A 62 year-old male with a history of hepatitis C cirrhosis complicated by hepatocellular carcinoma s/p radiofrequency ablation presenting after referral from hepatology clinic for hyponatremia. One week ago, the patient developed abdominal distension and shortness of breath that resolved after large-volume paracentesis and was started on furosemide 40mg p.o. daily and aldactone 100mg p.o. daily. After initiating diuretics, the patient noted worsening lower extremity edema, and increased thirst/fluid intake.

He reports two days of fatigue and intermittent confusion supported by family members who reported slowed speech. He otherwise denies abdominal pain, distension, nausea/vomiting, diarrhea/constipation, chest pain or shortness of breath. In the ED, the patient received 1L NS bolus.

Physical Exam:

Labs/Studies:

• BMP (admission): 112/5.6/88/22/28/1.1/97
• BMP (+10h): 118/5.4/93/23/26/1.0/133
• sOsm: 264
• Urine: Na <20, K 26, Osm 453
• BNP: 40
• AST/ALT/AP/TB/Alb: 74/57/91/2.4/2.2

Assessment/Plan:

62M with HepC cirrhosis, with e/o decompensation (new-onset ascites) and hyponatremia.

1. #Hyponatremia: Sodium 114, likely chronic, patient currently asymptomatic without concerning findings on neurological exam. Clinical findings suggestive of hypervolemic hyponatremia 2/2 decompensated cirrhosis resulting in decreased effective arterial blood volume and volume retention. However, the recent initiation of diuretics, mild AKI and early response to isotonic fluids in the ED suggests possible hypovolemic component.
   • 1L fluid restriction
   • q.4.h. sodium check, goal increase of 8mEq per 24h
   • hold diuretics
2. #Hyperkalemia: Potassium 5.6, asymptomatic, AKI vs. medication-induced (aldactone). Continue monitoring.
3. #AKI: Elevated creatinine 1.1 from baseline 0.7. Likely pre-renal given recent initiation of diuretics. Consider hepatorenal syndrome given decompensated cirrhosis. Follow-up repeat creatinine after 1L NS bolus in ED.
4. #Hepatitis C: decompensated with new-onset ascites. No e/o encephalopathy, continue home rifaximin.

Physiology of Hyponatremia: ^1,2,3,4

Differential Diagnosis of Hyponatremia: ⁵

Evaluation of Hyponatremia: ²

1. Identification of onset (acute vs. chronic)
2. Presence of symptoms (HA, nausea, confusion, seizures)
3. Assessment of volume status (edema, JVD, skin turgor, postural BP)
4. Medical history (cardiac, liver, renal disease), drug history

References:

1. Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatremia: a little physiology goes a long way. Cleve Clin J Med. 2004;71(8):639–650.
2. Biswas M, Davies JS. Hyponatraemia in clinical practice. Postgrad Med J. 2007;83(980):373–378. doi:10.1136/pgmj.2006.056515.
3. Adrogué HJ, Madias NE. Hyponatremia. N. Engl. J. Med. 2000;342(21):1581–1589. doi:10.1056/NEJM200005253422107.
4. Marx JA, Hockberger RS, Walls RM, Adams JG. Rosen’s emergency medicine: concepts and clinical practice. 2010;1.
5. Milionis HJ, Liamis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ. 2002;166(8):1056–1062.

The post Hyponatremia appeared first on Differential Diagnosis of.

A 62 year-old female with a history of hypertension, diabetes and coronary artery disease is brought to the emergency department with altered mental status. The patient is confused and unable to provide history. Her family note that symptoms have been gradually worsening for the past one day and she had previously been in her usual state of good health. There was no history of recent illness, medication changes, recreational substance use, sick contacts, or travel.

On evaluation, vital signs were notable for hypertension (224/120mmHg, comparable on all extremities) though otherwise normal including afebrile core temperature – capillary glucose was 114mg/dL. On examination, the patient was awake and alert, making coordinated movements symmetrically in all four extremities without hyperreflexia or increased tone. Speech was unintelligible and the patient was unable to follow simple commands.

Labs/Imaging

Laboratory tests were notable for a serum creatinine of 1.2mg/dL (baseline unknown) but otherwise normal including CBC, troponin, TSH, and UA. ECG demonstrated left ventricular hypertrophy without acute ischemic changes. Imaging including chest radiograph and CT head non-contrast and CTA brain/neck were normal. Lumbar puncture was performed and CSF was normal.

Hospital Course

The patient was initiated on a continuous infusion of nicardipine for presumed hypertensive encephalopathy and admitted to the medical intensive care unit. An MRI was performed on hospital day 1 and demonstrated chronic microvascular ischemic changes. The patient’s mental status gradually improved over the course of her hospitalization and she was discharged home on hospital day 4.

An Algorithm for the Evaluation and Management of Hypertensive Emergencies

References

General

1. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2017 Focused Update of the 2016 ACC Expert Consensus Decision Pathway on the Role of Non-Statin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. In: Vol 70. 2017:1785-1822. doi:10.1016/j.jacc.2017.07.745.
2. Janke AT, McNaughton CD, Brody AM, Welch RD, Levy PD. Trends in the Incidence of Hypertensive Emergencies in US Emergency Departments From 2006 to 2013. J Am Heart Assoc. 2016;5(12). doi:10.1161/JAHA.116.004511.
3. Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiology in Review. 2010;18(2):102-107. doi:10.1097/CRD.0b013e3181c307b7.
4. Katz JN, Gore JM, Amin A, et al. Practice patterns, outcomes, and end-organ dysfunction for patients with acute severe hypertension: the Studying the Treatment of Acute hyperTension (STAT) registry. Am Heart J. 2009;158(4):599–606.e1. doi:10.1016/j.ahj.2009.07.020.
5. Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48(5):316-325. doi:10.1016/j.pcad.2006.02.004.
6. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. 2006;24(1):135-146. doi:10.1016/j.ccl.2005.09.002.
7. Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003;7(5):374-384. doi:10.1186/cc2351.
8. Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. YMEM. 2003;41(4):513-529. doi:10.1067/mem.2003.114.
9. Vaughan CJ, Delanty N. Hypertensive emergencies. The Lancet. 2000;356(9227):411-417. doi:10.1016/S0140-6736(00)02539-3.

Ischemic Stroke

1. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2018;49(3):e46-e110. doi:10.1161/STR.0000000000000158.

Hemorrhagic Stroke

1. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060. doi:10.1161/STR.0000000000000069.

Subarachnoid Hemorrhage

1. Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737. doi:10.1161/STR.0b013e3182587839.

Renal

1. Gillies MA, Kakar V, Parker RJ, Honoré PM, Ostermann M. Fenoldopam to prevent acute kidney injury after major surgery-a systematic review and meta-analysis. Crit Care. 2015;19(1):449. doi:10.1186/s13054-015-1166-4.
2. Tumlin JA, Dunbar LM, Oparil S, et al. Fenoldopam, a dopamine agonist, for hypertensive emergency: a multicenter randomized trial. Fenoldopam Study Group. Academic Emergency Medicine. 2000;7(6):653-662.
3. Shusterman NH, Elliott WJ, White WB. Fenoldopam, but not nitroprusside, improves renal function in severely hypertensive patients with impaired renal function. Am J Med. 1993;95(2):161-168.

Aortic Disease

1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13):e266-e369. doi:10.1161/CIR.0b013e3181d4739e.

Pregnancy

1. Townsend R, O’Brien P, Khalil A. Current best practice in the management of hypertensive disorders in pregnancy. Integr Blood Press Control. 2016;9:79-94. doi:10.2147/IBPC.S77344.
2. Al-Safi Z, Imudia AN, Filetti LC, Hobson DT, Bahado-Singh RO, Awonuga AO. Delayed Postpartum Preeclampsia and Eclampsia. Obstet Gynecol. 2011;118(5):1102-1107. doi:10.1097/AOG.0b013e318231934c.
3. Hypertension in pregnancy: diagnosis and management. National Institute for Health and Care Excellence. https://www.nice.org.uk/guidance/cg107. Published August 1, 2010. Accessed May 20, 2019.

The post Hypertensive Emergency appeared first on Differential Diagnosis of.

Endotracheal Tube Size^1-3

Simplified Formula

Estimated gestational age in weeks ÷ 10 = round to nearest half-size uncuffed tube

NRP Recommendation

Laryngoscope Blade Size

Umbilical Vein Catheter Placement⁴

ED Indications

Unstable neonate

Contraindications

Omphalocele

Gastroschisis

Necrotizing enterocolitis

Depth

4-5cm or until blood return (for emergent placement)

Umbilical artery/vein catheter position on plain radiograph.

Umbilical catheter size

Umbilical catheter positioning on plain radiographs

Umbilical venous catheter position can be verified with a plain radiograph. Positioning within the umbilical vein can be confirmed by tracing a cephalad trajectory from the insertion point at the umbilicus. An umbilical artery catheter will first pass caudally into the internal iliac artery before travelling cephalad into a common iliac artery and the abdominal aorta.

Medications⁵

Neonatal Physiology and Transition to Extrauterine Life⁶

An important principle in neonatal resuscitation is supporting the appropriate transition from intra- to extra-uterine life which is dependent on several key anatomic and physiologic changes occurring in an optimal environment.

Anatomy⁷

Fetal Circulation

In the fetal circulatory system, oxygenated blood is delivered via the umbilical vein, entering the inferior vena cava via the ductus venosus. The majority of this oxygenated blood passes through the right atrium and into the left atrium through the foramen ovale to enter the systemic circulation.

Meanwhile, high pulmonary pulmonary vascular resistance (due to hypoxic vasoconstriction in fluid-filled alveoli) means that most of the deoxygenated right ventricular output is routed through the ductus arteriosus and enters into the systemic circulation – mixing with oxygenated blood distal to the highest priority end-organs (brain and heart), to be reoxygenated at the placenta.

Post-transition Circulation

The transition to extra-uterine life involves several key steps detailed below and is supported by appropriate ventilation, oxygenation and temperature regulation.

1. Alveolar Fluid Clearance
   Catecholamine and hormone changes (predominantly corticosteroids) during the process of labor induce changes in enzymatic expression that result in the resorption of alveolar fluid into the interstitial space. At the time of delivery, negative intra-thoracic pressure from inspiration further promotes the resorption of alveolar fluid. Mechanical thoracic compression from delivery may also contribute.
2. Respiration and Breathing
   Disconnection from the placenta ceases the transfer of placenta-derived factors including prostaglandins. The withdrawal of tonic inhibition of central respiratory drive from prostaglandins with cord clamping stimulates rhythmic breathing. The infant’s initial breaths and resultant lung expansion promotes alveolar expansion and stimulates surfactant production – this decreases alveolar surface tension, increases lung compliance and further facilitates breathing.
3. Circulatory Changes
   At delivery, clamping the umbilical cord removes a large bed of low-resistance circulation, increasing systemic vascular resistance and systemic blood pressure. At the same time, lung expansion and alveolar aeration decreases pulmonary vascular resistance and pulmonary arterial pressures. At the ductus arteriosus, increased systemic vascular resistance combined with decreased pulmonary vascular resistance decreases shunting and contributes to closure. Similarly, as left atrial pressure approaches and exceeds right atrial pressure, right-to-left flow across the foramen ovale ceases. Collectively, these changes serve to effectively separate the left- and right-sided circulations.

NRP Resuscitation Algorithm^5,8

References

1. Luten R, Kahn N, Wears R, Kissoon N. Predicting Endotracheal Tube Size by Length in Newborns. J Emerg Med. 2007;32(4):343-347. doi:10.1016/j.jemermed.2007.02.035.
2. Peterson J, Johnson N, Deakins K, Wilson-Costello D, Jelovsek JE, Chatburn R. Accuracy of the 7-8-9 Rule for endotracheal tube placement in the neonate. J Perinatol. 2006;26(6):333-336. doi:10.1038/sj.jp.7211503.
3. Kempley ST, Moreiras JW, Petrone FL. Endotracheal tube length for neonatal intubation. Resuscitation. 2008;77(3):369-373. doi:10.1016/j.resuscitation.2008.02.002.
4. Anderson J, Leonard D, Braner DAV, Lai S, Tegtmeyer K. Videos in Clinical Medicine. Umbilical Vascular Catheterization. Vol 359. 2008:e18. doi:10.1056/NEJMvcm0800666.
5. Association AAOPAAH. Textbook of Neonatal Resuscitation. 2016.
6. Caraciolo J Fernandes MD. Physiologic transition from intrauterine to extrauterine life. UpToDate.
7. Sadler TW. Langman’s Medical Embryology. Lippincott Williams & Wilkins; 2011.
8. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 7: Neonatal Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. In: Vol 132. American Heart Association, Inc.; 2015:S204-S241. doi:10.1161/CIR.0000000000000276.

The post Principles of Neonatal Resuscitation appeared first on Differential Diagnosis of.

A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.

Imaging

Algorithm for the Evaluation of Hypotension¹

This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.

1. The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
2. The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
3. If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
4. Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
5. Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.

Guided Lecture

Watch “The Transiently Hypotensive Patient: Who Cares?” from EM Ed. In this lecture Dr. Basrai reviews the diagnostic pathway for a patient who presents with transient hypotension.

References

1. Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.

The post Hypotension appeared first on Differential Diagnosis of.

Tachycardia

Bradycardia

References

1. Hazinski, M., Samson, R., & Schexnayder, S. (Eds.). (2010). 2010 Handbook of Emergency Cardiovascular Care for Healthcare Providers. Dallas, TX: American Heart Association.
2. WikEM: Adult pulseless arrest
3. WikEM: ACLS: Tachycardia
4. WikEM: ACLS: Bradycardia

The post Simplified ACLS Algorithms appeared first on Differential Diagnosis of.

34 year-old male brought in by ambulance s/p assault. Field GCS reportedly 7, in trauma bay assessed as E2-V4-M6. Witnessed seizure in CT scanner, resolved with lorazepam. Intubated for airway protection, underwent external ventricular drain placement and transferred to surgical ICU.

Initial imaging revealed bifrontal subdural hematomas and right temporal hemorrhagic contusion with generalized edema. Repeat imaging one hour later showed interval development of large extra-axial hemorrhage overlying the right occipital and parietal lobes (2.2cm), representing subdural or epidural hematoma.

The patient’s ICU course was complicated by continued seizures and refractory elevation in intracranial pressure. A pentobarbital infusion was started and titrated to adequate burst suppression and hyperosmolar therapy with both mannitol and hypertonic saline continued. Additional imaging revealed stable hemorrhage but continued diffuse cerebral edema evidenced by sulcal effacement.

On hospital day 5, examination revealed bilateral fixed and dilated pupils. Imaging revealed effacement of basilar cisterns, pre-pontine cistern, and cisterna magna suggestive of impending/ongoing transtentorial and tonsillar herniation. Pentobarbital was weaned and conventional cerebral angiography as well as cerebral perfusion studies were consistent with brain death.

Images

Algorithm for the Management of Severe Traumatic Brain Injury^1,2

References

1. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney, N. A., & Ghajar, J. (2007). Guidelines for the management of severe traumatic brain injury. Introduction. Journal of neurotrauma, 24 Suppl 1, S1–2. doi:10.1089/neu.2007.9997
2. Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
3. WikEM: Severe traumatic brain injury

The post Severe Traumatic Brain Injury appeared first on Differential Diagnosis of.

Differential Diagnosis and Evaluation of Hyponatremia

Differential Diagnosis and Evaluation of Hypernatremia

Differential Diagnosis and Evaluation of Hypokalemia

Differential Diagnosis of Hyperkalemia

Differential Diagnosis of Hypo and Hypercalcemia

Differential Diagnosis of Hypo and Hypermagnesemia

Differential Diagnosis of Hypo and Hyperphosphatemia

References:

1. Marino, P. (2014). Marino’s the ICU book. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
2. Fulop, M. (1998). Algorithms for diagnosing some electrolyte disorders. American Journal of Emergency Medicine, 16(1), 76–84.
3. WikEM: Hypokalemia
4. WikEM: Hyponatremia

The post Electrolyte Abnormalities appeared first on Differential Diagnosis of.

25M with a history of mild asthma transferred from an outside hospital after 10 days in the intensive care unit for continued management of ARDS.

The patient was well until one week prior to admission when he developed intermittent subjective fevers and general malaise associated with a non-productive cough and nausea/vomiting. He presented to the emergency department of an outside hospital with difficulty breathing and was noted to have respiratory distress and was subsequently admitted. Initial CT at the outside hospital revealed pneumomediastinum but no evidence of pulmonary embolism. Results from the outside hospital reveal a wide array of bacterial/fungal cultures and viral serologies including bronchoscopy but no obvious infectious source. The patient was treated with broad spectrum antibiotics for several days but his condition worsened requiring intubation, mechanical ventilation and transfer to the ICU. Further imaging was suggestive of ARDS, and the patient was transferred for additional management.

The patient was well until one week prior to admission when he reported development of malaise and fatigue. On the day of hospitalization, the patient presented to primary care doctor with complaint of cough and shortness of breath and was found to be in respiratory distress and was admitted. The patient received IV antibiotics (cefepime, vancomycin) and was intubated when respiratory distress worsened. Found to have evidence of ARDS on CXR.

Physical Exam:

Labs/Studies:

• CBC: 25.06/7.0/21.3/426
• BMP: 132/3.3/88/32/18/1.1/103
• ABG: 7.30/97/76/18
• Blood/sputum/urine cultures: Negative
• Aspergillus, crypto, cocci: Negative
• EBV, HIV, influenza, RSV: Negative

Imaging

Assessment/Plan:

25M with ARDS transferred from outside hospital for further management.
# ARDS: Severe (P/F ratio <100). Etiology unclear, thorough infectious workup without obvious source. Consider autoimmune or allergic cause.

• Ventilator: PRVC lung-protective ventilation
• Consider NMB for dyssynchrony despite sedation
• Monitor strict I/O, maintain net negative fluid balance.

# Sepsis: Leukocytosis, tachycardia. Continue broad-spectrum antibiotics and monitor cultures.
# Acidosis: Largely respiratory, place dialysis catheter if acute need arises.
# Pneumomediastinum: Possible Boerhaave syndrome given reports of nausea/vomiting.

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):¹

ARDS represents a stereotyped response to multiple insults. It is characterized by damaged capillary endothelium and alveolar epithelium resulting in increased permeability and the accumulation of fluid in the alveolar space. This causes diffuse alveolar damage and triggers the release of various cytokines (TNF, IL-1, IL-6) which recruit and activate neutrophils causing oxidative cell damage.

Definition of ARDS (Berlin):^2,3

Causes of ARDS:^2,4

An Introduction to Mechanical Ventilation:^5,6,7

This is a simplification of the general principles underlying the most common ventilator modes. For more detail, see the articles cited in the references.

Breath Sequences:

Continuous Mandatory Ventilation (CMV)

All breaths controlled by ventilator, no triggered breaths.

Assist-Control Ventilation (AC)

Every patient-triggered breath is fully supported, a backup rate is set. In the absence of patient-triggered breaths, AC acts like CMV.

Synchronized Intermittent Mandatory Ventilation (SIMV)

Preset minimum mandatory breaths are “synchronized” to patient’s efforts. The patient is allowed to breathe spontaneously between supported breaths.

Pressure Support (PS)

All breaths are triggered by the patient and each is supported by preset pressure.

Continuous Positive Airway Pressure (CPAP)

Spontaneous breathing at elevated baseline pressure.

Control Variables:

Volume Control (VC)

Volume Control (VC)

Volume is set, pressure is variable. With a drop in compliance, the preset minimum volume is maintained with an increase in pressure.

Pressure Control (PC)

Pressure Control (PC)

Pressure is set, volume is variable. With a drop in compliance, a smaller volume is delivered to maintain pressures at the preset limit.

Pressure-Regulated Volume Control (PRVC)

Pressure-Regulated Volume Control (PRVC)

Pressure is targeted with a set minimum volume. The ventilator makes breath-to-breath adjustments of pressure to maintain minimum volumes. Breath mechanics are therefore comparable to pressure-control as a defined pressure is delivered based on prior breath’s respiratory mechanics (note pressure and flow tracings for PRVC/PC vs. VC)

References:

1. Pierrakos C, Karanikolas M, Scolletta S, Karamouzos V, Velissaris D. Acute respiratory distress syndrome: pathophysiology and therapeutic options. J Clin Med Res. 2012;4(1):7–16. doi:10.4021/jocmr761w.
2. Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5(3):326–334. doi:10.3978/j.issn.2072-1439.2013.04.05.
3. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition. In: Vol 307. 2012:2526–2533. doi:10.1001/jama.2012.5669.
4. Ware LB, Matthay MA. The acute respiratory distress syndrome. N. Engl. J. Med. 2000;342(18):1334–1349. doi:10.1056/NEJM200005043421806.
5. Deng, J. (10/20/13). Principles of Mechanical Ventilation. Medical Intensive Care Unit Lecture. Los Angeles, CA.
6. Singer BD, Corbridge TC. Basic invasive mechanical ventilation. South. Med. J. 2009;102(12):1238–1245. doi:10.1097/SMJ.0b013e3181bfac4f.
7. Hamed HMF, Ibrahim HG, Khater YH, Aziz ES. Ventilation and ventilators in the ICU: What every intensivist must know. Current Anaesthesia & Critical Care. 2006;17(1-2):77–83. doi:10.1016/j.cacc.2006.07.008.

The post Acute Respiratory Distress Syndrome appeared first on Differential Diagnosis of.