The LOSt DiarY........

Bradyarrhythmias-Complete Heart Block

2012-03-27T22:58:00.001-07:00

Complete Heart Block

Third-degree AV block or complete heart block is the most clinically significant AV block associated with ACLS. Complete heart block occurs when the electrical impulse generated in the SA node in the atrium is not conducted to the ventricles.

When the atrial impulse is blocked, an accessory pacemaker in the ventricles will typically activate a ventricular contraction. This accessory pacemaker impulse is called an escape rhythm.

Because two independent electrical impulses occur (SA node impulse & accessory pacemaker impulse), there is no apparent relationship between the P waves and QRS complexes on an ECG.

Characteristics that can be seen on an ECG include:

P waves with a regular P to P interval
QRS complexes with a regular R to R interval
The PR interval will appear variable because there is no relationship between the P waves and the QRS Complexes

In the image above note that the p-waves are independent of the QRS complexes. Also note the 4th QRS complex (impulse) looks different from the others. This is because it is from a different accessory pacemaker in the ventricle than the other QRS complexes.

Common Causes

The most common cause of complete block is coronary ischemia and myocardial infarction. Reduced blood flow or complete loss of blood flow to the myocardium damages the conduction system of the heart, and this results in an inability to conduct impulses from the atrium to the ventricles.

Those with third-degree AV block typically experience bradycardia, hypotension, and in some cases hemodynamic instability.

The treatment for unstable third-degree AV block in ACLS is transcutaneous pacing.

Bradyarrhythmias-Second-Degree (AV) Heart Block (Type 2)

2012-03-27T22:57:00.002-07:00

Second-Degree (AV) Heart Block (Type 2)

Also called Mobitz II or Hay is a disease of the electrical conduction system of the heart. Second-degree AV block (Type 2) is almost always a disease of the distal conduction system located in the ventricular portion of the myocardium.

This rhythm can be recognized by the following characteristics:

nonconducted p-waves (electrical impulse conducts through the AV node but complete conduction through the ventricles is blocked, thus no QRS)
P-waves are not preceded by PR prolongation as with second-degree AV block (Type 1)
fixed PR interval
The QRS complex will likely be wide click here to see why»

Second-degree AV block (Type 2) is clinically significant for ACLS because this rhythm can rapidly progress to complete heart block

Secocnd-degree AV block (Type 2) should be treated with immediate transcutaneous pacing or transvenous pacing because there is risk that electrical impulses will not be able to reach the ventricles and produce ventricular contraction.

Bradyarrhythmias-Second-Degree Heart Block (Type 1)

2012-03-27T22:56:00.002-07:00

Second-Degree Heart Block (Type 1)

Also called Mobitz 1 or Wenckebach is a disease of the electrical conduction system of the heart in which the PR interval» has progressive prolongation until finally the atrial impulse is completely blocked and does not produce a QRS electrical impulse.

Once the p-wave is blocked and no QRS is generated, the cycle begins again with the prolongation of the PR interval.

One of the main identifying characteristics of second degree heart block type 1 is that the atrial rhythm will be regular.

In the above image, notice that the p-waves are regular, the PR-interval progressively gets longer until a QRS is dropped and only the p-wave is present.

Although second degree heart block type-1 is not clinically significant for ACLS, recognition of the major AV blocks is important because treatment decisions are based on the type of block present.

Bradyarrhythmias-First-Degree Heart Block

2012-03-27T22:54:00.001-07:00

Also called first-degree AV block is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds.

This lengthening of the PR interval is caused by a delay in the electrical impulse from the atria to the ventricles through the AV node

Normally and in the case of ACLS, first-degree heart block is of no consequence unless it involves myocardial infarction or an electrolyte imbalance.

Although first-degree heart block is not clinically significant for ACLS, recognition of the major AV blocks is important because treatment decisions are based on the type of block present.

H’s and T’s of ACLS

2012-03-27T22:49:00.003-07:00

H’s and T’s of ACLS

Knowing the H’s and T’s of ACLS will help prepare you for any ACLS scenario. Don’t forget your H’s and T’s when using the ACLS Megacode Simulator.

The H’s and T’s of ACLS is a mnemonic used to help recall the major contributing factors to pusleless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. These H’s and T’s will most commonly be associated with PEA, but they will help direct your search for underlying causes to any of arrhythmias associated with ACLS. Each is discussed more thoroughly below.

The H’s include:

Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper-/hypokalemia, H~~ypoglycemia~~, Hypothermia.

The T’s include:

Toxins, Tamponade(cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), and T~~rauma~~.

Hypovolemia

Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac arrest. Looking for obvious blood loss in the patient with pusleless arrest is the first step in determining if the arrest is related to hypovolemia. After CPR, the most import intervention is obtaining intravenous access/IO access. A fluid challenge or fluid bolus may also help determine if the arrest is related to hypovolemia.

Hypoxia

Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest. You must ensure that the patient’s airway is open, and that the patient has chest rise and fall and bilateral breath sounds with ventilation. Also ensure that your oxygen source is connected properly.

Hydrogen ion (acidosis)

To determine if the patient is in respiratory acidosis, an arterial blood gas evaluation must be performed. Prevent respiratory acidosis by providing adequate ventilation. Prevent metabolic acidosis by giving the patient sodium bicarbonate.

Hyper-/hypokalemia

Both a high potassium level and a low potassium level can contribute to cardiac arrest. The major sign of hyperkalemia or high serum potassium is taller and peaked T-waves. Also, a widening of the QRS-wave may be seen. This can be treated in a number of ways which include sodium bicarbonate (IV), glucose+insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. All of these will help reduce serum potassium levels.

The major signs of hypokalemia or low serum potassium are flattened T-waves, prominent U-waves, and possibly a widened QRS complex. Treatment of hypokalemia involves rapid but controlled infusion of potassium. Giving IV potassium has risks. Always follow the appropriate infusion standards. Never give undiluted intravenous potassium.

Hypoglycemia

Hypoglycemia or low serum blood glucose can have many negative effects on the body, and it can be associated with cardiac arrest. Treat hypoglycemia with IV dextrose to reverse a low blood glucose. Hypoglycemia was removed from the H’s but is still to be considered important during the assessment of any person in cardiac arrest.

Hypothermia

If a patient has been exposed to the cold, warming measures should be taken. The hypothermic patient may be unresponsive to drug therapy and electrical therapy (defibrillation or pacing). Core temperature should be raised above 86 F (30 C) as soon as possible.

The T’s include:

Toxins

Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most common include: tricyclics, digoxin, betablockers, calcium channel blockers, and erythromycin). Street drugs and other chemicals can precipitate pulseless arrest. Cocaine is the most common street drug that increases incidence of pulseless arrest. ECG signs of toxicity include prolongation of the QT interval. Physical signs include bradycardia, pupil symptoms, and other neurological changes. Support of circulation while an antidote or reversing drug is obtained is of primary importance. Poison control can be utilized to obtain information about toxins and reversing agents.

Tamponade

Cardiac tamponade is an emergency condition in which fluid accumulates in the pericardium (sac in which the heart is enclosed). The buildup of fluid results in ineffective pumping of the blood which can lead to pulseless arrest. ECG symptoms include narrow QRS complex and rapid heart rate. Physical signs include jugular vein distention (JVD), no pulse or difficulty palpating a pulse, and muffled heart sounds due to fluid inside the pericardium. The recommended treatment for cardiac tamponade is pericardiocentesis.

Tension Pneumothorax

Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping naturally. This leads to a build up of tension that causes shifts in the intrathroacic structure that can rapidly lead to cardiovascular collapse and death. ECG signs include narrow QRS complexes and slow heart rate. Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with ventilation, and no pulse felt with CPR. Treatment of tension pneumothorax is needle decompression.

Thrombosis (heart: acute, massive MI)

Coronary thrombosis is an occlusion or blockage of blood flow within a coronary artery caused by blood that has clotted within the vessel. The clotted blood causes an Acute Myocardial Infarction which destroys heart muscle and can lead to sudden death depending on the location of the blockage.

ECG signs indicating coronary thrombosis are 12 lead ECG with ST-segment changes, T-wave inversions, and/or Q waves. Physical signs include: elevated cardiac markers on lab tests, and chest pain/pressure. Treatments for coronary thrombosis include use of fibrinolytic therapy, PCI (percutaneous coronary intervention). The most common PCI procedure is coronary angioplasty with or without stent placement.

Thrombosis (lungs: massive pulmonary embolism)

Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can rapidly lead to respiratory collapse and sudden death. ECG signs of PE include narrow QRS Complex and rapid heart rate. Physical signs include no pulse felt with CPR. distended neck veins, positive d-dimer test, prior positive test for DVT or PE. Treatment includes surgical intervention (pulmonary thrombectomy) and fibrinolytic therapy.

Trauma

The final differential diagnosis of the H’s and T’s is trauma. Trauma can be a cause of pulseless arrest, and a proper evaluation of the patients physical condition and history should reveal any traumatic injuries. Treat each traumatic injury as needed to correct any reversible cause or contributing factor to the pulseless arrest. Trauma was removed from the T’s but is still to be considered important during the assessment of any person in cardiac arrest.

Other Tachycardia Rhythms

2012-03-27T22:47:00.005-07:00

Other Tachycardia Rhythms

There are several other tachycardia rhythms that can be seen with both stable and unstable tachycardia. These rhythms includemonomorphic ventricular tachycardia and polymorphic ventricular tachycardia both of which are wide-complex tachycardias.
Wide complex tachycardias are defined as a QRS of ≥ 0.12 second. Expert consultation should be considered with these rhythms.

These wide-complex tachycardias are the most common forms of tachycardia that will deteriorate to ventricular fibrillation.

Monomorphic Ventricular Tachycardia

With monomorphic VT all of the QRS waves will be symmetrical. Each ventricular impulse is being generated from the same place in the ventricles thus all of the QRS waves look the same.
Treatment of monomorphic VT is dependent upon whether the patient is stable or unstable. Expert consultation is always advised, and if unstable, the ACLS tachycardia algorithm should be followed.

Polymorphic Ventricular Tachycardia

With polymorphic ventricular tachycardia, the QRS waves will not be symmetrical. This is because each ventricular impulse can be generated from a different location. On the rhythm strip, the QRS might be somewhat taller or wider.
One commonly seen type of polymorphic ventricular tachycardia is torsades de pointes. Torsades and other polymorphic VT are advanced rhythms which require additional expertise and expert consultation is advised.
If polymorphic VT is unstable the ACLS tachycardia algorithm should be used to treat the patient. Unstable polymorphic ventricular tachycardia is treated with unsynchronized shocks (defibrillation). Defibrillation is used because synchronization is not possible.

These wide complex tachycardias tend to originate in the ventricles rather than like a normal rhythm which originates in the atria.

Supraventricular Tachycardia (SVT)

2012-03-27T22:47:00.001-07:00

Supraventricular Tachycardia (SVT)

SVT is a broad term for a number of tachyarrhythmias that originate above the ventricular electrical conduction system (purkinje fibers).

Classic Paroxysmal SVT has a narrow QRS complex & has a very regular rhythm. Inverted P waves are sometimes seen after the QRS complex. These are called retrograde p waves

The heart fills during diastole, and diastole is normally 2/3 the cardiac cycle. A rapid heart rate will significantly reduce the time which the ventricles have to fill. The reduced filling time results in a smaller amount of blood ejected from the heart during systole. The end result is a drop in cardiac output & hypotension.

With the drop in cardiac output, a patient may experience the following symptoms. These symptoms occur more frequently with a heart rate >150 beats per minute:

The pathway of choice for SVT in the tachycardia algorithm is based on wheter the patient is stable or unstable. The symptoms listed above that would indicate the patient is unstable are noted with the letter (U). Stable but serious symptoms are indicated with the letter (S).

Unstable patients with SVT and a pulse are always treated with cardioversion

Atrial Flutter

2012-03-27T22:45:00.002-07:00

Atrial Flutter will usually present with atrial rates between 240-350 beats per minute. These rapid atrial rates are caused by electrical activity that moves in a self-perpetuating loop within the atria.

The impact and symptoms of atrial flutter depend upon the ventricular rate of the patient (i.e. cardiac output). Usually, with atrial flutter, not all of the atrial impulses will be conducted to the ventricles, and the more atrial impulses that are conducted, the greater the negative effect.

Symptoms

Symptoms of atrial flutter are similar to those of atrial fibrillation and may include the following:

palpitations, chest pain or discomfort
shortness of air
lightheadedness or dizziness
nausea
nervousness and feelings of impending doom
symptoms of heart failure such as activity intolerance and swelling of the legs occur with prolonged fast flutter)

Complications

As with its symptoms, atrial flutter shares the same complications as atrial fibrillation. These complications are usually due to ineffective atrial contractions and rapid ventricular rates. Ineffective atrial contractions can lead to thrombus formation in the atria and rapid ventricular rates can cause decompensation and heart failure.

Prevent complications from atrial flutter with early cardioversion.

Treatment

For the purposes of ACLS, atrial flutter is treated the same as atrial fibrillation. When atrial flutter produces hemodynamic instability and serious signs and symptoms, it is treated using ACLS protocol.

For the patient with unstable tachycardia due to this tachyarrhythmia (atrial flutter), immediate cardioversion is recommended. Drugs are not used to manage unstable tachycardia.

Cardioversion

Atrial flutter is considerably more sensitive to electrical direct-current cardioversion than atrial fibrillation, and usually requires a lower energy shock. 20-50J is commonly enough to revert to sinus rhythm.

PEA

2012-03-27T22:40:00.000-07:00

PEA rhythm occurs when any heart rhythm that is observed on the electrocardiogram (ECG) does not produce a pulse. PEA can come in many different forms. Sinus Rhythm, tachycardia, and bradycardia can all be seen with PEA.

Performing a pulse check after a rhythm/monitor check will ensure that you identify PEA in every situation.

Pulseless electrical activity usually has an underlying treatable cause. The most common cause in emergency situations is hypovolemia.

PEA is treated by assessing and correcting the underlying cause. These causes can be summed up in the 6 H’s and 6 T’s of ACLS. Use the link to review the H’s and T’s.

When an underlying cause for pulseless electrical activity cannot be determined, PEA should be treated in the same fashion as asystole

#pulseless rhtm-vent fib

2012-03-27T22:29:00.001-07:00

Ventricular fibrillation or VF occurs when there are uncoordinated contractions within the ventricles of the heart. The primary cause of VF is hypoxia (lack of oxygen) to the heart muscle which causes hyperirritability in the cardiac muscle tissue.

As a result, multiple muscles cells within the ventricles simultaneously fire as pacemakers causing a quivering or fibrillation that is ineffective for adequate cardiac output.

The two images above show what ventricular fibrillation will look like on a EKG rhythm strip.

VF can rapidly lead to heart muscle ischemia and there is a high likelihood that it will deteriorate into asystole.

VF should be treated per the pulseless arrest algorithm which is also used for pulseless ventricular tachycardia.

Ventricular fibrillation is always pulseless and must be confirmed by EKG or defibrillator monitor. Defibrillation is the treatment of choice and should occur as soon as possible.

Vent. Fib./Tach.

Epinephrine
Vasopressin
Amiodarone
Lidocaine
Magnesium

# pulseless rhytm

2012-03-27T22:27:00.000-07:00

The pulseless ventricular tachycardia rhythm is primarily identified by several criteria. First, the rate is usually greater than 180 beats per minute and the rhythm generally has a very wide QRS complex.

Second, the patient will be pulseless and third, the rhythm originates in the ventricles or AV node. This is in contrast to other types of tachycardias which have origination above the ventricular tissue (in the atria).

Not all ventricular tachycardias are pulseless and therefore, pulselessness must be established prior to beginning an algorithm. This is accomplished simply by checking a carotid or femoral pulse.

Pulselessness with a tachyarrhythmia occurs because the ventricles are not effectively moving blood out of the heart and there is therefor no cardiac output. Many tachyarrhythmias of a rate >150 will deteriorate into pulselessness if timely treatment is not given

Tachycardia

adenosine
Diltiazem
Beta-blockers
amiodarone
Digoxin
Verapamil
Magnesium

pediatric v-fib

2012-03-27T00:40:00.001-07:00

pulseless electrical activity

2012-03-27T00:39:00.001-07:00

V-fib and V-tac

2012-03-27T00:37:00.002-07:00

2012-03-27T00:33:00.000-07:00

# neck and airway trauma

2012-03-27T00:16:00.000-07:00

Approach to the Patient

     Every trauma victim is considered to have both cervical spine and airway injury until proven otherwise. The standard ABC approach to the initial survey, followed by automatic C-spine x-rays, either identifies or rules out C-spine or airway problems.
     The discussion in the section on general management of the trauma patient details the sequence of examination and stabilization of the airway and cervical spine.
In dealing with the trauma victim, airway management takes first priority. Assessment of the patient’s airway is the very first action taken on encountering the patient. Three questions should be answered:

     1. IS THE PATIENT BREATHING?
     2. IS THERE OBSTRUCTION?
     3. IS THE AIRWAY AT RISK?

     As you walk up to the trauma victim, ask “How are you?” Any answer at all indicates the patient is breathing and has a reasonably intact airway.
     Before you touch the patient, insure that the C-spine is immobilized. An assistant can hold the head pending formal immobilization.
     If the patient isn’t breathing, open the airway by chin lift or jaw thrust. Insert an oropharyngeal airway. Begin artificial ventilations. DO NOT MOVE THE NECK while attempting to open or clear the airway!
     You can secure the airway with endotracheal intubation if the neck, jaw, and mouth are sufficiently intact. The nasal route is preferred on conscious patients, and is the route of choice if C-spine injury is suspected.
     Nasal intubation can only be accomplished if the patient is breathing. If the patient isn’t breathing, use either oral intubation or establish a surgical airway.
     Important: If the patient is not breathing, and C-spine injury is suspected, establish a surgical airway by cricothyrotomy.

     Method of Securing Airway in C-Spine Injury:
          With facial trauma — Surgical Airway
          Not breathing         — Surgical Airway
          Breathing               — Nasotracheal Intubation
          Ruled out by x-ray — Oral Intubation Allowed
     Indications for Surgical Airway
           Failure to Intubate
           Apneic with Suspected C-spine Injury
           Facial Trauma with Suspected C-spine Injury
           Severe Facial + Neck Trauma, altered anatomy

Criteria for intubation

     Intubation is necessary whenever the patient cannot maintain adequate ventilation on his own, or when he cannot protect his airway from secretions and foreign matter. Intubate when there is risk to the airway, such as an airway burn. The trachea should be intubated if the patient has, or likely will have, ongoing respiratory distress — for example, the COPD patient with a pulmonary contusion.

     Examples of inadequate respirations:
          Cardiac arrest
          Respiratory arrest (such as narcotic overdose)
          Respiratory failure (such as status asthmaticus)
          Severe lung injury (such as pulmonary contusion)
          Traumatic respiratory distress
     Examples of protection:           Prolonged unconsciousness
           Inadequate gag reflex (such as drug overdose)
           Airway encroachment (such as burn or bleeding)
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Laryngeal Injury

     The larynx may be fractured by contact with the steering wheel. The airway is at risk, as bleeding into the larynx, hematomas, or swelling may occur.
     Clinical Findings: The “Adam’s apple” area may be puffy, distorted, or crepitant on palpation. Subcutaneous air may be palpable in the neck. The voice may be hoarse, or stridor may be present.
     Diagnosis: The clinical findings are usually sufficient to diagnose injury to the larynx. Additional findings may be soft tissue air in the neck (but not in the chest) or deformity of the air column on lateral neck x-ray.
     Treatment: In the multiply-injured patient, intubation should be performed on any patient suspected to have laryngeal injury. If the injury is isolated, and judged to be not severe, the patient may be observed (while prepared to intubate if signs of airway encroachment develop).

Airway Burn

     Airway burns are most likely to occur in enclosed-space burn injuries. They are not as likely (but must be screened for) in “flare-up” burns, such as when gasoline in a carburetor flares into the face. Once swelling begins, it may progress so rapidly that intubation becomes extremely difficult.
     Clinical Findings: Assume the airway is burned if there are burns within the mouth, nose or throat, or if the victim had significant time in an enclosed-space fire or explosion. Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
     Diagnosis: Based on history and clinical examination.
     Treatment: If airway burn is suspected, intubate the patient nasally at the first opportunity.

Severe Facial Fractures

     Severe facial trauma often results in unstable tissues, which can occlude the airway. While lifting the jaw and inserting an oral or nasal airway may help temporarily, the airway will continue to be at risk due to bleeding, swelling, and hematoma formation. Patients with severe facial fractures will usually have a decreased level of consciousness due to intracranial injury. Neck fracture is also common in these patients.
     Clinical Findings: Facial fractures sufficient to put the airway at risk will almost always be unstable. Palpate the jaw for crepitance and instability. Grasp the upper teeth between your thumb and knuckle of your index finger and test for maxillary instability. Bilateral eyelid swelling and a sunken facial appearance suggest a cranio-facial fracture.
     Diagnosis: The diagnosis of risk to the airway is made based on the finding of significant fracturing and soft tissue injury. The airway is the critical issue — the nature of the fracturing can be determined at leisure once the airway is safe.
     Treatment: If trauma involves both the mandible and upper face, and the C-spine is still at risk, you are probably better off performing cricothyrotomy. If the C-spine is OK, oral intubation may be attempted first. Nasal intubation may cause complications such as entry into open fractures, and may restart bleeding into the airway.
     Gastric tubes may be passed orally in the presence of facial trauma. If trauma is not too severe, a nasal airway can be inserted to guide a nasally-inserted NG tube downward — the nasal airway prevents the NG from entering into tissue tears such as an open cribriform plate fracture.

Cervical Spine Injury

     The cervical spine is considered injured in all trauma victims until proven otherwise. In the multiply-injured or intoxicated patient, absence of pain or tenderness does NOT exclude cervical fracture.
     Clinical Findings: The presence of a step-off deformity may indicate a fracture or dislocation. Complete spinal cord injury will result in a flaccid areflexia, flaccid sphincters, and diaphragmatic breathing. The patient may be able to flex, but not extend the arms. Painful stimulation may be felt only above the clavicle.
     Neurogenic shock results from loss of sympathetic nerve stimulation of the blood vessels and heart. This is often described as a “warm hypotension.” Typically, both pulse rate and systolic pressure are around 80, with warm, pink extremities. However, hypotension in the injured patient should first be assumed due to hemorrhage. Only after fluid challenge, ruling out intraperitoneal hemorrhage, and measuring a normal CVP and normal urine output, should the hypotension be blamed on spinal cord injury.
     Diagnosis: By cross-table cervical spine x-ray.
     Treatment: Treatment of life-threatening injuries continues, with cautions to continue cervical protection. Gardner-Wells tongs may be applied in the emergency room for patients who are to undergo surgery. Obtain neurosurgical consultation. Placement of a CVP or Swan-Ganz catheter to monitor fluid resuscitation is advisable for those with spinal cord injury. Give immediate high-dose steroids.

#physical examination - lung

2012-03-26T23:39:00.001-07:00

The 4 major components of the lung exam (inspection, palpation, percussion and auscultation) are also used to examine the heart and abdomen. Learning the appropriate techniques at this juncture will therefore enhance your ability to perform these other examinations as well. Vital signs, an important source of information, are discussed elsewhere.

Inspection/Observation: A great deal of information can be gathered from simply watching a patient breathe. Pay particular attention to:

The position of the patient. Those with extreme pulmonary dysfunction will often sit up-right. In cases of real distress, they will lean forward, resting their hands on their knees in what is known as the tri-pod position.

Patient with emphysema bending over in Tri-Pod Position

General comfort and breathing pattern of the patient. Do they appear distressed, diaphoretic, labored? Are the breaths regular and deep?
Use of accessory muscles of breathing (e.g. scalenes, sternocleidomastoids). Their use signifies some element of respiratory difficulty.

Color of the patient, in particular around the lips and nail beds. Obviously, blue is bad!

Cyanosis of nail beds

- Breathing through pursed lips, often seen in cases of emphysema.
- Ability to speak. At times, respiratory rates can be so high and/or work of breathing so great that patients are unable to speak in complete sentences. If this occurs, note how many words they can speak (i.e. the fewer words per breath, the worse the problem!).
- Any audible noises associated with breathing as occasionally, wheezing or the gurgling caused by secretions in large airways are audible to the "naked" ear.
- The direction of abdominal wall movement during inspiration. Normally, the descent of the diaphragm pushes intra-abdominal contents down and the wall outward. In cases of severe diaphragmatic flattening (e.g. emphysema) or paralysis, the abdominal wall may move inward during inspiration, referred to as paradoxical breathing. If you suspect this to be the case, place your hand on the patient's abdomen as they breathe, which should accentuate its movement.
- Any obvious chest or spine deformities. These may arise as a result of chronic lung disease (e.g. emphysema), occur congenitally, or be otherwise acquired. In any case, they can impair a patient's ability to breathe normally. A few common variants include:
  - Pectus excavatum: Congenital posterior displacement of lower aspect of sternum. This gives the chest a somewhat "hollowed-out" appearance. The x-ray shows a subtle concave appearance of the lower sternum.
  - Barrel chest: Associated with emphysema and lung hyperinflation. Accompanying xray also demonstrates
    increased anterior-posterior diameter as well as diaphragmatic flattening.

Spine abnormalities:

Kyphosis: Causes the patient to be bent forward. Accompanying X-Ray of same patient clearly demonstrates extreme curvature of the spine.
Scoliosis: Condition where the spine is curved to either the left or right. In the pictures below, scoliosis of the spine causes right shoulder area to appear somewhat higher than the left. Curvature is more pronounced on x-ray.

Review of Lung Anatomy: Understanding the pulmonary exam is greatly enhanced by recognizing the relationships between surface structures, the skeleton, and the main lobes of the lung. Realize that this can be difficult as some surface landmarks (eg nipples of the breast) do not always maintain their precise relationship to underlying structures. Nevertheless, surface markers will give you a rough guide to what lies beneath the skin. The pictures below demonstrate these relationships. The multi-colored areas of the lung model identify precise anatomic segments of the various lobes, which cannot be appreciated on examination. Main lobes are outlined in black. The following abbreviations are used: RUL = Right Upper Lobe; LUL = Left Upper Lobe; RML = Right Middle Lobe; RLL = Right Lower Lobe; LLL = Left Lower Lobe.

Anterior View

Posterior View

Right Lateral View

Left Lateral View

Palpation: Palpation plays a relatively minor role in the examination of the normal chest as the structure of interest (the lung) is covered by the ribs and therefore not palpable. Specific situations where it may be helpful include:

Accentuating normal chest excursion: Place your hands on the patient's back with thumbs pointed towards the spine. Remember to first rub your hands together so that they are not too cold prior to touching the patient. Your hands should lift symmetrically outward when the patient takes a deep breath. Processes that lead to asymmetric lung expansion, as might occur when anything fills the pleural space (e.g. air or fluid), may then be detected as the hand on the affected side will move outward to a lesser degree. There has to be a lot of plerual disease before this asymmetry can be identified on exam.
Detecting Chest Excursion

Tactile Fremitus: Normal lung transmits a palpable vibratory sensation to the chest wall. This is referred to as fremitus and can be detected by placing the ulnar aspects of both hands firmly against either side of the chest while the patient says the words "Ninety-Nine." This maneuver is repeated until the entire posterior thorax is covered. The bony aspects of the hands are used as they are particularly sensitive for detecting these vibrations.

Assessing Fremitus

Pathologic conditions will alter fremitus. In particular:

Lung consolidation: Consolidation occurs when the normally air filled lung parenchyma becomes engorged with fluid or tissue, most commonly in the setting of pneumonia. If a large enough segment of parenchyma is involved, it can alter the transmission of air and sound. In the presence of consolidation, fremitus becomes more pronounced.
Pleural fluid: Fluid, known as a pleural effusion, can collect in the potential space that exists between the lung and the chest wall, displacing the lung upwards. Fremitus over an effusion will be decreased.

In general, fremitus is a pretty subtle finding and should not be thought of as the primary means of identifying either consolidation or pleural fluid. It can, however, lend supporting evidence if other findings (see below) suggest the presence of either of these processes.

Effusions and infiltrates can perhaps be more easily understood using a sponge to represent the lung. In this model, an infiltrate is depicted by the blue coloration that has invaded the sponge itself (sponge on left). An effusion is depicted by the blue fluid upon which the lung is floating (sponge on right).

Investigating painful areas: If the patient complains of pain at a particular site it is obviously important to carefully palpate around that area. In addition, special situations (e.g. trauma) mandate careful palpation to look for evidence of rib fracture, subcutaneous air (feels like your pushing on Rice Krispies or bubble paper), etc.

Percussion: This technique makes use of the fact that striking a surface which covers an air-filled structure (e.g. normal lung) will produce a resonant note while repeating the same maneuver over a fluid or tissue filled cavity generates a relatively dull sound. If the normal, air-filled tissue has been displaced by fluid (e.g. pleural effusion) or infiltrated with white cells and bacteria (e.g. pneumonia), percussion will generate a deadened tone. Alternatively, processes that lead to chronic (e.g. emphysema) or acute (e.g. pneumothorax) air trapping in the lung or pleural space, respectively, will produce hyper-resonant (i.e. more drum-like) notes on percussion. Initially, you will find that this skill is a bit awkward to perform. Allow your hand to swing freely at the wrist, hammering your finger onto the target at the bottom of the down stroke. A stiff wrist forces you to push your finger into the target which will not elicit the correct sound. In addition, it takes a while to develop an ear for what is resonant and what is not. A few things to remember:

If you're percussing with your right hand, stand a bit to the left side of the patient's back.
Ask the patient to cross their hands in front of their chest, grasping the opposite shoulder with each hand. This will help to pull the scapulae laterally, away from the percussion field.
Work down the "alley" that exists between the scapula and vertebral column, which should help you avoid percussing over bone.
Try to focus on striking the distal inter-phalangeal joint (i.e. the last joint) of your left middle finger with the tip of the right middle finger. The impact should be crisp so you may want to cut your nails to keep blood-letting to a minimum!
The last 2 phalanges of your left middle finger should rest firmly on the patient's back. Try to keep the remainder of your fingers from touching the patient, or rest only the tips on them if this is otherwise too awkward, in order to minimize any dampening of the perucssion notes.
When percussing any one spot, 2 or 3 sharp taps should suffice, though feel free to do more if you'd like. Then move your hand down several inter-spaces and repeat the maneuver. In general, percussion in 5 or so different locations should cover one hemi-thorax. After you have percussed the left chest, move yours hands across and repeat the same procedure on the right side. If you detect any abnormality on one side, it's a good idea to slide your hands across to the other for comparison. In this way, one thorax serves as a control for the other. In general, percussion is limited to the posterior lung fields. However, if auscultation (see below) reveals an abnormality in the anterior or lateral fields, percussion over these areas can help identify its cause.

#physical examination - lymph nodes

2012-03-26T23:22:00.001-07:00

Lymph Nodes: The major lymph node groups are located along the anterior and posterior aspects of the neck and on the underside of the jaw. If the nodes are quite big, you may be able to see them bulging under the skin, particularly if the enlargement is asymmetric (i.e. it will be more obvious if one side is larger then the other). To palpate, use the pads of all four fingertips as these are the most sensitive parts of your hands. Examine both sides of the head simultaneously, walking your fingers down the area in question while applying steady, gentle pressure. The major groups of lymph nodes as well as the structures that they drain, are listed below. The description of drainage pathways are rough approximations as there is frequently a fair amount of variability and overlap. Nodes are generally examined in the following order:

Palpating Anterior Cervical Lymph Nodes

Anterior Cervical (both superficial and deep): Nodes that lie both on top of and beneath the sternocleidomastoid muscles (SCM) on either side of the neck, from the angle of the jaw to the top of the clavicle. This muscle allows the head to turn to the right and left. The right SCM turns the head to the left and vice versa. They can be easily identified by asking the patient to turn their head into your hand while you provide resistance. Drainage: The internal structures of the throat as well as part of the posterior pharynx, tonsils, and thyroid gland.

Posterior Cervical: Extend in a line posterior to the SCMs but in front of the trapezius, from the level of the mastoid bone to the clavicle. Drainage: The skin on the back of the head. Also frequently enlarged during upper respiratory infections (e.g. mononucleosis).
Tonsillar: Located just below the angle of the mandible. Drainage: The tonsilar and posterior pharyngeal regions.
Sub-Mandibular: Along the underside of the jaw on either side. Drainage: The structures in the floor of the mouth.
Sub-Mental: Just below the chin. Drainage: The teeth and intra-oral cavity.
Supra-clavicular: In the hollow above the clavicle, just lateral to where it joins the sternum. Drainage: Part of the throacic cavity, abdomen.

Lymph nodes of the head and neck

A number of other lymph node groups exist. However, palpation of these areas is limited to those situations when a problem is identified in that specific region (e.g. the pre-auricular nodes, located in front of the ears, may become inflamed during infections of the external canal of the ear).

What are you feeling for? Lymph nodes are part of the immune system. As such, they are most readily palpable when fighting infections. Infections can either originate from the organs that they drain or primarily within the lymph node itself, referred to as lymphadenitis. Infected lymph nodes tend to be:

Firm, tender, enlarged and warm. Inflammation can spread to the overlying skin, causing it to appear reddened.

If an infection remains untreated, the center of the node may become necrotic, resulting in the accumulation of fluid and debris within the structure. This is known as an abscess and feels a bit like a tensely filled balloon or grape (a.k.a. fluctuance). Knowledge of which nodes drain specific areas will help you search efficiently. Following infection, lymph nodes occasionally remain permanently enlarged, though they should be non-tender, small (less the 1 cm), have a rubbery consistency and none of the characteristics described above or below. It is common, for example, to find small, palpable nodes in the submandibular/tonsilar region of otherwise healthy individuals. This likely represents sequelae of past pharyngitis or dental infections.

Malignancies may also involve the lymph nodes, either primarily (e.g. lymphoma) or as a site of metastasis. In either case, these nodes are generally:

Firm, non-tender, matted (i.e. stuck to each other), fixed (i.e. not freely mobile but rather stuck down to underlying tissue), and increase in size over time.

The location of the lymph node may help to determine the site of malignancy. Diffuse, bilateral involvement suggests a systemic malignancy (e.g. lymphoma) while those limited to a specific anatomic region are more likely associated with a local problem. Enlargement of nodes located only on the right side of the neck in the anterior cervical chain, for example, would be consistent with a squamous cell carcinoma, frequently associated with an intra-oral primary cancer.

#physical examination - Eye

2012-03-26T23:12:00.001-07:00

Occular Symmetry: Occasionally, one of the muscles that controls eye movement will be weak or foreshortened, causing one eye to appear deviated medially or laterally compared with the other

Sclera: The normal sclera is white and surrounds the iris and pupil. In the setting of liver or blood disorders that cause hyperbilirubinemia, the sclera may appear yellow, referred to as icterus. This can be easily confused with a muddy-brown discoloration common among older African Americans that is a variant of normal.

Conjunctiva: The sclera is covered by a thin transparent membrane known as the conjunctiva, which reflects back onto the underside of the eyelids. Normally, it's invisible except for the fine blood vessels that run through it. When infected or otherwise inflamed, this layer can appear quite red, a condition known as conjunctivitis. Alternatively, the conjunctiva can appear pale if patient is very anemic. By gently applying pressure and pulling down and away on the skin below the lower lid, you can examine the conjunctival reflection, which is the best place to identify this finding.

Pale Conjunctiva, due to severe anemia.

Conjunctivitis

Blood can also accumulate underneath the conjunctiva when one of the small blood vessels within it ruptures. This may be the result of relatively minor trauma (cough, sneeze, or direct blow), a bleeding disorder or idiopathic. The resulting collection of blood is called a subconjunctival hemorrhage. While dramatic, it is generally self limited and does not affect vision.

Subconjunctival Hemorrhage

# DVT

2012-03-25T22:01:00.000-07:00

DVT is very common complication after fracture and major orthopedic operation.

** Site: leg, thigh and pelvic vein.

**Risk factors:

à Knee and hip replacement

à Elderly

à Immobility

à Malignancy and CV disease

à Trauma ( fracture of spine , pelvis , femur and tibia)

à hypercoagulable status

Symptoms and signs

Pain and tenderness in calf or thigh usually unilateral

swelling

hotness

positive homan’s sign.

5. pulmonary embolism as primary presentation ( dyspnea, hemoptysis , tachypnea and fever).

Diagnosis:
Duplex ultrasonography , V-Q scan,
spiral CT and angiography.

Prevention:
1.Elastic stockings.

2.Elevation the foot.

3.Early mobilization.

4.Low molecular weigh heparin 40mg\day

# A simple Classification of Fractures of Long Bones

2012-03-25T21:26:00.000-07:00

Transverse Fracture:

A fracture in which the break is across the bone, at a right angle to the long axis of the bone. Adjoining figure would illustrate.

Oblique Fracture:

Instead of break being at right angle, it goes in oblique direction to the long axis of the bone.The fracture is confined to one plane. In other words the bone has broken at an angle.

Spiral Fracture :

This fracture is easily confused with the oblique fracture. Instead of a straight break as in oblique fracture that is only in one plane, the break in this case traverses both the planes. To understand this you need to imagine a three dimensional view of the bone.

If you take a stick and slice it at an angle so that it is divided in two, it is similar to oblique fracture. But if you twist and break that stick it would result in a break pattern that would start from one point, move obliquely in on direction, reach the other end and then continue in other side of the stick in a spiral fashion to meet the original point.

Adjoining diagram would give you rough idea of what I am trying to say. Compare it with the oblique fracture diagram and you would be able to appreciate the difference.

Comminuted Fracture :

If the injury results in multiple breaks in the bone, they are visible as different fragments. These kind of fractures are called comminuted fractures.

Apart from this, fracture can be displaced or undisplaced. If bone fragments stay together maintaining structural alignment of the bone , it is called an undisplaced fracture. A hairline fracture is an example of an undisplaced fracture.

But fragment of the bone may move from their original position resulting separation of the fragments. Such a fracture is called a displaced fracture

churp..churp

2012-03-25T06:07:00.001-07:00

Bookmark this website, cause you'll definitely be hooked! #ChurpChurp, one of your fav sites.

# syncope

2012-03-25T00:54:00.002-07:00

Blood Flow to the Brain and Heart

Sometimes the heart tries to raise blood pressure by increasing the force or rate of its muscle contractions. This just makes things worse. As the heart beats faster and stronger, it sends the wrong message to the heart's chambers, ie that the ventricle is filled with blood. This hasn't actually happened - in fact it's the opposite, the blood pressure is too low because the ventricle is not full.

When the brain receives the faulty message, it slows the heart rate down and further dilates the blood vessels. The blood pressure drops even lower, less blood is pumped to the brain, and the risk of fainting increases.

Diagnosing Fainting Disorders

NCS is the most common cause of fainting in young people. Many Electrophysiologists will agree that most young people diagnosed with this fainting disorder will 'outgrow' it by the time they hit their mid-20s, but this is just an average. Many people afflicted with this disorder have it for their lifetime. NCS is often misdiagnosed unless a 'tilt table' procedure is used.

In this test, a person is strapped to a flat table and 'tilted' backwards to a 70-degree upright tilt for 40 minutes. People who have NCS usually do not last that long and faint before the test is even completed. Prior to fainting, NCS patients exhibit;

fatigue,

weakness,

nausea,

sweating,

pale pallor,

visual disturbances,

abdominal discomfort,

headache,

pins-and-needles,

light-headedness or vertigo,

palpitations,

vomiting,

disorientation,

and difficulty speaking clearly or coherently.

There is much controversy and confusion regarding NCS, and many reports have been published that contradict past findings. It is now thought that patients may have a genetic predisposition toward NCS.

Assess whether the patient was standing, sitting, or lying when the syncope occurred. Syncope while seated or lying is more likely to be cardiac.^[19]

The following questions should be answered:

Was loss of consciousness complete?
Was loss of consciousness with rapid onset and short duration?
Was recovery spontaneous, complete, and without sequelae?
Was postural tone lost?

A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:

Agents that reduce blood pressure (eg, antihypertensive drugs, diuretics, nitrates)
Agents that affect cardiac output (eg, beta-blockers, digitalis, antiarrhythmics)
Agents that prolong the cardiac output (QT) interval (eg, tricyclic antidepressants, phenothiazines, quinidine, amiodarone)
Agents that alter sensorium (including alcohol, cocaine, analgesics with sedative properties)
Agents that alter serum electrolytes (especially diuretics)
Causes
Cardiac (cardiopulmonary) syncope may be due to vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction and predicts a worse short-term and long-term prognosis. Obtaining an initial ECG is mandatory if any of these causes are possible for the differential diagnosis.
Low flow states, such as those associated with advanced cardiomyopathy, CHF, and valvular insufficiency, may result in hypotension and cause transient global cerebral hypoperfusion. Often, these patients are on medications that reduce afterload, which may contribute to the cause of syncope.
Ventricular arrhythmias, such as ventricular tachycardia and torsade de pointes, tend to occur in older patients with known cardiac disease. These patients tend to have fewer recurrences and have a more sudden onset with few, if any, presyncopal symptoms. Associated chest pain or dyspnea may be present. This type of syncope is generally unrelated to posture and can occur during lying, sitting, or standing. Often, these arrhythmias are not revealed on the initial ECG but may be captured with prolonged monitoring.
Supraventricular tachyarrhythmias include supraventricular tachycardia and atrial fibrillation with rapid response. These may be associated with palpitations, chest pain, or dyspnea. Patients typically have prodromal symptoms and may have syncope while attempting to stand or walk because of resultant hypotension. These symptoms may spontaneously resolve prior to evaluation but are often noted during initial triage and assessment. Be sure to scrutinize ECG findings for evidence of Wolff-Parkinson-White syndrome, Brugada syndrome, and long QT syndrome.
Bradyarrhythmias include sick sinus syndrome, sinus bradycardia, high-grade atrioventricular blocks, pacemaker malfunction, and adverse medication reactions. Generally, these patients have a history of cardiac problems and are symptomatic. Chest pain, dyspnea, decreased exercise tolerance, and fatigue may all be present. Consider cardiac ischemia and medication side effects as additional causes.
Cardiac outflow obstruction may also result in sudden-onset syncope with little or no prodrome. One critical clue is the exertional nature, and the other is the presence of a cardiac murmur. Young athletes may present with this etiology for syncope. Specific pathology includes aortic stenosis, hypertrophic obstructive cardiomyopathy, mitral stenosis, pulmonary stenosis, pulmonary embolus, left atrial myxoma, and pericardial tamponade.
Syncope can also result from an acute MI, acute aortic dissection, and pulmonary embolus. These conditions can have associated chest pain, neck pain, shoulder pain, dyspnea, epigastric pain, hypotension, alteration of mental status and can result in sudden death.
Reflex (neurally mediated) syncope may be due to vasovagal syncope, which is mediated by emotional distress such as fear or physical pain. Situational syncope describes syncope that occurs with a fixed event such as micturition, deglutition, exercise induced, and carotid sinus syncope. These causes tend to be more benign and do not predict poor outcomes.
Vasovagal syncope is the most common type in young adults but can occur at any age. It usually occurs in a standing position and is precipitated by fear, emotional stress, or pain (eg, after a needlestick). Autonomic symptoms are predominant. Classically, nausea, diaphoresis, fading or "graying out" of vision, epigastric discomfort, and light-headedness precede syncope by a few minutes. Syncope is thought to occur secondary to efferent vasodepressor reflexes by a number of mechanisms, resulting in decreased peripheral vascular resistance. It is not life threatening and occurs sporadically.
Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defecation, deglutition, tussive, and carotid sinus syncope are types of situational syncope. These stimuli result in autonomic reflexes with a vasodepressor response, ultimately leading to transient cerebral hypotension. These are not life-threatening but can cause morbidity. The treatment involves avoidance of the precipitant when possible and the initiation of counter maneuvers when anticipated.
Syncope due to orthostatic hypotension can occur through several mechanisms. Pure autonomic failure can be associated with Parkinson's disease or dementia. Secondary autonomic insufficiency can be due to diabetes, uremia, or spinal injury. Drugs such as alcohol cause orthostatic intolerance and medications such as vasodilators and antidepressants block orthostatic reflexes. Volume depletion due to blood loss, vomiting, diarrhea, poor oral intake, and diuretics also cause orthostatic syncope.
Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relationship between orthostatic hypotension and syncope. Orthostatic hypotension increases in prevalence with age as a blunted baroreceptor response results in failure of compensatory cardioacceleration. In elderly patients, 45% of these cases are related to medications. Limited evidence suggests that polydipsia may reduce recurrences. Orthostasis is a common cause of syncope and tends to be recurrent. Bedside orthostatics cannot exclude this as an etiology; if suspected, patients should be referred to a primary care provider for outpatient tilt-table testing.
Prehospital Care
Prehospital management of syncope covers a wide spectrum of acute care and includes rapid assessment of airway, breathing, circulation, and neurologic status.
Treatment may require the following:
- Intravenous access
- Oxygen administration
- Advanced airway techniques
- Glucose administration
- Pharmacologic circulatory support
- Pharmacologic or mechanical restraints
- Defibrillation or temporary pacing
Medication Summary
The goals of pharmacotherapy are to prevent complications and to reduce morbidity.
Anticholinergics
Class Summary
These agents improve conduction through the atrioventricular node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective.

Atropine (Atropair, Isopto Atropine, Atropisol)
Anticholinergic (or parasympatholytic) drug that exerts its action by competitively inhibiting acetylcholine at muscarinic receptors on postganglionic smooth muscle. Can counteract rapidly heightened vagal tone in response to pathologic carotid sinus syndrome. Additionally, can reverse bradycardia and lessen degree of heart block when vagal activity is etiologic factor. Usual doses are used to reduce severe bradycardia and syncope associated with hyperactive carotid sinus reflex.
Nutrient Supplements
Class Summary
Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations.

Dextrose (D-Glucose)
Nutrient replenisher, serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose, whereas each 100 mL of 10% dextrose contains 10 g of dextrose.
Should be given only after demonstrated hypoglycemia.
Benzodiazepines
Class Summary
CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis.

Alprazolam (Xanax)
Indicated for treatment of anxiety and management of panic attacks. Following PO administration, absorbed readily. Peak concentrations in plasma occur 1-2 h following administration.
Vasopressor
Class Summary
Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist that acts on receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of BP. This drug has minimal beta effects and diffuses poorly across the blood-brain barrier.

Midodrine HCl (ProAmatine)
Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect persisting for 2-3 h. Has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure

Hypertensive Emergency

2012-03-25T00:42:00.000-07:00

Severe elevation of blood pressure with acute damage of an organ system (usually the brain, heart and/or kidneys) and possibly permanent damage. To reverse the damage the blood pressure should be lowered aggressively over minutes to hours. Typically the blood rises rapidly and can be caused by not taking blood pressure medications, abruptly stopping a blood pressure medication, drugs of abuse (cocaine, methamphetamine), severe elevation of thyroid hormone, and taking certain over the counter medications.

Symptoms

Chest pain, shortness of breath, headache, confusion, weakness, fatigue, lethargy, decreased urine output.

Tests

A history and physical exam will be performed. Tests will be done to determine the elevation of the blood pressure and to identify any end-organ damage.

Standard Workup

CBC
Chem 12
Troponin
X-Ray
EKG
CT Scan

# ABG

2012-03-25T00:38:00.000-07:00

Arterial Blood Gases

An arterial blood gas (ABG) test measures the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery. This test is used to check how well your lungs are able to move oxygen into the blood and remove carbon dioxide from the blood.

As blood passes through your lungs, oxygen moves into the blood while carbon dioxide moves out of the blood into the lungs. An ABG test uses blood drawn from an artery, where the oxygen and carbon dioxide levels can be measured before they enter body tissues.

Normal Arterial Blood Gas Values

pH	7.35-7.45
PaCO₂	35-45 mm Hg
PaO2	80-95 mm Hg
HCO3	22-26 mEq/L
O2 Saturation	95-99%
BE	+/- 1

Why It Is Done

An arterial blood gas (ABG) test is done to:

Check for severe breathing problems and lung diseases, such as asthma, cystic fibrosis, or chronic obstructive pulmonary disease (COPD).
See how well treatment for lung diseases is working.
Find out if you need extra oxygen or help with breathing (mechanical ventilation).
Find out if you are receiving the right amount of oxygen when you are using oxygen in the hospital.
Measure the acid-base level in the blood of people who have heart failure, kidney failure, uncontrolled diabetes, sleep disorders, severe infections, or after a drug overdose.

The LOSt DiarY........

Bradyarrhythmias-Complete Heart Block

Complete Heart Block

Common Causes

Bradyarrhythmias-Second-Degree (AV) Heart Block (Type 2)

Second-Degree (AV) Heart Block (Type 2)

Bradyarrhythmias-Second-Degree Heart Block (Type 1)

Second-Degree Heart Block (Type 1)

Bradyarrhythmias-First-Degree Heart Block

H’s and T’s of ACLS

H’s and T’s of ACLS

Hypovolemia

Hypoxia

Hydrogen ion (acidosis)

Hyper-/hypokalemia

Hypoglycemia

Hypothermia

Toxins

Tamponade

Tension Pneumothorax

Thrombosis (heart: acute, massive MI)

Thrombosis (lungs: massive pulmonary embolism)

Trauma

Other Tachycardia Rhythms

Other Tachycardia Rhythms

Monomorphic Ventricular Tachycardia

Polymorphic Ventricular Tachycardia

Supraventricular Tachycardia (SVT)

Supraventricular Tachycardia (SVT)

Atrial Flutter

Symptoms

Complications

Treatment

Cardioversion

PEA

#pulseless rhtm-vent fib

Vent. Fib./Tach.

# pulseless rhytm

Tachycardia

pediatric v-fib

pulseless electrical activity

V-fib and V-tac

# neck and airway trauma

#physical examination - lung

#physical examination - lymph nodes

#physical examination - Eye

# DVT

# A simple Classification of Fractures of Long Bones

churp..churp

# syncope

Blood Flow to the Brain and Heart

Diagnosing Fainting Disorders

Causes

Prehospital Care

Medication Summary

Anticholinergics

Class Summary

Atropine (Atropair, Isopto Atropine, Atropisol)

Nutrient Supplements

Class Summary

Dextrose (D-Glucose)

Benzodiazepines

Class Summary

Alprazolam (Xanax)

Vasopressor

Class Summary

Midodrine HCl (ProAmatine)

Hypertensive Emergency

Symptoms

Tests

# ABG

Arterial Blood Gases

Why It Is Done