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Critical Care Board Review

Critical Care Board Review. Pulmonary and Critical Care. Normal Pulmonary Physiology. The upright lung can then be divided into 3 zones: Zone 1: (apex) the pulmonary artery pressure is less than the alveolar pressure and therefore there is essentially no blood flow – P A > P a > P v

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Critical Care Board Review

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  1. Critical Care Board Review Pulmonary and Critical Care

  2. Normal Pulmonary Physiology • The upright lung can then be divided into 3 zones: • Zone 1: (apex) the pulmonary artery pressure is less than the alveolar pressure and therefore there is essentially no blood flow – PA > Pa > Pv • Zone 2: (middle part of the lungs) the pulmonary artery pressure is greater than the alveolar pressure, which in turn is greater than the pulmonary venous pressure. In this zone, the blood flow is due to the difference between pulmonary arterial pressure and alveolar pressure - Pa > PA > Pv • Zone 3: (base) the venous pressure exceeds alveolar pressure which results in the distension of capillaries. In this zone, a small increase in venous pressure can cause pulmonary edema - Pa > Pv > PA

  3. Normal Pulmonary Physiology • Boundaries between zones are not fixed and depend on physiologic conditions • ie. low cardiac output, positive pressure ventilation, proning • In normal persons, there is no zone 1 • Ideally, PCWP measurements should be done in Zone 3

  4. Respiratory Failure • Type I • Acute hypoxemic respiratory failure • Inability to provide adequate oxygen to the blood and tissues • Type II • Ventilatory failure • Failure of alveolar ventilation leading to a rising CO2 and a falling PaO2 • Type III • Mixed I and II

  5. Type I • Results when enough disease causing collapse, alveolar filling, or both occurs leading to an effective shunt • Will present with marked dyspnea and tachypnea • Can be divided into diffuse and focal diseases

  6. Diffuse Lung Lesions (Producing Pulmonary Edema) • Cardiogenic or increased-pressure edema  • Left-ventricular (LV) failure     • Acute LV ischemia     • Accelerated or malignant hypertension     • Mitral regurgitation     • Volume overload, particularly with coexisting renal and cardiac disease • Increased permeability or low-pressure edema (ARDS) • Sepsis and sepsis syndrome         • Mitral stenosis  • Acid aspiration         • Multiple transfusions for hypovolemic shock   • Near-drowning        •  Pancreatitis         • Air or fat emboli        • Cardiopulmonary bypass         • Pneumonia         • Drug reaction or overdose           • Inhalation injury         • Infusion of biologics (e.g., interleukin 2)        • Ischemia-reperfusion (e.g., postthrombectomy, posttransplantation) • Edema of unclear or "mixed" origin • Reexpansion     • Neurogenic     • Postictal     • Tocolysis-associated • Diffuse alveolar hemorrhage    • Microscopic angiitis     • Collagen vascular diseases     • Goodpasture's syndrome     • Severe coagulopathy and bone marrow transplantation    • Retinoic acid syndrome • Focal Lung Lesions • Lobar pneumonia • Lung contusion • Lobar atelectasis (acutely

  7. Type II • 3 underlying causes: • depressed respiratory drive (CNS) • neuromuscular incompetence • excessive respiratory work load • Consequences • Hypoxemia • PAO2 = FiO2(760 -47) – PaCO2/RQ • Acidemia • If HCO3 = 24, then pH decreases .08 for ever rise in CO2 by 10 • Effects – depression of cardiac and respiratory muscle contractility, arterial vasodilation, increased cerebral blood flow

  8. ALI/ARDS • 1st American and European Consensus Conference report in 1993 standardized the definition of ALI and ARDS: • ALI PaO2/FiO2 < 300 • ARDS PaO2/FiO2 < 200 • Bilateral chest infiltrates • PCWP < 18

  9. ALI/ARDS • Characterized by diffuse alveolar damage • Inflammatory cytokines and toxic mediators damage capillary-alveolar membranes • Disruption normal protective barrier results in alveolar filling with protein rich edema and hyaline membranes • Mortality 35-40% • Sepsis most common cause

  10. ALI/ARDS Causes • Increased permeability or low-pressure edema • Sepsis and sepsis syndrome         • Mitral stenosis  • Acid aspiration         • Multiple transfusions for hypovolemic shock   • Near-drowning        • Pancreatitis         • Air or fat emboli        • Cardiopulmonary bypass         • Pneumonia         • Drug reaction or overdose           • Inhalation injury         • Infusion of biologics (e.g., interleukin 2)        • Ischemia-reperfusion (e.g., postthrombectomy, posttransplantation) • Edema of unclear or "mixed" origin • Reexpansion     • Neurogenic     • Postictal     • Tocolysis-associated

  11. ALI/ARDS • Treatment consists of supportive care while reversing the underlying cause • Most patients require mechanical ventilation to support oxygenation and ventilation • Goal of ventilatory support is “lung protective strategies” to prevent barotrauma and alveolar distension • Low tidal volume ventilation +/- permissive hyperCO2 • Use of PEEP to improve oxygenation and prevent cyclical atelectasis

  12. ALI/ARDS • Low tidal volume ventilation • ARDSnet trial • 861 patients • Randomized to TV 6ml/kg ideal body weight and goal plat pressure <30 cmH2O versus 12ml/kg and plat pressure <50 • Study stopped early when significant mortality benefit in low TV group (31 vs 40%)

  13. ALI/ARDS • PEEP • Allows adequate oxygenation with lower fractions of inhaled oxygen • Improves oxygenation by preventing de-recruitment of alveoli thereby improving V/Q mismatch • Optimal PEEP varies from patient to patient and is unknown

  14. PEEP • Side effects • Overdistension of more normal areas of lung • Can result in barotrauma • Hypotension due to increased intrathoracic pressure and reduced venous return (preload) • Elevates ICP? (theoretical)

  15. Intrinsic PEEP (auto PEEP) • Patients with COPD often have elevated end expiratory pressure in the alveoli unlike normal patients in whom the end-expiratory pressure is usually zero • This elevated end-expiratory pressure is known as intrinsic PEEP or auto PEEP.

  16. Intrinsic PEEP • Intrinsic PEEP results in: • Decreased cardiac output due to increased intrathoracic pressure • Increased work of breathing • when the patient initiates a spontaneous breath while on the ventilator the patient has to generate an equal amount of negative pressure to overcome the positive intrinsic (auto) PEEP before pulmonary airflow can be initiated

  17. Intrinsic PEEP • In patients on ventilator, this intrinsic PEEP may be difficult to recognize unless the expiratory circuit on the ventilator is occluded at the end of expiration • When this is done, the pressure in the ventilator circuit and the lungs will equilibrate and hence, the ventilator manometer will display the amount of intrinsic PEEP.

  18. Intrinsic PEEP • Ways to correct auto PEEP: • Prolong the expiratory time • Increase inspiratory flow rate • Lower respiratory rate • Lower tidal volume • Treat the obstruction • Bronchodilators • Steroids • Disconnect from the ventilator

  19. Hemodynamic Monitoring • PA catheters provide capability to obtain direct measurements of central venous, right sided cardiac, pulmonary artery, and pulmonary capillary wedge pressure; thermodilution CO; mixed venous saturation • Controversial due to lack of any study demonstrating improved clinical outcome • Any decision to insert a Swan-Ganz catheter for monitoring must be carefully weighed against the potential risk of complications.

  20. Hemodynamic Monitoring • PA catheter indications: • Differentiation of shock • Determination of cardio- vs. noncardiogenic pulmonary edema • Evaluate pulmonary HTN • Diagnose tamponade • Diagnose intracardiac shunt • Periop management of complicated cardiac patients • Guide to pressor usage • Guide to nonpharmacologic management

  21. Hemodynamic Monitoring • PA catheter complications: • Trauma to heart or vessels during insertion • Dysrhythmias • Knotting • PA rupture due to “overwedging” • Pulmonary infarct • Thrombosis • Infection

  22. Hemodynamic Monitoring • Normal: 0-7 • Elevated RA: • RV infarct • Volume overload • Pulmonary HTN • R sided valve disease • L to R shunts • Cannon a’s: • AV dissociation • Cannon v’s: • TR

  23. Hemodynamic Monitoring • Normal: 15-25 over 3-12 • Elevated RV pressure: • Pulmonary HTN • Pulmonary stenosis • PE

  24. Hemodynamic Monitoring • Normal: 15-25 over 8-15 • Elevated PA pressure: • L heart failure • Lung disease • PE • L to R shunts • Pulmonary HTN • Mitral valve disease • Hypoxic vasoconstriction

  25. Hemodynamic Monitoring • Normal: 6-12 • Always performed at end exhalation • Elevated PCWP: • Volume overload • L heart failure • Mitral disease • Myocardial ischemia/infarct

  26. Hemodynamic Monitoring • Other normals: • CO 4-6 L/min • CI 2.2-4 L/min/m2 • SVR 1100-1500 dynes/sec/cm2 • PVR 120-250 dynes/sec/cm2 • SVO2 >65%

  27. Shock

  28. Common Signs and Symptoms of Shock • Hypotension • Skin changes • cool, clammy skin; livedo reticularis • Oliguria • decreased renal perfusion • Altered mental status • restlessness>agitation>obtundation>coma • Metabolic acidosis • poor clearance of lactate by kidney, muscle, liver

  29. Classification of Shock HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE OBSTRUCTIVE

  30. Hypovolemic Shock • Results from decreased preload > leads to decreased left ventricular filling and SV > leads to a fall in CO • 2 subtypes 1) fluid loss: diarrhea, vomitting, osmotic diuresis, burns, heat stroke, “third spacing” 2) hemorrhagic: major trauma, upper or lower GI bleed, surgery, ruptured aneurysm, hemorrhagic pancreatitis, fractures

  31. Cardiogenic Shock • Develops as a result of pump failure • Mortality rate is over 50% • 3 Subtypes 1) Cardiomyopathies: ischemic, infectious myocarditis, idiopathic 2) Arrhythmias: atrial or ventricular and tachy or brady 3) Mechanical: acute mitral regurgitation, critical aortic stenosis, aortic dissection, VSD

  32. Distributive Shock • Results from decreased SVR with a resultant abnormal distribution of blood flow • Associated with a normal to increased CO • Subtypes: - Sepsis - SIRS - Anaphylaxis - Neurogenic - Myxedema coma - Addisonian crisis - Drugs and toxins

  33. Anaphylactic/Anaphylactoid Shock • Reaction to an exogenous stimulus • Anaphylactic - IgE mediated • Anaphylactoid - non-IgE mediated • Massive release of mediators from mast cells and basophils • Most common causes: - Drugs (beta-lactam antibiotics, ACE-I, NSAIDs) - Insects (bees, wasps) - Contrast media - Foods (seafood, nuts, milk) - Blood products

  34. Anaphylactic/Anaphylactoid Shock • Onset of symptoms 5-60 minutes in majority • Clinical manifestations • Skin: flushing, pruritis, hives • Respiratory: rhinorrhea, wheezing, stridor, dyspnea • Cardiovascular: tachycardia, bradycardia, hypotension • GI: nausea, vomitting, diarrhea • CNS: dizziness, syncope, seizures • Can have a biphasic reaction 6-12 hours later (5-20%)

  35. Anaphylaxis • Treatment • ABC’s: • early intubation if stridor or laryngeal edema • IVF’s • Epinephrine – drug of choice: • .3 - .5ml of 1:1000 IM or SQ • Antihistamines – both H1 and H2 blockers • Steroids

  36. Sepsis • Clinical syndrome that complicates severe infection • Characterized by massive and uncontrolled release of proinflammatory mediators • Leads to widespread tissue injury • Estimated 750,000 cases annually • Incidence increased approx 8% per year 1979-2000 • Mortality rate increases along spectrum => 7% SIRS => 16% sepsis => 20% severe sepsis => 46% septic shock(Am J Resp Crit Care Med 1996; 154:617)

  37. Sepsis Definitions • SIRS – systemic response to variety of insults • 2 or more of following: • Heart rate >90 • Respiratory rate >20 or PaCO2 <32 • Temperature >38 or <36 • WBC >12K or <4K, or >10% band forms • Sepsis – SIRS with evidence of infection • Severe sepsis – sepsis asstd with organ dysfunction, hypoperfusion, or hypotension • Septic shock – sepsis with hypotension despite adequate fluid resuscitation • Multiple organ dysfunction (MODS) – the presence of altered organ function

  38. Sepsis Management #1 Resuscitation • Volume infusion due to relative intravascular hypovolemia • Early-goal directed – 1st 6 hours (Rivers, NEJM 2001) • Goals: CVP 8-12, MAP>65, UOP>.5ml/kg/hr, SVO2>70 • No advantage to colloid over crystalloid • Vasopressor usage after adequate volume replacement • Norepinephrine drug of choice • Support of oxygenation and work of breathing • Early intubation

  39. Sepsis Management #2 Antibiotics • Given within one hour optimal • Initial empiric broad spectrum drugs against most likely pathogens • Cultures ideally prior to antibiotics

  40. Sepsis Management #3 Source Control • Evaluation for focus of infection requiring intervention • Abdominal abscess • Infected devices • Necrotic tissue • Cholangitis

  41. Sepsis Managment #4 Adjunctive Measures • Steroids • Steroid replacement in non-responders (failure to increase cortisol >9microgr/dl after stim test) • Recombinant activated protein C • Has role in inflammatory and coagulation cascades • Recommended in patients at high risk of death (APACHE>25, septic shock, MOF) • Insulin • Goal glucose control 80-110

  42. Obstructive Shock • Due to extracardiac impediments to CO • Most common causes: • massive PE • tension pneumothorax • cardiac tamponade • constrictive pericarditis • severe pulmonary HTN with RHF

  43. PA Catheter and Shock BP CO PCWP SVR Decreased Decreased Decreased Increased Hypovolemic Decreased Increased Decr-Nl Decreased Distributive Decreased Decreased Increased Increased Cardiogenic Decreased Decreased Variable Increased Obstructive

  44. Pulse Oximetry Monitoring • Pulse oximetry is a way of measuring O2 saturation by a noninvasive method which relies on the different absorption characteristics of oxyhemoglobin and deoxy hemoglobin for red (or infrared) light. • The error of pulse oximetry is only around + or - 4% above the saturation of 70%. When used to measure O2 saturation below 70%, the error becomes unacceptably high.

  45. Pulse Oximetry Monitoring • Pulse oximetry can yield falsely elevated O2 saturation in smokers and victims of carbon monoxide poisoning • Pulse oximetry can yield falsely low values in methemoglobinemia, individuals given intravenous methylene blue or indocyanine green, in patients who are black, green or blue nail polish, and in patients who are in the presence of arc surgical lights, or fluorescent lights.

  46. Upper Airway Management Problems • The complications of intubation include: • Intubation of main stem bronchus • Can occur even after “properly positioning” the endotracheal tube because of inadequate stabilization of the patient’s neck or excessive neck movement • Neck flexion causes as much as 2 cm displacement of the tip of the endo-tracheal tube towards the carina • Ideally the tube should be positioned with its tip at least 3 cm above the carina to avoid this problem • If the carina is not easily seen, the tip of the endo-tracheal tube should be adjusted to be just below level of clavicles

  47. Upper Airway Management Problems • Laryngeal ulceration • Laryngeal ulceration occurs in almost all intubated patients to a lesser or greater degree. • Damage is usually more to the posterior surfaces than the anterior surfaces. • The extent of the damage is proportional to the duration of the intubation. • Tracheal stenosis • Sinusitis • May occur in up to 42 % of patients who have a nasal tube and in up to 6% of patients who have an oral tube

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