Anda di halaman 1dari 25

DD of chest pain:

First exclude any potentially life threatening causes virtue of history, brief examination & limited investigations. Then consider other potential causes.

Life threatening:

Acute myocardial infarction Angina Aortic dissection Tension Pneumothorax Pulmonary embolism Esophageal rupture


Pneumonia Empyema Chest pain: Muscular Rib fracture Bone metastases Costochondritis Pleurisy Gastroesophageal reflux Pericarditis Esophageal spasm Herpes zoster Cervical spondylosis Intra- abdominal cholecystitis Peptic ulceration Pancreatitis Sickle cell crisis

Before discharging patients with undiagnosed chest pain be sure in your own mind that the pain is not cardiac( this pain is usually dull, may radiate to jaw , arm or epigastrium & is usually associated with exert on). Do CXR, ECG, FBC, U&E & cardiac enzymes including troponin T. Discuss options with colleague & the patient. Dont simply turn people out on the street.

Management of acute MI:

Attach ECG monitor & record a 12 lead ECG

High flow O2 by face mask (caution: if COPD)

IV access Bloods for FBC, U & Es, glucose, lipids, cardiac enzymes (CK,AST,LDH)

Brief assessment History of cardiovascular ds, risk factors for IHD, # to thrombolysis. Examination: pulse, BP, JVP, crdiac murmurs, signs of heart failure, Peripheral pulses, scars from previous cardiac surgery

Aspirin 300mg chewed (unless already given by GB) Morphine 5-10mg IV + antiemetic e.g. metoclopramide 10 mg IV GTN sublingually 2 puffs or 1 tab. as required B- blocker e.g. atenolol 5 mg IV (unless asthma of lt ventricular failure) Thrombolysis CXR

Dont delay thrombolysis while waiting unless aneurysm suspected Consider glucose, insulin,& potassium infusion for patients with DM

Consider DVT prophylaxis

Continue medication except Ca channel blockers (unless specific indications) - If pain is uncontrolled, esp. if continuing ST elevation, consider re- thrombolysis with rtPA (no bolus) or rescue PTCA/ angioplasty.

Symptoms suggestive of acute coronary syndrome

1-Check electrocardiogram 2- Aspirin 3- Supplement O2 4- Sublingual nitroglycerine 5- Morphine pm 6- Check cardiac enzymes

No ST segment changes Initial enzymes normal

ST segment depression Consistent with unstable angina or NSTEMI

ST segment elevation Consistent with STEMI

Observe 1-Nitroglycerin pm 2-Analgesia 3-Serial ECG & cardiac enzymes

Recurrent chest pain Or Serial studies +ve

1-IV Nitroglycerin 2-Heparin 3-IV B-blocker

1PCI not available

1PCI available

No recurrent chest pain Serial studies - ve Provocative stress test LMWH, consider GP IIb / IIIa inhibitor

Thrombolytic therapy Primary PCI

Pre discharge stress test

-ve results

search for other causes of chest pain

No high risk markers No recurrent chest pain Provocative stress test

High risk markers present: -elevated troponin -persistent/ recurrent chest pain -persistent ST elevation -associated heart failure -hemodynamic instability -LVEF < 40% -PCI in preceding 6 months

+ve results -ve results +ve results

Cardiac catheterization & coronary revascularization

+ve results

-ve results

Aggressive risk factor modification long term antianginal therapy

Summary of ttt of atrial fibrillation:

Treatment reversible cause. Control ventricular rate. Consider cardio version to sinus rhythm, if onset within last 12 months ( do echo first: Is heart structurally normal?). Prevent emboli: warfarin ( or aspirin).


Digoxin B- blocker Verapamil Amiodarone Dc shock

Continuous Digoxin B- blocker Amiodarone Anticoagulation

Chronic AF


Sotalol Amiodarone Consider anticoagulation

Algorithm for management of atrial fibrillation:

Chronic AF: -Treat underlying cause -Start risk based anticoagulation -Consider rhythm, control if not tolerated Atrial Fibrillation If no: cardiovert if instability AF- related Vs treat underlying cause


If yes: Rate control

1st time AF (< 48hrs)

1st time AF (< 48hrs)

PAF (< 48hrs)

PAF (< 48hrs)

-Evaluate /treat
underlying cause -Early conversion ,risk based anticoagulation

Start Coumadin and convert in 3 weeks vs TEE + Herparin , then 4 wks Coumadin ,or rate control & anticogulate if rhythm not tolerated

-Early cardioversion vs observation -Risk-based anticoagulate -Rate control or antiarrhythmic to patient unable to tolerate symptoms

Risk based long term anticoagulation conversion requires anticoagulation 3 weeks with Coumadin vs TEES/Heparin, then Coumadin for 4 weeks Convert if AF poorly tolerated

AF= atrial fibrillation PAF= persistent atrial fibrillation TEE= transesopageal echocardiography

Management of massive pulmonary embolism:


Morohine 10 mg IV if the patient is in pain or very distressed

if critically ill: consider immediate surgery

IV access & start Heparin Either unfractionated Heparin 5000U IV bolus Then 1000- 2000U/h IVI as guided by APTT Or low molecular wt Heparin e.g. Tinzaprin 175U/Kg/24h SC2

Whats the systolic BP?

< 90 mmHg start rapid colloid infusion**

> 90 mmHg Start Warfrain 10mg/24h PO

If BP still after 500ml colloid dobutamine 5-10 ug/Kg/min IV: aim for systolic BP > 90 mmHg

Confirm diagnosis

If BP still consider noradrenaline

If the systolic BP < 90mmHg after 30-60min of standard treatment, clinically definite PE & no CL Consider thrombolysis*

*A standard regimen is: loading dose: Streptokinase 250000 IVI over 30 min. Maintenance dose: Streptokinase 100000U/h IVI for 12-72h according to response. ** Controversial, but some aythroities say it is best to infuse plasma- expanding fluids even if CVP , to maintain BP & organ perfusion.

Diagnostic Algorithm for suspected Pulmonary Embolism:

Clinically Assess* Pretest Probability

Low probability

Moderate or high probability

D-dimer ELISA -ve < 500 Stop No treatment Search for alternative diagnosis

> 500 elevated

V/O scan

Normal scan

Non diagnostic (low or intermediate probability)

High probability

Clinically stable


+ve for PE

Bilateral lower extremity Doppler


Pulmonary angiogram
-ve for PE

+ve for DVT Treat

Stop ttt

* Clinical clues: 1- Sudden onset of dyspnea or worsening of chronic dyspnea. 2- Pleuritic chest painor pleural rub. 3- Hypoxemia (SaO2< 92%) 4- Hemoptysis. 5- Recent surgery or immobilization. 6- Prior Hx of DVT or PE. CT angiography can be considered.

Management of shock:
If BP unrecordable, call the cardiac arrest team

ABC (including high flow O2)

Raise foot of the bed

IV access* 2 ( wide bore: get help if it takes> 2 mins)

Identity & treat underlying cause

Infuse colloid or crystalloid fast to raise BP (unless cardiogenic shock)

Seek expert help early

Investigations: FBC, U&E, ABG, glucose, BL.culture , urine culture ECG, CXR, others e.g. lactate, echo, abd. CT. USS

Consider arterial line, central venous line& bladder catheter (aim for a urine flow > 30 ml/h)

Further management: treat underlying cause if possible Fluid replacement as dictated by BP, CVP, urine output Dont overload with fluids if cardiogenic shock If persistently hypotensive consider inotropes N.B.- Remember that higher flow rates can be achieved through peripheral lines than that through standard gauge central lines. -If in doubt as to the cause treat as hypovolemia as it is the most common cause & reversible. - Ruptured abdominal aortic aneurysm aim for a systolic BP of ~ 90 mmHg.

Management of anaphylxis
Secure the airway give 100%O2 Intubate if respiratory obstruction imminet

Remove the cause : raising the feet may help restore the circulation.

0.5mg(i.e. 0.5ml of 1:1000)

Repeat every5mins, if needed by BP, pulse, and respiratory function), until better Give adrenaline IM

secure IV access

Chlorpheniramine* 10mg IV and hydrocortisone 200mg IV

IVI (0.9%saline, e.g. 500ml over h: up to 2L may be needed ) Titrate against blood pressure

If wheeze, treat for asthma, May require ventilatory support

If still hypotensive admission to ITU and an IVI of adrenaline may be needed aminophlline & nebulized salbutamol: get expert help.

Bleeding management :
Any suspicion of variceal bleeding?



Endoscope (at <24 h if shock)

emergency endoscope (at<4hif shock) Are there bleeding varices?

Peptic ulcer

other diagnosis



Are risk factors present: - 6 units transfused - Haematemesis & melaena - Rebleeding - Bleeding vessel seen on endoscope, or clot in an ulcer


No risk factors 1 risk factor

conservative treatment surgery (or endoscopic diathermy if fail)

Immediate management if shocked:

Protect airway and keep NBM

Insert 2 large bore cannulae 14- 16G

Draw bloods, Cross match 6 units FBC, U&E, LET, glucose, clotting screen

Give high-flow O2

Rapid IV colloid infusion up to 1 L

If remains shocked give blood group specific or ORh -ve until cross match done

Otherwise slow saline infusion* (to keep lines open)

transfuse as dictated by haemodynamics

correct clotting abnormalities (vitamin K, FFP, platelet concentrate)

Set up CVP line to guide fluid replacement Aim for >5cm H2O CVP may mislead if there is ascites or ccf A Swan- Ganz catheter may help

Catheterize and monitor urine output (aim for >30mL/h)

Monitor vital signs every 15 mins until stable then hourly

Notify surgeons of all severe bleeds

Urgent endoscope for diagnosis control of bleeding

Avoid saline in patients with decompensted liver disease (ascites, peripheral edema) as it worsens ascites & despite a low serum sodium, patients have a high body sodium. Use whole blood or salt-poor albumin for resuscitation & 5%dextrose for maintenance. ** Poor prognostic signs: - Age > 60 - chronic liver disease - signs of shock - consciousness level

- bradycaria or rate 120 bpm - significant co-morbidity - bleeding diathesis

Management of infective diarrhea:


No systemic signs

Systemic illness: - fever >39 C - blood diarrhea lasting >2 wks - dehydration

Special circumstances: - Food poisoning outbreak - Travel - Recent antibiotic use - Recent intercourse - Immunocompromised host - Raw sea food ingested

symptomatic treatment

Consider noninfectious causes Admit to hospital Give oral fluids Consider presumptive antimicrobial therapy *

Stool culture not needed

prompt direct faecal smear (then culture)

routine stool culture & microscopy

confer with microbiologist

polymorphs seen

no polymorphs

parasites seen

likely culture : - Shigella ** - Campylobacter - E coli (Yersinia rare) (Salmonella rare) (C. difficile*)

likely culture : - Salmonella ** - E coli

specific therapy

** prompt, specific treatment (e.g. ciprofloxacin) may be needed before sensitities are known be guided by likely diagnosis following microscopy * pseudo membranous colitis is caused by overgrowth of Clostrium difficile , following any antibioyic .treatment :Vancomycin 125mg/6h po metronidazole 400 mg /8h po (cheaper ; more palatable ).liaise with a microbiologist. Note : another classification distinguishes secreory diarrhoea (eg infections ,us/crohn's etc) from osmotic causes (water drawn into the gut , as in laxative use).

Algorithm for patient with diarrhea:

Acute diarrhea

Bloody diarrhea Systemic symptoms & signs Immunosuppressed host

Early mild course No blood in stool

Stool for pathogens

Stool for pathogens

Observe symptomatic therapy

- ve

+ ve

- ve

+ ve

Sigmoidoscopy & biopsies


Observe symptomatic therapy


Specific therapy

Chronic diarrhea

History, physical examination, laboratory tests, stool for pathogens

Clinical signs of malabsorption/ wt loss



Exclude lactose inolerance

Blood in stool

Exclude: Pancreatic/ liver ds, small bowel ds

Colonic biopsies ( microscopic coliis) Treat for IBS

Test for: -Cancer colon -IBD

- ve

Small bowel radiography/ biopsies Evaluate laxative use/abuse Celiac serology Circulating hormone levels

- ve

Empirical therapy (antibiotics, bile salts, binding resin, pancreatic enzymes)

Managing dyspepsia those 45 yrs not on NSAIDs, with no weight loss, dysphagia, repeated vomiting, anaemia ,masses or bowel habit change*
Simple antacids antireflux measures (p200) if symptoms of reflux (e.g. pain stooping)

symptoms still persistent previous peptic ulcer no past ulcer

symptoms still not persistent no further action

Test for H. pylori but see caveats in text

H pylori found to be present

H pylori absent

Eradicate H pylori (if past DU no test for H Pylori is needed before eradication therapy ,see above)

Give H2blocker for 2 wks

Review symptoms at about 3-4 wks

Patient well

Patient still has symptoms

No further action

Upper GI endoscope

Do endoscope urgently in dyspeptic adults not falling into this group, or stop NSAIDs & monitor closely. Why dont we give under 45s with dyspepsia a helicobacter ttt?
NNT ~ 9 for nonulcer dyspepsia & peptic ulcers are prevented. But we dont know enough about longterm effects of such a strategy for clear recommendations. We also know that nonulcer dyspepsia doesnt improve with eradication therapy. In known peptic ulceration, test before treating if its a gastric ulcer & treat before testing if its a duodenal ulcer. The 13C- urea breath test is the best noninvasive method for detecting H. pylori even when monitoring efficacy of ttt. Serology methods are less good here, as antibodies stay months after eradication. An immunoassay detecting bacterial antigen in faeces is a new ( under evaluated), noninvasive method for determining efficacy of eradication.

DD of headache:
No signs on examination: Tension headache Migraine Cluster headache Post traumatic Drugs (nitrates, Ca channel antagonists) Carbon monoxide poisoning or anoxia Signs of meningism: Meningitis (may not have fever or rash) Subarachnoid Hge Decreased conscious level or localizing signs: Encephalitis/ meningitis Stroke Cerebral abscess Subarachnoid He Tumor Subdural haematoma TB meningitis Papilloedema Tumor Malignant HTN Benign IC HTN Any CNS infection, if prolonged (e.g.> 2 wks) >>>>e.g. TB meningitis Others: Temporal arteritis ( ESR elevated) Glaucoma Pagets ds Sinusitis Altitude sickness Cervical spondylosis

Two vital questions: - where have you been? (malaria) - Might you be pregnant? ( eclampsia especially if proteinuria & BP)

* Wheezing? - Asthma - COPD - Heart failure - Anaphylaxis * Stridor? - Foreign body - Acute epiglottitis - Anaphylaxis - Trauma e.g. laryngeal fracture * Crepitations? - Heart failure - Pneumonia - Brochiectasis - Fibrosis * Chest clear? - Pulmonary embolism - Hyperventilation - Metabolic acidosis e.g. DKA - Anemia - Drugs e.g. salicylates - Central causes * Others - Pneumothorax - Pleural effusion

pain, increased resonance stony dullness

Management of acute COPD

Controlled oxygen therapy Start at 24- 28%; vary according to ABG. Aim for a Pa O2 > 8.0 KP a rise in Pa CO2 <1.5 KPa

Nebulized bronchodilators : Salbutamol 5mg/4h and Ipratropium 500ug/6h

Steroids IV hydrocortisone 200mg and oral prednisolone 30-10mg

Antibiotics: Use if evidence of infection, e.g. amoxicillin 500mg/6hPO

Physiotherapy to aid sputum expectoration

If no response: Repeat nebulizer& consider IV amiophylline*

If no response: 1- Consider nasal intermittent +ve pressure ventilation If resp. rate > 30 or PH < 7.35. It is delivered by nasal mask & a flow generator.

2- Consider intubation**& ventilation if PH < 7.26 and P CO2 is rising

3-Cosinder a respiratory stimulant drug , e.g. doxapram 1-2mg /min IV SE.: agitation, confusion tachycardia , nausea Only for patients who are not suitable for mechanical ventilation A short-term measure only * Aminophylline: Do Not give a loading dose to patients on maintenance methylxanthines ( theophyllines/aminophylline). Load with 250mg over 20min, then infuse at a rate of ~ 500g/kg/hour. Check plasma levels if given for > 24h. ECG monitoring is required. ** A decision to ventilate will depend on the patients premorbid state, exercise capacity, home oxygen and comorbidity. Ask at out this information before you need to make this decision.

Oxygen therapy:
The greatest danger is hypoxia, which probably accounts for more deaths than hypercapnia . Dont leave patients severely hypoxic. However, in some patients, who rely on their hypoxic drive to breathe, too much oxygen may lead to a reduced respiratory rate, and hypercapnia, with a consequent fall in conscious level. Therefore, care is required with O2 , especially if there is evidence of CO2 retention. Start with 24-28% O2 in such patients. Reassess after 30min. Monitor the patient carefully. Aim to raise the Pa O2 above 8.0 KPa with a rise in Pa CO2 < 1.5 KPa. In patients without evidence of retention at baseline use 28-40% O2 but still monitor and repeat APG.

Algorithms for ttt of bronchospasm A)Emergency department treatment of acute bronchospasm

Oxygen inhaled 2 against consider inhaled anticholinergic oral or iv corticosteroids

Inadequate response

good response

Inhaled anticholinergic If not given previously

discharge on inhaled 2 against inhaled anticholinergic Corticosteroids x 5days arrange outpatient follow up with in 5 days

persistent bronchospasm

admit to hospital

respiratory failure

consider aminophylline heliox (helium =oxygen )iv magnesium Endotracheal intubation and mechanical ventilation

B)Outpatient treatment of chronic/stable bronchospasm

Asthma COPD

Inhaled PRN short-acting 2 agonist

Inhaled PRN short-acting 2 agonist Inhaled anticholinergic

Continued symptoms

Continued symptoms

Add inhaled Corticosteroids

trial of inhaled Corticosteroids

Continued symptoms

Continued symptoms

Increase dose of inhaled Corticosteroids add long acting 2 agonist

oral antibiotics if chronic bronchitis is a prominent component consider trial of theophylline

Continued symptoms

Continued symptoms

Add leukotriene antagonist

trial of oral Corticosteroids

Continued symptoms

Add oral corticosteroids

Algorithm for the diagnosis & ttt of chronic cough;

Chronic cough
History & physical exam.

Cough gone

Stop ACEI Cough persists

Chest radiography


Abnormality may not be related to cough

Order according to likely clinical possibility

Avoid irritant

Cough gone

Cough persists

Sputum ,cytology, HRCT scan, modified BaE bronchoscopy, cardiac studies

Treat accordingly Evaluate for three most common conditions singly in the following order, or in combination: 1- PNDS 2- Asthma 3- GERD

Cough persists

Cough gone

Cough gone

Cough persists

Consider postinfectious cough

Evaluate for uncommon conditions

Sputum tests, HRCT scan, modified BaE, bronchoscope, cardiac studies

Cough gone

Cough persist Reconsider adequacy of treatment regimens before considering habit or psychogenic cough

Management protocol for patients with idiopathic nephrolithiasis:

First Stone Episode Detailed dietary history. Serum electrolytes, creatinine, calcium, phosphorus, uric acid. Urinalysis, crystallographic studies. Non-contrast CT scan. Advise > 3 liters of fluid/24hours. Protein 1-1.5 g/kg/24 hours. Moderate salt restriction

High recurrence risk

6-8 weeks

Low recurrence risk

24-hour urine collection for volume, calcium, phosphorus, uric acid, citrate, oxalate, creatinine, magnesium, cystine

Continue dietary & fluid management





No abnormalities

Reduce purine intake

Consider allopurinol if hyperuricemic

Restrict dietary oxalate and add calcium carbonate

Further protein restriction and potassium citrate

Restrict salt Consider thiazide and amiloride

Continue dietary and fluid management

Algorithm of syncope evaluation:


Stable Patient

Unstable Patient

Perform EKG

Perform EKG Abnormal EKG, or history suggestive of serious pathology (no clear prodrome), age >60 years, history of cardiac disease (especially congestive heart failure), exertional syncope, chest pain, dyspnea, neurological findings. Arrhythmia

Perform EKG Airway, breathing, circulation, oxygen, monitor, IV access

Normal EKG, plus reassuring historical features (vasovagal, situational, orthostatic, young, no comorbidities)

Discharge with primary care follow up

Apply appropriate ED testing (such as echo, V/Q scan, CT, Doppler studies, labs)

Noncardiac ( hypovolemia, anemia, pulmonary embolism, abdominal aortic aneurysm, aortic dissection, toxicologic)


Strongly consider admission, but discharge with expedient outpatient follow up may be appropriate depending on the specific scenario

Apply diagnostic modalities, consult appropriate services, treat emergently