5. Management of important cardiac emergencies in the ED

#### 5.1. Acute coronary syndrome

Acute coronary syndrome includes a spectrum of clinical presentations which range from unstable angina to non-ST elevation MI and ST elevation MI. They can be differentiated on the basis of history, ECG changes and blood investigations. The management started should be according to the diagnosis.

#### 5.1.1. Spectrum of ACS

4. Metabolic/electrolyte abnormalities

5. Arrhythmias b. Bed-side Ultrasound: 1. Pneumothorax

216 Essentials of Accident and Emergency Medicine

2. Pneumonia

4. Pleural effusion

4. Aortic dissection

7. Ejection fraction

1. Cardiomegaly

3. Pneumonia

7. Lung mass

g. ABG: PE

h. D-Dimer: PE

8. Myxoma/thrombus

9. Cardiac outflow obstruction

2. CCF/pulmonary edema

4. Wide mediastinum

8. Diaphragmatic hernia e. Cardiac enzymes: Acute MI f. Pro-BNP: Acute heart failure

5. Pleural effusion 6. Pneumothorax

5. Valvular heart disease 6. Ventricular thickening

1. Wall-motion abnormality

2. Pericardial effusion/tamponade

3. PE

c. Bed-side Echo

3. PE

d. X-Ray:

Unstable angina: It is referred to as pre-infarction angina or pre-occlusive syndrome. It is a warning sign of infarction.

Myocardial infarction: It is defined as cell death and necrosis. Below mentioned are the criteria satisfying the diagnosis of acute, evolving or recent MI.

	- a. Symptoms of ischemia
	- b. ECG changes (either Q waves or changes consistent with ischemia like ST or T wave changes)
	- c. Coronary artery interventions

#### 5.1.2. Diagnosis

Diagnosis is done based on the history and physical examination and finally after diagnostic testing. The diagnostic testing includes ECG, chest X-Ray, serum cardiac markers, echocardiography, scintigraphy and CT angiography depending on the requirement and the availability.

ECG findings of MI:

#### 5.1.3. Management

The management goal is early revascularization and reperfusion using either fibrinolysis or primary angioplasty. In places where PCI is available, quick cardiologist consultation and activation of PCI code are needed so that the cardiologist is involved to decide which pathway to follow. Delay in getting PCI does not justify avoiding thrombolysis. If, for any reason, expected time for PCI is more than 90 min, then thrombolysis is the choice of treatment. Medical management is divided into two categories:

#### 5.1.3.1. Pharmacologic intervention

Oxygen should be administered when blood oxygen saturation is 90% or if the patient is in respiratory distress. In patients whose ischemic symptoms are not relieved by nitrates and beta-blockers, opiate administration is reasonable while waiting for immediate coronary angiography, with the caveat that morphine may slow down the intestinal absorption of oral platelet inhibitors.

5.2. Heart failure

filling pressures to accomplish this goal.

monary capillary membrane.

5.2.2. Compensatory mechanisms

5.2.3. Treatment of heart failure

ing cardiac contractility.

• nitrates

• IABP

• morphine

• loop diuretics • nitroprusside

• stabilization of patient and resuscitation

• identify the underlying and precipitating cause and treat it

• Acute pulmonary edema with adequate perfusion:

• noninvasive or invasive ventilation [3, 7] • Acute pulmonary edema in hypotensive patients

• vasopressors and inotropes to maintain coronary perfusion

by cardiac index and pulmonary artery outflow pressure)

• judicious fluid challenge if low PAOP (<15 mm Hg)

phy.

5.2.1. Pathophysiology of acute pulmonary edema

It is defined as the pathophysiologic state in which the heart is not capable of pumping sufficient supply of blood to meet the body requirements or else requires elevated ventricular

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Cardiogenic pulmonary edema is due to increased capillary hydrostatic pressure secondary to acute ischemia or infarction, cardiomyopathy, valvular heart disease or hypertensive emergencies. Non-cardiogenic pulmonary edema occurs due to alteration in the permeability of pul-

The compensatory mechanisms secondary to heart failure include increase in stroke volume in response to increased pre-load, increased systemic vascular resistance and cardiac hypertro-

• control the symptoms and acute congestive state by reducing the cardiac work load (reducing pre-and after load), controlling excessive salt and water retention and improv-

• manage hypotension due to cardiogenic shock or due to volume depletion (identified


Subcutaneous(SC) enoxaparin for the duration of hospitalization or until PCI is performed (level of evidence: A);

Bivalirudin until diagnostic angiography or PCI is performed in patients with early invasive strategy only (level of evidence: B);

SC fondaparinux for the duration of hospitalization or until PCI is performed (level of evidence: B);

IV unfractionated heparin (UFH) for 48 h or until PCI is performed (level of evidence: B).

#### 5.1.3.2. Reperfusion therapy

Reperfusion therapy, either by using thrombolytics or primary PCI, increases the opportunity to salvage ischemic myocardium. Fibrinolytic therapy improves coronary flow, limits infarct size and improves survival.

#### 5.2. Heart failure

beta-blockers, opiate administration is reasonable while waiting for immediate coronary angiography, with the caveat that morphine may slow down the intestinal absorption of oral

• Nitroglycerine: It is a coronary vasodilator and reduces myocardial pre-load and after

• Pain management: If the patient is in severe pain and not responding to NTG and beta-

• Beta-blockers: Early administration of beta-blockers should be avoided in these patients if the ventricular function is unknown and should not be administered in patients with symptoms possibly related to coronary vasospasm or cocaine use, as they might favor spasm by leaving alpha-mediated vasoconstriction unopposed by beta-mediated vasodi-

• Calcium channel blockers (CCBs): CCBs are recommended for ischemic symptoms when beta-blockers are not successful, are contraindicated or cause unacceptable side effects. Long-acting CCBs and nitrates are recommended for patients with coronary artery spasm. They can be used for rate control in patients with SVT when beta blockers are not

• ACE inhibitors: ACE inhibitors should be started and continued indefinitely in all patients with a left ventricular ejection fraction (LVEF) below 40% and in those with hypertension,

• Antiplatelet: Antiplatelet therapy reduces progression to acute infarction in patients with non-AMI ACS patients. Aspirin or GP11b/111a inhibitors may be used. Antiplatelet treat-

• Anticoagulation: Administer anticoagulation, in addition to antiplatelet therapy, for all patients, irrespective of the initial treatment strategy. Treatment options include the fol-

Subcutaneous(SC) enoxaparin for the duration of hospitalization or until PCI is

Bivalirudin until diagnostic angiography or PCI is performed in patients with early

SC fondaparinux for the duration of hospitalization or until PCI is performed (level of

IV unfractionated heparin (UFH) for 48 h or until PCI is performed (level of evidence: B).

Reperfusion therapy, either by using thrombolytics or primary PCI, increases the opportunity to salvage ischemic myocardium. Fibrinolytic therapy improves coronary flow, limits infarct

diabetes mellitus or stable chronic kidney disease (CKD), unless contraindicated.

platelet inhibitors.

218 Essentials of Accident and Emergency Medicine

blockers.

lation.

tolerable.

ment reduces mortality.

lowing (all Class I):

evidence: B);

5.1.3.2. Reperfusion therapy

size and improves survival.

performed (level of evidence: A);

invasive strategy only (level of evidence: B);

load.

It is defined as the pathophysiologic state in which the heart is not capable of pumping sufficient supply of blood to meet the body requirements or else requires elevated ventricular filling pressures to accomplish this goal.

#### 5.2.1. Pathophysiology of acute pulmonary edema

Cardiogenic pulmonary edema is due to increased capillary hydrostatic pressure secondary to acute ischemia or infarction, cardiomyopathy, valvular heart disease or hypertensive emergencies. Non-cardiogenic pulmonary edema occurs due to alteration in the permeability of pulmonary capillary membrane.

#### 5.2.2. Compensatory mechanisms

The compensatory mechanisms secondary to heart failure include increase in stroke volume in response to increased pre-load, increased systemic vascular resistance and cardiac hypertrophy.

#### 5.2.3. Treatment of heart failure

	- nitrates
	- morphine
	- loop diuretics
	- nitroprusside
	- noninvasive or invasive ventilation [3, 7]
	- vasopressors and inotropes to maintain coronary perfusion
	- manage hypotension due to cardiogenic shock or due to volume depletion (identified by cardiac index and pulmonary artery outflow pressure)
	- judicious fluid challenge if low PAOP (<15 mm Hg)
	- IABP
	- Manage hypertension
	- Reverse remodeling by beta-blockers, ACE-I, aldosterone antagonists, ARB
	- Vasodilator therapy (ACE-I, ARB, Nitrates)
	- Diuretics
	- Cautious use of calcium blockers for hypertension, angina and dysrhythmia management

• Systemic reperfusion therapy for stroke or MI

as emergency physicians' expertise in managing them.

Diagnosis: 12 Lead ECG (see Images 1, 2, 3, 4 for NCT and WCT)

• Hypotension and or features of hypo-perfusion

• Chest pain suggesting myocardial ischemia

• Altered sensorium (agitation to coma)

• Dyspnea or pulmonary edema

Hypertensive encephalopathy Nicardipine

Intracranial Hemorrhage Nicardipine

Acute Pulmonary Edema Nitroglycerine

Ischemic Stroke Nicardipine

Acute Kidney Injury Fenoldapam

Preeclampsia/eclampsia Hydralazine

Sympathetic Crisis Phentolamine

Table 3. Management of hypertensive emergencies (Crack Cast).

Drugs of choice in treatment of hypertensive emergencies: Crack Cast (Table 3)

Dysrhythmias present in the emergency department as chest pain, breathlessness, palpitation, sweating, pre-syncope, syncope and thromboembolic complications [8]. Managing dysrhythmias is very challenging in the emergency department. Timely intervention saves life. The first challenge is to diagnose the type of arrhythmias and categorize them as narrow complex or broad complex tachycardias or brady cardiac. The next step in management is to categorize them as stable or unstable. The type of management depends on the stability of patient as well

a. Symptoms and signs of unstable patients in the emergency department includes:

Emergencies Drug of choice Alternatives

Esmolol Enalaprilat

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Esmolol

Esmolol Enalaprilat

Labetalol

Nicardipine

Fenoldapam Clevidipine Nicardipine Sodium nitroprusside

Nicardipine Sodium Nitroprusside

Esmolol and Nicardipine Diltiazem, Verapamil

Sodium Nitroprusside

Labetalol

Labetalol

Furosemide Enalaprilat

Labetalol

Labetalol

Labetalol

Nitroglycerine

Nicardipine, Clevidipine

Aortic Dissection Esmolol and Sodium Nitroprusside

• Postoperative state

5.4. Dysrhythmias


#### 5.3. Hypertensive emergencies

In the Emergency Department hypertension presents as one of the four varieties:


Only hypertension crisis requires treatment in the emergency department within 90 min of their presentation. Patients presenting with hypertensive emergencies will have markedly elevated BP and evidence of acute dysfunction in the cardiovascular, neurologic or renal system. Following are the conditions defined as hypertensive crisis:

	- Hypertensive encephalopathy
	- Microangiopathic hemolytic anemia
	- Acute renal failure
	- Myocardial ischemia
	- LVF
	- Uncontrolled hemorrhage

Drugs of choice in treatment of hypertensive emergencies: Crack Cast (Table 3)

#### 5.4. Dysrhythmias

• Emergency revascularization if ischemic cardiogenic shock

• Vasodilator therapy (ACE-I, ARB, Nitrates)

• Reverse remodeling by beta-blockers, ACE-I, aldosterone antagonists, ARB

• Beta-blocker therapy: Carvedilol may be effective agent in chronic HF

In the Emergency Department hypertension presents as one of the four varieties:

Only hypertension crisis requires treatment in the emergency department within 90 min of their presentation. Patients presenting with hypertensive emergencies will have markedly elevated BP and evidence of acute dysfunction in the cardiovascular, neurologic or renal

1. Hypertensive emergency or crisis with acute end organ ischemia

4. Transient hypertension which is related to anxiety or complaint

system. Following are the conditions defined as hypertensive crisis:

1. Accelerated or malignant hypertension: • Hypertensive encephalopathy

4. Severe hypertension in the setting of:

• Uncontrolled hemorrhage

• Acute renal failure

3. Eclampsia/pre-eclampsia

• Myocardial ischemia

2. Aortic dissection

• LVF

• Microangiopathic hemolytic anemia

2. Hypertensive urgency: Patients with poorly controlled hypertension

• Cautious use of calcium blockers for hypertension, angina and dysrhythmia manage-

• Treatment of chronic heart failure:

• Manage hypertension

220 Essentials of Accident and Emergency Medicine

• Diuretics

ment

• Digoxin

3. Mild hypertension

5.3. Hypertensive emergencies

Dysrhythmias present in the emergency department as chest pain, breathlessness, palpitation, sweating, pre-syncope, syncope and thromboembolic complications [8]. Managing dysrhythmias is very challenging in the emergency department. Timely intervention saves life. The first challenge is to diagnose the type of arrhythmias and categorize them as narrow complex or broad complex tachycardias or brady cardiac. The next step in management is to categorize them as stable or unstable. The type of management depends on the stability of patient as well as emergency physicians' expertise in managing them.

Diagnosis: 12 Lead ECG (see Images 1, 2, 3, 4 for NCT and WCT)

	- Hypotension and or features of hypo-perfusion
	- Chest pain suggesting myocardial ischemia
	- Dyspnea or pulmonary edema
	- Altered sensorium (agitation to coma)


Table 3. Management of hypertensive emergencies (Crack Cast).

Image 1. Narrow complex tachycardia: Courtesy Dr. smith ECG blog.

Image 3. SVT with aberrancy: Courtesy the blunt dissection.

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Image 4. Polymorphic V-Tac.

Image 2. Wide complex tachycardia (courtesy Dr smith blog).


Image 3. SVT with aberrancy: Courtesy the blunt dissection.

Image 4. Polymorphic V-Tac.

b. Management of stable patients: Management of stable patients requires proper assessment and evaluation by detailed history and examination, ECG and then treatment depending on the type of rhythm, whether it's narrow complex or broad complex tachycardias. The treatment options are some maneuvers like vagal or valsalva and medications like adenosine, amiodarone, procainamide, verapamil and diltiazem. Narrow complex tachycardias are treated with drugs which slow AV nodal conduction like class 11 agents (betablockers) or class 1 V agents (calcium blockers) and adenosine or Class 1A (procainamide) and 1C (flecainide) drugs which are useful in converting narrow complex tachycardias to

c. Management of unstable patients: Unstable patients are managed more aggressively. Again, treatment options depend on whether it's narrow complex tachycardias or wide complex tachycardias and an emergency physician's expertise with the drugs and syn-

a sinus rhythm. See Table 4 for treatment of NCT and WCT

Image 1. Narrow complex tachycardia: Courtesy Dr. smith ECG blog.

222 Essentials of Accident and Emergency Medicine

Image 2. Wide complex tachycardia (courtesy Dr smith blog).

chronized cardioversion.

Type of Rhythm Management Options


5.5. Aortic dissection

classification)

• Syncope

c. Physical examination:

• Severe hypertension

• Findings of stroke

artery)

specific.

• Pain management

intervention.

60/m.

d. Diagnostic tests:

b. Presentation:

treating as MI may kill the patient.

• Chest pain/back pain (interscapular)

• Aortic regurgitation findings on auscultation

• Acute inferior or posterior MI (RCA dissection)

tion of aortic knob, displaced NG-Tube

and 95% specific. It is operator dependent.

• ECG: LVH, MI, ischemia, non-specific ST-T changes

• Discrepancy in BP and pulse deficits between limbs

Aortic dissection is one of the most serious cardiovascular emergencies, presenting in ER, mimicking cardiac ischemia [9]. Failure to diagnose is catastrophe for the patient and may lead to death. Thrombolysis is contraindicated. Wrongly diagnosing them as cardiac ischemia and

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a. Types: Type A involves ascending aorta; Type B does not involve ascending aorta (Stanford

• Ischemic paraparesis or ischemic peripheral neuropathy (dissection of anterior spinal

• CXR: Normal or widened mediastinum, calcium sign, double density aorta, oblitera-

• Echocardiography: Transthoracic echo is an insensitive tool but TEE is 98% sensitive

• Helical CT: It's a reliable test for diagnosis. It is almost 100% sensitive and 98%

• Blood pressure management: The goal is to reduce blood pressure and to decrease the rate of rise of arterial pulse. The target BP is 100/60 and heart rate of less than

e. Management: Medical management is needed in Type B, whereas type A requires surgical

• Neurologic symptoms like weakness or change in mental status

Table 4. Treatment of Arrhythmias.

#### 5.5. Aortic dissection

Type of Rhythm Management Options

224 Essentials of Accident and Emergency Medicine

SVT (AV nodal)

Wide Complex V-Tach (stable) Monomorphic:

SVT with Aberrancy

Table 4. Treatment of Arrhythmias.

Fibrillation

Pharmacologic cardioversion: 1. Procainamide (1A) or 2. Propafenone (1C) or 3. Flecainide (1C) or 4. Amiodarone (111) or 5. Ibutilide (111) Rate Control:

2. Beta Blockers

Vagal Maneuvers Pharmacologic Treatment: 1. Adenosine 2. Calcium Blockers 3. Beta Blockers Electrical Cardioversion:

a. Rate Control: b. Beta Blockers c. Calcium Blockers

(25-50 J)

2. IV MgSO4

4. Amiodarone 5. Overdrive Pacing

Beta Blockers Digoxin

V-Tac (Pulseless) Treat as Ventricular Fibrillation

a. Use: Amiodarone Procainamide

a. Electrical Cardioversion

b. If Unstable: Treat as V Tac

50-100 J (increase by 50–100 if no response till 360 J)

e. Procainamide (1A) f. Ibutilide (111) g. Amiodarone (111) h. Electrical Cardioversion:

1. Treat underlying cause 2. Amiodarone 3. Procainamide 4. Lidocaine 5. Magnesium SO4

Polymorphic with Torsade de Pointes 1. Treat Underlying Causes

3. Beta-Adrenergic Infusion

Atrial Fibrillation with aberrancy: a. Avoid: calcium Blockers

d. Pharmacologic Cardioversion

Electrical Cardioversion:

or chronic.

(50–100 J)

(50-100 J)

Atrial Flutter Pharmacologic:

1. A calcium blocker (Verapamil or diltiazem) may be used before type 1A agent

Anticoagulation: anticoagulation in ED is needed depending on whether AF is new

Narrow complex Atrial

Aortic dissection is one of the most serious cardiovascular emergencies, presenting in ER, mimicking cardiac ischemia [9]. Failure to diagnose is catastrophe for the patient and may lead to death. Thrombolysis is contraindicated. Wrongly diagnosing them as cardiac ischemia and treating as MI may kill the patient.

	- Chest pain/back pain (interscapular)
	- Syncope
	- Neurologic symptoms like weakness or change in mental status
	- Severe hypertension
	- Aortic regurgitation findings on auscultation
	- Discrepancy in BP and pulse deficits between limbs
	- Findings of stroke
	- Ischemic paraparesis or ischemic peripheral neuropathy (dissection of anterior spinal artery)
	- Acute inferior or posterior MI (RCA dissection)
	- ECG: LVH, MI, ischemia, non-specific ST-T changes
	- CXR: Normal or widened mediastinum, calcium sign, double density aorta, obliteration of aortic knob, displaced NG-Tube
	- Echocardiography: Transthoracic echo is an insensitive tool but TEE is 98% sensitive and 95% specific. It is operator dependent.
	- Helical CT: It's a reliable test for diagnosis. It is almost 100% sensitive and 98% specific.
	- Pain management
	- Blood pressure management: The goal is to reduce blood pressure and to decrease the rate of rise of arterial pulse. The target BP is 100/60 and heart rate of less than 60/m.

• Use beta-blockers with vasodilators to avoid tachycardia. Esmolol is used to control heart rate. Labetalol can be used. Sodium nitroprusside is used as a vasodilator. Nitroglycerin can be used as a vasodilator but needs beta-blocker in conjunction.

V/Q Scan: It is used when CTPA is either contraindicated or not possible to perform.

• Anticoagulation: Anticoagulation with IV Heparin (bolus then infusion), fractionated heparin (Enoxaparin) or the Factor Xa inhibitor (Fondaparinux) is the current standard

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• Thrombolytic therapy: This is used in patients who present with severe symptoms, with features of massive PE who are not responding to standard treatment and are unstable and or go into cardiac arrest (PEA/asystole). Patients who show evidence of massive PE can be given thrombolytics provided they do not have contraindications of thrombolysis.

Cardiovascular emergencies present as most challenging emergencies in the emergency department. Presence of atypical signs and symptoms and presentations resembling many other benign medical conditions make it very challenging to timely diagnose them few times. Choosing inappropriate or unnecessary investigations will delay the disposition of the patient which may lead to a busy emergency department. It may lead to prolonged length of stay, delay in diagnosing serious emergencies and discharging patients inappropriately resulting in mortality or morbidity cases. This will compromise the credibility of the department. Taking proper history with systematic and symptomatic approach and doing a detailed examination and choosing the right investigations will reduce the length of stay of patient and on the other hand will help the physician in avoiding inappropriate discharges or referrals to subspecialty. Sound medical knowledge and awareness of differential diagnosis help in avoiding delayed patient disposition.

[1] Kim I, Kim MC, Park KH, Sim DS, Hong YJ, Kim JH, Jeong MH, Cho JG, Park JC, Cho MC, Kim JJ, Kim YJ, Ahn Y. Korea acute myocardial infarction registry investigators. Prognostic significance of non-chest pain symptoms in patients with non-ST-segment elevation myocardial infarction. The Korean Journal of Internal Medicine. 2017 Nov 10 PMID: 29117666

• IVC filters: These can be used in patients who have recurrent PE even on treatment.

5.6.4. Management:

6. Conclusion

Author details

Shahzad Anjum

References

treatment for patients presenting with PE.

Address all correspondence to: shahzad177@yahoo.com

Hamad Medical Corporation, Doha, Qatar

• Consultation with thoracic surgery for possible intervention in type A dissection.

#### 5.6. Pulmonary embolism

Pulmonary embolism is the result of clot dislodgement which formed hours, days or weeks earlier in the deep veins and traveled through the venous system to traverse the right-sided heart, finally lodging in the pulmonary vasculatures.

#### 5.6.1. Risk factors

The risk factors for pulmonary embolism are:


#### 5.6.2. Signs and symptoms:

#### 5.6.3. Diagnosis:

ECG: ECG may show S1, Q3, T3, non-specific ST-T changes, RV strain pattern, sinus tachycardia, pulmonary Hypertension changes (T inversion in V1-V4), incomplete or complete RBBB.

CXR: It may help in ruling out other causes of chest pain or breathlessness. Features of pulmonary infarction may indicate underlying PE (Hamptons Hump). Rarely an oligemic lung is seen.

Echocardiography: It helps in identifying features of right ventricular strain and right ventricular dilatation (indirect evidence of PE).

D-Dimer: It is used as a screening test. Negative D-Dimer is more helpful than positive D-Dimer which occurs in many other medical conditions as well.

CTPA: It's a gold standard to diagnose or rule out PE.

Doppler Ultrasound can be used to look for the primary source of thrombus when CTPA or V/ Q scan is absolutely contraindicated or is considered a high-risk procedure.

V/Q Scan: It is used when CTPA is either contraindicated or not possible to perform.

#### 5.6.4. Management:

• Use beta-blockers with vasodilators to avoid tachycardia. Esmolol is used to control heart rate. Labetalol can be used. Sodium nitroprusside is used as a vasodilator. Nitroglycerin can be used as a vasodilator but needs beta-blocker in conjunction.

• Consultation with thoracic surgery for possible intervention in type A dissection.

Pulmonary embolism is the result of clot dislodgement which formed hours, days or weeks earlier in the deep veins and traveled through the venous system to traverse the right-sided

• Hypercoagulability like inherited thrombophilia, acquired thrombophilia, carcinomas,

ECG: ECG may show S1, Q3, T3, non-specific ST-T changes, RV strain pattern, sinus tachycardia, pulmonary Hypertension changes (T inversion in V1-V4), incomplete or complete RBBB. CXR: It may help in ruling out other causes of chest pain or breathlessness. Features of pulmonary infarction may indicate underlying PE (Hamptons Hump). Rarely an oligemic lung

Echocardiography: It helps in identifying features of right ventricular strain and right ventric-

D-Dimer: It is used as a screening test. Negative D-Dimer is more helpful than positive D-

Doppler Ultrasound can be used to look for the primary source of thrombus when CTPA or V/

• Inflammation (connective tissue disorders, trauma, surgery, smoking)

Pulse oximeter reading <95%. Unilateral leg or arm swelling. Signs of right heart failure

5.6. Pulmonary embolism

226 Essentials of Accident and Emergency Medicine

5.6.2. Signs and symptoms:

Chest Pain Breathlessness Syncope Hemoptysis

is seen.

5.6.3. Diagnosis:

5.6.1. Risk factors

heart, finally lodging in the pulmonary vasculatures.

• Vascular stasis (limb or generalized immobility)

Pulse >100.

Dimer which occurs in many other medical conditions as well.

Q scan is absolutely contraindicated or is considered a high-risk procedure.

CTPA: It's a gold standard to diagnose or rule out PE.

The risk factors for pulmonary embolism are:

estrogen, pregnancy/postpartum

ular dilatation (indirect evidence of PE).

