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Description : Acute cardiogenic pulmonary edema = acute breathlessness with orthopnea due to cardiac disease......

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ACUTE MEDICINE CASES DR. ABOUBAKER ALDHIB
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Sudden dyspnea .! A 61 year old man presents with sudden onset of severe dyspnea grade 4 , on the background of exertional dyspena and orthopnea in the preceding 3 months . His medical history is significant for anterior STEMI 4 years ago. He is currently on aspirin , prasugrel , metoprolol, telmisartan and rosuvastatin. O/E = apex beat deviated , gallop rhythm , pansystolic murmur radiated to the axilla . Lungs = bilateral diffuse fine crackles . Pulse = irregular iiregular. B.P = 100 / 60 , JVP = elevated , cyanosis , o2 saturation = 85% on room air.
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… DX ? Acute cardiogenic pulmonary edema = acute breathlessness with orthopnea due to cardiac disease that leads to elevation of the hydrostatic pressure in the pulmonary capillaries causing pulmonary edema . Steps of management ? Ask your self 2 Q = .Is there respiratory failure . Is there cardiogenic shock. 1. Seat the patient upright to reduce venous return 2. administer100% O2 by simple mask to achieve O2 saturation above 90% . Assisted ventilation may be needed. insert 2 large pore canula and send blood for invx “ CBC , RFT , LFT , CE , ABG” . Admit to the ccu , ECG monitoring.
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3. IV loop diuretic “furosemide 40 _ 100 mg”. If BP > 90. 4. IV morphine 4_ 8 mg with 10 mg metoclopromide. 5. Nitroglycerin ( sublingual 0.4mg every 3_5 min ) followed by 5 _ 10 microgram / min iv . If systolic BP > 90. 6. Treat underlyning cause or PPS “ acute arrhythmia , infection , infarction ” 7. Inotropic agents ex . Dopamine and dobutamine in cardiogenic shock. To summarize = admit to the CCU and give :_ LEMON nitrate LASIX erect position morphine O2
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Sudden dyspnea . 2 A 66 year old lady who underwent an uncomplicated hemicolectomy for colorectal carcinoma last week. She is brought complaining of sudden onset dyspnea of 2 hours duration. There is no associated fever, cough , chest pain , nausea , vomiting , syncope, or calf pain. This her 1st episode , she is doesn’t smoke and is only in paracetamol for analgesia . Pulse = 110 , BP= 100 / 70 . , JVP= not raised. Lung = clear . ECG= sinus tachycardia.
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.. Next steps ? Well’s score , d_dimer , CTPA. Dx ? Acute pulmonary embolism = obstruction of the pulmonary artery or one of it’s branches by any material “thrombus , fat , amniotic fluid , air , tumour or septic emboli” that originate elsewhere in the body resulting in obstruction of pulmonary blood flow with the following results = #massive PE = acute RV failure and decrease in COP with resultant shock “SBP < 90 or decreased by > 40 from the baseline” or cardiac arrest or syncope. #Submassive PE= obstruction of segmental pulmonary artery can result in infarction +_ effusion +_ atelectasis. #Chronic recurrent PE may present with chronic pulmonary HTN and progressive RV failure
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.. causes = most common 75 _ 95% is DVT in femoral and pelvic veins. Risk factors = stasis , vascular injury , hypercoagulable state. Mx = . Admit and insert 2 large pore canula , send blood for invx “ d_dimer , ABG , …..”. . O2 if hypoxemic , MV may be needed if not improving by simple O2 musk. . Analgeia if there is chest pain ex= iv morphine.
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Indication of IVC filter = Proximal DVT + absolute CI to anticoagulant. Recurrent PE despite anticoagulant.
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Sudden dyspnea . 3 A 25 year old man presents with left sided pleuritic chest pain and dyspnea of sudden onset , soon after exercise. His medical hostory is completely unremarkable . He regularly engages in sports , and smokes a couple of cigarettes every day. O/E= confused , diaphoretic , pulse = 104 , BP=90/60 , JVP= elevated , prominent neck veins. Respiratory system = trachea deviated toward right , normal percussion note B/L , reduced chest expansion and absent breath sounds on left side , No added sounds.
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.. DX ? Tension pneumoathrax NEXT STEP ? Needle thoracocentesis = O2 100% , prompt decompression via a large bore needle should be performed immediately ; this shouldn’t delayed pending investigations . This will convert the tension pneumthorax into a more benign open pneumothorax . Subsequently , air should be evacuated until the patient is no longer compromised ; a chest drain should be inserted later.
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his CXR ????
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Sudden dyspnea . 4 A 28 year old man presents with severe dyspnea and wheezing for 1 day . He was diagnosed with mild persistent bronchial asthma in childhood , and is currently on sulbutamol inhaler. He also experienced a mild productive cough , rinorrhea and a sore throat during the preceding week. He doesn’t smoke and has no other comorbidites or allergies. O/E= dyspnic ,using accessory muscle to breath , can’t complete a sentence in one breath , not pale or cyanotic , no clubbing. Pulse = 120 , BP= 140/90 , SO2 = 92% on o2 musk, RR= 30. Chest = diffuse inspiratory and expiratory wheeze with prolonged expiratory phase.
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.. Dx ? Acute exacerbation of bronchial asthma “ asthma with an increase in chest tightness , wheezing and dyspnea ” . Precipitating factors = . no clear cause. . Exposure to known allergen , irritatnt or smoke . . Upper or lower respiratory tract infection. . Poor compliance with medication. . NSAID , Bblockers , emotinal stress , cold air.
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How to treat acute severe bronchial asthma? We can manage acute severe asthma by the followings— Urgent hospitalization and send blood for ABG. Nebulized salbutamol Adult: 5 mg 2–4 hourly Children: 0.15–0.3 mg/kg/dose every 20 minutes for 3 times or continuously. Propped up position/ head up position Oxygen High-flow/60%. In children, 4–6 L/min (40–60%) through oxygen hood/ head box Prednisolone 40 mg orally (or hydrocortisone 200 mg IV if patient cannot swallow or vomit). Child dose: Inj. hydrocortisone 3–4 mg/kg/dose 4–6 hourly or, Prednisolone 2 mg/kg/day for 3–5 days or as necessary.
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. IV access, chest X-ray, send blood for urea and electrolytes, theophylline level. If condition does not improve, nebulized ipratropium bromide may be added Administer repeat salbutamol 5mg + ipratropium bromide 0.5 mg nebulizer. If failure to respond, continuous salbutamol nebulizer 5–10 mg/hr. If not respond, consider IV magnesium sulfate 1.2–2 gm over 20 mins, or Aminophylline 5 mg/kg loading dose over 20 mins followed by a continuous infusion at 1 mg/kg/hr. Correct fluid and electrolytes (esp. K+ ) (repeated use of salbutamol may cause hypokalemia). In refractory cases Mechanical ventilation
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Sudden dyspnea . 5 A 60 year old libyan man presents with dyspnea at rest for 1 month , with increasing in severity in the last week. Close questioning reveals a history of exertional dyspnea for 2 years and ankle swelling for the last 3 months. He has smoked for a total of 62 pack years , and has not been medically evaluated for many years. O/E= dyspnic , RR= 40 , plethoric and cyanosed , B/L ankle edema. So2 = 66% . Respiratory system = barrel chest , both lung fields hyperresonant to percussion , diffuse reduction of breath sounds and polyphonic wheeze. Abdomen = mild tender hepatomegaly . CVS= pulse 88 regular , BP=150/80 , JVP= elevated , S2 = palpable , loud = S2.
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The radiological findings in COPD are: Hyperinflated lung field Low flat diaphragm Long tubular heart shadow Hyperlucent lung fields Horizontal ribs Widened intercostal spaces Roomy apex Emphysematous bullae
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… DX ? Acute exacerbation of COPD , complicated by corpulmonale . What are the presentations of COPD? Usually the patient is above 40 years, male and smoker. There is: Chronic cough and sputum production, which is .progressively increasing .Progressive breathlessness There may be hemoptysis if complicated by lung cancer, .edema and morning headache (due to hypercapnia)
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Causes of exacerbation : Infection of the tracheobronchial tree. Pneumothorax. Air pollution Sputum retention with lobar or segmnetal collapse. Air pollution. Expansion of large bullae. Excessive sedation or opioid analgesia. In one third the cause cant be identified.
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. What organisms are associated with acute exacerbation of COPD? Common organisms: Haemophilus influenzae and Streptococcus pneumoniae. Other less common organisms are = Moraxella catarrhalis, Chlamydia pneumoniae. Pseudomonas aeruginosa. Viral infections ‘’ rhinovirus , influenza , coronavirus , adenovirus‘’
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How can you predict acute infective exacerbation? We can predict acute infective exacerbation by— Increased breathless and cough Increased sputum volume and purulence Fever
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Respiratory failure What are the causes of type I respiratory failure? The causes of type I respiratory failure are: Acute asthma Emphysema Pulmonary edema Pneumonia Lung fibrosis
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Respiratory failure 2 What are the causes of type II respiratory failure? The causes of type II respiratory failure are: Acute severe asthma COPD “chronic bronchitis” Ankylosing spondylitis Kyphoscoliosis. Drug overdose. Neuromusculr diseases “ GBS, myastheni gravis , …”
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Mx of acute COPD Hospitalization Oxygen 24% or 28% (Continuous low concentration oxygen via Venturi mask) Bronchodilators: Nebulized short-acting β2-agonists combined with an anticholinergic agent (e.g. salbutamol with ipratropium). Sulbutamol 5mg every 2_4 hours by nebulizer , ibratropium bromide 500 microgram every 4_6 hours by nebulizer. IV aminophylline if not improved by nebulizer. Corticosteroids: Oral prednisolone—30 mg daily for 10 days. Antibiotics: Amoxicillin or macrolide. Respiratory support: Noninvasive ventilation for severe hypercapneic respiratory failure (pH<7.35) Respiratory stimulant, i.e. doxapram if noninvasive ventilation is not available. If no improvement : INVASIVE MV .
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What are the principles of O2 therapy in respiratory failure? The principles are: In type I, high concentration (i.e.>35%, usually 60%)/high flow (6–8 L/min) In type II, low concentration (24%–28%)/low flow(1–2L/min).
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CONTROLLED O2 ? Why low concentration O2 given in COPD? Or what happens when high flow O2 given? A small percentage of patients with severe chronic COPD and type II respiratory failure develop abnormal tolerance to raised PaCO2. The patient may become dependent on hypoxic drive for respiration High flow oxygen blunts the chemoresponsiveness of the respiratory center in the medulla (part of the brainstem) and thus aggravates respiratory failure (Type 2 respiratory failure). To avoid this, in these patients, lower concentrations of oxygen 24%–28% by Venturi mask should be used to avoid precipitating worsening respiratory depression
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What are the complications of COPD? The complications of COPD are: Pulmonary hypertension Cor pulmonale Respiratory failure Polycythemia Pneumothorax Secondary infection CA lung.
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dx X-ray chest PA view showing: Dense homogenous opacity in left lower zone with a curvilinear upper border (concave upper margin). There is obliteration of left costophrenic angle. Trachea and heart (mediastinum) are shifted to the right. Rest of the lung field is normal and bony case and soft tissue shadows are normal. Radiological diagnosis: Left-sided pleural effusion.
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What is pleural effusion? The accumulation of serous fluid within the pleural space is termed pleural effusion. What is the Light’s criteria? Light’s criteria is for distinguishing pleural transudate from exudate. Plural fluid is likely exudate if one or more of the following criteria are met: Pleural fluid protein : serum protein ratio > 0.5 Pleural fluid LDH : serum LDH ratio > 0.6 Pleural fluid LDH > two-thirds of the upper limit of normal serum LDH
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hat are the types of pleural effusion according to the color? According to color, pleural effusion may be: Serous (hydrothorax) Purulent (empyema or pyothorax) Hemorrhagic (hemothorax) Straw Milky or chylous (chylothorax)
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Empyema = pus in the pleural fluid . Characteristics of empyema fluid: Fluid is purulent Thick Biochemical—glucose low, < 3.3 mmol/L, protein exudative, LDH > 1000 U/L C/S—organism may be found Pleural biopsy may be done to exclude tuberculosis.
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If the patient is young, common causes are Pulmonary tuberculosis Parapneumonic Others—Lymphoma and SLE in female (also pulmonary infarction). If the patient is middle age or elderly, common causes are Heart failure Pulmonary tuberculosis Parapneumonic Bronchial carcinoma
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. What are the causes of exudative and transudative pleural effusion? As follows: Exudative (protein >3 g%) : Pneumonia (para-pneumonic effusion) Pulmonary tuberculosis Pulmonary infarction Malignant disease, e.g. bronchial carcinoma, lymphoma Collagen disease (SLE, rheumatoid arthritis) Dressler’s syndrome (post-myocardial infarction syndrome characterised by pain, pyrexia, pericarditis, pleurisy and pneumonitis). Others—acute pancreatitis, subphrenic abscess, liver abscess, pleural mesothelioma, secondaries in the pleura, yellow nail syndrome, etc.
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Transudative (protein <3 g%): Congestive cardiac failure (CCF) Nephrotic syndrome Cirrhosis of liver Malnutrition Hypothyroidism Meig’s syndrome (ovarian fibroma, ascites and right sided pleural effusion) Chronic constrictive pericarditis Acute rheumatic fever
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What are the causes of predominantly right or left sided pleural effusion? As follows: Causes of right-sided pleural effusion Liver abscess Meig’s syndrome Dengue hemorrhagic fever. Causes of left-sided pleural effusion Acute pancreatitis Rheumatoid arthritis Dressler’s syndrome (pleurisy, pericarditis, and pyrexia-3P) Esophageal rupture (Boerhaave’s syndrome) Dissecting aneurysm
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. What are the causes of bilateral effusion? As follows: All causes of transudative effusion (CCF, nephrotic syndrome, cirrhosis of liver, malabsorption or malnutrition or hypoproteinemia). Collagen diseases (rheumatoid arthritis and SLE). Lymphoma Bilateral extensive pulmonary TB. Pulmonary infarction. Malignancy (usually multiple metastases involving both lungs).
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What are the causes of hemothorax (blood stained fluid)? As follows: Chest injury or trauma Bronchial carcinoma Pulmonary infarction Pleural mesothelioma Others – SLE, lymphoma, acute pancreatitis.
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What are causes of empyema? As follows: Bacterial pneumonia Lung abscess (bursting in pleural cavity) Bronchiectasis Tuberculosis Secondary infection after aspiration Rupture of subphrenic abscess or liver abscess Infected hemothorax
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empyema How to diagnose empyema thoracis clinically? As follows: From history: High fever, sometimes hectic, may be associated with chill, rigor and sweating. Fever is persistent or recurrent despite treatment with a suitable antibiotic. Malaise, weight loss. Pleuritic chest pain, breathlessness. Copious purulent sputum if empyema rubtures into a bronchus (bronchopleural fistula). On examination: Toxic, emaciated. Tachypnea. Tachycardia. Features of pleural effusion. Clubbing. To be confirmed—aspiration which shows pus or purulent fluid.
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What are causes of chylothorax (milky or whitish fluid due to lymph)? Injury or obstruction of thoracic duct due to any of the following causes: Traumatic (surgery and trauma to the thoracic duct) Neoplastic (bronchial carcinoma and metastasis) Infective (tuberculosis and filariasis) Lymphoma involving thoracic duct.
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What are the causes of recurrent pleural effusion? As follows: Bronchial carcinoma Pleural mesothelioma Lymphoma Collagen disease (SLE) All causes of transudate (CCF, nephrotic syndrome, cirrhosis of liver)
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What are the mechanisms of pleural effusion? Excess pleural fluid accumulation occurs when pleural fluid formation exceeds absorption or normal pleural fluid formation with reduced absorption. Probable mechanisms are: Increased hydrostatic pressure (as in CCF) Reduced plasma colloidal osmotic pressure (as in hypoproteinemia) Involvement of pleura causing increased permeability (as in TB and tumor) Impaired lymphatic drainage of pleural space (as in obstruction of lymphatic system by tumor, TB and radiation) Transdiaphragmatic passage of fluid (in liver disease, ascites and acute pancreatitis).
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Clinical findings : Stony dullness on percussion and reduced or absent breath sound (confirmed by aspiration). What findings will you get by examining the patient with right-sided pleural effusion? Inspection Movement diminished on right side Palpation Trachea and apex beat deviated to left Expansibility reduced on right side Vocal fremitus diminished on right side Percussion Stony dull on right side Auscultation Breath sound diminished or absent on right side Vocal resonance diminished or absent on right side.
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invx What investigations do you suggest? As follows: X-ray chest P/A view Hb%, TC, DC, ESR (high ESR in TB, leukocytosis in pneumonia) Mantoux test (MT) Aspiration of pleural fluid for analysis- Physical appearance (straw colored, serous, hemorrhagic, chylous) Gram-staining, cytology (routine) and exfoliative cytology (malignant cells) Biochemistry (protein and sugar), also a simultaneous blood sugar, protein and lactate dehydrogenase (LDH) may be done ADA (high in tuberculosis) Culture and sensitivity (C/S) AFB and mycobacterial C/S
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cont Pleural biopsy by Abram’s or Cope’s needle Other investigation of pleural fluid (according to suspicion of cause): Cholesterol, LDH and rheumatoid factor (in rheumatoid arthritis) Amylase (high in acute pancreatitis, esophageal rupture, malignancy) Trigycerides (in chylothorax) Sputum (if present) for Gram staining, C/S, AFB, mycobacterial C/S and malignant cells (exfoliative cytology) If palpable lymph node: FNAC or biopsy (for lymphoma, metastasis) Other investigations according to suspicion of causes include: ANF, anti-ds DNA (SLE) Liver function tests Urine for protein and serum total protein (nephrotic syndrome) Bronchoscopy and biopsy (if needed in bronchial carcinoma) CT scan in some cases (it helps to clarify pleural abnormalities more readily than chest X-ray and ultrasonogram, and also helps to distinguish between benign and malignant diseases).
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? How to confirm if there is small effusion? (if not detected by chest X-ray PA view.) By doing: X-ray in lateral decubitus position Ultrasonogram (USG) of lower part of the chest Occasionally, CT scan of chest may be needed. Pleural effusion Pleural fluid normally present: 5 to 15 mL At least 500 mL of fluid is necessary to detect clinically At least 300 mL of fluid is necessary to detect radiologically in PA view At least 100 mL of fluid is necessary to detect radiologically in lateral decubitus position Less than 100 mL or small amount of fluid is detected by ultrasonography (even 20 to 25 mL fluid can be detected).
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What are the purposes of aspiration? Diagnostic purposes To detect the cause. Therapeutic purposes To reduce breathlessness How much fluid should be drawn in case of diagnosis and therapeutic purposes? At least 50 mL for diagnostic purpose and not more than 1.5 L on first occasion
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What are the characteristics of tuberculous pleural effusion? As follows: Straw or amber color Exudative High lymphocyte in pleural fluid AFB is found in 20% cases Culture for AFB is found in one-third cases Pleural biopsy is positive in 80% cases
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What are the causes of low pH and low glucose in pleural fluid? As follows: Infection (empyema) Tuberculosis Advanced malignancy SLE Rheumatoid arthritis Esophageal rupture.
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What is the role of pleural fluid amylase? Pleural fluid amylase may be higher than serum amylase in acute pancreatitis, bacterial pneumonia, esophageal rupture and malignancy. It is high in adenocarcinoma of lung and may be useful in differentiating it from mesothelioma.
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Pleural fluid analysis.. Increased TAG= chylothorax. Increased cholesterol = RA. Increased ADA , Gamma interferon=T.B. Increaesed RF = RA. Increased ANA= SLE.
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How can you suspect malignant effusion? As follows: Clincally—elderly emaciated or cachexic patient having clubbing with nicotine stain, palpable lymph node, radiation mark on the chest, etc. Pleural fluid is hemorrhagic and there is rapid accumulation after aspiration
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mx. Large pleural effusion causing dyspnea should be drained with not more than 1500 ml at one set. Treatment should be according to cause.For example Parapneumonic pleural effusions : _ uncomplicated : it should improve clinically with the appropriate antibiotics . Doesn’t need drainage. _ complicated parapneumonic pleural effusion and empyema : antibiotics and urgent drainage to avoid organization into fibrous peels ( fibrous encasement of lung ) . If loculated , do intrapleural injection of fibrinolytic agent or thoracoscopy to lyse adhesions and improve drainage.
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Surgery is required : _ for thick parapneumonic pleural effusion tha cant be drained by small bore tube. _ to drain loculated pleural fluid. _ decortication to remove thick , inelastic pleural peels that restrict ventilation. ________________________________________ Uncomplicated = sterile , LDH < 500 , WBC 5000 _ 25,000 /ml PMN , small to moderate size ( < ½ hemithorax ) , free flowing and not loculated , pleural fluid glucose = serum glucose.
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Complicated = Sterile , PH < 7.3 , glucose < 60 mg% , LDH > 1000 , large size (> ½ hemithorax ) , loculation , air fluid level or high PMN count. Empyema = Pus in pleural space or pleural fluid with organism on gram stain or culture . WBC 25,000 _ 100, 000 , glucose < 60 mg % (often very low ) , low PH , thick pleura on CT scan.
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If tuberculosis:Full course antitubercular therapy ( improvement within 6 weeks ) . Prednisolone 20 to 30 mg daily may be given for 4 to 6 weeks, especially in large effusion, will increase absorption and prevent fibrosis. Drainage if empyema.
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How to treat recurrent pleural effusion? Malignant ? Treatment of recurrent pleural effusion is done by pleurodesis in the following way: A plain rubber tube is introduced in the intercostal space, and fluid is removed as far as possible. Introduce the drug, tetracycline (500 mg) or kaolin or talc through the tube, clamp it and keep for 4 to 8 hours (may be overnight). In malignant pleural effusion, bleomycin 30 to 60 mg is introduced. Patients’ posture should be changed 2 hourly to allow the drug to spread in pleural space. After 4 to 8 hours, remove any remaining fluid and take out the drainage tube at the height of inspiration. The patient usually complains of severe chest pain after pleurodesis. In such case, analgesic should be given.
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What will happen if you aspirate more than 1.5 L or rapidly? Re-expansion pulmonary edema. Mechanism Because of effusion, lung is compressed and there is ischemia to lung parenchyma and necrosis of pulmonary vessels. If more fluid is drawn, there is rapid expansion of the lung, as no regeneration of necrotic vessels. As a result, more leakage of fluid causing pulmonary edema
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CHEST PAIN ?
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ACS . What is ACS? Why both of them known as collectively? ACS means acute coronary syndrome. Acute coronary syndrome is a term that encompasses both unstable angina and MI (STEMI and NSTEMI). These two are considered collectively as initial emergency management is same done by using ACS triage therapy. It is also a dynamic process, i.e. unstable angina if not treated appropriately in time, may progress to MI
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What is unstable angina? Unstable angina is characterized by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the absence of myocardial damage. Cardiac enzymes are not raised. What is myocardial infarction (MI)? Acute ischemic necrosis of an area of myocardium is called myocardial infarction. Cardiac enzymes are raised.
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Oxygen Supply Oxygen Demand Normal Myocardial Balanced Oxygen Supply and Demand Coronary Blood Flow
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Oxygen Supply Oxygen Demand Myocardial IschemiaUnbalanced Oxygen Supply and Demand Reduced Coronary Blood Flow
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Atherosclerosis , most important cause
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STEMI . A 50 year old man presents with sudden onset of central chest pain , crushing , diffuse , radiated to the jaw of 2 hours duration . PMH = DM poorly controlled , HTN poorly controlled . Smoking history = 30 pack years. O/E= dyspnic , no pallor , jaundice or edema . CVS = normal Lung = clear . Pulse = 110 , regular . JVP = not elevated. Abdomen = normal
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ECG
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Extensive STEMI Steps of mx ? 1. Hospitalization in CCU with continuous ECG monitoring 2. IV line and extract blood for invx “ CBC , RFT , LFT , LIPID PROFILE , GLUCOSE , INR , APTT , Cardiac enzymes ” don’t wait cardiac enzyme result . ! 3. High flow O2 if SO2 < 90 % . 4. Crushed aspirin 300 mg PO , clopidogrel 300 mg PO. 5. Pain control : “ kill the pain before pain killing pt” _ iv morphine 5 mg every 5 _ 10 min until pain is releived or side effect developed + 10 mg iv metoclopromide. S/E of morphine : nausea and vomiting. respiratory depression hypotrnsion and bradycardia
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Mona ! _ Nitroglycerine 0.5 mg S/L if SBP>100 . If pain persists after 3 doses given 5 minute apart , start IV NG (10 microgram / min ) also IV NG is indicated if there BP > 180 / 110 “ crisis”. MONA Iv morphine Aspirin O2 if saturation < 90% Nitrate N.B= avoid IM injections . !
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Cont. 6. B. blockers : IV metoprolol (5 mg every 5_10 min to a total dose of 15 mg ) , followed by PO regimen (25 _ 100 mg 12 hourly ) , aim of resting heart rate 60 _ 70 or less , it decrease myocardial O2 consumption , limit infarct size and decrease motility. Contraindication of BB = . CCF. . SBP < 90 . . PR < 60 . . AV block. . Bronchospasm .
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What are the roles of β-blocker in MI? β-blocker can – Relieve pain Reduce arrhythmias Reduce blood pressure Improve short-term mortality in patients who present within 12 hours of the onset of symptoms
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7. Reperfusion therapy ( most important ) mechanical pharmacological (Primary PCI ) (IV fibrinolytics) If available in < 120 min it’s the golden standard. if PCI not available then its treatment of choice
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Thrombolytics Indications : . < 12 hours of onset of chest pain . . Characteristic ST segment elevation > 1 mm in the limb leads or 2 mm in the chest leads. ? . New onset LBBB. ? . No contraindications.
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CONTRAINDICATION (AHA/ACCF)
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What are the thrombolytic agents? Streptokinase, alteplase,reteplase and tenecteplas
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8. ACE inhibitor can counteract ventricular remodelling and thus – Prevent the onset of heart failure Improve survival Reduce recurrent MI Avoid rehospitalization. Continued in patient with CCF or EF < 40% .
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9. Lipid lowering agents = statins . 10. Full dose of IV heparin until APTT is 2 times the control or LMWH (eg= enoxaparin 1mg/kg S/C every 12 hr) .
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summary 1.All patient with suspected STEMI should have continuous ECG monitoring in an area with full resuscitation facilities 2.Patient should receive immediate aspirin 300 mg PO and clopidogrel 300 mg or 600 mg according to reperfusion strategy , or other P2y12 inhibitors. 3.O2 only given if saturation less than 90% or HF. 4. good Analgesia “ IV morphine 4 mg “ kill the pain before the pain killing the patient. “ don’t give IM voltarine in suspected ACS”. 5. S/L Nitarate , heparin “UFH or LMWH”. 6. Most important step in STEMI management is = REPERFUSUION “ either by PCI or fibrinolysis ”
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Complications What are the immediate complications of MI? Arrhythmia LVF Right ventricular infarction Cardiogenic shock
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Early complications are: Pericarditis Re_ infarction Mechanical complications are: Rupture of chorda tendinae or papillary muscle damage leading to MR Rupture of interventricular septum leading to VSD. Late complications are: Ventricular aneurysm Dressler’s syndrome (pleurisy, pericarditis, and pyrexia-3P) Shoulder hand syndrome.
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Points to be noted Most dangerous complication of MI is ventricular fibrillation. Immediate cause of death after MI is ventricular fibrillation and cardiac arrest/ asystole. Anterior MI is worse, because it causes arrhythmia. Inferior MI causes bradycardia and heart block .? In inferior MI, heart failure is common.
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Right ! A 45 year old man presents with severe central chest pain for 3 hours associated with sweating. His PMH= HTN , Smokre. O/E= looks ill , diaphoretic . Pulse = 110 , regular. BP= 80 / 60 JVP = elevated. Lung = clear Heart = normal heart sound , well heard.
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Inferior STEMI with right ventricular infarction. mx= as previous . But = note that patient with right ventricular infarction are preload sensitive . So treatment of shock here is = IV fluid (fluid challenge ). Avoid = nitrate , lasix , ACEI.
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ACS “NSTEMI OR UA” 1. Hospitalization in CCU with continuous ECG monitoring 2. IV line and extract blood for invx “ CBC , RFT , LFT , LIPID PROFILE , GLUCOSE , INR , APTT , Cardiac enzymes ” don’t wait cardiac enzyme result . ! 3. High flow O2 if SO2 < 90 % . 4. Crushed aspirin 300 mg PO , clopidogrel 300 mg PO. 5. Pain control : “ kill the pain before pain killing pt” _ iv morphine 5 mg every 5 _ 10 min until pain is releived or side effect developed + 10 mg iv metoclopromide. S/E of morphine : nausea and vomiting. respiratory depression
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Cont.. _ Nitroglycerine 0.5 mg S/L if SBP>100 . If pain persists after 3 doses given 5 minute apart , start IV NG (10 microgram / min ) also IV NG is indicated if there BP > 180 / 110 “ crisis”. MONA Iv morphine Aspirin O2 if saturation < 90% Nitrate N.B= avoid IM injections . !
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Cont. 6. B. blockers : IV metoprolol (5 mg every 5_10 min to a total dose of 15 mg ) , followed by PO regimen (25 _ 100 mg 12 hourly ) , aim of resting heart rate 60 _ 70 or less , it decrease myocardial O2 consumption , limit infarct size and decrease motility. Contraindication of BB = . CCF. . SBP < 90 . . PR < 60 . . AV block. . Bronchospasm .
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Cont… 7. Anticoaglants : UH OR LMWH. The main Rx is = ASPIRIN + PLAVIX + HEPARIN. 8. Risk stratification and PCI. “NO ROLE FOR THROMBOLYSIS IN NSTEMI OR UA.”
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AF with RVR .
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Common causes The six common causes of atrial fibrillation are: Hypertension. Ischemic heart disease. Chronic rheumatic heart disease, particularly mitral stenosis. Thyrotoxicosis. Alcohol . Lone atrial fibrillation.
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Complication ? What are the complications of atrial fibrillation? Thromboembolism – CVA, acute limb ischemia Heart failure ( tachycardia in induced cardiomyopathy).
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Mx. Treat the underlying cause . ( drug , cardiac, thyroid or pulmonary ). If unstable :_ Electrical DC cardio version (200j ). If stable :_ Rate control :_ B.Blockers Or Rate limiting CCB (verapamil or diltiazem) Or Digoxin or amiodarone if heart failure.
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Rhythm control Rhythm control :_ chemical cardioversion : (amiodarone , propafenone or flecainide ). electrcial cardioversion ± anticoagulant according to the following guidelines :_ If < 48 hours , you can usually cardiovert without anticagulation. If > 48 hours : Do transesophageal echo if negative for thrombous , cardiovert. Or Anticoagulate the patient for 3 weeks before and 4 weeks after cardioversion. If cardioverted start anti arrhythmic ( amiodarone , flecainide or propafenone ) . To prevent recurrence
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Anticoagulants . How can you assess risk of thromboembolism in atrial fibrillation? By using the CHADS score: Congestive heart failure (1 point) Hypertension (1 point) Age ≥ 75 (1 point) Diabetes mellitus (1 point) Stroke or transient ischemic attack (2 points) Score: 0 = aspirin therapy only, 1= warfarin or aspirin, and ≥ 2 = warfarin
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Causes of V.TAHC
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Mx. Pulseless V. TACH or V.FIB = DC SHOCK(200 J ) AND CPR(chest compression). Hemodynimacally unstable = immediate DC cardioversion (200j). Hemodynimically stble = Amiodarone or procainamide , lidocaine , mexilitine, magnesium sulphate. IV . IF unsuccessful DC shock. Treat the underlying cause = MI = Reperfusion. Electrolyte = k , mg If severe Acidosis = iv sodium bicarbonate treat the recurrent V.TACH with = radiofrequency ablation /OR ICD implantation.
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BLS
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CHB The most important aetiologies are: Inferior wall myocardial infarction. AV-nodal blocking drugs (e.g. betablockers , CCB , digoxin) Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)
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Toxic megacolon . It is a severe colitis " pan colitis " It is defined as dilatation of the transverse colon more than or equal to 6 cm at it is widest point radiologicaly on andominal X ray or CT scan.If there is delay in surgery toxic dilatation of the colon carries the risk of perforation which has a high mortality.It is most often occur in the context of ulcerative colitis but also can occur in CD , pseudomembranous colitis , ischemic colitis.It is absolute C/I of barium enema b/c risk of bowel perforation .Mortality rate 20% .PPS = hypokalemia.HypomagnesimiaUnder treatmentPurgative bowel preparation for colonoscopyNSAID and opiods.Anti cholinergic and anti diarrheal ..
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Cont. C/P = abd pain , vomiting , abdominal distension , tender rigid abdomen . TTT = ICU High dose iv steroids rectal steroids IVF + LMWH ± cyclosporin ± infliximab ± surgery ( colectomy ).
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Total confusion A 55 year old man , presents with sudden onset of hematemesis . He has vomited bright red blood during the past 3 hours , he has also become increasingly confused since the onset of symptoms . He was dignosed with HCV ten years ago , which was believed secondary to blood transfusion. on arrival , there is tachycardia , BP 90/50 , flapping tremor were positive , fetor hepaticus , pedal edema , looks ill , pale , icteric , moderate splenomegaly and positive shifting dullness. Invx. Blood glucose ans serum electrolytes normal. CBC = anemia , thrombocytopenia. , albumin= 2 , t.bilirubin = 6 ,
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Dx ? Acute upper GIT bleeding complicated by hypovolemic shock (requiring immediate fluid resuscitation and gastric decompression) . The long standing history of HCV along the presence of confusion , icterus , asterixis suggest significant liver disease ( liver cirrhosis ) which has been acutely complicated by hepatic encephalopathy . The cause of upper GIT bleeding is = esophageal varices. ( B/C of portal HTN suggested by ascitis , splenomegaly , bicytopenia ). The precipitating factor for encephalopathy is upper GIT bleeding.
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What is the role of flumazenil ? benzodiazipine recepetor antagonist that can be used in the management of hepatic enchaphalopathy.
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Next steps . ? Sulphonylurea screen = in this patient it was negative. Supervised 72 – h fast test = the patient become symptomatic after 16 hours of fasting. Investigation shows = RBS = 39 mg/dll. S.insulin = 16 uU / ml (high) S. c – peptide = 2.9 ng / ml (high) No ketone bodies. No insulin antibodies .
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More confusion.! A 53 year old male nurse presents with drowsiness and confusion for several hours. Prior to become drowsy , he complained of palpitation and sweating. PMH = free. He doesn’t drink or use any recreational drugs. CBC and electrolytes are normal , but his capillary blood sugar is 40 mg/dl. Following administration of glucose , he recocers completely. O/E =was drowsy and confused , diaforetic , no pallor or jaundice or stigmata of chronic liver or renal diseases , no pedal edema , CNS = normal, no neck stiffness or focal signs. PULSE = 110 , regular , BP= 120/80 , JVP= normal , other systems =free.
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What is DX ?
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Why insulinoma .? High insulin , high C peptide. Negative screen for sulphonylurea and antibodies. Next step = Always in endocrine confirm the abnormality biochemicaly then proceed to imaging , so the action suggested now is = CT scan of abdoemn with contrast which showing enhancing lesion in pancreatic body.
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