Adult and Pediatric Respiratory Emergency. Christopher Martella, DO FACOEP. Adult and Pediatric Respiratory Emergency. Discuss the differential diagnosis of Adult and Pediatric Respiratory Emergencies Pathophysicology Epidemiology History Physical findings Treatments.
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Christopher Martella, DO FACOEP
Chest wall Rib fractures Flail chest
Pulmonary COPD exacerbation Asthma exacerbation Pulmonary embolism Pneumothorax Pulmonary infection ARDS Pulmonary contusion or other lung injury Hemorrhage
Cardiac ACS ADHF Flash pulmonary edema High output failure Cardiomyopathy Arrhythmia Valvular dysfunction Cardiac tamponade Neurological Stroke Neuromuscular disease
Use of accessory muscles
Brief fragmented speech
Inability to lie supine
Cyanosis, depressed mental status, inability to maintain respiratory effort
Pulmonary Index in pediatrics patients
I to E ratio
Hypoxia -nearly all asthma patients have hypoxia as a result of V/Q mismatch. Beta 2 agonist may worsen this mismatch by causing pulmonary vasodilation in areas of the lung that are poorly ventilated
Marked hypoxia PO2<60 SaO2<90
Infrequent but potential cause of complications and death. Recommendations for continuous Pulse ox monitoring for patients with PEFR <40 % of baseline
Asthma patients are usually tachynic therefore normal or high PaCO2 could be an ominous sign
Chest x-ray rarely helpful unless patient with fever suspected PTX
Labs not helpful
Treatment for Adult patient
Nebs vs MDI essentially no difference and MDI maybe better
Ipratopium 500mcg neb q 20 minutes for three doses, then as needed or 8 puffs via MDI q 20 min then as needed for up to 3 hours.
Usually reserved for severe obstruction failing to improve despite beta agonists
Speeds rate of recovery with patients with persistent wheezing despite intensive bronchodilator therapy likely secondary to airway flow obstruction due to airway inflammation and intraluminal mucous plugging
Current guidelines encourage early systemic glucocorticoids for all patients who have a moderate (PEFR of < 70%) or severe exacerbation ( PEFR<40%)
Optimal dose unknown
Corticosteroids: give methylprednisolone 60-125 mg IV or prednisone 40-60 mg po; alternatives include: dexamethasone 6-10 mg IV or hydrocortisone 150-200 mg IV; steroids may be given IM or orally if IV access is unavailable
PO absorbed rapidly with similar bioavailability to IV
IV dosing can be used for vomiting or severely ill patients
IM as effective as PO
Duration rough guide 10-14 days for severe attacks
Tapering is not necessary
Treatment in Peds
Similar approach to adults
Levalbureol vs Racemic albuterol
Parental beta 2-agonist Epinephrine and Terbutaline
May be superior to inhaled beta 2-agonists for children with severe exacerbations and poor inspiratory flow or anxious young children who are uncooperative with or have suboptimal response to initial aerosolized therapy.
The intramuscular route may provide for more rapid drug absorption, although direct comparisons are lacking. In this setting, terbutaline may be expected to produce fewer adverse effects than epinephrine.
Heart failure (HF) is a common clinical syndrome representing the end-stage of a number of different cardiac diseases. It can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. There are two mechanisms by which reduced cardiac output and HF occur:
The New York Heart Association's classification:
Class I describes a patient who is not limited with normal physical activity by symptoms.
Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms.
Class III is characterized by a marked limitation in normal physical activity.
Class IV is defined by symptoms at rest or with any physical activity.
Labs Chem 7, CBC, Cardiac enzymes, BNP
ABG levels may be of benefit in evaluation of hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis.
ECG nonspecific tool but may be useful in diagnosing concomitant cardiac ischemia, prior myocardial infarction (MI), cardiac dysrhythmias, chronic hypertension, and other causes of left ventricular hypertrophy
ECHO Emergency transthoracic echocardiography may help identify regional wall motion abnormalities as well as globally depressed or myopathic left ventricular function.
ECHO may help reveal cardiac tamponade, pericardial constriction, and pulmonary embolus.
ECHO is also useful in revealing valvular heart disease, such as mitral or aortic stenosis or regurgitation.
CXR Chest radiography is the most useful tool diagnostic tool. A recent study showed that 1 out 5 patients admitted to the hospital with CHF lacked signs of congestion on chest radiograph.
Treatment Acute Decompensated Heart Failure
HOSPITALIZATION — Hospital admission is recommended for patients with ADHF with the following clinical conditions:
Worsened congestion, even if without dyspnea; typically reflected by a weight gain of ≥5kg
Signs and symptoms of pulmonary or systemic congestion, even in the absence of weight gain
Major electrolyte disturbance
Associated comorbid conditions such as pneumonia, pulmonary embolus, diabetic ketoacidosis, or symptoms suggestive of TIA or stroke
Repeated ICD firings
Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion
High BNP levels
Poor compliance or ability to manage symptoms as an outpatient
Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. However, the role of beta-blockers in the acute setting is currently unclear; limit use until hemodynamic studies indicate that further deterioration is not possible.
Digoxin has no place in the treatment of acute HF
Potassium sparring diuretics such as Spironolactone are generally reserved for class III or IV HF, aggressive use could result in hypokalemia
Nitroprusside Cardiac steal syndrome
Angiotensin-Coverting Enzyme Inhibitor
DDX of CHF based upon age
1 min anemia, acidosis, hypoxia, hypoglycemia,
1 hour hypocalcemia, sepsis
1 day PDA
1 week hypoplastic L verntricle
2 weeks Coarctation
1 month VSD
3 months SVT
1 year Myocarditis, Cardiomyopathy, severe anemia
10 year Rheumatic fever
DEFINITIONS — PE refers to obstruction of the pulmonary artery or one of its branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body
Acute or Chronic
Submassive or Massive which is defined as causes hypotension, defined as a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15 minutes
NATURAL HISTORY — Untreated PE is associated with a mortality rate of approximately 30 percent. Recurrent embolism is the most common cause of death.
RV dysfunction — RV dysfunction due to PE predicts increased PE-related mortality
Brain natriuretic peptides (BNP) — An elevated BNP or N-terminal pro-brain natriuretic peptide (NT-proBNP) predicts RV dysfunction and mortality, according to three meta-analyses
RV thrombus have a higher 14-day mortality
PATHOPHYSIOLOGY — Most PE arise from thrombi in the deep venous system of the lower extremities. However, they may also originate in the right heart or the pelvic, renal, or upper extremity veins.
It is estimated that 50 to 80 percent of iliac, femoral, and popliteal vein thrombi
Fortunately, most calf vein thrombi resolve spontaneously and only 20 to 30 percent extend into the proximal veins if untreated
SYMPTOMS / SIGNS
Dyspnea most common symptoms were at rest or with exertion (73 percent),
Pleuritic pain (44 percent)
cough (34 percent)
>2-pillow orthopnea (28 percent)
Calf or thigh pain (44 percent)
Calf or thigh swelling (41 percent)
Wheezing (21 percent)
Tachypnea (54 percent)
Tachycardia (24 percent),
Rales (18 percent),
Recreased breath sounds (17 percent),
Accentuated pulmonic component of the second heart sound (15 percent)
Troponins, BNP, ECG, CXR
Lower Extremity Ultrasound
Angiography — Pulmonary angiography is the definitive diagnostic technique or "gold standard" in the diagnosis of acute PE. It is performed by injecting contrast into a pulmonary artery branch after percutaneous catheterization, usually via the femoral vein. A filling defect or abrupt cutoff of a small vessel is indicative of an embolus. A negative pulmonary angiogram excludes clinically relevant PE.
Spiral CT 98 percent of patients with PE were detected by CT-PA
The frequency of negative CT-PA among patients without PE was more consistent, around 90 percent
Duration of Therapy