Archer Critical care for USMLE Step 3


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Archer Critical care for USMLE Step 3

  1. 1. Archer Critical Care Step 3 Archer USMLE reviews Visit us at To receive more free videos, slides and questions, Like us on FACEBOOK at
  2. 2. Critical Care Aspects <ul><li>Shock </li></ul><ul><li>Respiratory Failure </li></ul><ul><li>Acute coronary Syndrome </li></ul><ul><li>Acid-Base problems </li></ul><ul><li>Neurological Emergencies </li></ul><ul><li>GI Bleeding </li></ul>
  3. 3. Shock - Objectives <ul><li>Recognize the clinical manifestations of shock - the major classifications of shock </li></ul><ul><li>Identify the IV solution type that is best suited for water and electrolyte loss </li></ul><ul><li>Describe conditions that may indicate successful volume resuscitation </li></ul>
  4. 4. Shock <ul><li>Hypovolemic </li></ul><ul><li>Distributive – Septic, Drug overdose ( opiod, BZDs, Ethanol), Hepatic failure </li></ul><ul><li>Obstructive – PE, Cardiac tamponade, Pneumothorax, Air Embolism </li></ul><ul><li>Cardiogenic – Acute LHF, RHF </li></ul><ul><li>Miscellaneous – think about Adrenal insufficiency, hypocalcemia, Autonomic dysfunction in a shock that is refractory to pressor support and in a shock that tends to persist even after correction of the initial etiology </li></ul>
  5. 5. Distributive Shock <ul><li>1. Distributive (maldistribution of blood flow) - Warm Shock – Warm extremities </li></ul><ul><li>a. Septic </li></ul><ul><li>b. Neurogenic – Drug overdose, vasovagal </li></ul><ul><li>c. Anaphylactic </li></ul><ul><li>d. Toxic shock syndrome </li></ul><ul><li>e. Metabolic </li></ul>
  6. 6. Hypovolemic Shock <ul><li>Hypovolemic (decreased cardiac output) Secondary to loss of intravascular volume </li></ul><ul><li>a. Hemorrhagic </li></ul><ul><li>b. Nonhemorrhagic </li></ul><ul><li>1 . GI fluid loss (e.g., diarrhea, vomiting) </li></ul><ul><li>2. Renal loss (e.g., diabetes insipidus, osmotic diuresis) </li></ul><ul><li>3. Evaporative loss (e.g., hyperthermia, severe burns) </li></ul><ul><li>4. Third space loss (e.g., peritonitis, pancreatitis) </li></ul>
  7. 7. Cardiogenic Shock <ul><li>Cardiogenic (decreased cardiac output due to cardiac factors) </li></ul><ul><li>a. Impaired left ventricular contractility (e.g., ischemia, infarct, congestive myopathy) </li></ul><ul><li>Impaired right ventricular contractility (e.g., right ventricular infarction) </li></ul><ul><li>Acute regurgitant lesions (e.g., mitral or aortic regurgitation, intraventricular septal rupture) </li></ul><ul><li>d. Obstructive cardiac lesions (e.g., aortic stenosis, subaortic stenosis) </li></ul><ul><li>e. Bradyarrhythmias or tachyarrhythmias </li></ul>
  8. 8. Obstructive Shock <ul><li>Obstructive (decreased cardiac output due to factors extrinsic to the heart) </li></ul><ul><li>a. Pericardial tamponade </li></ul><ul><li>b. Tension pneumothorax </li></ul><ul><li>c. Pulmonary embolism </li></ul><ul><li>d. Severe pulmonary hypertension </li></ul>
  9. 9. Shock <ul><li>Pulmonary Embolism </li></ul><ul><li>Etiology </li></ul><ul><li>Clinical Features </li></ul><ul><li>Investigations – BEDSIDE ECHO THE BEST INITIAL SCREENING TEST IF U SUSPECT SHOCK DUE TO PE IN A CRITICALLY ILL PATIENT – Can give you information on other causes – Acute MI, Cardiac tamponade, Acute corpulmonale ( ARDS, PE) </li></ul><ul><li>Treatment </li></ul>
  10. 10. Shock <ul><li>Cardiac Tamponade </li></ul><ul><li>Etiology – Trauma,Rapid Effusions - tumor </li></ul><ul><li>Clinical features </li></ul><ul><li>Investigations – X-Ray, CT chest, 2D echo </li></ul><ul><li>Treatment </li></ul>
  11. 11. Shock <ul><li>Pneumothorax ( obstructive phenomena) </li></ul><ul><li>Etiology – usual scenario- an icu patient on ventilator – sudden hypotension </li></ul><ul><li>Others – trauma, rupture emphysemal bullae </li></ul><ul><li>Clinical features – auscultate – SILENT!! </li></ul><ul><li>- look at the ventilator parameters ----- high peak pressures as well as plateau pressures </li></ul><ul><li>Investigations – CXR, Needle thoracentesis </li></ul><ul><li>Treatment – tube thoracostomy, high fio2 </li></ul>
  12. 12. Shock <ul><li>Acute Corpulmonale </li></ul><ul><li>- ARDS </li></ul><ul><li>- Pulmonary Embolism </li></ul><ul><li>Rx – IV fluids, correct the cause </li></ul>
  13. 13. Shock <ul><li>Cardiogenic - Right Heart Failure </li></ul><ul><li>Symptoms, EKG, Signs, Enzymes </li></ul><ul><li>Treatment – fluids, fluids, fluids </li></ul><ul><li>cardiac cath, fix the lesion </li></ul>
  14. 14. Shock <ul><li>Cardiogenic – Left Heart Failure </li></ul><ul><li>Causes - Acute MI </li></ul><ul><li>Rx – IABC – To buy time </li></ul><ul><li>- Dopamine, Dobutamine </li></ul><ul><li>- then cardiac cath, fix the lesion - ptca </li></ul>
  15. 15. Shock <ul><li>Distributive </li></ul><ul><li>SEPSIS ---- distributes to periphery  WARM shock, systemic vasodilation -  reduced SVR ( Swan Ganz ) </li></ul><ul><li>Investigations – pan cultures, cxr, --- consider random cortisol…if requiring pressor support for a long time  rule out relative adrenal insufficiency. </li></ul><ul><li>Rx – Fluids,fluids, fluids  antibiotics  hydrocortisone 100 q8hrs if relative/ absolute adrenal insufficiency. Remove the source -  ? IV Catheters, hemodialysis access, foley </li></ul><ul><li>Pressor support – norepinephrine, dopamine, vasopressin </li></ul><ul><li>Distributive/ Anaphylactic – Epinephrine, corticosteroids, beta agonists, Antihistamines </li></ul>
  16. 16. Shock <ul><li>Hypovolemic – </li></ul><ul><li>Hypovolemia Vs. Dehydration </li></ul><ul><li>GI blood loss, vomiting, excessive diarrhea,Other trauma/ blood loss, Diabetes Insipidus, Diuretics ( overdiuresis), Diuretic abuse, Laxative abuse, Bulimia nervosa, Surreptious vomiting </li></ul><ul><li>Rx: Fluids, blood if required, Correct hypernatremia slowly < 0.5 meq/hr if present </li></ul><ul><li>Rx the underlying cause – fix GI bleeds, any ? coagulopathy, consults if required </li></ul><ul><li>? Renal failure – prerenal – indicators Urine Na+, FeNa, urine sp gravity, </li></ul>
  17. 17. Shock – Case studies <ul><li>A 38-year old female on birth control pills, has suddenly become extremely short of breath. Someone has seen her collapse and called 911. She was diaphoretic and complained of severe chest pain before she collapsed. She is now in the ER/ED and you have been asked to evaluate her. Her old records show that she is a cocaine abuser and was admitted for subarachnoid hemorrhage 6 weeks ago from which she completely recovered. Clinical findings. Vitals : B.P 65/ palpable, R.R 45. Pulse 140, Tm: 99.2 F. Chest showed decreased breath sounds in right lower lobe and distant heart sounds. Pulse oximetry revealed 88%. EKG showed sinus tachycardia with s wave in lead I, q wave in lead III and T wave inversion in lead III. 2D echo showed hypokinetic right ventricle with pulmonary hypertension. You started her on Intravenos fluids and her blood pressure has slightly improved to 66/30. Your next step in management ? </li></ul><ul><li>A) Transfer to cath lab and notify the interventional cardiologist stat </li></ul><ul><li>B) Intra aortic balloon counterpulsation </li></ul><ul><li>C) Thrombolytic therapy </li></ul><ul><li>D) Surgical Embolectomy and Inferior vena cava filter </li></ul><ul><li>E) Obtain cardiothoracic surgery consult for subxiphoid window </li></ul>
  18. 18. Case study <ul><li>Absolute Contraindications to Fibrinolytic Therapy </li></ul><ul><li>Active internal bleeding </li></ul><ul><li>CNS neoplasm, AV malformation, or aneurysm. </li></ul><ul><li>CNS procedure or CVA within two months. </li></ul><ul><li>Severe uncontrolled hypertension (over 200/130 or complicated by retinovascular disease or encephalopathy) </li></ul><ul><li>Known bleeding diathesis </li></ul><ul><li>MI due to aortic dissection </li></ul><ul><li>Allergy to either streptokinase or anistreplase, if streptokinase or anistreplase will be used </li></ul>
  19. 19. Shock Case 2 <ul><li>A 55 y/o male with history of lung cancer recently had a porta cath placed in the SVC. However, one week later he presents to your office with increasing swelling of this face, neck and upper extremities and increasing jugulovenos distension. You diagnose SVC syndrome and your suspicion is confirmed by an SVC venogram. You send the patient to interventional radiologist for SVC dilatation. In the radiology OR patient suddenly becomes unresponsive and hypotensive. His heart rate was 140 and B.P 78/40. He responds well to IV fluids but tachycardia persists. He is then transferred to ICU. You pay him a visit in the ICU and examine him. At the time of your exam he suddenly becomes unresponsive again and his blood pressure drops to 80/40. You restart IV fluids. Chest is clear to auscultation. Heart sounds are audible and normal. He has increased JVD but wife reports he has had this for past one week. The EKG is shown. The most important test that will best help you in diagnosis: </li></ul><ul><li>A) 2D ECHO </li></ul><ul><li>B) Cardiac enzymes </li></ul><ul><li>C) Chest X-ray </li></ul><ul><li>D) Electrocardiogram </li></ul><ul><li>E) Blood cultures </li></ul><ul><li>Next Step in management : </li></ul><ul><li>A) Tube thoracostomy </li></ul><ul><li>B) Pericardiocentesis </li></ul><ul><li>C) Intraaortic balloon counterpulsation </li></ul><ul><li>D) Percutaneous transluminal coronary angioplasty </li></ul><ul><li>E) IV Antibiotics </li></ul>
  20. 21. Shock – case study <ul><li>A 35 y/o woman was admitted for Thrombotic thrombocytopenic purpura and was receiving plasmapheresis. She became agitated one evening and pulled off her right jugular catheter which has been her plasmapheresis access. On examination her B.P is 60/32., HR: 120, Tm: 102, RR 24. Physical examination revealed a remnant of jugular catheter that’s still bleeding. You remove the catheter immediately. The patient is now crashing and blood pressure is no longer recordable but palpable at 60. Your immediate step in management? </li></ul><ul><li>A) Pericardiocentesis </li></ul><ul><li>B) Start IV fluids </li></ul><ul><li>C) Put patient in trendelenberg position </li></ul><ul><li>D) Needle thoracentesis </li></ul><ul><li>E) Portable chest x-ray </li></ul><ul><li>F) 2D echo </li></ul>
  21. 22. Respiratory Failure <ul><li>Hypoxemic – Type I </li></ul><ul><li>Hypercapnic – Type II </li></ul><ul><li>Mixed </li></ul>
  22. 23. How to classify? <ul><li>Look at Co2 </li></ul><ul><li>Calculate A-a gradient ( Alveolar – arterial gradient )  (PAo2 is alveolar po2 where as Pa02 is arterial po2) </li></ul><ul><li>Look at bicarbonate ( helps you to know if there is Chronic/ acute retention of co2) </li></ul><ul><li>Formula for A-a Gradient </li></ul><ul><li>= PAo2 – Pao2 = {(Atm Pressure – Watervapor)Fio2 – paC02 – pao2} </li></ul><ul><li>= 150 – pao2 – paco2/0.8 ( At room air) </li></ul><ul><li>At room air; </li></ul><ul><li>PA02 = 150 – PaCO2/O.8 </li></ul><ul><li>( 713X0.21 = 150; FIO2 = 21% ( or 0.21)} </li></ul>
  23. 24. Hypoxemic Respiratory Failure <ul><li>Increased A-a gradient  suggests gas exchange problem  anything that interferes with gas exchange i.e; reduced lung surface area, V/Q mismatch ( Pulmonary embolism), Shunting (infiltrates; Pneumonia, ARDS; atlectasis; Pulmonary edema; lung collapse) </li></ul><ul><li>These guys need OXYGENATION sufficient to rise their Sa02 > 90% ( usually po2 >60) </li></ul><ul><li>Modes for oxygenation </li></ul><ul><li>Nasal cannula </li></ul><ul><li>Venturi Mask ( adjust flow i.e; Fio2 as needed) </li></ul><ul><li>Non Rebreather’s mask ( can provide close to 100% Fio2) </li></ul><ul><li>Mechanical ventilator ( if non invasive modes fail to raise the sa02, pt is tachypneic; having altered mental status  intubate!!) </li></ul>
  24. 25. Hypercapnic Respiratory Failure <ul><li>Hypoventilation is the principal mechanism ( Minute Ventilation = Vt x RR)  reduction in Minute ventilation rises your C02 </li></ul><ul><li>Examples : COPD; acute attack of Asthma ( acute bronchoconstriction); Neuromuscular diseases ( GBS; Myasthenia Gravis); Hypermagnesemia; hypophosphatemia; opiod overdose; coma; severe cerebral edema </li></ul><ul><li>Here, hypoxemia occurs secondary to Hypercapnia ( remember the formula for A-a gradient . Alveolar Po2(PAo2) = {(713)Fio2 – Paco2/0.8}. So, your alveolar Po2 depends on your pco2. You are starting with a low alveolar po2 and as a result you will have low arterial po2  the A-a gradient as such, will not be significantly increased </li></ul>
  25. 26. Hypercapnic Respiratory Failure <ul><li>Management : </li></ul><ul><li>Oxygenation to maintain Pao2 > 60 i.e; sao2 >90 </li></ul><ul><li>Make sure not to over oxygenate COPD patients as you can precipitate severe co2 retention and there by, worsening respiratory failure. </li></ul><ul><li>Always, repeat blood gases after placing oxygen on COPD pt ( look for co2 retention and ph changes) </li></ul><ul><li>Ventilation </li></ul><ul><li># Try Non –invasive positive pressure ventilatory modes (NPPV) first if the patient is awake and alert ( Pressure support+PEEP; BIPAP, CPAP) and if there are no contraindications for NPPV (such as excessive secretions, uncooperativeness or acute ischemic changes on electrocardiography) </li></ul><ul><li># Intubation ( Invasive ventilation ) </li></ul><ul><li> if pt has altered mental status/ if ontraindications for NPPV are present </li></ul><ul><li>if non invasive modes fail </li></ul><ul><li>if Ph is too acidic ( Severe acute respiratory acidosis) </li></ul><ul><li># Always, repeat blood gases after ventilating a COPD pt  r/o posthypercapnic alkalosis  ( your ideal blood gas is the one without posthypercapnic alkalosis; so, do not overventilate or do not quickly drop co2 to less than baseline )  REMEMBER, alkalosis can inhibit respiratory drive and there by, makes it difficult to wean off a pt from the ventilator! </li></ul>
  26. 27. BIPAP <ul><li>A mode of NPPV. </li></ul><ul><li>Consists of IPAP+ EPAP ( Inspiratory positive airway pressure + expiratory positive airway pressure) </li></ul><ul><li>EPAP is usually equal to PEEP ( For eg: EPAP of 5 equals a PEEP of 5cm h20 on ventilator) </li></ul><ul><li>IPAP is equivalent to PEEP + Pressure support ( for eg: an IPAP of 13 with EPAP 5 is equal to a standard ventilatory setting of a pressure support of 8cmh20) </li></ul>
  27. 28. PEEP <ul><li>Helps in preventing normally occurring collapse of alveoli at the end of expiration i.e; keeps them open </li></ul><ul><li>Prevents recruitment – derecruitment injury </li></ul><ul><li>Helps both in oxygenation as well as in Ventilation </li></ul><ul><li>High PEEP  strategy used in ARDS </li></ul><ul><li>High PEEP can lead to barotrauma and pneumothorax </li></ul>
  28. 29. Case Study 1 <ul><li>A 58-year-old woman is evaluated because of increased dyspnea. Her exercise tolerance has been severely limited for years secondary to spinal scoliosis. She denies coughing or wheezing, and has never smoked. Her only previous surgery was Harrington rod spinal fixation at 18 years of age for scoliosis. On physical examination, she has marked spinal curvature and acral and labial cyanosis. Her heart rate is 110/min and respiration rate is 28/min. The lungs have scattered coarse crackles. The pulmonic component of the S2 is increased, there is persistent splitting of the S2, neck veins are distended, abdominojugular reflux is present, and there is dependent edema. Arterial blood gases with the patient breathing room air are PaO2, 33 mm Hg; PaCO2, 75 mm Hg; pH, 7.32; and bicarbonate, 37 meq/L. Spirometry shows severe restriction with markedly reduced maximum respiratory pressures. Chest radiography shows marked thoracic scoliosis and an enlarged heart with no pulmonary infiltrate. In addition to low-flow oxygen, which of the following initial interventions is most appropriate? </li></ul><ul><li>( A ) Pulmonary rehabilitation program </li></ul><ul><li>( B ) Furosemide, intravenously </li></ul><ul><li>( C ) Methylprednisolone and bronchodilators </li></ul><ul><li>( D ) Noninvasive mechanical ventilation </li></ul><ul><li>( E ) Nasotracheal intubation and mechanical ventilation </li></ul>
  29. 30. Case study 2 <ul><li>A 60-year-old man is hospitalized because of progressive dyspnea during the past month. He also has morning headache, poor sleep, and nightmares. He has a 45-pack-year smoking history, but no other medical problems. On physical examination, his body mass index is 32.7, heart rate is 105/min, respiration rate is 28/min and shallow, and blood pressure is 140/78 mm Hg. He is cyanotic and has paradoxical respiratory movements of his rib cage and abdomen. Expiratory wheezes, jugular venous distention, and moderate ankle edema are present. The remainder of the examination is normal. On pulse oximetry, oxygen saturation is 85%. Arterial blood gases are PO2, 42 mm Hg; PCO2, 55 mm Hg; pH, 7.33; and bicarbonate, 28 meq/L.Pulmonary function tests show forced expiratory volume in 1 sec (FEV1), 2.15 L (63% of predicted); forced vital capacity (FVC), 2.61 L (60% of predicted); FEV1/FVC, 82.6% (105% of predicted); total lung capacity (TLC), 5.49 L (85% of predicted); residual volume/total lung capacity (RV/TLC), 52% (163% of predicted); diffusing lung capacity for carbon monoxide (DLCO), 22.7 mL/sec/mm Hg (82% of predicted); maximum inspiratory pressure, 40 cm H2O (36% of predicted); and maximum expiratory pressure, 93 cm H2O (45% of predicted). Which of the following is the most likely cause of his respiratory failure? </li></ul><ul><li>( A ) Unilateral diaphragmatic paralysis </li></ul><ul><li>( B ) Chronic obstructive pulmonary disease </li></ul><ul><li>( C ) Idiopathic pulmonary fibrosis </li></ul><ul><li>( D ) Amyotrophic lateral sclerosis </li></ul><ul><li>( E ) Chronic thromboembolic pulmonary hypertension </li></ul>
  30. 31. Case Study 3 <ul><li>A 63-year-old woman is evaluated in the emergency department for a three-day history of increasing dyspnea. She is a former heavy smoker and has severe chronic obstructive pulmonary disease (COPD) requiring long-term oxygen therapy. Her baseline PaCO2 is 48 mm Hg. She has had increasing cough productive of yellowish phlegm but is expectorating without difficulty. She has no chest pain. </li></ul><ul><li>On physical examination, she is in moderate respiratory distress and using accessory muscles to breathe, but she is alert and cooperative. Her blood pressure is 144/82 mm Hg, her pulse rate is 122 beats/min and her respiration rate is 28 breaths/min. There is no jugular venous distention. Examination of the lungs reveals bilateral rhonchi and a prolonged expiratory phase. Heart sounds are distant, and the abdomen is soft without masses. She is not cyanotic (using oxygen at 4 L/min by nasal cannula), and she has 1+ pedal edema. Laboratory results show a hemoglobin level of 13 g/dL and a serum bicarbonate level of 31 meq/L. Arterial blood gases show a PO2 of 64 mm Hg, a PCO>2 of 56 mm Hg and a pH of 7.28. </li></ul><ul><li>Electrocardiography shows multifocal atrial tachycardia without acute ischemic changes. Respiratory treatments and intravenous corticosteroids and antibiotics are started. In addition to the supplemental oxygen and intravenous corticosteroids and antibiotics, which of the following would be most appropriate in the patient? </li></ul><ul><li>A. Close observation B. Continuous positive airway pressure (CPAP) C. Prompt intubation D. Noninvasive positive pressure ventilation (NPPV) </li></ul>
  31. 32. Ans. D <ul><li>This patient is the ideal candidate for NPPV. Numerous controlled trials as well as meta-analyses have demonstrated significant benefits of NPPV compared to standard therapy in such patients, including more rapid improvements in respiratory and heart rate, gas exchange, avoidance of intubation, reduced rates of morbidity and mortality and shorter hospital lengths of stay. The patient has the usual features of patients benefiting from NPPV in the studies, including moderate respiratory distress, use of accessory muscles, tachypnea, and acute-on-chronic carbon dioxide retention. She also has none of the contraindications, such as excessive secretions, uncooperativeness or acute ischemic changes on electrocardiography (the multifocal atrial tachycardia is not a problem as long as the patient is hemodynamically stable). </li></ul><ul><li>Close observation is not the most appropriate next step because, although she has roughly a 50% of responding to medical therapy, waiting to see if she worsens increases the likelihood of NPPV failure. CPAP alone has been shown to reduce work of breathing by counterbalancing auto-PEEP in patients with COPD, but is less effective at doing so than the combination of pressure support plus PEEP . </li></ul><ul><li>Intubation should be avoided in patients with COPD because of the increased morbidity and mortality associated with its use. </li></ul>
  32. 33. Key Points <ul><li>Noninvasive positive pressure ventilation in selected patients with moderate respiratory distress has been shown to improve heart and respiration rates and gas exchange and to reduce morbidity and mortality rates, the need for intubation, and the length of hospital stay. </li></ul><ul><li>Contraindications to noninvasive positive pressure ventilation in patients with moderate respiratory distress include excessive secretions, uncooperativeness and acute ischemic changes on electrocardiography. </li></ul>
  33. 34. Case Study 4 <ul><li>A 77-year-old man on chronic hemodialysis is evaluated in the emergency department for severe dyspnea. He is in respiratory distress, but is alert and responsive. His blood pressure is 216/92 mm Hg, his pulse rate is 122 beats/min and his respiration rate is 44 breaths/min. He is using accessory muscles to breathe. He has jugular venous distention; examination of the lungs reveals bilateral crackles, and cardiac examination reveals a summation gallop with a 3/6 systolic ejection murmur. There is no edema. Arterial blood gases on 50% oxygen by high-flow mask are a PO2 of 64 mm Hg, a PCO2 of 50 mm Hg and a pH of 7.24. Electrocardiography shows sinus tachycardia with nonspecific STT wave abnormalities, and chest radiograph is pending. He receives oxygen supplementation, nitroglycerin, furosemide and small doses of morphine, but remains very dyspneic. Which of the following interventions would most likely avoid intubation in this patient? </li></ul><ul><li>A. Increasing the dose of morphine; continue nitroglycerin and furosemide B. Starting noninvasive continuous positive airway pressure (4 cm H2O) C. Starting noninvasively administered pressure support (8 cm H2O) and positive end-expiratory pressure (4 cm H2O) D. Increase the FIO2 via face mask </li></ul>
  34. 35. Ans. C <ul><li>This patient presents with typical features of acute cardiogenic pulmonary edema. Randomized, controlled trials on such patients have demonstrated that both CPAP and NPPV more rapidly improve dyspnea, vital signs and gas exchange, and avoid intubation more effectively than oxygen therapy plus standard therapy. NPPV would be the preferred initial therapy to &quot;buy time&quot; until hemodialysis can be started. It is important to understand that bilevel ventilation using portable noninvasive devices and pressure support plus PEEP administered by a critical ventilator (used mainly in intubated patients) are essentially the same but use different terminology. With bilevel devices, the inspiratory pressure is the total inspiratory pressure, whereas with critical ventilators, the pressure support is added to the PEEP. Thus, a pressure support of 10 cm H2O and PEEP of 5 cm H2O using critical care ventilator terminology is the same as an inspiratory pressure (IPAP) of 15 cm H2O and expiratory pressure (EPAP) of 5 cm H2O using bilevel terminology. </li></ul><ul><li>A recent meta-analysis concluded that neither CPAP nor NPPV was superior to the other in patients with acute pulmonary edema, although some individual trials have suggested that NPPV can more rapidly reduce the sensation of dyspnea and improve gas exchange compared to CPAP alone. Thus, CPAP alone would be a reasonable choice here, except that a level of 4 cm H2O would be considered inadequate (10 to 12.5 cm H2O was used in the randomized studies). </li></ul><ul><li>Additional medical therapy or more supplemental oxygen would be unlikely to help much because the patient has not responded to adequate doses of medication and PAO2 is in an acceptable range. Furthermore, the patient is on chronic hemodialysis and the definitive therapy is emergent dialysis. </li></ul>
  35. 36. Key point In patients with cardiogenic pulmonary edema, continuous positive airway pressure (CPAP) and noninvasive positive pressure ventilation more rapidly improve dyspnea, vital signs and gas exchange, and avoid intubation more effectively than oxygen supplementation plus standard therapy.
  36. 37. Case Study 5 <ul><li>A 72-year-old man is hospitalized for gradually increasing dyspnea on exertion for the past several days. On the morning of admission, he develops marked dyspnea, associated with fever, chills and a nonproductive cough. He has no chest pain, and has taken only a ß-blocker for systemic hypertension. On admission to the intensive care unit, he is mildly disoriented and severely dyspneic. His blood pressure is 132/80 mm Hg, his pulse rate is 112 beats/min, his respiration rate is 40 breaths/min and his oxygen saturation is 85% on 100% oxygen by high-flow mask; he is using accessory muscles to breathe. There is no jugular venous distention; examination of the lungs reveals bilateral dry crackles, and cardiac examination reveals no murmur or gallop and a normal point of maximal intensity. There is no edema. Arterial blood gases are a PO2 of 52 mm Hg, a PCO2 of 44 mm Hg and a pH of 7.17. Chest radiograph shows bilateral interstitial infiltrates, which are new since a radiograph done 3 months ago, without cardiomegaly. Electrocardiography shows ST with nonspecific ST and T changes. Which of the following would be the most appropriate management for this patient? </li></ul><ul><li>A. CPAP (10 cm H2O) via full face mask B. Intubation with conventional mechanical ventilation C. Noninvasive ventilation using a full face mask with a pressure support (15 cm H2O) and positive end-expiratory pressure (5 cm H2O) D. Nonrebreather mask with 100% FIO2 </li></ul>
  37. 38. Ans. B <ul><li>This patient has a number of risk factors for noninvasive ventilation failure. In one study, odds ratios for failure were 3.75 if the patient had ARDS or severe community-acquired pneumonia, 2.51 if the PAO2/FIO2 ratio was less than 146 and 1.72 if the age was above 40 years. This patient has all three features. </li></ul><ul><li>Noninvasive ventilation is a consideration for patients like this one, with some studies demonstrating avoidance of intubation and infectious complications as well as reduced mortality. However, there is wide agreement that success rates are much lower than when NPPV is used to treat patients with COPD. </li></ul><ul><li>In this case, the poor prognostic factors combined with the mild disorientation and low pH shifts the balance in favor of prompt intubation. CPAP alone and a 100% nonrebreather mask would be less desirable choices because this patient’s PaCO2 is inappropriately high for the levels of hypoxemia and pH. He needs ventilatory assistance immediately. </li></ul>
  38. 39. Key Points <ul><li>Risk factors for noninvasive ventilatory failure include </li></ul><ul><li>the acute respiratory distress syndrome </li></ul><ul><li>severe community-acquired pneumonia </li></ul><ul><li>PAO2/FIO2 ratio less than 146 </li></ul><ul><li>age greater than 40 years. </li></ul>
  39. 40. Case Study 6 <ul><li>38-year-old woman with hypertriglyceridemia is admitted to the intensive care unit from the emergency department where she presented with the acute respiratory distress syndrome (ARDS) associated with severe acute pancreatitis and required intubation. Initially, her oxygenation had been adequate on an FIO2 of 60% and positive end-expiratory pressure (PEEP) of 7 cm H2O, but her oxygen saturation dropped to the low 80% level despite an increase in FIO2 to 100%.On physical examination, she is intubated and sedated. Examination of the lungs reveals diffuse crackles and rhonchi. Cardiac examination is normal except for tachycardia (heart rate, 112 beats/min). Her abdomen is very tender with diminished bowel sounds, and she has 2+ peripheral edema. A chest radiograph shows diffuse bilateral infiltrates. She is being ventilated with a &quot; lung protective strategy&quot; using an assist/control mode with a tidal volume of 6 mL/kg and plateau pressure of 25 cm H2O. Which of the following strategies for PEEP would be most appropriate for this patient? </li></ul><ul><li>A. PEEP should be increased in 2- to 3-cm H2O increments to lower FIO2 to at most 60%, if possible, and to maintain an arterial oxygen saturation of at least 88% and 95% or less B. PEEP should be set below the lower inflection point on a pressure volume curve of the lung C. PEEP should be set to correspond to the expiratory pressure that minimizes compliance of the lung D. PEEP should be at least 14 cm H2O and PEEP up to 20 cm H2O for FIO2 of 0.5 to 0.8 as long as cardiac output is monitored using a pulmonary artery catheter </li></ul>
  40. 41. Ans. A <ul><li>The best strategy for setting PEEP continues to be a matter of debate. Increasing PEEP in 2- to 3-cm H2O increments to lower FIO2 to 60%, if possible, and to maintain an arterial oxygen saturation of at least 88% and 95% or less is the strategy used by the ARDSnet and has been associated with improved outcomes when provided with a lung protective strategy. </li></ul><ul><li>In the ALVEOLI trial, the ARDSnet compared a lower to a higher PEEP strategy to treat ARDS. No differences in major outcome variables were detectible between the two strategies, including hospital mortality, ventilator-free days and barotrauma. Therefore, there is no apparent advantage to the higher PEEP strategy, at least as used in the ARDSnet trial, and the risk of barotrauma and increasing the plateau pressure to more than 30 cm H2O are theoretically higher than in the lower PEEP strategy. Furthermore, there is no indication for a pulmonary artery catheter when PEEP is used. </li></ul><ul><li>Use of the lower inflection point (thought to correspond to the opening of many alveoli) has been advocated to set PEEP, but no evidence shows it to be superior to other methods. Furthermore, lower inflection points may be hard to identify precisely, and the level chosen should be above, not below, the inflection point. </li></ul><ul><li>Thirty years ago, the expiratory pressure that optimizes lung compliance was proposed as the best PEEP. This may be easier and safer to determine than the lower inflection point, but that option is incorrect in this case because using this approach, PEEP should be set to maximize lung compliance, not minimize it. </li></ul><ul><li>LOW VT STRATEGY  VT OF < 6 CC/KG  LUNG PROTECTIVE STRATEGY FOR ARDS </li></ul>
  41. 42. Key Point In patients with acute lung injury/acute respiratory distress syndrome on mechanical ventilation with a lung protective strategy, positive end-expiratory pressure should be increased in 2- to 3-cm H2O increments to lower FIO2 to 60%, if possible, and to maintain an arterial oxygen saturation of at least 88% and 95% or less.
  42. 43. Case Study 7 <ul><li>A 23-year-old man with Duchenne muscular dystrophy is evaluated in the emergency department for difficulty clearing secretions and episodic feelings of asphyxiation. The patient has been using NPPV at home for the past two years. For eight hours a night, he has been using a &quot;bilevel&quot; portable positive pressure device at pressures of 16 cm H2O inspiratory, 4 cm H2O expiratory and a backup rate of 15, delivered via a nasal mask. His most recent forced vital capacity was 540 mL (14% of predicted), and daytime arterial blood gases obtained while he was sitting breathing room air revealed a PO2 of 82 mm Hg, a PCO2 of 48 mm Hg and a pH of 7.42. He felt well until three days ago when he developed a sore throat and nasal congestion. For the past two days, he began coughing more. On physical examination, he is afebrile, but his respiration rate is 32 breaths/min. He has crackles at both lung bases, and a very weak cough. Chest radiograph shows some basilar atelectasis. His arterial blood gas on 2 L/min of oxygen by nasal cannula reveals a PO2 of 86 mm Hg, a PCO2 of 48 mm Hg and a pH of 7.39. A decision is made to admit the patient to the intensive care unit. </li></ul><ul><li>Which of the following should be included in this patient’s management? </li></ul><ul><li>A. Antibiotic therapy with ampicillin/sulbactam and gentamicin B. Prompt endotracheal intubation C. Techniques to assist cough D. Therapy with intravenous theophylline </li></ul>
  43. 44. Ans.C <ul><li>Patients with chronic respiratory failure due to neuromuscular disease must be treated with extreme caution when they develop upper respiratory tract infections that cause chest congestion. Their risk for secretion retention is determined by the severity of cough impairment. In order to cough effectively, these patients must have an adequate inspiratory capacity and preserved expiratory muscle and bulbar function. During cough, a deep inspiration allows for sufficient expiratory volume and takes advantage of lung elasticity. Expiratory muscles then compress the air against a closed glottis that abruptly opens to permit an explosive release that mobilizes secretions. In patients with advanced Duchenne muscular dystrophy, inspiratory capacity is too small for an adequate cough. Also, even though bulbar involvement is usually minimal, expiratory muscles cannot sufficiently compress expired gas. Therefore, despite the stable arterial blood gases, this patient is at very high risk of secretion retention that could prove fatal. </li></ul><ul><li>Such patients should be placed on round-the-clock NPPV, and provision of cough assistance is imperative. Manually assisted coughing, consisting of a modified Heimlich maneuver timed with the patient’s attempts at coughing, and the cough insufflator-exsufflator should be used to enhance airflow during cough. The latter device administers a deep breath via a mask and then abruptly switches to a negative pressure to enhance expiratory flow and simulate a cough. Randomized, controlled trials of these approaches are lacking, but a historically controlled series indicates that patients managed in this manner can avoid intubation and return to their previous regimen of nocturnal nasal ventilation within a few weeks. It is possible to manage such patients at home as long as family and caregivers are adequately trained and willing. If the patient is hospitalized, intensive care unit admission is necessary because regular wards would be insufficient to provide the requisite level of pulmonary care. </li></ul><ul><li>Although the patient should be treated with antibiotics, ampicillin/sulbactam and gentamicin are the wrong antibiotic choice for a community-acquired respiratory infection, which should include coverage for atypical organisms. Also, although the patient could need intubation eventually, the lack of blood gas deterioration justifies holding off to see if noninvasive approaches will be successful. Theophylline is a bronchodilator and strengthens weakened respiratory muscles, but it also often causes adverse gastrointestinal side effects and there is no evidence that it is likely to help in this situation </li></ul>
  44. 45. Acute Coronary Syndrome <ul><li>Will be discussed in detail in Cardiology section. </li></ul>
  45. 46. Acid – Base/ Electrolytes <ul><li>Refer Nephrology </li></ul><ul><li>Electrolytes  hyper/hyponatremia, hyper/hypokalemia, hyper/hypocalcemia  will be discussed in detail in Nephrology. </li></ul>
  46. 47. GI Bleeding <ul><li>Refer Gastroenterology section </li></ul>
  47. 48. Neurological Emergencies <ul><li>Status Epliepticus </li></ul><ul><li>Ischemic Stroke  Thrombolytic therapy </li></ul><ul><li>Hemorrhagic Stroke  Intracerebral, Cerebellar hemorrhage </li></ul><ul><li>Cord Compression  Urgent management </li></ul><ul><li>Head Injury  Extracerebral ( Subdural, Epidural Hemorrhage) </li></ul><ul><li>Subarachnoid Hemorrhage </li></ul><ul><li>Spinal Cord Hemorrhage </li></ul><ul><li>Spinal Cord Infarction </li></ul><ul><li> All discussed in detail in NEUROLOGY </li></ul>