Critical Care Board Review Pulmonary and Critical Care

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 – 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

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

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

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

• 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

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

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

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

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

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

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%)

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

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)

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.

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

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.

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

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.


• 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


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

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


• Normal: 15-25 over 3-12

• Elevated RV pressure:– Pulmonary HTN

– Pulmonary stenosis

– PE


• 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


• Normal: 6-12• Always performed at

end exhalation• Elevated PCWP:

– Volume overload

– L heart failure

– Mitral disease

– Myocardial ischemia/infarct


• 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%

Shock

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

Classification of Shock

HYPOVOLEMICHYPOVOLEMIC

CARDIOGENICCARDIOGENIC

DISTRIBUTIVEDISTRIBUTIVE

OBSTRUCTIVEOBSTRUCTIVE

Hypovolemic Shock

• Results from decreased preload > leads to decreased left ventricular filling and SV > leads to a fall in CO

• 2 subtypes1) 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

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

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

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

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%)

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

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)

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

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

Sepsis Management

#2 Antibiotics

• Given within one hour optimal

• Initial empiric broad spectrum drugs against most likely pathogens

• Cultures ideally prior to antibiotics

Sepsis Management

#3 Source Control

• Evaluation for focus of infection requiring intervention– Abdominal abscess– Infected devices– Necrotic tissue– Cholangitis

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

Obstructive Shock

• Due to extracardiac impediments to CO

• Most common causes:– massive PE– tension pneumothorax– cardiac tamponade– constrictive pericarditis– severe pulmonary HTN with RHF

PA Catheter and Shock

BP CO PCWP SVR

Decreased Decreased Decreased Increased

HypovolemicDecreased Increased Decr-Nl Decreased

DistributiveDecreased Decreased Increased Increased

CardiogenicDecreased Decreased Variable Increased

Obstructive

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.

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.

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


– 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


• Tracheostomy– Should be considered in all patients requiring

prolonged mechanical ventilation– The main complication of tracheostomy is

innominate artery rupture which occurs in less than 0.5% of such patients but which has a mortality of about 90%.

– Tracheal stenosis may also be a complication of tracheostomy and occurs particularly if a large stoma is made or excessive traction is applied.

Ventilator Management

• The most important goals of mechanical ventilation include:– Maximize pulmonary gas exchange– Reduce the work of breathing– Allow the lungs to heal– Minimize ventilator induced lung injury


• The following are the most important facts regarding the various types of ventilators:– There are essentially two types of ventilators:

Volume-cycled and pressure-cycled.– Volume-cycled ventilators are designed to

deliver a fixed volume (operator-selected) of air and/or oxygen using whatever (within reason) pressure needed to achieve that goal during each cycle.


– Pressure-cycled ventilators are designed to deliver whatever volume they can using a constant pressure (operator-selected) during each cycle.

• Since these ventilators use constant pressure, the amount of air and/or oxygen delivered during any cycle can vary depending on various factors such as compliance of the lungs.


• The three most common modes of mechanical ventilation include:– Assist control (AC) ventilation

• Refers to the mode in which the ventilator recognizes when the patient is trying to breathe and immediately initiates a fully supported ventilatory cycle

• If patient does not make any attempt to initiate a breath, the ventilator delivers a set number of respirations per minute

Ventilator Management– Pressure-support ventilation (PSV)

• Refers to the ventilator mode in which a fixed amount of pressure is added during each breath.

• The airway pressure is maintained at a preset level until the patient’s inspiratory air flow falls to a preset level such as 25% of peak flow for example.

• The tidal volume is dependent on the patient effort, pulmonary mechanics and the amount of pressure-support.

– Intermittent mandatory ventilation (IMV)• Refers to the mode in which the patient is allowed to initiate

and complete his own breaths but nevertheless the patient is given a periodic predetermined number of mechanical ventilations with the set volume and rate


• The initial setting of FiO2 in a patient newly intubated should be between 0.9 and 1.0 until the first set of Arterial Blood Gases (ABG) results are available and then adjusted down to maintain a pO2 of at least 60 mm Hg.

• The initial tidal volume setting should 6-8ml/kg based on ideal body weight


• The inspiratory flow rate of approximately 60 L/min is adequate for most patients. However, patients with COPD may have to have a higher inspiratory flow rate (helps decrease autoPEEP)

• The ventilatory rate setting varies with the clinical scenario

Trouble-shooting Peak Airway Pressures

Peak and Plateau Pressures1) Elevated peak and plateau pressures:

Low compliance:- endobronchial (right main stem) intubation- pulmonary pathology (pna, pulm edema,

hemorrhage, etc)- pneumothorax

- hyperinflation: dynamic, excessive PEEP- ascites or other abdominal compartment syndrome

2) Elevated peak pressure only with normal plateau pressure: Increased system resistance:

- obstruction to flow in circuit, tracheal tube- malplaced ETT- bronchospasm- aspiration/secretions

Weaning

• Used to describe process of removing patient from ventilator assistance

• Weaning can be short…..– eg. general anesthesia, drug overdoses

• ….or protracted (up to a third of vent time)– eg. COPD, asthma, sepsis, multiple organ failure

• Optimal method is controversial• No great objective parameter to identify patients

ready for extubation

Assessing Weaning Potential

• Evidence for reversal of the underlying cause of respiratory failure

• Adequate oxygenation and pH– PaO2/FiO2 ratio >200, PEEP < 5-8, FiO2 < .4– pH > 7.25

• Stable hemodynamics– No active cardiac ischemia– No significant hypotension

• Ability to initiate an inspiratory effort

Weaning Parameters

• Respiratory rate– < 30

• Vital capacity– > 10 mL/kg

• Minute ventilation– Respiratory rate X tidal volume– < 10-15 L/min

• Negative inspiratory force (NIF)– < -20 to –30cm H2O

Weaning Parameters

• Rapid shallow breathing index (RSBI)– Respiratory rate divided by tidal volume in

milliliters– If < 105 then 78-83% success rate– Most accurate predictor of failure

Methods of Weaning

• SBT or T-piece trials– Trials done and duration of trial gradually increased each time– Interval between trial unknown but does not appear to be

difference between daily and multiple trials during day

• Intermittent Mandatory Ventilation (IMV)– Set machine rate reduced in steps of 1-3 breaths/min– Gradual reduction in amount of vent support with progressive

work done by the patient

• Pressure Support Ventilation (PSV)– Machine augments spontaneous breaths with fixed amount of

positive pressure– Theoretic comfort advantage to patient

Which is the Best?

• Esteban, et al. NEJM 1995– 130 patients assigned randomly to 4 groups– Gr 1- IMV – started at 10br/min, then decreased twice a

day by 2-4 breaths: wean = 5 days– Gr 2 – PSV – started at 18cmH2O, then decreased

twice a day by 2-4 cm: wean = 4 days– Gr 3 – Intermittent SBT – 2 or more times a day: wean

= 3 days– Gr 4 – Once daily SBT: wean = 3 days– Conclusion: SBT groups the same and better than IMV

and PSV. IMV performed the worst.

• W eaning parameters

• E lectrolytes

• A BG – acid/base, PaO2

• N utrition

• S ecretions

• N euromuscular factors – drugs

• O bstruction – bronchodilator treatments

• W akefulness

Upper GI Bleed

• Commonly presents with hematemesis and/or melena

• NG lavage can confirm diagnosis and predict high risk lesion– Can be negative if bleeding stopped or present

beyond a closed pylorus

Upper GI Bleed

• #1 Resuscitation– 2 large bore IV’s (18 gauge or larger)– Crystalloids to start– Elderly with multiple comorbidities or

ASCADz goal HCT close to 30

Upper GI Bleed

• #2 Reverse any coagulopathy– Check coags…if elevated INR (coumadin, liver

dz, etc) then fresh frozen plasma (goal <1.5)– Check CBC….if platelets <50K, then transfuse

plts– Check chemistries…if renal failure/uremia,

then give DDAVP (causes release of Vwf…”platelet glue”)

Upper GI Bleed

• #3 Adjunctive therapies– Intravenous infusion PPI – reduces rebleeding– Octreotide or somatostatin if known varices or

suspected based on EtOH hx – shunts blood away from varices

– Look for and tap any ascites – high rate of SBP; if negative will at least need prophylactic abx

– ENDOSCOPY

DKA

• Present with nause, vomiting, abdominal pain, polyuria, polydipsia, wgt loss

• Precipitants: EtOH and drug abuse, infection, MI, dehydration, stroke, pancreatitis, trauma, noncompliance

• Labs: variable glucose (usually <800), hypoNa+, hyperK+, gap acidosis, serum ketones, mildly elevated amylase/lipase

DKA

• Treatment– Resuscitation – IVF’s with NS initially– Insulin infusion

• Need some IVF’s on board first then insulin• Do not turn off drip until gap resolved

– Potassium and phosphorous replacement• Start replacing K+ when <5

– Switch IVF’s to ½ NS after first 2-3L to prevent hyperchloremic acidosis

– Search for precipitant

Carbon Monoxide Poisoning

• Colorless, odorless, nonirritating gas• Sources: vehicle exhaust, gas heating/cooking, smoke

inhalation• Binds Hb with affinity 200X greater than O2• Symptoms: HA, dizziness, nausea, CP, confusion,

weakness, dyspnea, ataxia, sz’s, coma• Diagnosis: blood level by cooximeter• Treatment:

– 100% O2 – reduces ½ life from 5-6 hrs to 60-90 mins

– Hyperbaric O2 – reduces ½ life to 20-25 mins

Chemical Warfare AgentsAgent Properties Syndrome Tx

Nerve agents vaporized liquid miosis,salivation, atropine,2-pam

sarin lacrimation, mm weak, soman bronchorrhea, diarrhea tabun VXChlorine pungent yellow or bronchospasm, pulm supportive

green gas edema, resp failureSulfur mustard vaporized liquid rhinorrhea, topical supportive

irritation, tracheobronchPhosgene colorless gas tracheobronch, topical supportive

irritation, pulm edema

Overdoses and AntidotesAcetaminophen 4 hr level and use Rumack- N-acetylcysteine

Matthew nomogram, treat

regardless if >7.5g’s

Amphetamines Benzos

Arsenic/Hg/gold/Pb BAL

Benzos Flumazenil

B-blocker Glucagon, CaCl, pacing

Ca-blocker Ca, glucagon, pacing

Coumadin Vitamin K

Cyanide unexplained lactic acidosis Nitrites, thiosulfate

refractory to fluids and 100% O2

in setting of smoke inhalation

Digoxin Digoxin Fab

Overdoses and Antidotes

Ethylene glycol drunkeness, gap acidosis with Ethanol, fomepizole, osmolal gap dialysis

Heparin ProtamineIron DeferoxamineINH PyridoxineLithium DialysisMethanol vision complaints,gap acidosis Ethanol, fomepizole,

with osmolal gap dialysis

Narcotics AMS, depressed respirations, Naloxone pinpoint pupils

Organophosphates SLUDE Atropine, 2-PAMSalicylates respiratory alkalosis, gap acidosis, Alkalinization, dialysis

and hyperthermia

Tricyclics arrhythmia, hypotension, Alkalinization, alpha- anticholinergic toxicity agonist

Alcohol Withdrawal• Minor withdrawal

– Tremulous, anxiety, diaphoresis, nausea, HA– Appear within 6hrs, gone in 24-48 hrs

• Withdrawal seizures– Tonic-clonic– Occur within 48 hrs

• Alcoholic hallucinosis– Visual>auditory>tactile– Appear within 12-24 hrs, gone in 24-48 hrs

• Delirium tremens– Begin 48-96 hrs and last 1-5 days– 5% mortality– Hallucinations, agitation, tachycardia, HTN, fever– Treated with benzos

Questions?

Documents

Critical Care Board Review Pulmonary and Critical Care