Dyspnea N Resp Failure

1) 2) 3) 4) 5) 6)

Presented by: Muhamad Yusof Shazwani Norhana Khairunnisa Zafirah Nur Ashila Nor Amalina

Case 1 1) A 72-year old man presented with a complaint of worsening exertional dyspnea for several weeks. He feels short of breath after walking 100 feet. • No chest pain • He had felt lightheaded, nearly faint while climbing a flight • of stairs, but relieved when he sat down. Difficulty sleeping at night and has to prop himself up with • 2 pillows. Occasionally, he wakes up at night feeling quite short of • breath, which is relieved within minutes by sitting upright. He denies any significant medical history, • Not on regular medications, doesn’t smoke or drink alcohol. •

DIFFERENTIAL DIAGNOSIS

Congestive Heart Failure

Pros: - worsening exertional dyspnea - Orthopnea - Nocturnal episode of severe paroxymal dyspnea

Myocardial Infarction Pros: - worsening exertional dyspnea - nearly faint Cons: - severe chest pain

Cont….. Emphysema Pros: - Worsening exertional dyspnea progressing to dyspnea at rest Cons: - Progressing for many years Pulmonary Vascular Occlusive Diseases (eg. Pumonary Embolism) Pros: - Near syncope on exertion Cons: - Repeated episodes of dyspnea at rest (recurrent pulmonary embolism)

CARDIOVASCULAR CAUSES OF DYSPNEA Acute left heart failure cause acute pulmonary edema

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Increase central venous pressure

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Increase pulmonary venous and capillary pressure

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Hydrostatic pressure of pulmonary capillaries > oncotic pressure of plasma ( 25-30mmHg ) Fluids moves into interstitium and alveoli cause pulmonary congestion and edema •

Reduce lung compliance, lead to hypoxaemia •

Dyspnea

Myocardial ischaemia  Induce true breathlessness by provoking transient left ventricular dysfunction or heart failure transient left ventricular dysfunction increase left ventricular diastolic pressure Increase pulmonary congestion Hypoxeamia & Dyspnea

INVESTIGATIONS These tests may be helpful in determining whether dyspnea is produced by heart disease, lung disease, abnormalities of the chest wall, or anxiety: Echocardiography or radionuclide ventriculography Pulmonary function testing exercise treadmill test

MANAGEMENT Urgent treatment: i. ii. iii. iv.

Sit the patient Give oxygen Administer nitrates Administer a loop diuretic like furosemide

Clinical Scenario A 65-years-old man with a long history of smoking and alcohol intake, present to the emergency department with a 4 days history of fever, cough that is productive of thick, foul smelling sputum ,dyspnoea for 3 days at rest, and left pleuritic chest pain.

DIFFERENTIAL DIAGNOSIS???

Differential diagnosis:• Pneumonia • Chronic bronchitis • Bronchial asthma • Pulmonary embolism • Congestive heart failure

Physical examination On examination, he has a temperature of 38.8. He has dullness to percussion over the posterior left lower lung zone; bronchial breath sounds and crackles are noted over the same area.

Condition

History

Signs

Massive •Prolong bed rest or •Severe central cyanosis •Elevated JVP pulmonary other risk factor embolus •Severe central chest •Shock (tachycardia, reduce BP) pain •Previous pleurisy •Syncope •Dizziness •Immediate dyspnea

Acute severe asthma

•History of previous •Tachycardia •Cyanosis (late) episodes. •Family history of •Peak flow meter reading ↓ •Rhonci asthma •Asthma medications •Chest wall movement ↓at both •Wheeze side •Immediate dyspnea •Normal perccussion and vocal resonance

COPD

•Previous episodes of breathlessness and productive cough •Weeks to year dyspnea.

Pneumonia •Fever •Rigors •Pleuritis •Hours to day dyspnea

•Signs of COPD(expiratory wheezing, barrel chest,use accessory muscle) •Emphysema referred to as “pink puffers •Chronic bronchitis are classically labeled “blue bloaters •Chest wall movement ↓both side •Fever •Pleural rub •Cyanosis (severe case) •Reduced chest wall movement at effected side •Dullness on percussion at effected site •Bronchial breath sound

Congestive heart failure

•Dyspnea on exertion •Orthopnea • Nocturnal episode of severe paroxymal dyspnea

•JVP distension •hepatomegaly •Tachycardia and tacypnea •Displaced apex beat

Pathophysiology of pneumonia Infection ↓ Proliferation of microorganisms within the alveolar space ↓ Acute inflammatory response ↓ Increase alveolar capillary permeability ↓ Impaired ventilation ↓ Decreased lung compliance ↓ Increased the work of breathing ↓ Dyspnoea

Pathophysiology of COPD Loss elasticity and alveolar attachment

Inflammation and scarring of small airway

Block airway

Reduce elastic recoil Airway collapse during expiration

Mucus secretion

Narrowing of small airway and air trapping Hyperinflation of lung and breathlessness

Investigation • • • • • •

Chest X-Ray Electrocardiogram Arterial Blood Gases Full blood count Sputum and blood culture Echocardiogram

Principles of management Treatment of pulmonary infection • Antibiotic Treatment of airway obstruction • Bronchodilator Pleuritic pain • Analgesia Hypoxaemia • Oxygen Others • Vaccination, diuretics for oedema, exercise training to improve sense of wellbeing and breathlessness

Clinical Scenarios • SYAHID, 14 year old boy presents to ED complaining of severe shortness of breath. He has long standing poorly controlled, Diabetes Mellitus type 1 for the past 6 years • About 3 days before admission, he had several episodes of vomiting, 5 times per day.

• Associated with generalize severe sudden burning abdominal pain 1 days prior to admission • Since then he has noted progressive SOB. Initially the SOB only occur on minimal exertion. • He also complain of passing massive volume of urine ,drinking so much of water per day, feel tired every day

• He had history of coma before • He is on regular insulin supplement since 6 years ago • Both Parent have history of diabetes mellitus

On examinations: Patient look very thin, fast breathing, obvious sub costal resection • BP = 100/75 mmHg, RR = 32/min, O2 saturation = 88%. • Pulse rate =95/ min • Capillary refill time = 3 second • Impression = tachypnoe, dehydration

• Provisional diagnosis? • Differential diagnosis? • What investigations that you would like to do?

Come with shortness of breath ??? Why???

Differential diagnosis? • • • • • •

Asthma Bronchitis Diabetic ketoacidosis Chronic obstructive pulmonary disease pulmonary edema Pulmonary embolism

Diabetic ketoacidosis •

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Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. It happens predominantly in those with type 1 diabetes,

Cause • • • • •

who already have diabetes inadequate insulin administration diabetes mellitus type 1 diabetes mellitus type 2 eating disorder

Symptoms of Diabetic ketoacidosis • • • • • •

nausea and vomiting increased respiratory rate. Shortness of breath dry mouth abdominal pain decrease in the level of consciousness • lethargy

How ketoacidosis cause dyspnea??? • In ketoacidosis pH is low and acidic so cause • The body buffers this with a mechanisms to compensate for the acidosis, • such as hyperventilation to lower the blood carbon dioxide levels. This hyperventilation cos dyspnea

• , in its extreme form, may be observed as Kussmaul respiration. • deep and labored breathing pattern associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also renal failure.

• Oooo….so the acidosis associate with occumulation of co2,,so body try to lower partial pressure of co2 by increase respiration ..then cause dyspnea..

investigation • • • • • • •

plasma glucose …glucose level Urea and electrolyte ….na usually increase Blood culture..infection by what? FBC…infection?? Urine test.. keturia, glycosuria, Chest x ray…lung normal??? Renal function test….cross react with keton?

Management • • • • • • •

Monitor vital sign Monitor glucose level..insulin supplement Fluid replacement to correct dehydration Ventilation support,o2 Antibiotic …if infection Iv bicarbonate Recheck atrial pH

DYSPNOEA

DEFINITIONS: feeling of uncomfortable need to breath INSATIABLE RESPIRATORY DISTRESS DESPITE MAXIMAL EFFORTS TO BREATHE

Dyspnoea occurs whenever the work of breathing is excessive

Mechanisms of DYSPNOEA

Dyspnea is characterized by an excessive or abnormal activation of the respiratory centers in the brainstem

STIMULI:(1) Intrathoracic receptors via the vagal nerves; (pneumothorax, intestitial inflammation, pul. Embolus) (2) Afferent somatic nerves,particularly from the respiratory muscles and chest wall, but also from other skeletal muscles and joints; (increased mech. load on ms.-obstruction, pul. Fibrosis ) (3) Chemoreceptors in the brain, aortic, and carotid bodies, and elsewhere in the circulation; (HYPOXIA, HYPERCAPNIA OR ACIDOSIS) (4) Higher (cortical) centers; (5) Afferent fibers in the phrenic nerves harrison’s text book

harrison’s text book

Dyspnoea may present either with • Chronic dyspnoea on exertion or • Acute dyspnoea at rest

Some causes of dyspnoea

System

Acute dyspnea at rest Chronic exertional dyspnea

CVS

*Acute pulmonary edema

Chronic heart failure

*Acute on COPD

*Chronic asthma

*Pneumothorax

Bronchial carcinoma

*Pulmonary Embolus

Intestitial lung disease

ARDS

Chronic pulmonary thromboembolism

RS

Myocardial ischemia *Acute severe asthma *COPD

Inhale foreign body Laryngeal edema

Lymphatic carcinomatosis

Metabolic acidosis

Severe anemia

Psychogenic hyperventilation

obesity

Lobar collapse

others

Large pleural effusion

Types • • • •

Nocturnal dyspnoea Orthopnoea Trepopnoea platypnoea

Grades (NYHA) • • • •

1- while doing more than normal activity 2- regular activity (moderate exercise) 3- mild exertion ( household work) 4- at rest.

• How to diagnose?????

Diagnosis: History • Pulmonary embolus suggested by sudden onset of shortness of breath or chest pain • COPD exacerbation suggested by history of Heavy smoking, cough, sputum production • Cardiogenic pulmonary edema suggested by chest pain, paroxysmal nocturnal dyspnea, and orthopnea

Diagnosis: Physical Findings 1. Wheezing suggests airway obstruction:

– Bronchospasm – Fixed upper or lower airway pathology – Secretions – Pulmonary edema

2. Stridor suggests upper airway obstruction 3. Elevated jugular venous pressure suggests right ventricular dysfunction due to accompanying pulmonary hypertension 4. Tachycardia and arrhythmias may be the cause • of cardiogenic pulmonary edema

Diagnosis: Laboratory Workup ABG • Quantifies magnitude of gas exchange abnormality Complete blood count • Anemia • Polycythemia suggests may chronic hypoxemia • Leukocytosis, a left shift, or leukopenia suggestive of • infection

Cardiac serologic markers • Troponin, Creatine kinase- MB fraction (CK- MB) Microbiology • Respiratory cultures: sputum/tracheal • aspirate/broncheoalveolar lavage (BAL) • Blood, urine and body fluid (e.g. pleural) cultures

Diagnostic Investigations Chest radiography • Identify chest wall, pleural and lung parenchymal pathology; and distinguish disorders that cause primarily V/Q mismatch (clear lungs) vs. Shunt (intra- pulmonary shunt; with opacities present) Electrocardiogram • Identify arrhythmias, ischemia, ventricular dysfunction Echocardiography • Identify right and/or left ventricular dysfunction

RESPIRATORY FAILURE Definition Classification Etiology Management Monitoring

Components of respiratory system • • • • • • *

CNS (Brain stem, spinal cord) Neuromuscular Airway Lung parenchyma (alveolar-capillary unit) Pulmonary circulation Chest wall (pleura, respiratory muscle, bones) Defect in each of these components may result in respiratory failure.

Definition • A syndrome of inadequate pulmonary gas exchange which leads to hypoxia with or without hypercarbia due to dysfunction of any component of the resp system. • PaO2 < 8 kPa (60mmHg). • PaCO2 > 7 kPa (55 mmHg).

Classification • Type 1 • Acute hypoxic • O2↓, CO2 normal or low • Due to condition that affect/damage lung tissue

• Type 2 • Ventilatory failure • O2↓, CO2↑ • Alveolar hypoventilation (decreased alveolar minute ventilation)- fail to remove CO2

• Type 3 • Due to lung atelectasis in perioperative period. • After GA, functional residual capacity decreases and lead to collapse of dependent lung units. • A.k.a. Perioperative respiratory failure

• Type 4 • Due to hypoperfusion of respiratory muscles in patients who are in shock.

Etiology • Type 1: – Pneumonia – Pulmonary edema • Cardiogenic e.g. LVF • Non-cardiogenic e.g. ARDS, ALI

– Pulmonary embolism – Pulmonary fibrosis – Atelectasis

Impaired component: lung tissue & pulm. circulation.

• Type 2: – Central hypoventilation: • Drug overdose • Brainstem injury • Hypothyroidism

– Airway: Asthma, COPD – Impaired neuromuscular transmission: • Myasthenia Gravis • Guillain-Barre Syndrome • Phrenic nerve injury

– – – –

Resp. muscle weakness: Myopathy, hypophospathemia Chest wall deformity: kyphoscoliosis Pleura: Pneumo/hydro/haemothorax Morbid obesity ( Obesity Hypoventilation Syndrome)

Impaired components: CNS, airway, n/muscular transmission, chest wall.

• Type 3: – Inadequate post-op anelgesia, upper abdominal incision (attemp to ↓ intraabdominal pressure) – Pre-op tobacco smoking – Obesity, ascites – Excessive airway secretions • Type 4 – Cardiogenic/ septic/ hypovolemic shock.

Outline of Management • Treat underlying cause(s): • Infection: antibiotics • Airway obstruction: bronchodilator, corticosteroids • Improve cardiac function: diuretics, vasodilator, inotropy.

• Oxygen therapy via simple face mask or nasal canulla. (O2 conc. 35-55%; O2 flow rate 6-10L/min.) if not improve/ PaCO2 ↑, need urgent

• Respiratory support (Mechanical ventilation): • Non-invasive - via tight-fitting nasal or face mask. • Invasive - need endotracheal intubation/ tracheostomy.

Monitoring of Respiratory Failure •

Clinical assessment of respiratory distress – signs: • Use if accessory muscle • Intercostal recession • Tachypnoea, tachycardia, sweating • Unable to speak, unwillingness to lie flat • Restlessness, reduced conscious level

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Pulse oximetry- measure the arterial O2 saturation (SaO2) Blood gas analysis Capnography – analysis of expired CO2 conc.