RESPIRATORY DISTRESS

September 8, 2005

Prepared by Christina M. Cabott D.O.

RESPIRATORY DISTRESS

DYSPNEA HYPOXIA HYPERCAPNEA WHEEZING COUGH HICCUPS CYANOSIS PLEURAL EFFUSION

DYSPNEA

Common complaint described as – “shortness of breath”– “breathlessness”– “not getting enough air”

2/3 of patients presenting to ED with dyspnea have either a cardiac or pulmonary disorder

DYSPNEA

Definitions:– Tachypnea: rapid breathing– Orthopnea: dyspnea in a recumbent

position• Most often a result of LV failure• May be associated with diaphragmatic

paralysis or COPD

DYSPNEA

Definitions:– Paroxysmal nocturnal dyspnea: orthopnea

that awakens the patient from sleep– Trepopnea: dyspnea associated with only

one of several recumbent positions• can occur with unilateral diaphragmatic

paralysis• ball-valve obstruction• after surgical pneumonectomy

DYSPNEA

Definitions:– Platypnea: dyspnea in the upright position

• Result from loss of abdominal wall muscular tone

• Rarely, from left-to-right intracardiac shunting (e.g. patent foramen ovale)

– Hyperpnea: hyperventilation with a minute ventilation in excess of metabolic demand

DYSPNEA

Pathophysiology– No defined neural pathway, derived from

mechanical, chemical, and vascular receptors

DYSPNEA

Processes involved in sensation of dyspnea:

1. Conscious sense of voluntary peripheral skeletal and respiratory muscular efforts with increased work of breathing

2. Stimulation of upper airway mechanical and thermal receptors

DYSPNEA

3. Decreased stimulation of chest all afferents

4. Stimulation of central hypercapneic chemoreceptors in the central medulla

5. Stimulation of peripheral hypoxic chemoreceptors, in carotid body and aortic arch

DYSPNEA

6. Stimulation of intraparenchymal pulmonary stretch receptors, airway irritant receptors, and unmyelinated receptors, responding to interstitial edema or changes in compliance

7. Stimulation of peripheral vascular receptors

• right and left atrial mechanoreceptors• pulmonary artery baroreceptor

DYSPNEA

Input from all of these receptors is integrated in the CNS at subcortical and cortical levels

DYSPNEA

Clinical features that may signify impending respiratory failure– Presentation:

• shortness of breath or breathlessness• tachypnea• tachycardia• use of accessory respiratory muscles• stridor

DYSPNEA

Clinical features that may signify impending respiratory failure– Presentation:

• inability to speak, secondary to breathlessness• agitation or lethargy• paradoxical abdominal wall movement with

inspiration (abdominal wall retracts inward)

DYSPNEA

Clinical features– Evaluation

• abnormal vital signs• ABCs

– Need rapid airway control and intervention• airway obstruction• ineffective respiratory effort• changes in mental status

CAUSES OF DYSPNEA

Most Common Causes– Asthma & COPD– CHF/ cardiogenic

pulmonary edema– Ischemic heart dz

• Unstable angina &MI

– Pneumonia– Psychogenic

Most Immediately Life Threatening– Foreign body– Angioedema– Hemorrhage– Tension pneumo– PE– Myasthenia gravis– Guillain-Barre– Botulism

Ancillary Tests Used for Dyspnea Diagnosis

– pulse oximetry and ABG

– CXR– EKG– peak flows– Hgb and Hct– BNP (>100 pg/ml)– spirometry

– pulmonary function tests

– cardiac stress tests– echocardiography– exercise testing– electromyography– V/Q scan– pulmonary biopsy

DYSPNEA

ED treatment– Supplemental O2: PaO2 >60 mm Hg; pulse

ox >91 to 93%– CPAP or BiPAP– Bag-valve-mask ventilation– Intubation with mechanical ventilation– Patients with unclear cause of dyspnea and

hypoxia require admission for monitoring

HYPOXEMIA

Pathophysiology– Def: inadequate delivery of oxygen to tissues – Amount of oxygen available to the tissues is a

function of the arterial oxygen content (CaO2)

CaO2 = 0.0031 X PaO2 + 1.38 X Hb X SaO2

– PaO2 < 60 mm Hg

HYPOXEMIA

Relative hypoxemia– Arterial oxygen tension is lower than

expected for a given level of inhaled oxygen

– Can be calculated by doing A-a gradient

HYPOXEMIA

– Simplified formula P(A-a)O2 = 145 - PaCO2 - PaO2

– Normal P(A-a)O2 is under 10 mm Hg in young, healthy patients and increases with age

– Predicted A-a gradient with age • P(A-a)O2 = 2.6 + 0.21 (age in years) (+ 11)

HYPOXEMIA

Pathophysiology– 5 distinct mechanisms

1. Hypoventilation

2. Right-to-left shunt

3. Ventilation/perfusion mismatch

4. Diffusion impairment

5. Low inspired oxygen

HYPOXEMIA

Hypoventilation– Rising PaC02 displaces O2 from the aveolus

PaO2 O2 diffusion gradient across the pulmonary membrane

– Normal A-a O2 gradient

HYPOXEMIA

Right-to-left shunting– Unoxygenated blood enters the systemic

circulation– May occur secondarily to under ventilated

lung or with congenital heart anomalies

– Increase in A-a O2 gradient

– Will have failure of arterial oxygen levels to increase in response to supplemental O2

HYPOXEMIA

Ventilation/Perfusion Mismatch– Regional alterations of ventilation or

perfusion– Etiologies: PE, pneumonia, asthma,

COPD, extrinsic vascular compression

– Increased A-a O2 gradient

– Hypoxemia improves with supplemental O2

HYPOXEMIA

Diffusion impairment– Impairment of alveolar-blood barrier

– Increased A-a O2 gradient

– Hypoxemia improves with supplemental O2

HYPOXEMIA

Low inspired oxygen– High altitude hypoxia– Nonobstructive asphyxia

– Normal A-a O2 gradient

– Hypoxemia improves with supplemental O2

HYPOXEMIA

Acute compensatory mechanisms– 1. Minute ventilation – 2. Pulmonary artery vasoconstriction

perfusion to hypoxic alveoli– 3. Sympathetic tone oxygen delivery

by HR and cardiac output

HYPOXEMIA

Chronic compensatory mechanisms– 1. Red blood cell mass– 2. Tissue oxygen demand

HYPOXEMIA

Clinical Features– Signs and symptoms are nonspecific

• Cardio-pulm: tachycardia and tachypnea• CNS: aggitation, seizures, and coma

– At PaO2 < 20 mm Hg, paradoxical depression of respiratory drive

– Dyspnea may or may not be present

HYPOXEMIA

Diagnosis and Differential– Pulse ox = screening test– ABG = defines diagnosis– Similar tests used to determine cause of

dyspnea may be useful in evaluating hypoxia

HYPOXEMIA

ED treatment– Treatment: support, identify, and aggressively

treat underlying cause

– Maintain PaO2 >60 mm Hg with supplemental O2

– Arterial line if frequent ABGs

Patients with persistent hypoxia require hospitalization

HYPERCAPNEA

Pathophysiology– def: PaO2 >45 mm Hg

– Caused by hypoventilation• rapid shallow breathing

• small tidal volumes

• underventilation of lung reduced respiratory drive

– Never due to intrinsic lung disease or increased CO2 production

HYPERCAPNEA

Causes of Hypercapnea– Depressed central respiratory drive

• Structural CNS disease: brainstem lesions• Sedating drugs: opiates, sedatives, anesthetics• Exogenous toxins• Endogenous toxins: tetanus

HYPERCAPNEA

Causes of Hypercapnea– Thoracic cage disorders

• Kyphoscoliosis• Morbid obesity

– Neuromuscular impairment• Neuromuscular disease: myasthenia gravis,

Guillain-Barre syndrome• Neuromuscular toxins: organophosphate

poisoning, botulism

HYPERCAPNEA

Causes of Hypercapnea– Intrinsic lung disease associated with

increased dead space• COPD

– Upper airway obstruction

HYPERCAPNEA

Pathophysiology– Alveolar ventilation

• Less than minute ventilation• Dependent on the tidal volume less the

anatomic dead space and the respiratory rate

– Efferent neuronal imput from the medulla’s chemoreceptors control tidal volume and respiratory rate

HYPERCAPNEA

Clinical Features– Signs and symptoms are dependent on

rate and degree of elevation– Acute rise in elevation

• increase in ICP, confusion, lethargy, asterixis, seizures, and coma

– Acute changes to PaCO2 >100 mm Hg may lead to cardiovascular collapse

HYPERCAPNEA

Clinical Features– Acute retention:

• For each 10 mm Hg increase of PaCO2, the pH will decrease by 0.1 U

• For each 10 mm Hg increase of PaCO2, the HCO3 will increase by 1 mEq/L

HYPERCAPNEA

Clinical Features– Chronic retention:

• May be well tolerated

• Kidneys retain HCO3

• For every 10 mm Hg of PaCO2 over 40 mm Hg, HCO3 increases by 3.5 meq/L

HYPERCAPNEA

ED treatment– Identify threats to life, evaluate, and

aggressively treat deficiencies in the ABCs• e.g. narcotic overdose - tx with naloxone• e.g. neuromuscular disease - tx with assisted or

mechanical ventilation

HYPERCAPNEA

ED treatment– Supplemental oxygen should be given to

maintain level normal for the patient• Don’t withhold oxygen based on worry of

“decreased respiratory drive”• Hypoxia and extreme hypercapnea will kill

– Bipap or CPAP - use as a bridge, not definitive care

– Mechanical ventilation

WHEEZES

Pathophysiology– Def: musical adventitious lung sounds

produced by turbulent flow through the central and distal airways

– Obstruction: bronchospasm, smooth muscle hypertrophy, increased secretions, and peribronchial inflammation

WHEEZES

Clinical features– Usually occurs in asthma and other

obstructive pulmonary diseases– “Not all that wheezes is asthma.”– Not every obstructive pulmonary disease

will cause wheezing• e.g. severe asthma - quiet chest, not moving

enough air to produce turbulent flow

WHEEZES

Causes of wheezing– Upper airway (stridor most likely, may have

wheezing)• Angioedema: allergic, ACE inhibitor, idiopathic• Foreign body• Infection: croup, epiglottitis, tracheitis

WHEEZES

Causes of wheezing– Lower airway

• Asthma• Transient airway hyperreactivity (usually due to

infection or irritation)• Bronchiolitis• COPD• Foreign body

WHEEZES

Causes of wheezing– Cardiogenic

• Cardiogenic pulmonary edema (“cardiac asthma”)

• Noncardiogenic pulmonary edema – Adult respiratory distress syndrome [ARDS]

• Pulmonary embolus (rare)

– Psychogenic

WHEEZES

Diagnosis– Diagnosis is suspected in the proper

clinical situation– Patient improves with relief of airway

obstruction• Decreased work of breathing• Improvement of pulse ox• Decreased respiratory rate

WHEEZES

Diagnosis– Definitive diagnosis confirmed by

spirometric testing• Cannot be done at the bedside or during an

acute exacerbation

– Hand held peak-flow meter used as an adjunct to gauge response to treatment

• Value >80% predicted = normal• Limitations: effort and usefulness in kids

WHEEZES

Diagnosis– Other ancillary tests

• CXR and ABG• May not be needed during an uncomplicated

obstructive pulmonary disease

WHEEZES

ED treatment – Initial treatment: directed at identifying

threats to life and aggressively treating the underlying condition

– Supplemental oxygen: given if hypoxia and degree of obstruction

– Monitoring

WHEEZES

ED treatment– Initial treatment of wheezing

• inhaled beta-agonists (e.g. albuterol) and/or anticholinergic agents (e.g. ipratropium bromide)

– Acute setting• steroids to help reduce airway inflammation

WHEEZES

ED treatment– Admission of patients

• Oxygen requirements• Potential for quick decompensation• Failed treatment• Require mechanical ventilation

COUGH

Pathophysiology– Protective reflex that acts to clear

secretions and debris from tracheobronchial tree

– Initiated by stimulation of irritant receptors located in larynx, trachea, and major bronchi

COUGH

Pathophysiology– Receptor signal travel via vagus,

phrenic, and other nerves cough center of the medulla cough pattern

– Cough pattern:• deep inspiration expiration against closed

glottis glottis opens forceful exhalation of air, secretions and foreign debris from tracheobronchial tree

COUGH

Pathophysiology– Stimulation of receptors

• inhaled irritants (e.g. dust)

• allergens (e.g. ragweed pollen)

• toxic substances (e.g. gastric acid)

• hypo- or hyperosmotic liquids

• inflammation (e.g. asthma)

• cold air

• instrumentation

• excess pulmonary secretions

COUGH

Categories– Acute– Chronic

• Cough present more than 3 weeks without any periods of resolution

COUGH

Acute Causes– Upper respiratory infection: rhinitis, sinusitis– Lower respiratory infection: bronchitis, pneumonia– Allergic RXN– Asthma– Environmental irritants– Transient airway hyperresponsiveness– Foreign body

COUGH

Common Chronic Causes– Smoking and/or chronic bronchitis– Postnasal drainage– Asthma: reactive airway disease - worse at night– Gastroesophageal reflux– Angiotensin-converting enzyme inhibitor - b/c

accumulation of bradykinin and substance P– Angiotensin II receptor blocker

COUGH

Less Common Chronic Causes– Congestive Heart Failure– Bronchiectasis– Lung cancer or other intrathorcic mass– Emphysema– Occupational and environmental irritants– Recurrent aspiration or chronic foreign body– Cystic fibrosis– Interstitial lung disease

COUGH

Diagnosis– Most acute cough does not require routine

ancillary tests• CXR: if purulent sputum and/or fever• Spirometry: evaluation of airflow obstruction in

asthmatics

COUGH

Diagnosis– Chronic cough

• Treatment based on clinical assessment first• Ancillary tests performed only if symptoms

persist– Nasolaryngoscopy - document mucosal inflammation

and excessive mucous drainage– Sinus radiographs or CT - check for sinusitis– Spirometry - check for airflow obstruction

COUGH

Acute treatment– Cough suppressants

• opioids: dextromethorphan, codeine, and oxycodone

– Demuculants

COUGH

Chronic treatment

1. Reduce lung irritant exposure

2. Discontinue use of ACE inhibitors, ARBs, and B-blockers

3. Treat post-nasal drainage with oral antihistamine-decongestant and/or nasal steroid

COUGH

Chronic treatment

4. Evaluate and treat for asthma

5. Obtain CXR and sinus x-ray

6. Evaluate and treat GE reflux

7. Refer patient for bronchoscopy

HICCUPS

Hiccups a.k.a singultus– Def: an involuntary respiratory reflex with

spastic contraction of the inspiratory muscles against a closed glottis, producing the characteristic sound

– There is no specific protective purpose known for hiccups

HICCUPS

Pathophysiology– Afferent: phrenic and vagus nerves and thoracic

sympathetic chain– Intensive interconnection among the

hypothalamus, medullary reticular formation, respiratory center, and cranial nerve nuclei

– Efferent: phrenic nerve, recurrent laryngeal branch of the vagus nerve, and the motor nerves to the anterior scalene and intercostal muscles

HICCUPS

Pathophysiology– 30 to 40 msec after the onset of inspiration,

glottic closure is stimulated– In cases where a specific cause can be

assigned, hiccups appear to result from stimulation, inflammation, or injury to one of the nerves of the reflex arc

HICCUPS

Causes of Hiccups– Acute: benign, self-limited

• Gastric distention - from food, drinking (especially carbonated drinks), or air

• Alcohol intoxication• Excessive smoking• Abrupt change in environmental temperature• Psychogenic - excitement or stress

HICCUPS

Causes of Hiccups– Chronic: persistent, intractable

• Central nervous system structural lesions• Vagal or phrenic nerve irritation• Metabolic: uremia, hyperglycemia• General anesthesia• Surgical procedures: thoracic, abdominal,

prostate, urinary tract, craniotomy

HICCUPS

Diagnosis– Benign hiccups

• Resolves spontaneously or with simple maneuvers

• Do not seek medical attention• Do not require specific diagnosis

HICCUPS

Diagnosis– Persistent hiccups

• History to determine specific event associated with the onset

• Persistence during sleep– Suggests organic cause

• Resolution during sleep– Suggests psychogenic cause– Most patients with benign hiccups

• Inquiries about general anesthesia, surgical procedures, and metabolic diseases

HICCUPS

Diagnosis– Persistent hiccups

• Evaluate external auditory canal– hair in canal can press up against the tympanic

membrane and stimulate the auricular branch of the vagus nerve

• CXR– evaluate for intrathoracic pathology

• Fluoroscopy – evaluate unilateral vs bilateral diaphragmatic

movement during hiccups

HICCUPS

Treatment with physical maneuvers– Stimulating the pharynx will block vagal portion of

reflex arc and abolish hiccups

Treatment with medications– chlorpromazine– metoclopramide– nifedipine– valproic acid– baclofen

HICCUPS

chlorpromazine – 25 to 50 mg IV, with

repeated dose in 2 to 4 hours, if needed

– If improvement, 25 to 50 mg po tid or qid

– May cause extrapyramidal symptoms

– Usually works within 30 min

metoclopramide – 10 mg IV or IM– If effective, 10 to 20

mg po qid for 10 days– May cause

extrapyramidal symptoms or hypotension

– Usually works within 30 min

HICCUPS

nifedipine– 10 to 20 mg po tid or qid

valproic acid– 15 mg/kg per day po tid

baclofen– 10 mg po tid

These all work more gradually

CYANOSIS

Pathophysiology– Indicated by the bluish color of the skin and

mucus membranes– Resulting from an increased amount of

deoxyhemoglobin– Usually 5 g/ 100 mL of deoxyhemoglobin

must be present for cyanosis to occur– Amount of oxyhemoglobin does not matter

CYANOSIS

Pathophysiology– Various factors affect the presence or

absence of cyanosis• Skin pigmentation• Skin thickness• Subcutaneous microcirculation• Lighting• Ambient temperature

CYANOSIS

Clinical Features– Presence of cyanosis signals tissue

hypoxia, but not always • Sensitive indicator = tongue• Less sensitive indicators = earlobes,

conjunctiva, and nail beds

– Cause either central or peripheral cyanosis

CYANOSIS

Clinical Features– Central cyanosis

• Result of unsaturated arterial blood or abnormal hemoglobin (e.g. methemoglobin)

– Peripheral cyanosis• Caused by decreased peripheral circulation and

clinical situations that lead to an increased arterial oxygen extraction

CYANOSIS

Central cyanosis– Hemoglobinopathies

• Methemoglobin: acquired; hereditary• Sulfhemoglobinemia: acquired

– Decreased arterial oxygen saturation• Pulmonary etiologies: shunt , diffusion, V/Q

mismatch• Hypoventilation• High altitude

CYANOSIS

Central cyanosis– Anatomic right-to-left shunts

• Cardiac: Ventricular Septal Defect (VSD), Atrial Septal Defect (ASD), and Tetralogy of Fallot (TOF)

• Intrapulmonary• Intrapulmonary shunts

CYANOSIS

Peripheral cyanosis– Decreased cardiac output– Distributive shock– Cold exposure on extermities– Venous congestion– Arterial thrombosis or embolus

CYANOSIS

Diagnosis– Presence of cyanosis must be taken in

context with clinical situation– Tests

• ABG: will confirm the diagnosis• Hematocrit: check for polycythemia or anemia• CXR• EKG• Abnormal hemoglobin tests

PSEUDOCYANOSIS

Blue, gray, or purple cutaneous discoloration that may mimic cyanosis

Causes– Heavy metals: iron (hemochromatosis),

gold, silver, lead, and arsenic– Drugs: phenothiazines, minocycline,

amiodarone, and chloroquine

PSEUDOCYANOSIS

Chrysiasis– Gray, blue, or purple pigmentation of areas

exposed to light– Rare-dose dependent complication of gold

treatment that causes permanent discoloration of the skin

PSEUDOCYANOSIS

Argyria– Slate blue to gray coloration of skin– Results of chronic ingestion or local

application of silver salts or colloidal silver,

CYANOSIS

True cyanosis DOES blanch when direct pressure is applied to skin

Pseudocyanosis DOES NOT blanch when direct pressure is applied to skin

CYANOSIS

Diagnosis– Methemoglobin, sulfhemoglobin, and

carbon monoxide poisoning must be kept in mind

• Artificially alter peripheral pulse oximetry, secondary to pigment formation in the blood

CYANOSIS

Diagnosis– Methemoglobin,

• Causes– Drugs: most commonly by benzocaine and nitrates– Hereditary: rare genetic disorder affecting NADH

• Visible cyanosis with as little as 1.5 g/dL• Incapable of binding oxygen• Symptoms related to hypoxia

CYANOSIS

Diagnosis– Methemoglobin

• Severity of symptoms related to quantity, rapidity of onset, and pts cardiovascular system

• Need to consider if oxygen supplementation does not correct hypoxia

• Venous blood looks chocolate brown• Treatment: methylene blue

CYANOSIS

Diagnosis– Sulfhemoglobin

• Caused commonly by phenacetin or acetanilid• Inert as an oxygen carrier• Can produce deep cyanosis at level < 0.5 g/dL• Irreversible• Treatment

– symptomatic and supportive care– identification and removal of suspected causes

CYANOSIS

ED treatment– Central cyanosis

• Supplemental oxygen• supplied in appropriate conditions

– Methemoglobinemia• Methylene blue 1 to 2 mg/kg of body weight IV

over 5 minutes

PLEURAL EFFUSION

Result from fluid accumulating in potential space between visceral and parietal pleura

Most common causes in developed countries– CHF– Pneumonia– Cancer

PLEURAL EFFUSION

Pathophysiology– Normally, small amount of fluid is secreted

from parietal pleura into pleural space, where it is absorbed by visceral pleural microcirculation

– Small amount of fluid decreases friction between the pleural layers and allows for smooth lung expansion and contraction during respiration

PLEURAL EFFUSION

Pathophysiology– Transudates

• Result of imbalance in hydrostatic or oncotic pressure

• Produces an ultrafiltrate across the pleural membrane

• Low protein content

PLEURAL EFFUSION

Pathophysiology– Exudates

• Result of pleural disease, usually inflammation or neoplasm

• Active fluid secretion or leakage• High protein content

COMMON CAUSES OF PLEURAL EFFUSION

Transudates– CHF

Transudate or exudate– Diuretic therapy

Exudates– Cancer: primary or

metastatic– Bacterial pneumonia

with parapneumonic effusion

– Pulmonary embolism

LESS COMMON CAUSES OF PLEURAL EFFUSION

Transudates– Cirrhosis with ascites– Peritoneal dialysis– Nephrotic syndrome

Transudate or exudate– Pulmonary embolism

Exudates– Viral, fungal,

mycobacterial or parasitic infection

– SLE or RA– Uremia– Pancreatitis– Post-cardiac surgery

or radiotherapy– Amiodarone

PLEURAL EFFUSION

Clinical features– May be clinically silent– Detected by symptoms of underlying

disease– Increase in volume of effusion with

dyspnea– Development of inflammation and

associated pain with respiration

PLEURAL EFFUSION

Physical exam– Percussion dullness in dependent portions

of the lung– Decreased breath sounds at lung base

PLEURAL EFFUSION

Diagnosis– Upright CXR: in an adult, 150-200 mL of

pleural fluid in hemithorax required to produce signs

– Supine CXR: haziness in posterior pleural space

– Diagnostic thoracentesis• analyzed to determine cause

PLEURAL EFFUSION

Detection of exudative pleural effusion– Pleural fluid/serum protein ratio > 0.5– Pleural fluid/serum LDH ratio > 0.6– Pleural fluid LDH > 2/3 of upper limit for

serum LDH

PLEURAL EFFUSION

Additional tests– Gram stain and culture - detect bacteria– Cell count

Neutrophils- parapneumonic, PE, pancreatitis Lymphocytes- cancer, TB, post-cardiac sz

– Glucose: low in parapneumonic, malignancy, TB, and RA

PLEURAL EFFUSION

Additional tests– Cytology for malignancy

• Highest yield: adenocarcinoma• Lower yield: squamous cell, lymphoma, or

mesothelioma

– Pleural fluid pH• Normal: around 7.46• Parapneumonic: <7.10, predicted development

of or persistence of empyema

PLEURAL EFFUSION

Additional tests– Pleural fluid amylase

• Elevated in pancreatitis or esophageal rupture

– Mycobacterial and fungal stains and cultures– Tuberculosis pleural fluid markers:

• PCR for mycobacterial DNA• Pleural fluid adenosine deaminse• Pleural fluid interferon-

PLEURAL EFFUSION

Treatment– Dyspnea at rest

• Therapeutic thoracentesis with drainage of 1 to 1.5 L of fluid

– Empyema (gross pus or organisms on Gram stain)

• Drainage with large bore thoracostomy tubes

PLEURAL EFFUSION

Treatment– Parapneumonic effusions

• Thoracostomy tube drainage if + cultures, +Gram stain, or pleural fluid pH < 7.10

– CHF pleural effusions• Diuretic therapy• Usually resolves 75% of effusions within 2 to3

days

QUESTIONS

1. Causes of central cyanosis

2. Causes of peripheral cyanosis

1. B, D, F. 2. A, C, E, G

A. Decreased cardiac output

B. Methemoglobin

C. Hypothermia

D. Right-to-left shunt

E. Venous congestion

F. High altitude

G. Embolus

QUESTIONS

3. Causes of upper airway obstruction

4. Causes of lower airway obstruction

3. A, C, D, G. 4. B, C, E, F

A. Angioedema

B. Bronchiolitis

C. Foreign body

D. Croup

E. COPD

F. Asthma

G. Epiglotitis

QUESTIONS

5. If PaO2 < 20 mm Hg, what happens to the respiratory drive?.

6. In an acute setting, what should the pH be for a patient with a PaCO2 of 60?

5. B 6.C

A. Increases

B. Decreases

C. 7.15

D. 7.25

E. 7. 35

F. 7.55

G. 7.65