroidism due to hypothalamic or pituitary disease remains in the differential diagnosis, measurement of serum cortisol can be helpful as it would be elevated in critical illness and low (or inappropriately normal) in patients with true central hypothyroidism. Measurement of serum rT3 is only rarely useful in hospitalized patients to distinguish between nonthyroidal illness (high values) and central hypothyroidism (low values); the values are low in the latter patients because of low production of the substrate (T4) for rT3. TSH high — As noted above, some hospitalized patients have transient elevations in serum TSH concentrations (up to 20 mU/L) during recovery from nonthyroidal illness [48]. Few of these patients prove to have hypothyroidism when reevaluated after full recovery from their illness. Patients with serum TSH concentrations over 20 mU/L usually have permanent hypothyroidism [50]. Our approach depends on the degree of TSH elevation and the clinical suspicion for underlying hypothyroidism: ●TSH between upper limit of normal and <10 mU/L – If the patient appears to be recovering from the underlying illness, we repeat the TSH in one to two weeks. Few of these patients prove to have hypothyroidism when reevaluated after recovery from their illness. ●TSH 10 to 20 mU/L – Treatment with levothyroxine may be appropriate depending on the free T4 level, clinical suspicion of hypothyroidism, and degree of nonthyroidal illness. If uncertain, repeat the TSH and free T4 in one to two weeks. Thyroid function tests may improve in patients recovering from nonthyroidal illness. ●TSH ≥20 mU/L – Assess the free T4 level. •Free T4 low – Hypothyroidism is likely. Initiate thyroid hormone. In the absence of suspected myxedema coma, repletion should be cautious, beginning with approximately half the expected full replacement dose of T4 (levothyroxine). In suspected myxedema coma, or in critically ill patients who cannot ingest or absorb oral medications, thyroid hormone should be given intravenously. •Free T4 normal – Repeat TSH and free T4 in one to two weeks. Thyroid function tests may improve in patients recovering from nonthyroidal illness.
- They show you diagrams of the the three set-ups of CRRT (hemofiltration, hemodialysis and hemodiafiltraton. - They ask you to label each mode of renal replacement therapy (3). - With regard to hemofiltration, state one advantage and one disadvantage of pre-filter replacement fluid substitution (2). State one advantage and one disadvantage of post- filter replacement fluid substitution (2).
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 (slow continuous ultrafiltration) overall review here 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. o Pre-filter Advantage • Less clot, longer filter life Disadvantage • Less removal of solute as you have a dilute solution o Post-filter Advantage • More solute removal Disadvantage • Shorter filter lifespan
- What properties of a molecule or toxin, govern whether it would be dialysable or not (4)? B. What are the mechanisms of drug and toxin removal with hemofiltration, i.e. how does it work to clear toxins (3)?
- Size - Protein bound - Volume of distribution - Water solubility - +/-charge - +/- interaction with the dialysis membrane? - Blood passed through filter with large pores - Ultrafiltrate passes through the pores, drags toxins with it (CONVECTION = Convection is bulk-flow of solute across a semi-permeable membrane together with a solvent in a manner that is dependent on transmembrane pressure and membrane characteristics.) - Rate of fluid is equal to drug clearance
- When using inotropes or pressers in the ICU, what are the considerations for using each of the following. - Milrinone (3 considerations) - Dobutamine (3 considerations)
- Milrinone (3 considerations) = phosphodiesterase 3 inhibitor which decreases the rate of cAMP degradation –> increases Ca influx into cell o Renal function o Fluid status o Cardiac function o Presence/absence of pulmonary hypertension o Concurrent beta-blockade -slower onset and clearance - Dobutamine (3 considerations) = primarily beta-1 adrenergic o Cause of current shock (cardiogenic) o Heart rate, arrhythmia -can increase O2 demand in pts with pre-existing MI -hypotension o Fluid status -more rapid onset
- A lady after a prolonged delivery develops respiratory distress, hypoxemia, RV dilation and failure and DIC (disseminated intravascular coagulopathy). What is the diagnosis (1)? What are the diagnostic criteria for this condition?
-Amniotic fluid embolism Amniotic fluid embolism is a clinical diagnosis. The diagnosis should be suspected in pregnant or recently postpartum women who experience sudden cardiovascular collapse, severe respiratory difficulty and hypoxia, and/or seizures, particularly when followed by disseminated intravascular coagulopathy (DIC). The condition generally arises during labor or soon after delivery, in the absence of other explanations for these findings. In many cases, the diagnosis is made retrospectively, after all investigative data, including autopsy data, have been collected. ●Sudden onset of cardiorespiratory arrest OR hypotension (systolic blood pressure <90 mmHg) with evidence of respiratory compromise (eg, dyspnea, cyanosis, or peripheral oxygen saturation <90 percent). ●Documentation of overt DIC using the scoring system of the Scientific and Standardization Committee on DIC of the International Society on Thrombosis and Haemostasis (ISTH), modified for pregnancy [8]: •Platelet count >100,000/mL = 0 points, <100,000 = 1 point, <50,000 = 2 points •Prolonged prothrombin time or international normalized ratio <25 percent increase = 0 points, 25 to 50 percent increase = 1 point, >50 percent increase = 2 points •Fibrinogen level >200 mg/L = 0 points, <200 mg/L = 1 point A score ≥3 is compatible with overt DIC. Coagulopathy must be detected before hemorrhage itself can account for dilutional or shock-related consumptive coagulopathy. ●Clinical onset during labor or within 30 minutes of placental delivery. ●Absence of fever (≥38°C) during labor.
- A short obese lady undergoes cardiac surgery (CABG) with a size 8 endotracheal tube. The anesthesiologist documents an atraumatic, easy intuition inserted on the first pass. She is doing really well in the ICU and has passed her SBT, is awake, and fits all the criteria for extubation. The respiratory therapist however, tells you she has no cuff leak. - What would you do (1)? - Explain why you would do that (1)?
o Extubate o There is no strong evidence that a lack of a cuff leak implies failure to extubate, and given the large size ETT in a short woman it is very likely that she’ll never have a cuff leak. Also given the report from the anesthesiologist it is unlikely that there was significant trauma during intubation causing severe swelling from MV guidelines: Risk factors for PES include: traumatic intubation, intubation longer than 6 days, large endotracheal tube, female sex, and reintubation after unplanned extubation
- A gentleman is recovering from his critical illness in the ICU quite well. He is now awake and cooperative, feeding well, and looking good, except that he keeps failing his SBT’s. - What are the advantages of proceeding tracheostomy (4)? - His tracheostomy procedure goes well. The next day however, upon turning the patient, the tracheostomy is dislodged, and you are unable to pass it in again. His SpO2 is now 50’s. What do you do now?
o Decrease resistance to airflow with a shorter airway allowing for weaning in ventilation o Allow for reduced sedation o Allow for secretion management o Improved patient comfort (speech, mobility, swallowing enhanced) -can be nursed outside of ICU -ease of replacement once tract has formed o Cover the trach site and bag from above, then intubate from above o Have trach replaced in OR
- A. What are two different ways of performing an spontaneous breathing trial (2)? B. What parameters would indicate failure of a spontaneous breathing trial (4)?
- T-piece - PS ventilation -CPAP - Tachypnea, inc WOB, diaphoresis - Tachycardia, cardiac arrhythmia - ST changes - Desats -abrupt change in LOC from my paper -gas exchange (i.e. oxygenation: SpO2 ≥85-90%, PO2 ≥ 50-60mm Hg, and ventilation: pH≥7.32, increase in PCO2 ≤10mm Hg) -hemodynamic stability (HR <120-140bpm, HR not changed >20%, SBP <180-200mm Hg and >90mm Hg, BP not changed >20%, no vasopressor use) -respiratory pattern (RR≤30-35 breaths/min, RR not changed >50%) -Subjective variables showing success included the absence of: change in mental status, onset/increase in discomfort, diaphoresis, and signs of increased work of breathing.
- A lady had underwent a mitral valve replacement in and is now in the ICU. Other than the surgical wires and mitral valve, what other anomalies do you observe in this chest X ray (2)? Her right IJ line was going outward into her right subclavian and her right pleural base looked thickened i.e. had a pleural plaque. Her gastric air bubble was quite big, and some of my colleagues said she had some air under her right hemidiaphragm but, I’m not really sure that was the intended anomaly. To me it looked like the calcified pleura at the right lung base gave an impression of some air under the diaphragm that didn’t quite exist. In addition to that, in the OR chest tubes go from underneath anyways and a little bit of air under the diaphragm immediately postop in the setting of a benign exam, is usually not a big deal. That is if we were to say that she had free air…(which as I said, she might not have had). The chest X-ray showed sternal wires, so it was a conventional MVR via a sternotomy.
?nothing to add
- Several authors have investigated the use of PA catheters and have always concluded that their use increases mortality rate. Other than lack of power and lack of blinding, name 3 other methodological limitations of their analyses (3)?
-Lack of standardization of response to hemodynamic values -groups not balanced in terms of severity of illness -interpretative of PA catheter was not uniform o FACTT was done in ARDS/ALI patients only - Delayed insertion of PAC (PAC-Man trial) - Unclear control group (PAC-Man control group had a large number with some form of measured cardiac output)
- You are managing a trauma patient in emerg. that has a widened mediastinum on CXR, and you suspect an aortic tear. a. What other CXR findings (other than a widened mediastinum) make you suspect an aortic tear? List four (4). b. What site is most commonly affected in traumatic aortic injury i.e. where does the aorta usually tear (1)?
a. - left Apical capping - Pleural effusion - Loss of aortic knuckle - Deviated NG or paratracheal stripe - 1st rib fracture b.- aortic isthmus: Just distal to the ligamentum arteriosum (near left subclavian) Most blunt injuries of the thoracic aorta occur at the aortic isthmus just distal to the left subclavian artery [17]. A number of theories are used to explain the mechanism of thoracic aortic injury at the isthmus. It is likely that most injuries probably involve a combination of forces. ●The isthmus is thought to be a transition zone between the more mobile ascending aorta and arch and the relatively fixed descending thoracic aorta that allows for stretching with rapid deceleration [15]. ●The isthmus may be intrinsically weaker than the remainder of the aorta as evidenced by a series of tensile strength tests conducted on aortic samples [20]. ●Blunt aortic injury may be the result of a “water hammer” effect in which compression of the abdomen due to a sudden impact occludes the aorta, leading to rupture of the proximal, intrinsically weak isthmus or other susceptible portion of the aorta
- A patient with a brain tumour and a brainstem bleed (or tumour, I can’t remember) is now intubated, ventilated and unresponsive. He has lost all cranial nerve reflexes. How would you proceed to diagnose brain death (1)?
- Ensure no confounders - Proceed with apnea test o CO2 should increase to above >/=60 and by greater than >/=20mmHg above baseline and pH =7.28 ???
- They tell you about a depressed lady who is on clomipramine and then comes in for an appy and then for some reason, she is also on selegiline. And then the surgeons give her some dilauded. She gets an acute bout of irritability, fever (temperature 41 degrees), and they even tell you she has clonus, and has a CK of 50,000. - What is your diagnosis (1)? - What 3 things would you do to treat this (3)? - list ten drugs that can cause this condition?
Serotonin syndrome. o Stop the offending agents o Active cooling o Administer benzos o Consider cyproheptadine -see list Serotonin syndrome is often misdiagnosed as NMS, but the two can readily be distinguished on the basis of history, examination findings, and clinical course (table 3) [10]. NMS develops over days to weeks [10], whereas serotonin syndrome develops over 24 hours [3]. Serotonin syndrome is characterized by neuromuscular hyperreactivity (tremor, hyperreflexia, myoclonus), while NMS involves sluggish neuromuscular responses (rigidity, bradyreflexia). Hyperreflexia and myoclonus are rare in NMS [10]. In addition, resolution of NMS typically requires an average of nine days, compared with less than 24 hours (usually) for resolution of serotonin syndrome [10]. Hyperthermia, altered mental status, muscle rigidity, leukocytosis, elevated creatine phosphokinase, elevated hepatic transaminases, and metabolic acidosis are seen in severe cases of both conditions, which highlight the necessity of a thorough history and physical examination.
- With regards to Ringers lactate and normal saline (0.9%), they ask you about their composition and pH. They actually give you a table to fill in for both with the columns labeled: sodium, potassium, calcium, glucose, chloride, magnesium, lactate and pH.
see table—
- A lady collapsed at home, and they showing you her CT head, her CXR which shows pulmonary edema, and her EKG with some precordial ST elevation. They ask if a unifying diagnosis could explain all this, or they say how would you link all these findings pathophysiologally and they ask you to explain (3).
SAH –> Takotsubo’s –> CHF o Catecholamine excess induces coronary artery vasospasm leads to stress induced cardiomyopathy, leads to decreased LV function allowing for pulmonary edema The pathogenesis of this disorder is not well understood. It is not known why this disorder affects postmenopausal women disproportionately or why the left ventricular (LV) mid-cavity and apex are predominantly affected. Studies comparing LV systolic and diastolic function in patients with stress cardiomyopathy with function in patients with acute myocardial infarction (MI) have reached differing conclusions [21,22]. Initial systolic function may be similar [21] or worse [22] with stress cardiomyopathy compared with acute MI, while diastolic function may be similar [21] or better [22] with stress cardiomyopathy. Postulated mechanisms include catecholamine excess [8,23], microvascular dysfunction, and coronary artery spasm. Also, dynamic mid-cavity or LV outflow tract obstruction has been documented in some patients and may contribute to apical dysfunction. A number of features of stress cardiomyopathy, including its association with physical or emotional stress [4,5,7-10,16,20,24], suggest that this disorder may be caused by diffuse catecholamine-induced microvascular spasm or dysfunction, resulting in myocardial stunning [18], or by direct catecholamine-associated myocardial toxicity.
