Sunday, 22 November 2009

Miscellaneous conditions

Myocarditis:

The ECG findings that are mostly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations, these can also be seen in pericarditis.

Pericarditis

Types include:

  • Serous
  • Fibrinous
  • Purulent
  • Heamorrhagic
  • Caseous
Acute vs. chronic
Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or heart attack.


Clinical presentation


Chest pain, radiating to the back and relieved by sitting up forward and worsened by lying down, is the classical presentation. Other symptoms of pericarditis may include dry cough, fever, fatigue, and anxiety. Pericarditis can be misdiagnosed as myocardial infarction (heart attack), and vice versa.

The classic sign of pericarditis is a friction rub. Other signs include diffuse ST-elevation and PR-depression on ECG in all leads except aVR and V1;

PRINZMETALS ANGINA

Specific ECG ST segment changes in Prinzmetals angina are elevation rather then depression


PULMONARY EMBOLISM


ECG changes can develop in a very proportion of patient's with a pulmonary embolism, changes strongly suggestive of a diagnosis of pulmonary embolism are: 

  • S1Q3T3 pattern: large S waves in Lead I, large Q waves in V3 and T wave inversion in lead III.
  • Abnormal right axis deviationbnormal rigright

  • T wave inversion in the right precordial leads 

But, the commoner findings are non-specific T wave changes and non-specific ST segment elevation or depression. 



WOLFF-PARKINSON-WHITE SYNDROME

Wolff-Parkinson-White syndrome (WPW) is a syndrome of pr-excitation of the ventricles of the heart, this is due to an accessory abnormal electrical conduction pathway known as the bundle of kent, and vast majority of individuals remain asymptomatic throughout their entire lives, but there is a risk of sudden death associated with this syndrome, this is in rare cases due to the fact of the accessory tachyarrhythmia's   in these individuals.


LOWN-GANONG-LEVINE SYNDROME


HYPERTHYROIDISM


HYPOTHYROIDISM


BRUGADA SYNDROME


EARLY REPOLARISATION


TAKO-TSUBO SYNDROME


SUBARACHNOID HAEMORRHAGE


PIGGYBACK HEART TRANSPLANT (HETEROTOPIC)


PERICARDIAL EFFUSION


COPD


RESTRICTIVE CARDIOMYOPATHY



DILATED CARDMYOPATHY


EBSTEIN's ANOMALY


TRICUSPID ATRESIA


TETRALOGY OF FALLOT


PULMONARY STENOSIS


ANEURYSM



















Pacemakers



TERMINOLOGY


FAILURE TO CAPTURE OR PACE PROBLEMS


SENSING AND OVER SENSING


PACEMAKER-MEDIATED TACHYCARDIA


PACEMAKER CODES & MODES


TRANSCUTANEOUS PACEMAKERS


IMPLANTABLE CARDIOVERTER-DEFIBRILLOR



Hypertrophy chamber enlargement

COMING SOON:


ATRIAL ABNORMALITY


LEFT ATRIAL ABNORMALITY (p mitrale)


RIGHT ATRIAL ABNORMALITY (p pulmonale)


LEFT VENTRICULAR HYPERTROPHY (LVH)


RIGHT VENTRICULAR HYPERTROPHY (RVH)


BIVENTRICULAR ENLARGEMENT (p biatrial)


STRAIN PATTERNS

Conduction and bundle branch blocks

COMING SOON:


INCOMPLETE LEFT BUNDLE BRANCH BLOCK


INCOMPLETE RIGHT BUNDLE BRANCH BLOCK


COMPLETE LEFT BUNDLE BRANCH BLOCK


COMPLETE RIGHT BUNDLE BRACH BLOCK


INTRAVENTRICULAR CONDUCTION DELAY


HEMIBLOCK, (LEFT ANTERIOR)


HEMIBLOCK, (LEFT POSTERIOR)


FASCICULAR BLOCKS


LEFT ANTERIOR FASCICULAR BLOCK (LAFB)


LEFT POSTERIOR FASCICULAR BLOCK (LPFB)


MULTIFASCICULAR BLOCK


TRIFASCICULAR BLOCK

Acute coronary syndrome (ACS) rhythms





ISCHEMIA


INJURY


INFARCTION


LOCALIZING THE INFARCT


ESTIMATING THE EXTENT OF THE INFARCTION


ISCHEMIC HEART DISEASE


POSTERIOR WALL INFARCTION


ANTERIOR WALL


ANTEROLATERAL WALL


INFERIOR WALL


LATERAL WALL


RIGHT VENTRICULAR WALL


MYOCARDIAL ISCHEMIA (SUBENDOCARDIAL)


DIAGNOSIS OF INFARCTION IN SPECIAL CIRCUMSTANCES


WELLEN's SIGN


ST Segment Elevations in ECG

Toxic and systemic disorder effects on the ECG

COMING SOON:


HYPERCALCAEMIA ECG EFFECTS


HYPOCALCEMIA ECG EFFECTS


HYPERKALEMIA ECG EFFECTS


HYPOKALEMIA ECG EFFECTS


drugs effects on ECG:


ANTIARRHYTHIC DRUGS
DIGOXIN
QUINIDINE
OTHER
QTc MEASUREMENTS
PROLONGED QT INTERVAL SYNDROME

Supraventricular rhythms

COMING SOON:


SVT


ABERRANT VENTRICULAR CONDUCTION


AV NODAL RE-ENTRY TACHYCARDIA


AV NODAL RECIPROCATING TACHYCARDIA



































NON-PAROOXYSMAL TACHYCARDIA


ECTOPIC ATRIAL TACHYCARDIA


SINUS NODE RE-ENTRY TACHYCARDIA


PAROXYSMAL ATRIAL TACHCARDIA WITH BLOCK



Ventricular rhythms

COMING SOON:


SUSTAINED VT


VENTRICULAR ESCAPE BEATS


DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA's


DISTINGUISHING VT FROM SVT


IDIOVENTRICULAR RHYTHM


ACCELERATED IDIOVENTRICULAR RHYTHM


DISTINGUISHING ACCELERATED IDIOVENTRICULAR RHYTHM FROM JUNCTIONAL


POLYMORPHIC VT


TORSADES DE POINTES







Premature beats



PREMATURE ATRIAL CONTRACTIONS


PREMATURE ATRIAL CONTRACTION (PAC) OR ATRIAL PREMATURE BEAT (APB)


PREMATURE JUNCTIONAL CONTRACTION (PJC) OR JUNCTIONAL PREMATURE BEAT (JPB)


PREMATURE VENTRICULAR CONTRACTION (PVC) OR VENTRICULAR PREMATURE BEAT (VPB)


FUSION & PSEUDO-FUSION BEATS


DISTINGUISHING NON-CONDUCTED PAC'S FROM SINOATRIAL BLOCK 


DISTINGUISHING INTERMITTENT VENTRICULAR PACING FROM PVC's


BIGEMINY


TRIGEMINY


QUADGEMINY


MUTIFOCAL PVC's


COUPLETS


SALVO's


R-ON-T PHENOMENON







Junctional rhythm

COMING SOON:


JUNCTIONAL ESCAPE BEATS


JUNCTIONAL RHYTHM


JUNCTIONAL TACHYCARDIA


PREMATURE JUNCTIONAL CONTRACTION (PJC)


ACCELERATED JUNCTIONAL RHYTHM

Atrial rhythms



ATRIAL FIBRILLATION






ATRIAL FLUTTER







ATRIAL ESCAPE


ATRIAL BIGEMINY


SINUS ARREST


SINUS EXIT BLOCKS


WONDERING ATRIAL PACEMAKER


DISTINGUISHING WAP FROM PAC'S


SICK SINUS SYNDROME OR SINUS NODE DYSFUNCTION


MUTIFOCAL ATRIAL TACHYCARDIA


DISTINGUISHING MAT FROM AF


PARAOXYSMAL ATRIAL TACHYCARDIA


ATRIAL TACHYCARDIA WITH BLOCK


DISTINGUISHING ATRIAL FLUTTER FROM ATRIAL FIBRILLATION


DISTINGUISHING ATRIAL FIBRILLATION FROM JUNCTIONAL RHYTHM







Sinoatrial blocks





TYPE-1


FIRST-DEGREE ATRIOVENTRICULAR BLOCK


TYPE-2


SECOND-DEGREE (TYPE I) ATRIOVENTRICULAR BLOCK


SECOND DEGREE (TYPE II) ATRIOVENTRICULAR BLOCK


TYPE III


THIRD-DEGREE ATRIOVENTRICULAR BLOCK


ATRIOVENTRICULAR DISSOCIATION



Sinus node arrhythmias

NORMAL SINUS RHYTHM





SINUS ARRHYTHMIA







SINUS BRADYCARDIA







SINUS TACHYCARDIA







TACHYARRHYTHMIAS


BRADYARRHYTHMIAS


INTRINSIC CAUSES


EXTRINSIC CAUSES


BRADYCARDIA-TACHYCARDIA SYNDROME


ESCAPE RHYTHMS 


PARASYSTOLE


ASHMAN'S PHENOMENON


CATURE BEATS


FUSION BEATS







12-lead ECG interpretation

COMING SOON:


NORMAL ECG FINDINGS


LOCATING MYOCARDIAL DAMAGE
































THE RIGHT SIDED LEADS

Introduction to the 12-lead ECG



THE 12-LEAD ELECTRICAL AXIS


12-LEAD ELECTRODE POSITIONING/PLACEMENTS


WILSON'S (PRECORDIAL LEADS)


NEHB'S SPECIAL LEADS


HOW TO PERFORM A 12-LEAD ECG



Basic rhythm interpretation (arrhythmias)



DEFINITIONS


MECHANISM


ALTERED IMPULSE FORMATION


ALTERED IMPULSE CONDUCTION


CLASSIFICATION OF ARRHYTHMIAS


CAUSES OF ARRHYTHMIAS

Technical problems (troubleshooting)

Artifacts

Artifacts (disturbances) can have many causes. Common causes are:
  • Movement
  • Electrical interference

Filter settings

Although not a technical problem, filter settings influence the interpretation of the ECG.
Filter settings can influence the interpretation of ST elevation as these examples show. On the left side an ECG with normal settigns (0.01-40Hz), on the right side a rhythm strip from the same patient with a different high-pass filter setting (0.32-40Hz). Also, the P wave morphology is different between the two ECGs.
To reduce electrical interference ECG machine use two filters:
  • A high-pass filter reduces low frequency noise. This filter reduces base line drift on the ECG.
  • A low-pass filter reduces high frequency noise, such as produces by chest and extremity muscles and electrical interference from the power grid.
Depending on the purpose of the ECG these filters can be adjusted.
  • In the monitor mode the high-pass filter can be set higher at 0.5-1.0 Hz and the low-pass filter on 40 Hz. This is the strongest filter setting (only a narrow frequency range is passed by the filter). This setting is especially useful for rhythm monitoring where noise can be distracting and ST segment interpretation is not very important. In this mode, pacemakerspikes are sometimes invisible while filtered out.
  • In the diagnostic mode the high-pass filter is set at 0.05 Hz and the low-pass filter at 40, 100 or 150 Hz. This improves the diagnostic accuracy of the ST semgent. On the downside a base line drift occurs more easily.

Cardiac axis, leads and planes

LEADS I,II,III

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg. The limb leads form the points of what is known as Einthoven's triangle.
  • Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode.
  • Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode.
  • Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode. 

BIPOLAR & UNIPOLAR LEADS


There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one negative pole. In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson's central terminal) made up of signals from lots of other electrodes. In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).
Wilson's central terminal is produced by connecting the electrodes, RA; LA; and LL, together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e., zero).
LEADS avr, avl and avf

Leads aVR, aVL, and aVF are augmented limb leads. They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode" or a unipolar lead. This is possible because Einthoven's Law states that I + (−II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I − II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5, and V6.

  • Lead augmented vector right (aVR) has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm.
  • Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm.
  • Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.
The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane.
Einthoven's triangle


LEFT AXIS DEVIATION (LAD)


Left axis deviation occurs when additional electrical forces move to the left (hypertrophy), or when the time required for the electrical activity to move over the ventricle is prolonged (LBBB, left ventricular dilation).
Causes of left axis deviation include hypertension, aortic stenosis or regurgitation, subaortic stenosis, mitral regurgitation, and left ventricular conduction defects.
The QRS axis may shift during the respiratory cycle if elevation of the diaphragm changes the physical position of the heart. Beat-to-beat variation in QRS axis (an every-other-beat change in QRS shape) is called “electrical alternans.” This is thought to be caused by the heart physically swinging back and forth in a pericardial effusion.



RIGHT AXIS DEVIATION (RAD)

Right axis deviation is seen on the ECG when more electrical forces are moving to the right than normal. This is usually due to hypertrophy of the right ventricle (RVH). Causes of right axis deviation include COPD, pulmonary emboli, valvular disease, septal defects, and pulmonary hypertension.

An axis of +90 is common in persons with emphysema. This so-called “vertical heart” reflects both the rotation of the heart downward as the diaphragm position drops due to air trapping, and some degree of hypertrophy of the right ventricle.

EXTREME AXIS DEVIATION


RIGHT SUPERIOR AXIS DEVIATION (RARE CASES)


ROTATION OF THE CARDIAC AXIS


Axis Deviation:



The QRS axis is the “average” direction of electrical activity during ventricular depolarization. The QRS axis may shift due to physical change in the position of the heart, chamber hypertrophy, or conduction block.








ECG Waves & Segments components





P wave

The P wave represents right by left atrial depolarization and is low amplitude positive deflection preceding the QRS complex. Atrial repolarization occurs simultaneously with depolarization of the ventricular myocardium and is hidden by the QRS complex.

Assessment of the P wave allows an idea of where the atrial depolarization begins and whether or not the atrial are enlarged

  • The best leads to look for P waves in are leads II and V1.
  • Right Atrial Enlargement (RAE) tends to present as peaked P wave >2.5mm in lead II.
  • Left Atrial Enlargement (LAE) is seen as a biphasic P wave in V1 with a 1 small box deep and 1 small box deep negative deflecton.
  • Inverted P waves in leads II, III and aVF imply a negative axis of the P wave or retrograde conduction in the atrial due to a low atrial or junctional pacemaker.
PR interval


The PR interval is measured from the beginning of the P wave to the first part of the QRS complex. It includes time for atrial depolarization, conduction through the AV node, and conduction through the His-Purkinje system. Disruption at any point can prolong the PR interval. The length of the PR interval changes with heart rate, but is normally 0.12-0.20 seconds.


QRS complex


The QRS complex consists of the time needed for ventricular depolarization.

The first positive deflection of the QRS (R wave) is very steep, reflecting the quick distribution of electrical impulses through the His-Purkinje system. This represents depolarization of the left ventricular myocardium. The negative deflection following the R wave is the S wave which represents terminal depolarization of the high lateral wall. The lowercase letters are used for relatively small amplitude waves of less then 0.5mV or 5 mm (one large box).

A lengthened QRS complex can result from 3 possibilities:

  • Impairment of the conduction system exists so that the wave of depolarization coming down from the atria does not or cannot travel the normal conduction system (bundle branch block, abberrant ventricular conduction, or Wolff-Parkinson-White syndrome).
  • A beat initiated in the ventricle (PVC, Ventricular Tachycardia, or idioventricular).
In a normal ECG the R waves of the QRS complex begin small in V1-V2 and get larger as we progress through the precordial leads laterally. The R wave will be the dominant deflection in the QRS by V3-V4.

Early large R waves in V1-V2, as large as those in following leads, can reflect posterior wall infarction, lateral infarction, right ventricular hypertrophy or septal hypertrophy.

Poor R wave progression is when the R waves do not begin to dominate the QRS until V5 or V6. This may represent infarction or injury of the anterior left ventricle and carries almost as much significance as Q waves.

The size of the QRS can be determined by: the size of the patient (larger patients have smaller complexes), the left ventricular muscle mass, and the age of the patient (older patients tend to have smaller complexes).

ST segment


The ST segment occurs after ventricular depolarization has ended and before repolarization has begun. The ST segment is usually isoelectric and has a slight upward concavity. It is of particular interest in diseased states where it may have other configurations.

ST segments are measured for elevation or depression against the TP segment, not the PR interval. The TP segment is the true isoelectric line. The ST segment is always measure from the J point, where the QRS and ST segments meet. Many J points are an approximation with no clear transition from the QRS to the ST segment.

In young people, J-point elevation is seen as concave up-sloping ST segments that take off a bit above the isoelectric line and this is common. It does not indicate pathology.

T wave


The T wave represents the period of ventricular repolarization. Since repolarization is slower than depolarization, the T wave is broad and has a slow upstroke.

  • Flattened T waves may indicate ischemia.
  • T waves are normally upright in I, II, V3-V6 and inverted in lead aVR.
  • T waves can be observed for indications of ischemia or electrolyte disturbances.

QT interval


The QT interval consists of the QRS complex (representing only a brief part of the interval), along with the ST segment and T wave, which constitutes the majority of the duration. The QT interval is used primary as a measure of membrane repolarization. Since the QT interval varies with heart rate, the QT is "corrected" (QTc) to make comparisons between ECG's. The corrected QT interval equals the QT when the ventricular rate is 60 bpm (the RR=1).

Causes of prolonged QT intervals include:

  • Electrolyte abnormalities
  • hypothermia
  • Idiopathic long QT syndrome
  • Tricyclic antidepressants
  • Phenothiazines
  • Antiarrhytmics (quinine and procainamide)
U wave


The U wave may be seen in some leads, especially the right precordial leads: V2-V4. U waves are associated  with metabolic disturbances, typically hypokalemia and hypomagnesemia. Additionally, it may be seen following the T wave and can make interpretation of the QT interval especially difficult.


Determining heart rate


Standard ECG paper is standardized at 25mm/sec. The vertical lines on the ecg graph paper can be used to measure varying time intervals. There is a 0.20 sec between two of the large lines.

To count the number of heart beats (QRS complexes) in a regular rhythm, between 30 large boxes (6 seconds) you just multiply by 10, and this will give you a estimate of how many beats per minute. ECG paper also has additional markings every 3 seconds so you don't have to count 30 large boxes.

Other way that is quicker and easier to estimate the heart rate is to remember the table below:


Rhythm

Basic Electrocardiology

Basic ECG Interpretation


P wave- atrial depolarization
PR segment- conduction delay through AV node
PR interval- atrial depolarization and conduction delay through AV node
QRS- ventricular depolarization
ST segment- isoelectric; ventricles still depolarized
QT interval- ventricular depolarization and ventricular repolarization
T wave- Ventricular repolarization


Normal Cardiac Rhythm Parameters
Normal sinus rhythm -----------between 60 and 100 bpm
Sinus bradycardia-------------- less than 60 bpm
Sinus tachycardia --------------over 100 bpm
QRS width---------------------- between 0.08 and 0.12 sec
PR interval ----------------------between 0.12 and 0.20 sec
QT interval ----------------------0.30-0.40 sec
Atrial rate, inherent------------ 60-100 bpm
Junctional rate, inherent ------ 40-60 bpm
Ventricular rate, inherent ----- 20-40 bpm


FIGURING RATE (for regular rhythms only)
1. 1500 method
- divide 1500 by the number of small squares between two consecutive QRS complexes
2. R-R method
- find a QRS where the peak R wave falls on a heavy dark line. USe this QRS as reference then take note where the next QRS falls. Starting from the next heavy line, count 300, 150, 100, 75, 60, 50, 40.
3. 6-second method
- count the number of QRS complexes in a 6 second strip and multiply by 10
9:05 AM


ECG RULER
CALIPERS
MODERN ECG MACHINES

ABBREVIATIONS

α    alpha
AAL    Anterior axillary line
abd    Abdominal
ABC    Airway, Breathing, Circulation
ACA    Anterior cerebral artery
ACC    American College of Cardiology
ACCP    American College of Chest Physicians
ACE    Angiotensin converting enzyme
ACEI    ACE Inhibitor
ACLS    Advanced cardiac life support
ACS    Acute coronary syndrome
ACT    Activated clotting time
ACTH    Adrenocorticotrophic hormone
ACV    Assist control ventilation
AD    Aortic dissection
ADH    Antidiuretic hormone
AID    Automatic internal defibrillator
AFib    Atrial fibrillation
AFlut    Atrial flutter
Alb    Albumin
AHA    American Heart Association
AHF    Acute Heart Failure
ALI    Acute Lung Injury
AMI    Acute myocardial infarction
APACHE    Acute physiologic and chronic health evaluation
AP    Arterial pressure
APC    Activated protein C
APRV    Airway pressure release ventilation
aPTT    Activated partial thromboplastin time
ARB    Angiotensin Receptor Blocker
ARDS    Acute Resp. Distress Syndrome 
ARF     Acute Renal Failure
AS    Aortic stenosis
ASAP    As soon as possible
ASHP    American Society of Hospital Pharmacists
ASVD    Arteriosclerotic vessel disease
ATLS    Advanced trauma life support
ATN    Acute tubular necrosis
AV    Atrio-ventricular
AVB    Atrio-ventricular block
AVF    Augmented voltage of the feet
AVL    Augmented voltage of the left
AVR    Augmented voltage of the right
AVSP    Atrial-ventricular sequential pacing
β    beta
BB    Beta blocker  
BBB    Bundle branch block
BD    Base deficit
BG    Blood glucose
BiPAP    Bi-level positive airway pressure
BNP    Brain natriuretic peptide
BP    Blood pressure
bpm    Beats per minute
brady    Bradycardia
BUN    Blood urea nitrogen
C    Centigrade
Ca    Calcium
CA    Coronary artery
CABG    Coronary artery bypass graft
CAD    Coronary artery disease
CAM    Confusion assessment method
CaO2    Oxygen content of arterial blood
CCB    Calcium channel blocker
CCL    Cardiac Catheterization Lab
CHF    Congestive heart failure
CHO    Carbohydrate
CI    Cardiac index
Cl    Chloride
CK    Creatine phosphokinase
CMV    Control mode ventilation
CN    Cranial nerve
CNS    Central nervous system
CO    Cardiac output
Conc    Concentration
COP    Colloid osmotic pressure
COPD    Chronic obstructive     pulmonary disease
Cor PP    Coronary perfusion     pressure
CPAP    Continuous positive airway pressure
CPB    Cardiopulmonary bypass
CPK    Creatine phosphokinase
CPK-MB   CPK myocardial biomarker
CPP    Cerebral perfusion pressure
Cr    Creatinine
Cr Cl    Creatinine clearance
CRRT    Continuous renal replacement therapy    
Cryo    Cryoprecipitate
CS    Cardiogenic shock
CSF    Cerebrospinal Fluid
CT    Computed tomography
CV    Cardiovascular
CVAH    Continuous arterial to venous hemofiltration
CvO2    Oxygen content of venous blood
CVP    Central venous pressure
CVVH    Continuous venous to venous hemofiltration
CVVHD     CVVH with dialysate
CVVHDF     CVVD with filtration
d    day
DBP    Diastolic blood pressure
DC    Discontinue
DCC    Direct current cardioversion
DDAVP    Desmopressin acetate
Defib    Defibrillator
DI    Diabetes insipidus
Dias    Diastolic
Dig    Digoxin
DKA    Diabetic ketoacidosis
dL    deciliter
DOO    Dual chamber fixed rate 
    pacing
DO2    Oxygen Delivery
DP    Dorsalis pedis
2,3 DPG      2,3 Diphosphoglycerate
DTI    Direct thrombin inhibitor
DVI    Dual chamber pacing with
    ventricular inhibition
DVT    Deep vein thrombosis
EBL    Estimated blood loss
ECG    Electrocardiogram
Echo    Echocardiogram
ECMO    Extracorporeal membrane oxygenation
EF    Ejection fraction
EMG    Electromyelogram
EPS    Electrophysiology study
ET    Endotracheal
ETOH    Ethanol
F    Fahrenheit
FDA    Food & DrugAdministration
FeNa    Fractional excretion of sodium
FF    Filtration fraction
FFP    Fresh frozen plasma
FiO2    Fraction (%) of inspired O2
FM    Face mask
Fr.    French
FRC    Functional residual capacity
FUN    Filtrate urea nitrogen
fx    Fracture
g    gram 
G    Ground
GCS    Glasgow coma scale
GCSE    Generalized convulsive status epilepticus
GFR    Glomerular filtration rate
GI    Gastrointestinal
GP    Glycoprotein
GPRA    Glycoprotein receptor antagonist
GSW    Gunshot wound
h    hour
hr    hour
HA    Headache
Hct     Hematocrit
HF    Heart failure
HFJV    High frequency jet ventilation
Hg    Mercury
Hgb    Hemoglobin 
H/H    Hemoglobin/Hematocrit
HIT    Heparin-induced thrombocytopenia
HITT    HIT with thrombosis
HNAD    Hyperosmolar Nonacidic Diabetes
HR    Heart rate
HOB    Head of bed
HS    Hypertonic saline
Hx    History
IABP    Intra-aortic balloon pumping
ICD    Implanted Cardiodefibrillator
ICH    Intracerebral hemorrhage
ICP    Intracranial pressure
ICS    Intercostal space
I:E    Inspiration:Expiration
IJ    Internal jugular
IL-1    Interleuken 1
IMA    Internal mammary artery
IMV    Intermittent mandatory ventilation
INR    International normalization ratio
IO    Intraosseous
IRV    Inverse ratio ventilation
ITA    Internal thoracic artery
IV    Intravenous
IVC    Inferior vena cava    
IVP    Intravenous push
j    Joule
JCAHO    Joint Commission on the Accreditation of Health Organizations
JVD    Jugular venous distention
K    Potassium
kg    kilogram
lb    pound
L    Liter
LA     Left arm
LAP    Left atrial pressure
LAD    Left anterior descending
LBBB    Left bundle branch block
LDH    Lactate dehydrogenase
LDUH    Low dose unfractionated heparin
Lido    Lidocaine
LL    Left leg
LLL    Left lower lobe
LMWH    Low molecular weight heparin
LOC    Level of consciousness
LOS    Length of stay
LPM    Liters per minute
LR    Lactated Ringers
Lt    Left
LUQ    Left upper quadrant
LUL    Left upper lobe
LV    Left ventricle
LVEDP    Left ventricular end-diastolic pressure
LVEF    Left ventricular ejection fraction
LVHF    Left ventricular heart failure
LVSWI    Left ventricular stroke work index
mA    Milliamp
MAOI    Monoamine oxidase inhibitor
MAP    Mean arterial pressure
MAT    Multifocal atrial tachycardia
max    maximum
MCA    Middle cerebral artery
MCL    Midclavicular line
MCL1    Modified chest lead I
MDO2    Myocardial oxygen delivery
m2    square meter
mEq    milliequivalents
mg    milligrams
Mg    Magnesium
min    minute
mL    milliliter
mm    millimeter
mm2    cubic millimeter
MODS    Multiple organ dysfunction syndrome
MOF    Multiple organ failure
mOsm    milliosmoles
MPT    Minimum pacing threshold    
MR    Mitral regurgitation
MS    Morphine sulfate
mV    millivolt
MV    Minute ventilation
MVO2    Myocardial oxygen demand
Na    Sodium
NA    Not applicable
NC    Nasal cannula
NCR    Nasal cannula reservoir
NCSE    Nonconvulsive status epilepticus
ng    nanogram
NG    Nasogastric
NIBP    Noninvasive blood pressure
NIH    National Institutes of Health
NMB    Neuromuscular blockade
NMBA    Neuromuscular blocking agent
NS    Normal Saline
NSAID    Nonsteroidal antiinflammant
NSR    Normal sinus rhythm
NSTEMI    Non ST-elevation myocardial infarction
NTG    Nitroglycerin
N/V    Nausea/Vomiting
NYHA    New York Heart Association
OD    Overdose
OER    Oxygen extraction ratio
OPCAB    Off-Pump coronary artery bypass
OPC    Organ procurement coordinator
OPO    Organ procurement organization
PA    Pulmonary artery
PAC    Premature atrial contraction
PAD    Pulmonary artery diastolic
PAI    Plasminogen activator inhibitor
PAM    Pulmonary artery mean 
PaO2    Partial pressure of O2 in arterial blood
PAO2    Partial pressure O2 alveolar air
PAP    Pulmonary artery pressure
PAS    Pulmonary artery systolic
    pressure
PAT    Paroxysmal atrial tachycardia
Pb    Barometric pressure
PbtO2    Oxygen dissolved in brain tissue
PCI    Percutaneous coronary intervention
PCT    Pleural chest tube
PCWP    Pulmonary capillary wedge pressure
PDEI    Phosphodiesterase inhibitor
PE    Pulmonary embolism
PEA    Pulseless electrical activity
Peep    Positive end-expiratorypressure
PetCO2    Partial pressure of end-tidal carbon dioxide
P/F    ratio of PaO2 to FiO2
Phos    Phosphorus
PMI    Point of maximal impulse
PRBC’s    Packed red blood cells
PSA    Phlebostatic axis
PSV    Pressure support ventilation
PSVT    Paroxysmal Supraventricular Tachycardia
PT    Prothrombin time
PTCA    Percutaneous transluminal coronary angioplasty
PTT    Posterior tibial
PVC    Premature ventricular contraction
PVD    Peripheral vascular disease
PvO2    Partial pressure of O2 in venous blood
PVR        Pulmonary vascular resistance
Q    Blood flow, perfusion, or cardiac output
QS/QT    Shunted flow/total flow
RA    Right arm
RAP    Rapid atrial pacing
RBC    Red blood cell
RL    Ringer’s Lactate
RLL    Right lower lobe
RML    Right middle lobe
RSBI    Rapid shallow breathing index
RSI    Rapid Sequence Intubation
Rt    Right
r-tPA    recombinant tissue plasminogen activator 
RUL    Right upper lobe
RUQ    Right upper quadrant
RV    Right ventricle
RVEDF    RV end-diastolic volume
RVEF    RV ejection fraction
RVHF    Right ventricular heart failure
RVMI    RV myocardial infarction
Rx    Treatment
SA    Sino-atrial
SAH    Subarachnoid hemorrhage
SaO2    Arterial oxygen saturation
SBP    Systolic blood pressure
SBT    Spontaneous breathing trial
SC    Subcutaneously
SCCM    Society Critical Care Medicine
SCD        Sequential compression device
SCI    Spinal cord injury
SCIWORA   SCI without radiologic abnormality
SCUF    Slow continuous ultrafiltration
ScvO2    Central venous O2 saturation
SE    Status epilepticus
sec    Second
SGOT    Serum glutamic-oxaloacetic transaminase
SHI    Severe head injury
SIMV    Synchronized intermittent mandatory ventilation
SIRS    Systemic inflammatory response syndrome
SjvO2    Oxygen saturation of jugular venous blood
SK    Streptokinase 
SL    Sublingual
SpO2    Pulse oximetry of arterial oxygen saturation 
S & S    Signs and symptoms
SSS    Sick sinus syndrome
STBI    Severe traumatic brain injury
STEMI    ST-elevation myocardial infarction
SV    Stroke volume
SVG    Saphenous vein graft
SvO2     Mixed venous O2  saturation
SVR    Systemic vascular resistance    
SVT    Supraventricular tachycardia
Sx    Suction    
Sys    Systolic
TAFI    Thrombin activatable fibrinolysis inhibitor
TAT    Thrombin-Antithrombin
TBI    Traumatic brain injury
TBV    Total blood volume
TCP    Transcutaneous pacing
TdeP    Torsades de pointes
TEE    Transesophageal echocardiogram
TIMI    Thrombolysis in Myocardial Infarction
TNF    Tumor necrosis factor
TnI    Troponin I
TnT    Troponin T
t-PA    Tissue Plasminogen Activator
TRH    Thyrotropin releasing hormone
TSH    Thyroid stimulating hormone
TV    Tidal volume
TVP    Temporary ventricular pacing
UA    Unstable Angina
U    Unit
µg    microgram
UF    Ultrafiltrate
UFH    Unfractionated Heparin
UK    Urokinase
UO    Urinary output
UrCl    Urea clearance
VAP    Ventilator associated 
    pneumonia
VC    Vital capacity
Vent    Ventricular
VF    Ventricular fibrillation
VFib    Ventricular fibrillation
VKA    Vitamin K Antagonist
V/Q    Ventilation/perfusion
VSD    Ventricular septal defect
VT    Ventricular tachycardia
VTach     Ventricular tachycardia
VTE    Venous Thromboembolism
VOO    Ventricular fixed rate pacing 
VO2    Oxygen consumption
VP    Ventriculo-peritoneal
VVI    Ventricular demand pacing 
WBC    White blood cell
WPW    Wolf-Parkinson-White
Xa    Activated clotting factor X
yo    Years old