CARDIAC EMERGENCIES

Dr.L.Gopichandran,PhD,FCREBM(
AIIMS)
Associate Professor,CON,AIIMS
Faculty –ACLS,CCLS,
AIIMSITC,NEWDELHI
PRESIDENT-TNAI Delhi Branch
Founder President- Society of
Cardiac Nurses (India)
 Cardiac Emergency
Emergency:
Impending death OR risk of end organ damage in a short
time frame

• Cardiovascular emergencies are life-threatening disorders

that must be recognized immediately to avoid delay in
treatment and to minimize morbidity and mortality.
 Time Frame of Emergencies
Within Few Minutes : Arrhythmic Crisis
• Brady-arrhythmia – CHB, Asystole
• Tachyarrhythmia - PSVT, VT, VF
• Cardiac Arrest

Within Several Minutes : HT Crisis

Death / Organ
• Urgency, Emergency Damage

Within Several Minutes - Hours : Intractable Chest Pain

• Cadiac Tamponade
• Pulmonary Embolism
• Aortic Dissection
• ACS / AMI
• Cardiogenic Shock
 Classification
• Hypertensive Crisis
• Acute Pulmonary Edema
• Cardiogenic Shock
• Fatal Arrhythmias
• Sudden Cardiac Arrest
• Acute Myocardial Infarction
• Aortic Dissection And Aneurysm
• Cardiac Tamponade
• Pulmonary Embolism
• Pediatric Cardiac Emergencies
Fatal Arrhythmias
 Fatal Arrhythmias
• Death/Organ Damage occurs within few minutes

• Arrhythmic Crisis

Brady-arrhythmia
• CHB,
• Asystole

Tachyarrhythmia
• PSVT
• VT
• VF
VT And VF
 VT VF
• Ventricular tachycardia is • Ventricular fibrillation is
a rapid, regular heart an abnormal heart
rhythm that originates in rhythm that is
the lower chambers of the disorganized and
heart. irregular
• In ventricular tachycardia • In ventricular fibrillation,
electrical impulses electrical activity in the
circulate in an endless
heart muscle becomes
loop or fire from a single
chaotic, preventing the
focus, creating rapid heart
heart from contracting.
rhythms.
VT
VF
 Causes
VT VF
• Usually occurs with • AMI
underlying heart disease
• Untreated VT
• Commonly occurs with
myocardial ischemia or • Electrolyte imbalance
infarction • Hypothermia
• Certain medications may • Myocardial ischemia
prolong the QT interval
predisposing the patient to • Drug toxicity or overdose
ventricular tachycardia • Trauma
• Electrolyte imbalance
• Digitalis toxicity
• Congestive heart failure
 Sign and Symptoms
VT VF
• Chest discomfort (angina) • Loss of consciousness
• Syncope • Absent pulse
• Light-headedness or
dizziness
• Palpitations
• Shortness of breath
• Absent or rapid pulse
• Loss of consciousness
• Hypotension
 PEA
• Unresponsiveness and lack of palpable pulse in the presence
of organized cardiac electrical activity.
• Pulseless electrical activity has previously been referred to as
electromechanical dissociation (EMD).
• The overall prognosis for patients with pulseless electrical
activity (PEA) is poor unless a rapidly reversible cause is
identified and corrected
 PEA
• By definition, patients with pulseless electrical activity (PEA)
have no pulse in the presence of organized electrical activity.
• The physical examination should focus on identification of
reversible causes; for example, tracheal shift or the unilateral
absence of breath sounds indicates tension pneumothorax.
 PEA

• Electricity is working, but the mechanics and plumbing are not.

• The absence of a palpable pulse and absence of myocardial muscle
activity with presence of organized electrical activity on the cardiac
monitor. The patient is clinically dead despite some type of
organized rhythm on monitor.
 PEA
• Initiate CPR
• Place an intravenous line
• Intubate the patient
• Correct hypoxia by administering 100% oxygen
 Asystole

•Asystole is cardiac standstill with no cardiac output and no

ventricular depolarization, eventually occurs in all dying
patients.

•Primary asystole occurs when the heart's electrical system

intrinsically fails to generate a ventricular depolarization.

•Reflex bradyasystole/asystole can result from ocular surgery,

retrobulbar block, eye trauma, direct pressure on the globe,
maxillofacial surgery, hypersensitive carotid sinus syndrome.
 Asystole
• Secondary asystole occurs when factors outside the heart's
electrical conduction system cause a failure to generate any
electrical depolarization (hypoxia).

• If the rhythm is truly asystole and present for more than

several seconds, the patient will be unconscious and
unresponsive.
• A few agonal (final gasping) breaths may be noted, but
detectable heart sounds and palpable peripheral pulses are
absent.
 Asystole
Diagnosis
Made via ongoing cardiac monitoring or electrocardiogram
(ECG) and physical examination with pulselessness.
Management
Providing oxygenation and ventilation via endotracheal
intubation and circulation via cardiopulmonary resuscitation
(CPR).
SUDDEN CARDIAC DEATH
 Sudden Cardiac Death

• Unexpected death caused by cardiac causes that occurs within

1 hour of symptom onset.
• May or may not have preexisting heart disease.
• Cardiac arrest : sudden collapse, loss of consciousness & loss
of effective circulation that precedes biological death.
Why it is an
emergency
 Sudden Cardiac Death
Non structural
heart disease

Non cardiac
Arrhythmia Causes causes

Structural
Abnormalities
 Sudden Cardiac Death
 Arrhythmia
 Pulseless Ventricular Tachycardia (VT)
 Ventricular Fibrillation (VF)
 Pulseless Electrical Activity
 Asystole
 Structural abnormalities
 CAD
 Cardiomyopathy
 Valvular heart disease
 Sudden Cardiac Death
 Non structural heart disease
 Long QT syndrome
 Short QT syndrome
 Catecholaminergic polymorphic VT
 Non cardiac causes
 Cerebral or sub arachnoid hemorrhage
 Choking
 Dissecting aneurysm of aorta
 Electrolyte abnormality
 Metabolic disturbances
 Pulmonary hypertension
 Pulmonary embolism
 Nursing management

• Physiological nursing management

• Emotional support
• Patient and family education
HYPERTENSIVE CRISIS
 Hypertensive crisis

 Hypertension:

– Stage I: 140-159/90-99

– Stage II: >160/100

 Hypertensive Urgency:

Systolic BP >180 or Diastolic BP >120 in the absence of end-

organ damage.
 Hypertensive crisis
 Hypertensive Emergencies:
SBP >180 OR DBP>120 in the presence of end-organ
damage.

– Malignant Hypertension: End-organ damage--eyes,

kidneys, brain (hemorrhage/infarct) affected.
– Hypertensive encephalopathy: Cerebral edema leading to
neurological symptoms.
 Signs and Symptoms
Hypertensive Urgency
 Can be completely asymptomatic
 Symptoms
• Severe headache
• Shortness of breath
• Nose bleeds
• Severe anxiety
 Signs
• Elevated BP on consecutive readings
 Signs and Symptoms

Hypertensive Emergencies
 Symptoms:
• Nausea, vomiting (cerebral edema)
• Chest Pain
• SOB
• Blurring of vision
• Confusion
• Loss of consciousness
 Signs and Symptoms
Hypertensive Emergencies

 Signs
– Retinal hemorrhages, exudates or papilledema
– Renal involvement (malignant nephrosclerosis) with AKI,
proteinuria, hematuria
– Cerebral edema  seizures and coma
– Pulmonary Edema
– Myocardial Infarction
– Hemorrhagic Stroke, lacunar infarcts
– Cardiac failure
• Confirm BP on both arms using a properly sized BP cuff.
• Check pulses in all extremities.
• Perform physical exam to evaluate for end-organ damage and
to differentiate between hypertensive emergency and
hypertensive urgency (no end-organ dysfunction).
 Treatment
Hypertensive Urgency
 Goal: Reduce BP to <160/100 over several hours to day.
 Elderly are at high risk of ischemia from rapid reduction of BP,
so BP reduction should be slow.
 Previously treated hypertension:

- Increase dose of existing medication or add another

medication.
- Reinstitution of medication in non-compliant patients.
 Treatment
Hypertensive Emergency
• Goal: Mean arterial pressure should be reduced gradually by
about 10 to 20 percent in the first hour and by a further 5 to 15
percent over the next 23 hours. 
• More aggressive decrease can lead to ischemic stroke and
myocardial ischemia.
– Admission to ICU
– Parenteral antihypertensive (IV Drip) recommended over oral
agents in hypertensive emergency.(Nitroprusside, Nicardipine,
and Labetalol)
• Once BP controlled, switch to oral anti-hypertensives and
follow-up closely.
High risk for injury related to uncontrolled hypertension as evidenced
by high blood pressure

• Goal :to maintain normal blood pressure

Assessment
• Vitals,close and continuouse monitoring of BP
• S/S of decreased cardiac output
• Altered level of consciousness
• s/s of renal dysfunction
High risk for injury related to uncontrolled hypertension as evidenced
by high blood pressure

Interventions
• Administer fast acting antihypetensives
• Administer other antihypertensives as needed
• Maintain HOB slightly elevated
• Provide complete bed rest
• Explain about to avoid valsalva maneuver to prevent potential
increase in ICP
• Administer fluid as prescribed to maintain CO and renal
perfusion
 Acute coronary syndrome
Acute Coronary Syndrome refers to any rupture of plaque or
thrombotic event that leads to symptomatic ischemia or
infarction.
 Pathophysiology
Development of myocardial necrosis caused by a critical
imbalance between the oxygen supply and demand of the
myocardium
10 seconds of oxygen deprivation: Ischemia
1 minutes of Ischemia: Myocardial function affected
20 minutes of oxygen deprivation: Irreversible cell damage
 Aspirin consideration
Aspirin should be administered to all patients who are suspected
to have ACS, unless they are allergic or intolerant to aspirin or
have active gastrointestinal bleeding
 Nitrate Considerations
Contraindications
Systolic BP < 90 mm Hg or < 30 mm Hg below baseline
Bradycardia < 50 BPM
Tachycardia > 100 BPM (in absence of clinical HF)
Right ventricular infarct
Nitroglycerin should not be administered if the patient has taken
a phosphodiesterase inhibitor (e.g. Viagra™) within 24-48
hours.
 Morphine sulfate

• It should be given intravenously in small doses (2 to 4 mg),

which can be repeated every 5 minutes until relief is obtained.
• If the patient is particularly emotionally disturbed, a mild
tranquilizer should be given in addition to morphine to allay
anxiety
 Thrombolytic Agents
• Streptokinase

• Tissue plasminogen activators: tenecteplase, alteplase,

reteplase
CARDIAC TAMPONADE
 Cardiac Tamponade
• Cardiac tamponade is a clinical syndrome caused by the
accumulation of fluid in the pericardial space, resulting in
-compression of the heart,
-reduced ventricular filling and
-subsequent hemodynamic compromise.

Medical emergency
Cardiac Tamponade
Causes of Pericardial Tamponade

Malignancy
Trauma (penetrating or blunt chest trauma)
Uremia
Hypothyroidism
Tuberculosis
HIV infection, Infection - Viral, bacterial, fungal
Dissecting aneurysm
Drugs - Hydralazine, procainamide, isoniazid, minoxidil
Postcoronary intervention (ie, coronary dissection and
perforation)
 Sign and symptoms
• Feeling of faintness
• Dyspnea, tachycardia, tachypnea
• Cold, clammy extremities
• Shortness of breath
• Anxiety, syncope
• Pain from decreased CO
• Distended neck vein
• Cough due to pressure on the trachea
• Paradoxical pulse
• Muffled heart sound
 BECK’S TRIAD

Raised JVP

Muffled heart
Hypotension
sound
 Diagnosis
ECG
• low voltage,
• sinus tachycardia,
• PR depression,
• electrical alternation
Chest X ray
• Enlarge cardiac
silhouette
• Water bottle shaped heart
 Pericardial effusion Cardiac tamponade

Definition Is the accumulation of Acute form of PE.Resulting in

fluid in the pericardial cardiac compression, reduced
space without causing ventricular filling and
symptoms. subsequent hemodynamic
compromise
Amount Usually there is slow Fast accumulation of fluid (1
of fluid accumulation of fluid litre)Though slow accumulation
(100ml) of a large amount of fluid can
cause tamponade
Causes Malignancy, Uremia, Trauma, post cardiac
hypothyroidism , interventions, ARF, pericarditis
pericarditis, infections
Rx Antibiotics(tetracycline) Pericardiocentesis
instillation
MEDICAL MANAGEMENT
 Treatment
General Measures
 Oxygen
 Volume expansion with blood, plasma, or saline to maintain
adequate intravascular volume
 Bed rest with leg elevation only over pillow(This may help
increase venous return.)
 Inotropic drugs (Choose inotropes that do not increase systemic
vascular resistance while increasing cardiac output)
 Definitive Treatment

 Pericardiocentesis
- can be fluoroscopically or TTE guided
 Pericardial window
-involves the surgical opening of a communication between
the pericardial space and the intrapleural space
 Pericardiocentesis

Initial management is by pericardiocentesis.

The insertion of a needle through the skin and into the
pericardium and aspirating fluid under ultrasound guidance
preferably.
This can be done laterally through the intercostal spaces,
usually the fifth, or as a subxiphoid approach.
 Catheters used for drainage

• Two different types of catheters are commonly used: the

pigtail catheter and the straight catheter.
– pigtail catheter is curved and has a soft tip.
– straight catheter has side holes that help to increase
drainage and reduce the chances of blockage.
 Nursing care of Pericardiocentesis
• Pericardiocentesis aims at sharp weapon at the heart,therefore
certain protective measures are desirable
• Crash cart items should be available including pressure agents, IV
fluids, oxygen, tracheal tubes, defibrillator, pacemakerand ECG
monotor.
• A slow intravenous drip of saline or glucose in water should be
started to preserve a route for intravenous therapy.
• During Pericardiocentesis, the nurse should place the patient in
semi-Fowlers position
 Nursing care of Pericardiocentesis
• ECG pads should be placed on limbs and away from the chest
wall if possible
• Monitoring of ST-segment elevation is required and will be seen
when the needle touches the epicardium.
• Pain medication and sedation should be given when possible.
• Monitoring for other complications (pneumothorax, cardiac
rupture or cardiac laceration).
AORTIC DISSECTION
 Aortic Dissection
• Aortic dissection is the most common catastrophe of the aorta,
When left untreated, about 33% of patients die within the first
24 hours, and 50% die within 48 hours

• Clinically, the patient must be assessed frequently for

 hemodynamic compromise,
 mental status changes,
 neurologic or peripheral vascular changes,
 and development or progression of carotid, brachial, and
femoral bruits.
 Aortic Dissection
• BP should be lowered quite aggressively
• Goal: Systolic BP 100-120 mmHg within 20 minutes
• Aim
 lower BP
 decrease LV contraction so as to decrease Aortic shear
stress
• Drug Of Choice : labetalol or Esmolol
 Symptoms
• Sudden severe chest or upper back pain, often described as a
tearing, ripping or shearing sensation, that radiates to the neck
or down the back
• Loss of consciousness
• Shortness of breath
• Sudden difficulty speaking, loss of vision, weakness or
paralysis of one side of your body, similar to those of a stroke
• Weak pulse in one arm compared with the other
 Causes
• An aortic dissection occurs in a weakened area of the aortic
wall.
• Chronic high blood pressure may stress the aortic tissue,
making it more susceptible to tearing.
• condition associated with a weakened and enlarged aorta, such
as Marfan syndrome, bicuspid aortic valve
• Rarely, traumatic injury to the chest area
 Types

• Type A. This more common and dangerous type involves a

tear in the part of the aorta where it exits the heart or a tear in
the upper aorta (ascending aorta), which may extend into the
abdomen.
• Type B. This involves a tear in the lower aorta only
(descending aorta), which may also extend into the abdomen

Animation
 Diagnosis
• Transesophageal echocardiogram (TEE).
• Computerized tomography (CT) scan.
CT of the chest is used to diagnose an aortic dissection,
possibly with an injected contrast liquid.
• Magnetic resonance angiogram (MRA
 Management
Surgery
 Remove as much of the dissected aorta as possible, block the
entry of blood into the aortic wall and reconstruct the aorta
with a synthetic tube called a graft.
 If the aortic valve leaks as a result of the damaged aorta, it
may be replaced at the same time.
 The new valve is placed within the graft used to reconstruct
the aorta.
 Management
Medications
• Beta blockers and nitroprusside (Nitropress), reduce heart rate
and lower blood pressure, which can prevent the aortic
dissection from worsening.
CARDIOGENIC PULMONARY
EDEMA
 Pulmonary edema
• Pulmonary edema is the abnormal accumulation of fluid
in the interstitial spaces surrounding the alveoli.

• The advancement of fluid accumulation in the alveolar

sacs which leads to dyspnea.
 Types

 Cardiogenic: It is either due to direct damage to the cardiac

tissue or a result of inadequate functioning of the heart or
circulatory system.
 Non cardiogenic: Radiographic evidence of alveolar fluid
accumulation without hemodynamic evidence to suggest a non
cardiogenic etiology .
Causes of cardiogenic pulmonary edema

• Atrial outflow obstruction

• LV systolic dysfunction
• LV diastolic dysfunction
• Dysrhythmias
• LV hypertrophy and cardiomyopathies
• LV volume overload
• Myocardial infarction
• LV outflow obstruction
 Clinical manifestations
• Cough with thin and frothy sputum (combined with water)
• Sudden onset of dyspnea
• Noisy, wet respirations that do not clear with coughing.
• Chest auscultation reveals crackles.
• Tachypnea, Tachycardia, Orthopnea
• Breathing pattern shows use of accessory muscle.
• Cool, moist skin.
• The client may be anxious from dyspnea and restless.
• Pulse oximetry is commonly less than 85% and arterial Po2 of
30 to 50 mm Hg
 Diagnostic evaluation

• Repeated arterial blood gases should be done

• CBC
• Serial ECGs
• Echo
• CT scan of the chest
• Lung biopsy
• Pulmonary function tests
 Medical Management

1) Correction of hypoxia 2)Reduction in preload

(3) Reducing After load (4) Supporting Perfusion

 Medical Management
Correcting Hypoxemia :oxygen therapy at high Fi02 level and
may require mechanical ventilation of continuous or continuous
positive airway pressure ( CPAP)

Reducing The PRE-LOAD :

• The client is placed in an upright position..
• Diuretics are prescribed to promote fluid exertion to promote
fluid excretion.
• Nitrates, such as nitroglycerine are used for their vasodiltative
properties.
 Medical Management
Reducing After Load
• Antihypertensive agents, such as nitroprusside, are prescribed.
• Morphine is prescribed to reduce after load

Supporting Perfusion
• Using inotropic medication such as dobutamine supports left
ventricular failure.
• IABP may required in severe heart failure & pulmonary
edema.
 Impaired gas exchange related to pulmonary venous congestion as
evidence by
restlessness,irritability,hypoxia,cough,crackles,dyspnoea,pink frothy
sputum,and cyanosis
Goal :to improve oxygenation and ventillation
Assessment
• RR,rhythm,depth,presence of SOB
• Breath sounds
• Secretions
• ABG
• Saturation
• Mental status
• Monitor chest x ray (cloudy white lung fields)
 Impaired gas exchange related to pulmonary venous congestion as
evidence by restlessness,irritability,hypoxia,cough,crackles,dyspnoea,pink
frothy sputum,and cyanosis

Interventions
• High fowlers position
• Encourage slow ,deep breathing
• Assist with coughing
• Provide O2 as needed
• Administer prescribed medicines
CARDIOGENIC SHOCK
 Cardiogenic shock
The clinical definition of cardiogenic shock is
. decreased cardiac output and evidence of tissue
hypoxia in the presence of in adequate
intravascular volume and left ventricular filling

Cardiogenic shock manifests as circulatory failure from cardiac

dysfunction.
Cardiogenic shock is usually characterized by

◦ Decreased blood pressure (systolic less than 90 mmhg, or

reduction in mean arterial pressure over 30 mmhg)
◦ Decrease in urine output (less than 0.5 ml / kg / hour)
◦ Pulse rate of more than 60 beats per minute
◦ With or without the presence of organ congestion
 Causes
• MI (most common)
• Aortic dissection
• Pulmonary embolism
• Cardiac tamponade
• Hemorrhage
• Sepsis
• Cardiomyopathy (restrictive or dilated), myocarditis
• Medication overdose (beta/calcium-channel blockers)
• Cardiotoxic drugs (doxorubicin)
• Electrolyte abnormalities (calcium, phosphate)
• Valvular abnormalities (mitral/aortic stenosis)
Pathophysiology
 Systolic dysfunction
Decreased stroke volume, decreased EF

Decreased Decreased
BP CO

Sympatho-adrenal activation compensation

Increased
heart rate, Increased
ionotropy SVR
Increased
myocardial O2
demand
 Clinical features
Low cardiac output and hypotension
Poor peripheral perfusion
Oliguria
Altered mentation, restlessness and anxiety
Tachycardia and arrhythmias
Pulmonary congestion with widespread inspiratory crackles and
hypoxaemia
Dyspnoea and tachypnoea
Respiratory alkalosis (hyperventilation) or acidosis (respiratory
fatigue)
Lactic acidosis
Distended neck veins
 Diagnosis
• Chest X-ray- pulmonary congestion, cardiac tamponade.
• ECG
• ECHO
Invasive
• Swan-Ganz catheterization
PCWP > 15mm Hg and CI < 2.2 L/min/m2
Coronary artery angiography.
 Collaborative Management
1.Hemodynamic monitoring
PCWP > 15mmhg and CI < 2.2 L/min/m2
2.Oxygenation: Intubation, mechanical ventillation
3.CV Support
• Fluid support
• Inotropes
• Vasopressors
• IABP
• ECMO
• Anti shock dress
 Pharmacologic Treatment of Cardiogenic
Shock

• SBP <70 mm Hg + shock Norepinephrine

• SBP 70-100 mm Hg + shock Dopamine

• SBP 70-100 mm Hg – shock Dobutamine

• Refractory hypotension + shock Amrinone or

Milrinone
 IABP

• The use of an intra-aortic balloon pump (IABP) improves

coronary artery perfusion and reduces afterload.
• The IABP inflates during ventricular diastole (increasing
coronary artery perfusion) and deflates during ventricular
systole (decreasing afterload or the resistance against which
the heart has to pump).
• Animation
 Nutritional support

• Patients in shock require >3000cal/day

• Parenteral or enteral nutritional support
• Glutamine is important in the immunologic function of the GI
tract given through enteral nutrition
 Complications

 Brain damage

 Kidney damage

 Liver damage
 Assessment

 Frequent, thorough assessment of the patient’s status is

essential, focusing on:

– Identification of patients at risk of clinical deterioration;

– Assessment of the severity of shock and identification of
organ or system dysfunction;
– Assessment of the impact of treatment; and
– Identification of complications of treatment.
 Nursing management
• Haemodynamic management
• Respiratory support
• Cardiovascular support
• Biochemical stabilisation
 Nursing management
Monitoring a patient in cardiogenic shock
 Continuous cardiac monitoring –rhythm.
 Continuous arterial blood pressure monitoring.
 Hourly urine output.
 Strict fluid balance monitoring.
 Hourly temperature monitoring.
 Continuous central venous pressure monitoring.
 Respirations.
 Arterial blood gas.
 Blood sugar.
Nursing Process
Decreased cardiac output related to impaired left ventricular
contractility as evidenced by pale,coolclamy skin,oliguria
and mental status changes
Goal: To maintain the normal cardiac out put
Assessment
• Skin colour,temperature
• Mental status(early signs of cerebral hypoxia are restlessness and
anxiety)
• Vitals
• Oliguria
• ABG
• Hemodynamic monitoring (CVP,PAP,PCWP and CO)
Decreased cardiac output related to impaired left ventricular
contractility as evidenced by pale,coolclamy skin,oliguria
and mental status changes
Interventions
• Place pt in optimal position,supine with head end slightly elevated
(promote venous return and ventillation)
• Administer IV fluids to maintain optimal filling pressure
• Administer drug therapy as prescribed
- Positive inotropes
- Vasodilators
- Diuretics (if volume overload)

• Provide appropriate care of IABP

Impaired gas exchange related to altered blood flow/alveolar capillary
membrane changes as evidenced by tachypnoea ,decreased O2
saturation (<95),restlessness and confusion
Goal:To achieve adequate oxygenation
Assessment
• Rate ,rhythm and depth of respirations
• Abnormal breath sounds
• Check for cyanosis
• ABG
 Summary
• Cardiac tamponade
• Fatal arrhythmia
• SCD
• Hypertensive crisis
• Pulmonary edema
• Cardiogenic shock
 References
 Black MJ, Hawks JH, Medical Surgical nursing, 3 edition.
 Woods SL. Cardiac nursing. 6 edition. Philadelphia:
Lippincott Williams and Wilkins; 2010. P. 519-520
 www.google.com
 www.emedicine.medscape.com
 www.pubmed.com