Monday, June 20, 2011

ECG-AHA 2010

When the patient presents with symptoms and signs of potential ACS, the clinician uses ECG findings (Figure 1, Box 4) to classify the patient into 1 of 3 groups:

1. ST-segment elevation or presumed new LBBB (Box 5) is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men 40 years old); J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old); J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).113

2. Ischemic ST-segment depression >0.5 mm (0.05 mV) or dynamic T-wave inversion with pain or discomfort (Box 9) is classified as UA/NSTEMI. Nonpersistent or transient ST-segment elevation 0.5 mm for <20 minutes is also included in this category. Threshold values for ST-segment depression consistent with ischemia are J-point depression 0.05 mV (-.5 mm) in leads V2 and V3 and -0.1 mV (-1 mm) in all other leads (men and women).113

3. The nondiagnostic ECG with either normal or minimally abnormal (ie, nonspecific ST-segment or T-wave changes, Box 13). This ECG is nondiagnostic and inconclusive for ischemia, requiring further risk stratification. This classification includes patients with normal ECGs and those with ST-segment deviation of <0.5 mm (0.05 mV) or T-wave inversion of 0.2 mV. This category of ECG is termed nondiagnostic.

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Friday, June 17, 2011

TIMI Score

ARCA ACS



TIMI stands for 'Thrombolysis In Myocardial Infarction' and is the name of an Academic Research Organization (ARO) which was founded by Dr. Eugene Braunwald in 1984. It has conducted numerous practice-changing clinical trials in patients with cardiovascular disease or risk factors for cardiovascular disease.
The TIMI Study Group is affiliated with Brigham and Women's Hospital and Harvard Medical School, and is chaired by Dr. Marc Sabatine (founding Chairman Eugene Braunwald, MD (1982-2010)). Its headquarters are located in Boston, MA with a second location in Quincy, MA.

TIMI Risk Score is used in patients with Unstable Angina / Non-ST Elevation Myocardial Infarction. It is used to categorize a patient's risk of death and ischemic events and provides a basis for therapeutic decision making.

TIMI Score Calculation (1 point for each):
-Age >= 65
-Aspirin use in the last 7 days (patient experiences chest pain despite ASA use in past 7days)
-At least 2 angina episodes within the last 24hrs
-ST changes of at least 0.5mm on admission EKG
-Elevated serum cardiac biomarkers
-Known Coronary Artery Disease (CAD) (coronary stenosis >= 50%)
- At least 3 risk factors for CAD, such as: Hypertension -> 140/90 or on antihypertensives, Cigarette smoking, HDL < 40, Diabetes, Family history of premature CAD (CAD in male first-degree relative, or father less than 55, or female first-degree relative or mother less than 65).

Score Interpretation:
% risk at 14 days of: all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization.
Score of 0-1 = 4.7% risk Score of 2 = 8.3% risk Score of 3 = 13.2% risk Score of 4 = 19.9% risk Score of 5 = 26.2% risk Score of 6-7 = at least 40.9% risk
Reference: "The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI". JAMA. Website: [1]
Reference: "TIMI Study Group" [2]

'TIMI Grade Flow' is a widely adopted scoring system from 0-3 referring to levels of coronary blood flow assessed during percutaneous coronary angioplasty:
TIMI 0 flow (no perfusion) refers to the absence of any antegrade flow beyond a coronary occlusion.
TIMI 1 flow (penetration without perfusion) is faint antegrade coronary flow beyond the occlusion, with incomplete filling of the distal coronary bed.
TIMI 2 flow (partial reperfusion) is delayed or sluggish antegrade flow with complete filling of the distal territory.
TIMI 3 flow (complete perfusion) is normal flow which fills the distal coronary bed completely
'TIMI risk' estimates mortality following acute coronary syndromes. http://www.timi.org


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Angina-CCS

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Cardiac markers-Malaysian CPG


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Some Clinical Conditions in Which the Electrocardiogram Interpretation Can Be Difficult

Source:Tintinelli 7th

May have ST-segment elevation in the absence of acute myocardial infarction
Early repolarization
Left ventricular hypertrophy
Pericarditis
Myocarditis
Left ventricular aneurysm
Hypertropic cardiomyopathy
Hypothermia
Ventricular paced rhythms
Left bundle-branch block
May have ST-segment depressions in the absence of ischemia
Hypokalemia
Digoxin effect
Cor pulmonale and right heart strain
Early repolarization
Left ventricular hypertrophy
Ventricular-paced rhythms
Left bundle-branch block
May have T-wave inversions in the absence of ischemia
Persistent juvenile pattern
Stokes-Adams syncope or seizures
Post-tachycardia T-wave inversion
Postpacemaker T-wave inversion
Intracranial pathology (central nervous system hemorrhage)
Mitral valve prolapse
Pericarditis
Primary or secondary myocardial diseases
Pulmonary embolism or cor pulmonale from other causes
Spontaneous pneumothorax
Myocardial contusion
Left ventricular hypertrophy
Ventricular-paced rhythms
Left bundle-branch block
Right bundle-branch block

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Wednesday, June 15, 2011

Facial Nerve Block

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Monday, March 21, 2011

Hyponatremia

Source:http://www.globalrph.com/hyponatremia.htm
Sodium: (Normal range: 136 - 145 meq/l)

Sodium plays a vital role in maintaining the concentration and volume of the extracellular fluid (ECF). It is the main cation of the ECF and a major determinant of ECF osmolality. Sodium is important in maintaining irritability and conduction of nerve and muscle tissue and assists with the regulation of acid-base balance. The average daily intake far exceeds the normal daily requirements. The kidneys are responsible for excreting the excess and are capable of conserving sodium during periods of extreme sodium restriction. The kidneys accomplish this primarily through regulation of water intake/excretion. If the serum sodium falls, the kidneys respond by excreting water. If the serum sodium increases (increased osmolality)---thirst center is stimulated--increased ADH release by the posterior pituitary---acts on kidney to conserve water. Aldosterone also plays a key role by regulating Na+/ECF volume. Its release causes the kidneys to conserve water and sodium which results in increased ECF volume. Because changes in serum sodium levels typically reflect changes in body water balance, gains or losses of total body sodium are not necessarily reflected by the serum sodium level.
Hyponatremia: (Serum sodium less than 136 meq/L)
Clinical indicators and treatment depend on the cause of hyponatremia and whether or not it is associated with a normal, decreased or increased ECF volume.
Signs and symptoms: neurologic symptoms usually do not occur until the serum sodium level has dropped to approximately 120-125 meq/L. Hyponatremia with decreased ECF volume: irritability, apprehension, dizziness, postural hypotension, dry mucus membranes, cold and clammy skin, tremors, seizures. Hyponatremia with normal or increased ECF volume: headache, lassitude, apathy, confusion, weakness, edema, weight gain, elevated blood pressure, muscle cramps, convulsions.
History and risk factors: diarrhea, fistulas, vomiting, NG suction, diuretics, adrenal insufficiency, skin losses (burns, wound drainage), other. Note: hyperlipidemia, hyperproteinemia, and hyperglycemia may cause a pseudo-hyponatremia. This must be ruled out before determining therapy. For every 100 mg/dl increase in glucose, the sodium is diluted by 1.6 meq/L.
Diagnostic tests: serum sodium will be less than 136 meq/L. Serum osmolality will be decreased except in cases of pseudo-hyponatremia, azotemia, or toxins that increase osmolality (example: ethanol). Urine specific gravity will be decreased because of the kidneys attempt to excrete excess water. Urine sodium: decreased (except in SIADH and adrenal insufficiency).
Collaborative management: The goal of therapy is to get the patient out of immediate danger (eg return the sodium level to greater than 120 meq/L) and then gradually return the serum sodium to a normal level and restore normal ECF volume.
Hyponatremia with increased ECF volume and edema
Hypervolemia: low serum serum osmolality (< 280 ), urine sodium < 10 mmol/L, Usually associated with: CHF, cirrhosis, or acute/chronic renal failure.)

Therapeutic options:
1) For mild cases only (serum sodium > 120 meq/L): Water restriction (limit to 500 to 1500 ml/ 24 hours) and furosemide 40-80 IV/ oral once daily (20-400 mg/day).
2) Patients with CHF, cirrhosis, nephrotic syndrome who usually have excessive ECF volume have few symptoms referable to hyponatremia. Usually water restriction combined with treatment of the underlying disorder is successful.
3) If severe symptomatic hyponatremia is present (sodium level < 115 meq/L) in the volume overloaded patient: Continue water restriction. Also infuse 3% hypertonic saline.
Calculate sodium deficit: 0.6 x (weight in kg) x (desired sodium - Actual sodium)
Use 0.5 for females. Desired range= 120 - 125 meq/L.
When hyponatremia is symptomatic and acute (< 24 hours in duration), the serum sodium may be raised safely to 120-125 meq/L in 24 hours or less. In patients with symptomatic chronic hyponatremia, or hyponatremia of unknown duration, the serum sodium should be raised slowly (0.5 meq/L/hr) to about 120-125 meq/L in order to avoid CNS complications (cerebral edema, pontine myelinolysis, seizures) and/or pulmonary edema. The total increase in these patients should not exceed 10-12 meq/L in 24 hours or <20-25 meq/L over 48 hours. Thereafter, the hypertonic saline is stopped, and the serum sodium is allowed to rise more slowly (eg over several days) in response to continued restriction of free water. In all cases, the serum sodium should be corrected only halfway to normal in the initial 24 hours (120-125 meq/L) to prevent the complications listed above.

Example calculations:
80kg patient; serum sodium=110 meq\L ; male; desired target= 120 meq/L.
1) 0.6 x 80kg x (120-110)= 480 meq (total needed)
2) Amount needed to increase serum level by 0.5 meq/L/hr =
0.6 x 80 x 0.5= 24 meq. (rate should be 24 meq/hr)
3) 3% hypertonic saline contains 513 meq/Liter
[desired rate/hr]/513 x 1000= # ml/hr // Total meq/rate/hr
=infusion time.

Therefore: 24 meq/hr x 1000= 47 ml/hr
513
Length of infusion= 480 meq/ 24 meq= 20 hours
Final order: infuse 3% hypertonic saline at 47 ml/hr for 20 hours.
When infusion is complete, discontinue. Continue with fluid
restriction.
Hyponatremia with isovolemia
Low osmolarity (<280), urine sodium < 10 mmol: water intoxication; urine sodium > 20: SIADH, hypothyroidism, renal failure, addisons disease, drugs.
Mild: (serum level > 120 meq/L; asymptomatic): furosemide 80mg IV once or twice daily and Normal saline + 20-40meq KCL/liter infused at 65-150 ml/hr (correct deficit at 0.5 meq/L/hr or less.)
SIADH: fluid restriction 500-750ml/ day. Demeclocycline 300 to 600mg twice daily. Use caution in patients with hepatic disease. In emergency situations (sodium < 115) use hypertonic saline (see above) and furosemide.
Symptomatic patients: hypertonic saline and furosemide as above. or hypertonic saline and water restriction.

Hyponatremia with hypovolemia
Low serum osmolarity (<280). Urine sodium < 10 mmol: vomiting, diarrhea, 3rd space/respiratory/skin loss. Urine sodium > 20: diuretics, renal injury, RTA, adrenal insufficiency.
If volume depleted give 500 to 3000 ml of normal saline at 500 ml/hr until no longer orthostatic, then give normal saline ( + 20-40 meq KCL/ liter) at 65 to 150 ml/hr until desired level is reached (note: in mild cases, target a level of 130 meq/ Liter). Each liter of normal saline contains 154 meq. May use the calculations above to determine approximate length of therapy. If severe hyponatremia is present (<115 meq/L) start hypertonic saline using the dosing guidelines above.

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Was established since 25 Nov 09.Just to educate myself.

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