brain death .pptx presentation in King George's medical University Lucknow in emergency medicine department by Dr Rahul Kumar yadav

BRAIN DEATH
Dr Rahul
Moderator - Dr pranay
Guide - Dr H Abbas
Dr Mukesh

A 65-year-old male, a former smoker with a 30-pack-year
history.He has a known diagnosis of moderate to severe
COPD.The patient has a medical history of hypertension
and occasional use of short-acting bronchodilators.
C/O - The patient presents to the emergency department with complaints of worsening
shortness of breath, increased cough with purulent sputum production, and increased
wheezing for the past 48 hours.He reports that he has been feeling generally unwell and
more fatigued than usual.

Vital signs - vital signs reveal an elevated respiratory rate, increased heart rate, and
mild hypoxemia (low blood oxygen levels).
On physical examination - the patient appears distressed, with increased use of
accessory muscles for breathing, and there are diffuse
wheezes and decreased breath sounds on auscultation.
ABG - Arterial blood gas analysis shows respiratory acidosis with elevated carbon
dioxide levels (hypercapnia).
LABORATORY INVESTIGATION - Laboratory tests may reveal an elevated white
blood cell count, indicating possible infection.

Based on the clinical presentation
and history, the patient is diagnosed
with an acute exacerbation of COPD.

Acute Asthma and Status
Asthmaticus

INTRODUCTION AND EPIDEMIOLOGY
1. Asthma is a chronic inflammatory disorder characterized by increased
airway responsiveness to various stimuli.
2. It leads to recurrent episodes of symptoms, including wheezing,
breathlessness, chest tightness, and coughing, often occurring at night
or in the early morning.
3. Approximately 8% of the U.S. population has asthma, making it a
prevalent condition.
4. Asthma is the most common chronic disease in childhood, affecting
around 9% of children.
5. About half of asthma cases develop before the age of 10, and a third
develop by the age of 40.

PATHOPHYSIOLOGY
1. Cellular Accumulation: Asthma sufferers experience an abnormal accumulation of
various immune cells in their airways, including eosinophils, lymphocytes, mast
cells, macrophages, dendritic cells, and myofibroblasts.
1. Pathophysiologic Hallmark: The key characteristic of asthma is a reduction in
airway diameter due to several factors, including smooth muscle contraction,
vascular congestion, bronchial wall edema, and thick secretions.
These changes lead to alterations in pulmonary function, increased breathing effort,
and abnormal pulmonary blood flow distribution.

3 . Airway Plugs: Both large and small airways can contain plugs composed of
mucus, serum proteins, inflammatory cells, and cellular debris,
contributing to airflow obstruction.
4. Inflammation: Inflammation affects all parts of the bronchial and pulmonary
structures, leading to airway remodeling.
5. Airway Remodeling: Acute bronchospasm to airway inflammation and, ultimately
permanent airway remodeling.
This remodeling involves sub-basement membrane thickening, subepithelial fibrosis,
airway smooth muscle hypertrophy and hyperplasia, angiogenesis, and mucous gland
hyperplasia and hypersecretion. It can result in non-reversible loss of lung function.

Physiologic Consequences of Airflow
Obstruction in Acute Asthma

Triggers for Acute Asthma:
● Acute viral infections (most common stimulus)
● Exercise
● Environmental conditions (pollutants, indoor antigens)
● Occupational exposures (various chemicals and substances)
● Certain medications (aspirin, β-blockers, NSAIDs)
● Exposure to cold air
● Endocrine factors (hormonal changes during the menstrual cycle and
pregnancy)
● Emotional stress

CLINICAL FEATURES
The typical symptoms of acute asthma include-
● Dyspnea
● Wheezing
● Cough

PHYSICAL EXAMINATION IN ACUTE ASTHMA
● General Appearance:
-Signs of respiratory distress, which may include increased effort in breathing.
-The level of consciousness to evaluate mental status.
● Vital Signs:
-Tachycardia (elevated heart rate) as a sign of stress on the cardiovascular system
-Tachypnea (rapid breathing) as an indicator of increased respiratory effort.
● Chest Findings:
- Wheezing may be present but can be unreliable, especially in severe cases.
-Note that a silent chest, without wheezing, is indicative of extremely severe
airflow obstruction.

● Signs of Severe Acute Asthma:
1 Use of accessory muscles for breathing, indicating increased respiratory effort.
2 Inability to speak in full sentences or phrases due to breathing difficulties
3.Presence of pulsus paradoxus, a drop in systolic blood pressure during
inspiration, which can be a sign of severe airway obstruction.
● Concomitant Illnesses:
1 Pneumonia, which can present with fever and lung sounds consistent with
infection.
2 Pneumothorax, which may manifest as sudden chest pain and shortness of
breath.

DIAGNOSIS AND PATIENT MONITORING
● Subjective Symptoms
● Forced Expiratory Volume in 1 Second (FEV1)- FEV1 is a key objective measure
to assess the severity of acute asthma.
It can help distinguish between various lung disorders and obstructive disorders like
asthma.
● Peak Expiratory Flow Rate (PEFR)-PEFR, measured using a peak flow meter,
provides an estimate of acute asthma severity.
PEFR measurements are useful for monitoring treatment response.
● Comparison of FEV1 or PEFR- Comparing FEV1 or PEFR measurements at ED
presentation and 1 hour after treatment is a good predictor of hospitalization in
acute asthma patients.

● Patient Education and Cooperation- Reliable measurements of FEV1 and PEFR
require patient education and cooperation.
● Pulse Oximetry- Pulse oximetry is used to assess oxygen saturation during
treatment.
● Arterial Blood Gas (ABG) Measurement- ABG measurement is not needed for
mild to moderate asthma exacerbation.
It is reserved for cases with suspected hypoventilation, carbon dioxide retention,
and respiratory acidosis.
● Chest Radiographs- Chest radiographs are used to detect complications or other
causes of symptoms.
They are selectively used when conditions like pneumothorax,
pneumomediastinum, pneumonia, or acute heart failure are suspected.

● CBC (Complete Blood Count)- A CBC is not routinely needed in acute asthma
cases.
Modest leukocytosis may be observed due to β-agonist therapy or corticosteroids.
● Immunoglobulin E (IgE) and Eosinophil Quantification- In cases of severe acute
asthma, these measures can aid in chronic asthma management using biologic
agents.
● ECG (Electrocardiogram)- Routine ECG is usually unnecessary.
It may reveal certain abnormalities but often normalizes with treatment.
Cardiac monitoring is recommended for older patients and those with heart disease.

ACUTE ASTHMA STANDARD TREATMENT
● The primary goal is the rapid reversal of airflow obstruction in acute asthma.
(1) β-ADRENERGIC AGENTS - Rapid-onset β2-adrenergic agonists are the preferred
initial therapy for acute bronchospasm.
MOA - Stimulation of β2-receptors promotes bronchodilation and vasodilation.
This helps relax and open the airways.
Levalbuterol vs. Albuterol- Levalbuterol is more expensive than albuterol but does
not show a clear advantage in terms of symptom improvement, hospitalization
rates, or tachycardia.
Aerosol Therapy- Aerosol therapy with β2-adrenergic drugs is preferred over oral
or parenteral routes.
It achieves targeted delivery with minimal systemic absorption and fewer side
effects.

Delivery Methods- Aerosol delivery can be done with a metered-dose inhaler
coupled to a spacing device or a compressor-driven nebulizer.
Proper use of a spacing device with a metered-dose inhaler is highly effective.
Drug Retention- Even with optimal technique, a maximum of 15% of the drug dose
is retained in the lungs, regardless of the aerosol method used.
Alternative Options - Subcutaneous (SC) epinephrine and terbutaline are options
for patients who cannot coordinate aerosolized or metered-dose inhaler treatments,
often seen in severe airflow-limited states.
Long-Acting β2-Adrenergic AgonistsSalmeterol xinafoate and formoterol are
long-acting β2-adrenergic agonists used for maintenance, not acute, therapy.
Their bronchodilator effects last at least 12 hours and do not show tachyphylaxis
with long-term use.

Combination Therapy- Long-acting β2-adrenergic agonists are often used in
conjunction with inhaled corticosteroids for long-term control of asthma.
Short-acting β2-adrenergic agonists like albuterol are used for infrequent or
breakthrough symptoms despite long-acting therapy.
(2) CORTICOSTEROIDS- Corticosteroids are used in all cases of acute asthma except
for mild, easily fully reversed episodes.
Mechanism of Action - Corticosteroids produce beneficial effects by restoring β-
adrenergic responsiveness and reducing inflammation.
Peak Anti-Inflammatory Effect- The peak anti-inflammatory effect of
corticosteroids occurs at least 4 to 8 hours after intravenous (IV) or oral (PO)
administration.

Early Use- Early administration of corticosteroids is advisable; giving them within 1
hour of arrival in the emergency department (ED) reduces the need for
hospitalization.
Dosage- An initial dose of PO prednisone (40 to 60 milligrams) or IV
methylprednisolone (1 milligram/kg) is sufficient in acute asthma.
Higher doses do not offer a clear advantage.
Discharge Medication- Patients discharged after ED treatment are typically given
a 5- to 10-day nontapering course of prednisone (40 to 60 milligrams/d) or a 2-day
course of oral dexamethasone (16 milligrams/d).
A single dose of depot methylprednisolone (150 milligrams IM) is an alternative for
patients with compliance concerns.

Maintenance Corticosteroids- Inhaled corticosteroids are recommended for all
patients with mild persistent asthma or more severe chronic asthma.
Patients with mild persistent or more severe asthma should be discharged on
maintenance inhaled corticosteroids, in addition to any systemic bursts.
Inhaled Corticosteroid Options- Options for inhaled corticosteroids include
beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and
triamcinolone acetonide, with specific dosage ranges.

(3) ANTICHOLINERGICS- Anticholinergics are used as additive therapy alongside
β-adrenergic agents in ED patients with acute asthma.
Targeted Airway Effects- Anticholinergics primarily affect large, central airways,
while β-adrenergic drugs predominantly dilate smaller airways.
Commonly Used Anticholinergic- Inhaled ipratropium bromide is a commonly
used anticholinergic.
It is available as a nebulized solution, a metered-dose inhaler, or in combination
with albuterol.
Dosage in ED Patients- In ED patients with moderate to severe exacerbation, an
aerosolized ipratropium bromide solution (0.5 milligram) is used

Benefits- Adding multiple doses of ipratropium bromide to a short-acting selective
β-agonist may improve bronchodilation and reduce the rate of hospitalization in
patients with moderate-to-severe acute asthma.
However, this benefit may not be universal.
Potential Side Effects- Potential side effects of anticholinergics include dry mouth,
tachycardia, restlessness, irritability, confusion, difficulty in urination, ileus, blurring
of vision, and an increase in intraocular pressure.
Role of Long-Acting Anticholinergic Agents- Long-acting anticholinergic agents
do not have a role in acute asthma care and are not used for this purpose.

FOLLOW-UP OF PATIENTS WITH ACUTE ASTHMA
● A good response to treatment results in symptom resolution and PEFR >70%
predicted, allowing safe discharge.
● A poor response includes persistent symptoms and FEV1 or PEFR <40%
predicted, usually requiring observation or hospitalization.
● An incomplete response is common, with some persistence of symptoms and
FEV1 or PEFR between 40% and 69% predicted; most of these patients can be
discharged home, while some may benefit from prolonged

STATUS ASTHMATICUS (ACUTE SEVERE ASTHMA)
Status asthmaticus is an acute and severe form of asthma that does not
respond to usual doses of inhaled bronchodilators and corticosteroids.
Clinical Findings:
● Hypoxemia
● Tachypnea
● Accessory Muscle Use
● Wheezing

TREATMENT
● Rapid and aggressive bronchodilator treatment is crucial to prevent
cardiopulmonary arrest.
(1) IV Magnesium Sulfate:
-Indicated for acute, very severe asthma with FEV1 or PEFR <25% predicted.
-Dose: 1 to 2 grams IV over 30 minutes.
-Nebulized magnesium can be used in conjunction with β-agonists and
corticosteroids.
-Monitor blood pressure and reflexes during administration.

(2) Noninvasive Positive-Pressure Ventilation (NPPV)-
● Improves airflow and respiration compared to usual care.
● May reduce the need for tracheal intubation and improve clinical outcomes.
● Not suitable for patients with altered sensorium or near respiratory collapse.
● Pneumothorax should be ruled out before starting NPPV.
(3) Ketamine:
● Can be used to aid some severe acute asthma cases.
● IV bolus dose of 0.15 milligram/kg followed by an infusion of 0.25 milligram/kg/h.
● May also be used as premedication or sedative during intubation.
● Limited controlled trial data on ketamine's outcomes in treating severe acute
asthma.

(4) Epinephrine:
● Considered an adjunct treatment for status asthmaticus.
● Give epinephrine SC or IM (0.5 milligram in adults) for refractory situations.
(5) Mechanical Ventilation:
● Indicated when the patient exhibits progressive hypercarbia, acidosis, exhaustion,
or confusion to prevent respiratory arrest.
● Mechanical ventilation doesn't relieve airflow obstruction but reduces the work of
breathing.
● Potential complications include high peak airway pressures, barotrauma, and
hemodynamic issues.
● Sedation is required, and neuromuscular blocking agents may be needed.

Chronic Obstructive Pulmonary Disease

INTRODUCTION AND EPIDEMIOLOGY
● COPD is a common, preventable, and treatable respiratory disease characterized
by persistent respiratory symptoms and airflow limitation. It is primarily caused by
exposure to noxious particles or gases.
● COPD encompasses various conditions, including:
1 Chronic bronchitis
2 Emphysema
3 Bronchiectasis
4 Asthma
5 Most patients may have a combination of these different diseases.
● COPD is a widespread health issue and is a significant cause of morbidity and
mortality globally.

● In the United States, COPD is the third leading cause of death. Interestingly, more
than 50% of COPD-related deaths now occur in women.
● COPD is preventable through measures like avoiding exposure to harmful particles
or gases, particularly by quitting smoking. Treatment options are available to
manage symptoms and improve quality of life for those with COPD.

Risk Factors:
1. Tobacco Smoke: Major risk factor for COPD; however, only about 15% of smokers
develop the condition.
1. Occupational Exposure: Exposure to occupational dust and chemicals increases
the risk.
1. Air Pollution: Prolonged exposure to air pollution is another significant risk factors
1. α1-Antitrypsin Deficiency: Accounts for less than 1% of COPD cases.

Pathophysiology
1. Irritants: Such as tobacco smoke and air pollutants trigger inflammation.
1. Inflammatory Cells: Increase in airways, lung interstitium, and alveoli.
1. Cellular Changes:
Proteases: Enzymes that break down lung tissue and stimulate mucus production.
Cell Replacement: Mucus-secreting cells replace surfactant-secreting cells.
1. Consequences: Loss of lung elasticity, airway narrowing, and smaller airway
collapse.

CLINICAL FEATURES
Hallmark Symptoms:
1. Chronic and Progressive Dyspnea: A primary symptom that worsens over time
2. Cough: Persistent and often varies from day to day.
3. Sputum Production: Chronic and progressive; varies in quantity.
Additional Symptoms
1. Hemoptysis: Minor hemoptysis is frequent, especially in those with chronic
bronchitis and bronchiectasis, but it may also indicate the possibility of lung cancer.

5. Physical Findings: May include:
● Tachypnea: Rapid breathing.
● Accessory Respiratory Muscle Use: Due to increased effort in breathing
● Pursed-Lip Exhalation: A technique used to relieve shortness of breath.
6.Lower Airway Obstruction: Expiratory Wheezing: Especially prominent
during maximum forced exhalation.
7.Prolonged Expiratory Time: Due to obstruction, making exhalation slower.

DIAGNOSIS
1. Suspect chronic, compensated COPD based on symptoms and risk exposure
profiles.
2. Confirm COPD diagnosis with spirometry, showing a postbronchodilator
FEV1-to-forced vital capacity ratio of <0.7.
3. As the disease progresses, the percentage of predicted FEV1 becomes a
better measure of disease severity.
4. Radiographic Findings:
- Chronic bronchitis is not radiographically apparent unless bronchiectasis is
present.
-In emphysema, radiographs show hyperaeration, seen as increased
anteroposterior chest diameter, flattened diaphragms, increased parenchymal
lucency, and attenuation of pulmonary arterial vascular shadows.

Underdiagnosis of COPD:
1. COPD is often underdiagnosed due to various factors, with more than
50% of patients meeting spirometric criteria not receiving a COPD
diagnosis.
1. Patients may attribute respiratory declines or a chronic cough to aging
or smoking.

Distinguishing from Acute Heart Failure:
1. Distinguishing between acute heart failure and COPD can be
challenging.
1. A B-type natriuretic peptide (BNP) level <100 picograms/mL supports a
diagnosis of COPD.
1. BNP levels >500 picograms/mL have a sensitivity of 80% and a positive
predictive value of 47% for acute heart failure.
1. The electrocardiogram (ECG) detects dysrhythmias or ischemia but
does not accurately assess the severity of pulmonary hypertension or
right ventricular dysfunction.

TREATMENT OF COPD
(1) Oxygen Therapy:
● Long-term oxygen therapy is essential to reduce COPD mortality.
● The goal is to increase the baseline partial pressure of arterial oxygen (PaO2) to
≥60 mm Hg or arterial oxygen saturation (SaO2) to ≥90% at rest.
● Criteria for long-term oxygen therapy include-
- PaO2 ≤55 mm Hg, SaO2 ≤88%, or
-PaO2 between 56 and 59 mm Hg in the presence of pulmonary hypertension,
cor pulmonale, or polycythemia.

(2) Pharmacotherapy:
● Pharmacotherapy does not cure COPD but offers symptom relief, controls
exacerbations, improves quality of life, and enhances exercise performance.
● Long-acting inhaled β2-agonists (e.g., salmeterol, formoterol) are preferred for
baseline care.
● Short-acting inhaled β2-agonists (usually albuterol) are used as needed.
● Combining bronchodilators with different mechanisms and durations may improve
bronchodilation.
● Long-acting anticholinergic agents (e.g., tiotropium) are preferred over short-acting
ones.

● Inhaled corticosteroids are used daily for patients with documented spirometric
response, FEV1 <50%, or recurrent exacerbations.
● Combination inhalers with long-acting β2-agonists and corticosteroids are suitable
for high-risk patients.
● Daily azithromycin may reduce acute exacerbations, especially in older patients.
● Limit the use of antihistamines, antitussives, mucolytics, and decongestants.

(3) Smoking Cessation:
● Smoking cessation is the most effective intervention to slow lung function decline
and reduce respiratory-related mortality.
● The emergency department is a key site to initiate smoking cessation interventions.
● Combining nicotine replacement therapy or medications with behavioral
interventions can aid in quitting smoking.

(4) Pulmonary Rehabilitation:
● Pulmonary rehabilitation can enhance exercise capacity and quality of life,
particularly for moderate to severe COPD patients.
(5) Vaccination
● Pneumococcal and influenza vaccinations are crucial to reduce the risk of acute
respiratory infections in COPD patients.

ACUTE EXACERBATIONS OF CHRONIC
OBSTRUCTIVE PULMONARY DISEASE
Triggers for COPD Exacerbations:
1. Acute exacerbations of COPD are typically triggered by infections (viral or bacterial)
or respiratory irritants.
1. Gastroesophageal reflux disease is an additional risk factor.
1. Other triggers include hypoxia, cold weather, β-blockers, opioids, and sedative-
hypnotic agents.

Pathophysiology of COPD Exacerbations:
1. Exacerbations lead to the release of inflammatory mediators causing
bronchoconstriction, pulmonary vasoconstriction, and increased mucus production
1. Increased airway resistance and lung hyperinflation result in greater work of
breathing.
1. This leads to higher oxygen demand, increased carbon dioxide production, and
hypercapnia.

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