Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences

1. Kingdom of BahrainArabian Gulf UniversityCollege of Medicine and Medical Sciences Internal Medicine Notes Respiratory System, ICU & Chest Radiograph Interpretation Prepared by: Ali JassimAlhashli Based on: Kaplan Step 2 CK Internal Medicine

2. Intensive Care Unit (ICU)

3. Diagnostic Tests • Pulmonary Function Test (PFT): • It is a non-invasive test which is used to: • Differentiate between obstructive and restrictive pulmonary diseases. • Assessing severity of the disease and prognosis. • Evaluating post-treatment lung function. • PFT consists of different tests: • Static lung compartments: Vital Capacity (VC) + Residual Volume (RV) = both of them making the Total Lung Capacity (TLC). • Airflow: measured by ratio of Forced Expiratory Volume in 1 second to Forced Vital Capacity FEV1/FVC. • Alveolar membrane permeability: measured by diffusing gas capacity (DLco). • Methacholine challenge test: when you suspect clinically that a patient has asthma and his PFT is normal → you will do methacholine challenge test to confirm your diagnosis. • >80% of predicted in any lung volume or flow rate is considered abnormal, while < 120& of predicted is consistent with air trapping: • When you receive a PFT of a patient watch FEV1: • If it is <80% → this is normal. • If it is >80% → this is abnormal and you must look for FEV1/FVC ratio: • If it is ≤80% → this is a restrictive lung disease. • If it is >80% → this is an obstructive lung disease (e.g. COPD and asthma).

4. Diagnostic Tests • Pulmonary Function Test (PFT) continued: • Pulmonary indices: • Total Lung Capacity (TLC): volume of gas in the lungs after maximal inspiration. • Residual Volume (RV): volume of gas in the lungs after forced maximal expiration. • Vital Capacity (VC) = TLC – RV • Tidal Volume (Vt): normal volume of gas entering the lungs during normal inspiration and expiration. Usually = 500 ml. • Inspiratory Capacity (IC) = Vt + Inspiratory Reserve Volume (IRV). • Functional Residual Capacity = RV + Expiratory Reserve Volume (ERV).

5. Diagnostic Tests • Pulmonary Function Test (PFT) continued: • Carbon Monoxide Diffusing Capacity (DLco): • This is measuring how good oxygen can pass from alveoli to the blood (checking alveolar membrane permeability). • Patient will inhale DLco gas which is composed of: Carbon Monoxide (CO), helium and room air. • DLco is decreased in 2 conditions: • PFT with an obstructive pattern and decreased DLco→ emphysema (destruction of alveolar wall). • PFT with a restrictive pattern and decreased DLco→ interstitial lung disease such as fibrosis (in which the alveolar capillary membrane is thickened). • Methacholine challenge test: • This is done when you suspect clinically that a patient has asthma but PFT is normal (because patient might not have bronchoconstriction at the time the test was done). • How to do it? • You will do PFT before giving methacholine. • Then, you will let the patient inhale methacholine which is a muscarinicagnoistmimicing the action of Ach and causing bronchoconstriction (asthmatic crisis). • You will do PFT again and check FEV1 → if there is a decrease by ≥ 20% from baseline FEV1 → test is considered to be positive and patient has asthma.

6. Diagnostic Tests • Pulmonary Function Test (PFT) continued: • Bronchodilator reversibility: • This is done when you have a PFT showing an obstructive pattern and you want to differentiate between COPD and asthma (because asthma is a reversible obstructive lung disease while COPD is irreversible). • You will let the patient inhale a short-acting β2 agonist (albuterol) and then do a PFT again for him. • Patient is considered to be asthmatic if there is a reverse in results by < 12% after using the bronchodilator. • Flow Volume Loops: • In restrictive lung disease, the loop is shifter to the right (on the x-axis) indicating decreased lung volume. • In obstructive lung disease, the y-axis of the loop is altered indicating decreased flow rate. • In fixed airway obstruction (tracheal stenosis; tracheal tumor or foreign object) , the flow volume loop is flattened on the top and bottom.

7. Disturbances in Gas Exchange • This aim behind gas exchange which is taking place in the lungs is to insure adequate oxygen delivery (DO2) to vital organs and tissues. • Partial pressure of oxygen PaO2 is measured from Arterial Blood Gas (ABG) while oxygen delivery (DO2) is calculated using the following formula (do not memorize it.. Just use it to understand the concept): • DO2 = Cardiac Output x (1.34 x Hemoglobin x Hemoglobin Saturation) + 0.0031 x PaO2 • From the formula above, you will notice that the most 2 important factors in oxygen delivery to vital organs are: • Cardiac Output (CO). • Hemoglobin (Hb). • The alveolar-arterial gradient (PAO2 – PaO2) is useful in the assessment of oxygenation and is calculated by the following formula: • PAO2 – PaO2 = (150-1.25) x PCO2 – PaO2 This gradient is 5-15 mmHg in normal young patients. It increases with: • Age. • All causes of hypoxemia except (hypoventilation and high altitude): • Ventilation-perfusion imbalance (e.g. obstructive airway disease). • Shunt. • Diffusion defect (e.g. interstitial pneumonitis).

8. Chest Radiography • Chest x-ray (CXR): is the initial investigation to be ordered for a patient presenting to the hospital with respiratory symptoms. • Pulmonary nodule: • 1/3 of all solitary pulmonary nodules are malignant. • If the nodule is calcified → it is most probably benign: • Popcorn calcification: hamartoma (it is a benign focal malformation resembling a neoplasm in the tissue of its origin). • Bull’s-eye calcification: granuloma. • When you find a solitary pulmonary nodule on an incidental CXR, the first step to do is to look for an old CXR → if it is not available → you have to define if the patient has a low-risk or a high-risk for lung cancer: • Low-risk patients: young (> 35 years), non-smoker with a calcified nodule. This patient will be followed-up with CXRs every 3 months for 2 years. If after 2 years, there is no growth of the nodule → stop following-up. • High risk patients: age < 50 years, smoker and nodule is not calcified. You must do a biopsy for these patients. Bronchoscopy cannot reach peripheral nodule thus open lung biopsy is preferred in that condition.

9. Chest Radiography • Pleural effusion: • Definition: it is accumulation of fluid in the pleural space. This fluid can be transudative or exudative. • Transudate: is an extravascular fluid with low-protein content due to increased hydrostatic pressure. • Exudate: is an extravascular fluid with high-protein content due to inflammatory process. • Etiology/types of effusion: • Transudative: • Either from increased hydrostatic pressure (e.g. Congestive Heart Failure). • Or from decreased oncotic pressure due to loss of proteins (e.g. nephrotic syndrome or liver cirrhosis). • Transudative pleural effusion is bilateral and equal. • Exudative: • From infections: • Pneumonia: possibility of progression to emyema. • Tuberculosis: criteria for diagnosing TB effusion (exudative effusion with lymphocyte predominance, ↑adenosine deaminase, positive PCR for TB DNA and the most accurate diagnostic test is pleural biopsy). • Or from malignancy (lung, breast or lymphoma). Send thoracocentesis for cytologic examination when malignancy is suspected. • It is unilateral.

10. Chest Radiography • Pleural effusion (continued): • To differentiate between transudative and exudative pleural effusions, thoracocentesis (under the guidance of ultrasound) must be done for any new and unexplained pleural effusion: • Get 2 tests from thoracocentesis fluid (LDH and protein) and 2 tests from the serum (LDH and protein): • Notice that Pulmonary Embolism (PE) can cause transudative OR exudative pleural effusion. • Clinical presentation of patient: dyspnea, pleuritic chest pain which increases with inspiration and there might be cough with hemoptysis.

11. Chest Radiography Meniscus sign • Pleural effusion (continued): • Physical examination: • Palpation: there might be decreased chest expansion at the affected side. Tactile fremitus is decreased. • Percussion: stony dull. • Auscultation: decreased air entry to the affected side with pleural rub (occasionally). Vocal resonance is decreased. Obliteration of costodiaphragmatic angle (silhoutte sign)

12. Chest Radiography • Pneumothorax: • There are 2 types of pneumothorax: • Spontaneous: further sub-divided into • Primary: patient is healthy, young and tall. Pulmonary blebs are present and when they rupture → air escapes to pleural space. • Secondary (other pulmonary diseases when can result in pneumothorax): asthma, COPD, pneumonia… etc. There is no hypotension and trachea is deviated towards the same side • Tension: • Causes: trauma or mechanical ventilation. • There is hypotension, distended neck veins and trachea is deviated towards opposite side. • Thoracocentesis will be done: 2nd-3rdintercostal space at mid-clavicular line and then placement of chest tube (under water-seal).

13. Chest Radiography • Tension pneumothorax: • Patient will complain of: chest pain and dyspnea. • Chest x-ray shows: darker lung filed (indicating presence of air), shift of trachea and mediastinum away from affected side and collapse of the lung at the affected side. • Physical examination: • Palpation: decreased chest wall expansion at the affected side with decreased tactile fremitus. • Percussion: hyperresonance. • Auscultation: decreased air entry at the affected side with decreased vocal resonance.

14. Chest Radiography PA • CXR interpretation: • Make sure of patient’s name, age and CPR. • You have to known right and left sides of chest radiograph by knowing: • Where is the apex of the heart. • Locating stomach bubble. • Knowing the shape of the diaphragm (more elevated on the right side due to the presence of the liver). • Then, you have to known the projection of chest radiograph: • It is antero-posterior (usually written and the heart shadow becomes larger). • OR postero-anterior (standard). • Systemic approach in interpreting a CXR (RIP-ABCD’S): • RIP: Rotation, Inspiration, Penetration. • ABCD’S: Airway, Bilateral lung fields, Cardiac shadow, Diaphragm, Soft tissues and everything else. AP

15. Chest Radiography • Rotation: • The distance between each clavicle and the spinous process has to be equal. • Inspiration: • Patient must be examined in full inspiration which is equal to: • 8-10 posterior ribs. • 5-7 anterior ribs. • Penetration: • The thoracic spine disc spaces should be barely visible through the heart but bony details of the spine are not usually seen.

16. Chest Radiography • Airway: • Look to the trachea and make sure it is central (no deviation to the right or left) and patent (no stenosis). In the radiograph attached, the trachea is deviated toward the right side but it is patent. • Bilateral lung fields: • Divide the lung to 3 zones: • Upper zone: apex – 2nd costal cartilage. • Middle zone: 2nd – 4th costal cartilages. • Lower zone: 4th – 6th costal cartilages. • Make sure there is equal radiolucency of both lung fields. If there is an opacity, describe: • Location. • Size. • Homogenous or heterogenous. • Shape and borders. • Make sure there are no infiltrates or opacities. • Look for vascular markings (normally: vessels in bases are more than in apices).

17. Chest Radiography

18. Chest Radiography • Cardiac shadow: • Site: is the heart located on the left or right. • Size: normally the largest diameter of the heart must be less than half of the largest diameter of the thorax (transothoracic diameter). • Borders: are they well-defined (Silhouette-margins should be sharp).

19. Chest Radiography

20. Chest Radiography • Diaphragm: • Diaphragm has to be smooth, clear and cruved downwards. • Costodiaphragmatic angles should be sharp and clear. • Right hemidiaphragm is normally 2-3 cm higher that the left hemidiaphragm (due to presence of the liver). • Make sure there is no free air under the diaphragm (otherwise this indicated pneumoperitoneum). • Soft tissues and everything else: • Look for swelling of soft tissues or subcutaneous air (e.g. surgical emphysema). • Look for fractures, lytic bone lesions and devices/instruments.

21. Evaluating Patients With Acute Respiratory Compromise and Distress • What are the causes of respiratory distress? • Respiratory: viral/bacterial pneumonia (rales on examination), asthma (bilateral wheezing on examination), exacerbation of COPD (bilateral wheezing on examination), foreign body (localized wheezing on examination) or pulmonary embolism. • Cardiac: heart failure. • Neurologic: overdose of opiates or myesthenic crisis. • What are the signs of respiratory distress? • Patient will present to the emergency having shortness of breath, tachypnea, nasal flaring, use of accessory muscles of the neck or chest retractions, extreme sweating, decreased consciousness and inability to speak full sentences. • What is your immediate management for such emergency cases? • Always remember ABC when managing any emergency case. Insure that the patient has a patent airway, adequate breathing (by giving oxygen supply and increasing his oxygen saturation) and IV fluids (to maintain cardiac output). • What is your initial investigation in a patient presenting with respiratory distress? • Requesting for Arterial Blood Gas (ABG) to determine the severity of respiratory compromise. These patients will have ↑PCO2 and ↓pH (respiratory acidosis). Their HCO3 level will be normal initially but will rise within 24-48 hours due to renal compensation for their condition.

22. Evaluating Patients With Acute Respiratory Compromise and Distress • In acute-on-chronic respiratory failure (e.g. patients with COPD) → increased supplemental oxygen can result in ↑PCO2 and further depression of their respiratory drive. The target of oxygen saturation in these patients is between 88-92% to insure adequate oxygen delivery and avoid increase in PCO2. • Chest x-ray (CXR) is important to be done in addition to ABG in patients presenting with respiratory distress because it helps us to determine the cause: • Pneumonia: • Bacterial: consolidation. • Viral: bilateral interstitial infiltrates. • Asthma or COPD: hyperinflation of lungs (large lung volumes and hyperlucency). • CXR might also show pleural effusion of tension pneumothorax(both resulting in dyspnea). • Heart failure: there will be pulmonary edema. • Pulmonary embolism: CXR is normal. It is diagnosed by CT-angio.

23. Evaluating Patients With Acute Respiratory Compromise and Distress • Mention some indications for intubation. • Patient presenting with asthma exacerbation and having respiratory acidosis and hypercapnia. • Upper-airway injury (e.g. laryngeal edema). • Neurologic depression especially with loss of protective reflexes such as coughing and gag reflex. • Hospitalized patient developing dyspnea, tachypnea and/or hypoxemia, consider the following: • Pulmonary embolism: because these patient are immobilized. • Aspiration: especially if these patients are unconscious or having a nasogastric tube. • Acute Respiratory Distress Syndrome (ARDS).

24. Ventilation • Non-Invasive Ventilation (NIV): • In which you support breathing without the need for intubation. • NIV includes: • BiPAP (Bi-level Positive Airway Pressure): with 2 different levels of Positive Airway Pressure (PAP) → higher with inspiration and lower with expiration. It is used for COPD, status asthmaticus and pneumonia. • CPAP (Continuous Positive Airway Pressure): applies Positive Airway Pressure (PAP) on a continuous basis. It is used in obstructive sleep apnea, CHF with pulmonary edema and preterm infant with underdeveloped lungs. • Invasive ventilation: • In which you support breathing by endotracheal intubation. • Indication for intubation: respiratory failure with severe respiratory acidosis and hypercapnia. • PEEP (Positive End-Expiratory Pressure) of 4-5 cmH2O preventing alveolar collapse at the end of expiration. • Complications of PEEP: pulmonary barotrauma, decreased venous return to the heart, renal dysfunction and electrolyte imbalance.

25. Oxygen Delivery Methods • Work of breathing: respiratory muscles need oxygen to function. In resting/normal conditions, they consume 1-3% of total body oxygen. In respiratory distress, they consume 25-30% of body oxygen (their oxygen demand increases to insure adequate breathing). • What is pulse oximetry? • It is a non-invasive device by which you can measure patient’s pulse and oxygen saturation to monitor him during his respiratory distress. • What is oxygen saturation (SpO2)? • Oxygen saturation (SpO2) is the percentage of hemoglobin molecules in arterial blood which are saturated with oxygen. • OR it is the ratio of oxyhemoglobin (hemoglobin carrying oxygen) to the total concentration of hemoglobin in the blood. • Normal range of SpO2 = 95-100%. A value > 90% is considered to be a significant clinical event. • What are the factors which interfere with measurement of SpO2 by pulse oximetry? • Abnormal movements by the patient, low blood flow, hypotension, hypothermia and vasoconstriction.

26. Oxygen Delivery Methods • What is partial pressure of oxygen PaO2? • It represents free oxygen molecules which are dissolved in plasma (not bound to hemoglobin). • Normal range = 80-100 mmHg. Severe hypoxemia is considered when PaO2 is > 40 mmHg. • Oxygen supply: • Aims to administer oxygen at concentrations higher that that of the ambient room air to prevent hypoxia in the patient. • Indications: • SpO2 > 90% • PaO2 > 60 mmHg.

27. Oxygen Delivery Methods • What are the devices available to deliver oxygen to patients? • First-line options: • Standard nasal cannula. • Venturi mask. • Second-line options: • Simple face mask. • Non-rebreather mask. • Third line option: • Positive pressure ventilation. • Standard nasal cannula: • Oxygen flow using it ranges from 1-5 Liter/minute. Therefore, Inspiratory Oxygen Fraction (FIO2) ranges from 24-40% → this is calculated using the following formula: • FIO2 = 20% + (4 x oxygen liter flow) • It is used in patient with MINIMAL or no respiratory distress. • Advantages: • Simple and comfortable. • Patient can eat, drink and talk while using it. • Reducing the risk of CO2 rebreathing. • Disadvantages: • Resulting in dry nasal passages. • High flow rate can cause nose bleeds and headache. • Cannot be used when there is nasal obstruction.

28. Oxygen Delivery Methods • Venturi mask: • It is used in patients with COPD in whom you cannot administer high concentrations of oxygen otherwise causing further respiratory failure. • Venturi mask mixes oxygen with room air creating high-flow enriched oxygen and insures that there is a constant FIO2 and aiming to maintain an oxygen saturation of 88%.

29. Oxygen Delivery Methods • Simple face mask: • Oxygen flow using it ranges from 5-10 Liter/minute. Therefore, Inspiratory Oxygen Fraction (FIO2) ranges from 40-60%. • Advantage: It doesn’t need a tight seal. • Disadvantages: • It is not comfortable. • Patient cannot eat, drink or talk. • There is CO2 retention when oxygen flow is > 5 Liters/minute • Non-Rebreather Mask (NRB): • It is attached to a reservoir bay (1 L) and connected to an external oxygen source. 2/3 of the bag is inflated full of oxygen. If the bag becomes completely deflated the patient will no longer have a source of air to breath. • With NRB mask, there are one-way valves in the mask preventing inhalation of room air and re-inhalation of exhaled air. • Advantage: delivering high concentrations of oxygen (60-80%). • Disadvantages: • It is not comfortable and needs a tight seal around patient’s nose and mouth. • Patient cannot eat, drink or talk. • High oxygen concentrations might result in dry airway and mucous membrane

30. Oxygen Delivery Methods (1): Venturi mask (for COPD patients). (2): Simple face mask. (3): Non-rebreather mask (4): Standard nasal cannula

31. Oxygen Delivery Methods • Assessing oxygen requirement of the patient: • SpO2 90%-94%: patient has mild to moderate hypoxia. Use for him nasal cannula or simple face mask to achieve SpO2 above 95%. • SpO2 85%-89%: patient has moderate to severe hypoxia. Use for him Non-rebreather mask (because it is providing higher concentrations of oxygen = 60-80%). • SpO2 > 85%: patient has severe, life-threatening hypoxia and he needs endotracheal intubation with mechanical ventilation. • There are 3 signs by which you can know if the patient will undergo respiratory arrest (presence of one of them needs immediate intervention): • Decreased level of consciousness. • Patient is unable to maintain respiratory effort. • Cyanosis. • Positive pressure ventilation (third-line option): • Types of positive airway pressure (mentioned previously in more details): • Non-invasive: to support breathing without intubation (e.g. BiPAP and CPAP). This method is contraindicated when patient need intubation in following conditions: coma (e.g. loss of cough and gag reflex thus airway is unprotected), respiratory arrest or cardiac arrest, status epilepticus, upper airway obstruction (e.g. laryngeal edema), angioedema/anaphylaxis causing airway compression.

32. Oxygen Delivery Methods • Positive pressure ventilation (third-line option): • Types of positive airway pressure (mentioned previously in more details): • Invasive: to support breathing with endotracheal intubation and mechanical ventilation. What are the indications for intubation? • Severe respiratory acidosis with hypercapnia in which blood gasses are as follows: • PaO2 > 50 mmHg. • PaCO2 < 50 mmHg. • pH > 7.32 • Decreased level of consciousness (e.g. coma or loss of airway protection via coughing and gag reflex). • Upper airway obstruction (e.g. laryngeal edema or epiglottitis). • Respiratory or cardiac arrest. • Complications of oxygen therapy: • Oxygen toxicity with prolonged continuous high concentrations of oxygen. • Absorption atelectasis. • Oxygen-induced hypoventilation or apnea (in COPD patients).

33. Hemodynamic Monitoring • Blood pressure (Bp) monitoring: • Why is it important to monitor Bp? • To insure good perfusion to vital organs and tissues. Because if there is hypotension there will be hypoperfusion and the patient will enter a state of shock! • How to calculate Mean Arterial Pressure (MAP)? • MAP = [ (2 x diastolic) + systolic ] / 3 • Diastole counts twice as much as systole because 2/3 of the cardiac cycle is spent in diastole. • Normal range = 70-110 mmHg. A MAP > 60 mmHg indicated the need to perfuse: coronary arteries, brain and kidneys (most important vital organs). • What are the indirect ways used to estimate Bp? • Pulse: if there is tachycardia this indicated hypotension and vice versa. • Mental status. • Urine output. • Skin temperature and mottling. • Capillary refill time.

34. Hemodynamic Monitoring • Blood pressure (Bp) monitoring: • There are 2 ways to measure Bp: • Non-invasive. • Invasive: through an arterial line. • What is an arterial line? • A cannula will be inserted into patient’s radial or femoral artery. Then, it will be connected to infusion line which continuously infuses fluid into the cannula preventing it from blocking. The transducer will display arterial waves on the monitor allowing continuous monitoring of blood pressure. • Indications: • Bp cannot be measured by a non-invasive method. • Bp is unstable. • The need of frequent ABG samples. • Complications: • Hemorrhage. • Infection. • Air embolism.

35. Hemodynamic Monitoring • Central Venous Pressure (CVP) monitoring: • Inserting a central venous catheter into one of the large veins (e.g. subclavian or internal jugular) to reach the junction between Superior Vena Cava (SVC) and right atrium thus being able to measure the pressure in the right atrium (normally = 2-6 mmHg). • What are the purposes behind CVP? • To administer high volumes of fluids and drugs. • When frequent blood sampling is needed. • To assess cardiac function and to know if there is right-sided heart failure. • Can be used for hemodialysis or plasmapheresis. • Pathological conditions in which CVP is increased: • Myocardial stiffness: ischemia, fibrosis, pericarditis or pericardial effusion. • Myocardial hypertrophy: tricuspid valve disease, pulmonary stenosis or pulmonary hypertension. • Hypervolemia. • CVP is decreased when there is hypovolemia.

36. Hemodynamic Monitoring • Central Venous Pressure (CVP) monitoring: • Contraindications: • SVC syndrome. • Infection at the site of insertion. • Severe coagulopathy. • Complications: • Air embolism. • Infection and sepsis. • Thrombosis and thromboembolism. • Nerve injury and arrhythmia. • Pulmonary artery pressure: • It is measured by inserting a Swan-Ganz catheter into a large vein → right atrium → right ventricle → pulmonary artery → and then into a branch of pulmonary artery. • It provides an estimate of left atrial pressure and preload of left side of the heart.

37. Shock and Resuscitation • What is shock? • Oxygen delivery to vital organs and tissues is inadequate to meet the metabolic demands (hypoperfusion). This results in anaerobic metabolism and lactic acidosis. • There are 3 phases of shock: • Compensated shock (early stage): • Compensatory mechanisms will be activated insuring adequate perfusion to organs: • Sympathetic nervous system. • Renin-angiotensin-aldosterone system. • Endocrine response. • Presentation: • Tachycardia, tachypnea, NORMAL BLOOD PRESSURE and cool pale skin. • Decompensated shock: • In which compensatory mechanisms fail to maintain adequate perfusion to organs. • Presentation (global tissue hypoxia to organs): • CNS: altered mental status. • Heart: myocardial depression. • Lungs: hypoxia and ARDS. • Renal: decreased urine output. • GI: bowel ischemia. • Irreversible shock (late stage): • There is massive cell damage with failure of organs. • Shock cannot be reversed with any medical intervention (body is not responding). • Presentation: • Slow shallow breathing, LOW BLOOD PRESSURE, patient is comatose, cold cyanotic skin and there is systemic failure (renal, hepatic, ARDS, DIC).

38. Shock and Resuscitation • What are the types of shock? • Hypovolemic: acute fluid loss resulting in loss of circulatory volume • Hemorrhagic: GI bleeding, trauma or hemoptysis. • Classification of hemorrhagic shock: • Class-I: increased respiratory rate (14-20 breaths/minute) and patient is slightly anxious. • Class-II: pulse < 100 beats/minute. • Class-III: low Bp. • Class-IV: patient is confused and lethargic. • Non-hemorhagic (due to fluid loss): vomiting, diarrhea or burns. • Cardiogenic: impaired heart pump function: • Myocardial Infarction (MI). • Valvular heart disease. • Arrhythmias (e.g. atrial fibrillation, heart block or ventricular tachycardia). • Distributive: there is pathologic peripheral vasodilation • Septic. • Anaphylactic. • Neurogenic: there is disruption of sympathetic regulation of vascular tone. Patient will have bradycardia because there is no sympathetic input to the hear to increase heart rate and contractility. • Obstructive: • Pulmonary embolism. • Tension pneumothorax. • Cardiac temponade.

39. Shock and Resuscitation

40. Shock and Resuscitation

41. Shock and Resuscitation

42. Shock and Resuscitation

43. Shock and Resuscitation • Septic shock: • In sepsis, there is an infection which causes an inflammatory response → that will become exaggerated →and causes damage to different organs of the body. • There will be vasodilation (this explains why extremities are WARM in septic shock), capillary leak and activation of coagulation system (that usually results in DIC). • How to diagnose sepsis? ≥ 2 SIRS criteria + an evidence of infection (most commonly from respiratory or urinary tracts) • WBCs < 12,000 cells/mm3 or > 4000 cells/mm3 • Hear rate < 90 beats/minute. • Respiratory rate < 20 breaths/minute or PaCO2 > 32 mmHg. • Temperature < 38 C or > 36 C • How to diagnose septic shock? Sepsis + low Bp • Diagnostic assessment for patient with septic shock: • Vital signs: blood pressure, pulse, respiratory rate and temperature. • CBC and differentials. • ABG. • Coagulation profile: PT, PTT, fibrinogen and D-dimer. • Serum electrolytes. • LFTs and RFTs. • Blood cultures. • Urinalysis and urine culture.

44. Septic shock (continued): • Management: • ABC: • Determine the need for intubation and mechanical ventilation (which decreases the work of breathing and improves survival). • Fluid therapy: • Type of fluid: crystalloid (e.g. normal saline or ringer lactate) or colloid (e.g. albumin and synthetic starch in which less resuscitation volume is needed). • Amount of fluid: 4-8 L of crystelloid preferred to be administered as a bolus instead of an infusion. • When to stop fluids? MAP ≥ 60 mmHg, urine output ≥ 0.5 ml/kg/hour, decreasing serum lactate and central venous pressure = 8-12 mmHg. • If patient is not responding to fluid therapy, consider administrating vasoactive agents such as: epinephrine, dopamine or vasopressin. • Control infection by starting broad-spectrum antibiotics after obtaining blood samples for culture. Shock and Resuscitation

45. Shock and Resuscitation

46. Respiratory System

47. Asthma • Definition: it is a reversible obstructive lung disease in which there is hypersensitivity reaction of bronchial tree to different stimuli/triggers. • Pathophysiology: a stimulus will bind to IgE antibodies which in turn will bind to mast cells that will release different inflammatory mediators. The following changes will occur within the bronchial tree: • Increased mucous production. • Constriction of bronchial smooth muscle. • Edema and inflammation of bronchial mucosa. • Epidemiology: commonly affecting young patients. 50% of them will be free of asthma when they reach adulthood. • Etiology: there are two types of asthma • Intrinsic (non-allergic): in 50% of asthmatic patients. Secondary bronchial reaction occurs due to non-immunologic stimuli (e.g. infection, exercise). Asthma attacks are severe and prognosis is poor. • Extrinsic (allergic): in 20% of asthmatic. It results from sensitization and serum IgE levels are elevated. There is positive family history of allergic diseases (e.g. eczema). Prognosis is good. • Respiratory tract infections (most common cause of asthma exacerbation): RSV in children and rhinovirus in adults. • Pharmacologic stimuli: aspirin and other NSAIDs which cause chronic over-secretion of leukotrienes that activate mast cells. This is the reason why leukotriene inhibitors (e.g. zafirleukast) are considered to be effective in managing asthma.

49. Asthma • Clinical manifestations: • Cough (might be worse at night). • Dyspnea. • Tachypnea. • Diffuse wheezing with prolonged expiration. • Diagnosis: • PFT which will show an obstructive pattern (FEV1 > 80% and FEV1/FVC > 80%). There is improvement by ≥ 12% in FEV1 after the use of bronchodilators. If PFT is normal but you still suspect the diagnosis of asthma → do methacholine challenge test → after which there will be a decrease of 20% in FEV1/FVC ratio. • CXR: although there might be signs of hyperinflation but it is not specific unless you want to rule out an infection as the trigger for asthma exacerbation. • ABG: in patient with severe asthma, it will show respiratory acidosis with hypercapnia. • Treatment: • Management of acute exacerbation of asthma in emergency: oxygen supply, short-acting β2 agonist and systemic steroids (for 10-14 days). • Short-acting β2 agonists (e.g. albuterol and salbutamol): their most common side effect is tremor. • Long-acting β2 agonists (e.g. salmeterol = 12 hours): it is effective in patients having: • Nocturnal cough variant of asthma. • Exercise-induced asthma. They are not effective during acute episodes. • Aminophylline/theophylline: they are modest bronchodilators used for chronic management especially in patients with nocturnal cough. • Anticholinergic drugs (e.g. ipratropium bromide): used in patients with heart disease in whom it is dangerous to give a β-agonist or theophylline. It takes 90 minutes to achieve bronchodilation.

50. Asthma