Interpretation of EKG

Interpretation of EKG's
Five Cardinal Features

• (1) Rate
• (2) Rhythm – including intervals
• (3) Axis
• (4) Hypertrophy
• (5) Infarction

Rate

• Three ways to determine rate:
• (1) count number of thick lines that occur between QRS complexes: 300 if next QRS on thick lines, 150 if 2^nd, 100 if 3^rd, then 75, 60, 50
• say: "300, 150, 100" "75, 60, 50" as counting thick lines
• can also use thin lines (thick lines bolded): 300, 250, 214, 187, 167; 150, 136, 125, 115, 107; 100, 94, 88, 83, 79; 75, 71, 68, 65, 62; 60
• (2) if bradycardic (less than 60 bpm) or irregular: count 6 second strip (2 3-second marks) and multiply by 10
• can also count entire strip (10 seconds) and multiply by 6
• (3) calculate: 1500/number of small lines between similar waves
• must determine coexisting independent rates if there are more than one

Rhythm

• Automaticity – heart has automaticity foci that respond at different rates and produce different morphology on EKG
• atrial – preceeded by P wave (shape of P wave changes depending upon originating focus), narrow complex QRS, normal rate 60-80/min
• junctional – no P wave, narrow QRS, normal rate 40-60/min
• ventricular – no P wave, wide QRS, normal rate 20-40/min
• Intervals
• PR should be less than 0.2 seconds (one large square)
• QRS should be less than 0.12 seconds (three small squares)
• QT interval – must be corrected for rate (QTc); in general, QT should be less than half R-R interval
• Sinus Rhythm – P before each QRS, QRS after each P, P in correct orientation (up in II)
• normal sinus rate is 60-100 bpm; if sinus rhythm but greater than 100 bpm, it is sinus tachycardia; if less than 60 bpm, it is sinus bradycardia
• Irregular Rhythms
• Sinus Arrythmia – varies with respiration, P waves identical; not pathological
• Wandering Pacemaker – irregular rhythm, P waves change shape, rate less than 100 bpm
• Multifocal Atrial Tachycardia – same as wandering pacemaker with rate greater than 100 bpm
• Atrial Fibrillation – irregular ventricular rhythm without P waves; may see erratic atrial spikes or wavy baseline
• Escape – lower level of heart will automatically respond if not driven with faster rate from above (automaticity)
• Escape Beat – single beat after a pause; can be atrial, junctional, or ventricular
• ventricular escape beats can be caused by burst of excessive parasympathetic activity (parasympathetic innervation inhibits SA node and AV junction but NOT ventricular tissue)
• Escape Rhythms – persistent escape beats (sinus node not active or not conducting); can be atrial, junctional ("idiojunctional" rhythm), or ventricular ("idioventricular" rhythm)
• idiojunctional rhythms can produce retrograde atrial depolarization with an inverted P' before, during, or after the QRS
• idioventricular rhythms caused by complete block below AV junction (P waves present but not associated with QRS) or total failure of all tissue above ventricles (downward displacement of the pacemaker)
• idioventricular rhythms can cause loss of consciousness due to insufficient cardiac output (Stokes-Adams Syndrome)
• Premature Beats – from an irritable automaticity focus; can be atrial (PAB), junctional (PJB), or ventricular (PVC; 6 PVC's per minute is pathological)
• PAB/PJB – irritable atrial and junctional foci are caused by sympathetic stimulation, caffeine, amphetamines, cocaine, digitalis, toxins, ethanol, hyperthyroidism, and stretch receptors
• PAB resets from the new P' wave at previous rate (first cycle slightly lengthened due to transient baroreceptor reflex)
• PAB's can cause wide QRS (aberrent ventricular conduction)
• PAB and PJB still depolarize the SA node (either directly or through retrograde atrial depolarization) and reset the pacing, so rhythm begins again in phase with the premature beat
• if the beat is not conducted (due to refractoriness), the missed QRS in produces a long empty baseline (harmless)
• can occur every other beat (atrial or junctional bigeminy) or every third beat (atrial or junctional trigeminy)
• PVC – irritable ventricular foci are caused by low oxygen, hypokalemia, or muscle pathology (mitral valve prolapse, myocarditis, etc.)
• PVC's do not depolarize the SA node, so there is a "compensatory" pause after them (except for "interpolated" PVC's, where they occur exactly where the ventricular contraction would have)
• P waves continue unaffected and the next QRS occurs where it would have if there had been no PVC
• a PVC that falls on a T wave ("R on T phenomenon") can cause sustained ventricular tachycardia
• ventricular parasystole – ventricular tissue with entrance block (NOT an irritable focus) that starts PVC's at its own automatic firing rate
• Tachyarrhythmias
• Paroxysmal tachycardia – 150-250 bpm; can be atrial (PAT), junctional (PJT), or ventricular (PVT)
• atrial (PAT) or junctional (PJT) are also called paroxysmal superventricular tachycardia (PSVT)
• paroxysmal atrial tachycardia with block (PAT with more than one P wave before each QRS) – caused by digitalis
• AV nodal reentry tachycardia (AVNRT) is a type of PJT
• PJT may still have retrograde atrial depolarization and inverted P' waves
• PJT may involve somewhat widened QRS since one bundle branch may still be refractory when next beat arrives (aberrent ventricular conduction)
• PVT:
• during PVT, if the P wave appears at just the right time, can see normal QRS (capture beat) or QRS that degenerates into a PVC (fusion beat)
• PVT can be distinguished from PSVT with wide QRS (caused by BBB, etc.) by the following:
• presence of coronary artery disease
• very wide QRS (more than 0.14 sec)
• extreme RAD
• AV dissociation (see capture or fusion beats)
• Torsades des Pointes – "party streamer"; caused by two competitive, irritable foci in different ventricular areas
• Flutter – 250-350 bpm; can be atrial (sawtooth baseline with QRS's) or ventricular (sine wave; almost always leads to fibrillation unless treated)
• Fibrillation – greater than 350 bpm; can be atrial (jagged baseline with QRS's) or ventricular (no identifiable waves)
• no pumping occurs
• atrial fibrillation can produce a narrow-complex tachycardia (rapid ventricular response)
• Block – identify by pauses (sinus block), abnormal PR intervals (AV blocks), abnormal QRS interval (bundle branch block), or axis deviation (hemiblock)
• Sinus Block – spontaneous pause in electrical activity; can restart automatically or have an escape beat (see above)
• AV Block – causes abnormal PR interval
• 1^st degree block – PR too long (greater than 0.2 seconds, or one large square)
• 2^nd degree block – some P waves without QRS:
• Wenkebach (Mobitz I) – block at the node itself; PR gradually lengthens until a P does not produce a QRS
• Mobitz II – block beyond the node; PR length constant, but some P waves do not produce QRS (can be 2:1, 3:1, etc., or even intermittent)
• 2:1 block can be either of above; can use vagal maneuvers to differentiate (see below)
• 3^rd degree block – none of the P waves get through; there is an idioventricular or idiojunctional rate instead
• Bundle Brach Block – basically two out of phase QRS's (R R'); requires wide QRS for diagnosis (at least 3 small squares; best to use limb leads since low voltages allow for more accurate measurement)
• Right Bundle Branch Block (RBBB) – QRS has two peaks (R R') in V₁ or V₂ usually returning to lower than baseline between them
• Left Bundle Branch Block (LBBB) – QRS has two peaks (R R') in V₅ or V₆ with slight depression between them
• BBB makes ventricular hypertrophy criteria unreliable
• LBBB makes infarction difficult to determine
• BBB can cause SVT to degenerate more easily into VT
• Hemiblock – block of anterior or posterior fascicle of LBB; causes axis deviation and widened QRS
• Anterior hemiblock – left axis deviation with a Q wave in I and a prominent S wave in III
• Posterior hemiblock – right axis deviation with a prominent S wave in I and a Q wave in III
• can have bifascicular blocks (RBBB + hemiblock)
• must have previous EKG to diagnose so that other causes of axis deviation can be ruled out
• Vagal Maneuvers (gagging or carotid sinus massage) – inhibit irritable atrial or junctional foci or increase the refractoriness of the AV node
• abolishes PSVT, identifies 2:1 AV block (no effect if Mobitz II), and reveals flutter waves in atrial flutter

Axis

• find axis quadrant using below diagram (QRS above or below baseline in each lead):
• 
• axis is also 90 degrees from isoelectric QRS (same up as down) or in the direction of a QRS that only goes up (opposite direction of QRS that only goes down)
• Normal axis is "up in I and aVF" (some say "up in I and II")
• if I is down: right axis deviation (RAD)
• if aVF is down: left axis deviation (LAD)
• if both are down: extreme RAD
• Axis Rotation – find isoelectric QRS (same up as down) in chest leads (V₁ to V₆); normally occurs in V₃ or V₄
• if isoelectric in V₁ or V₂: rightward rotation
• if isoelectric in V₅ or V₆: leftward rotation

Hypertrophy

• Atrial Hypertrophy – diphasic P wave in V₁
• right atrial hypertrophy – large initial component of diphasic P wave in V₁
• left atrial hypertrophy – large terminal component of diphasic P wave in V₁
• Ventricular Hypertrophy – tall R wave in V₁ for RVH, deep S wave in V₁ and tall R wave in V₅ for LVH
• right ventricular hypertrophy – widened QRS with RAD, rightward rotation, and:
• R greater than S in V₁ but R gets smaller in V₂ through V₆
• S wave persists in V₅ and V₆
• left ventricular hypertrophy – widened QRS with LAD, leftward rotation, and:
• sum of depth of S in V₁ and height of R in V₅ is more than 35 small squares
• inverted T wave with gradual downslope and rapid upslope

Infarction – always requires previous EKG for comparison

• Identifying Injury
• (1) ischemia – inverted T waves (earliest sign) – symmetrical down- and upslope, opposite direction of QRS
• (2) acute injury – ST elevation
• can occur without Q waves: "non Q-wave MI"
• ST depression may indicate "subendocardial infarction" (small shallow area as opposed to entire wall of heart)
• (3) necrosis (non-conductive tissue) – Q-waves
• significant if more than one small square wide or greater than 1/3 the amplitude of the QRS
• remain even after acute infarction is over (unlike other two)
• Localizing Injury – leads where the above occur; also remember that axis points away from infarction
• Anterior – left anterior descending artery – V₁ to V₄
• Lateral – circumflex artery – I, aVL
• Inferior – right or left coronary artery – II, III, aVF
• Posterior – right coronary artery – V₁ and V₂, but changes are mirror image (R instead of Q, ST depression instead of elevation, etc.)
• for blocks and hemiblocks: AV node is supplied by the right coronary artery, RBB and anterior LBB is supplied by LAD, posterior LBB is supplied by either

Effects of Other Medical Conditions on EKG

• Pulmonary Embolism
• prominent S wave in I
• Q wave in III
• inverted T waves in III and V₁ through V₄
• ST depression in II
• acute incomplete RBBB
• RAD with rightward rotation
• Electrolyte Disturbances
• hyperkalemia
• wide flat P – P disappears entirely with severe hyperkalemia
• wide QRS
• peaked T wave
• hypokalemia
• flat T wave
• U wave (after T wave; represents Purkinje cell repolarization) – prominent with severe hypokalemia
• can cause torsades des pointes if extreme
• hypercalcemia – shortened QT interval
• hypocalcemia – prolonged QT interval
• Drugs
• Digitalis
• therapeutic – ST slopes below baseline, inverted T waves, shortened QT
• excessive – blocks: SA block, paroxysmal atrial tachycardia (PAT) with block, AV block (can be 3^rd degree)
• toxic – atrial fibrillation, junctional or ventricular tachycardia, frequent PVC's, ventricular fibrillation
• Quinidine (blocks potassium channels)
• wide notched P wave
• wide QRS
• very deep ST
• U wave
• long QT interval
• Pericarditis
• flat or concave downward ST segment elevation in leads where QRS is mainly negative (right chest leads – V₁ to V₃)
• elevated ST segment with T wave off baseline in leads where QRS is mainly positive (lateral/inferior limb leads – aVL, I, II, aVF, III)
• COPD
• all waves of minimal amplitude; often leads to RVH with RAD; MAT in some cases

Effect of Cardiac Syndromes on EKG

• Wolff-Parkinson-White Syndrome – caused by accessory bundle of Kent that bypasses the AV node to allow ventricular pre-excitation
• delta wave with apparently shortened PR interval
• can cause tachycardia through three mechanisms:
• (1) rapid conduction of rapid atrial beats (PSVT, atrial flutter, or atrial fibrillation)
• (2) automaticity foci within the bundle
• (3) re-entry of ventricular depolarization
• Lown-Ganong-Levine Syndrome – caused by James bundle (extention of the anterior internodal tract) that bypasses the AV node directly to the bundle of His
• no PR delay (so PR interval is minimal)
• QRS immediately responds to any atrial tachyarrythmias, so (for example) atrial flutter produces a rapid QRS response
• Brugada Syndrome – familial dysfunction of Na⁺ channels
• characterized by RBBB with ST elevation (downsloping) in V₁ through V₃
• can cause deadly arrythmias leading to sudden cardiac death with no apparent structural heart disease (responsible for half of all cases)
• Wellen's Syndrome – stenosis of LAD
• causes marked T-wave inversion in V₂ and V₃
• Long QT Syndrome – QT interval more than 1/2 the cardiac cycle
• predisposed to ventricular arrythmias

Hypertensive Urgency vs Emergrncy

-Urgency: is increase in BP > 180 / 120 w/o any signs of target organ damage
-while emergency: is increase in BP > 180/120 w s/o target organ damage , like:

1. Flash pulm edema- do CXR
2. CVA: get CTB
3. renal failure: get BUN and Cr
4. Coronary ischemia/ infarction: get EKG and Cardiac Enzymes

Management:

 for Urgency:: goal is to decrease BP by 25% in next 24 hrs

While for Emergency : goal is to decrease BP by 10% in next 1 hr and 25 in next 3- 4 hrs

Pathophysiology:

High BP--cause damage to endothelium---> Decrease NO secretion---> further exacerbates BP

Also Due to Endothelin damage ---> there will be Capillary leakage --> causing Flash Pulm Edema

New Onset Atrial Fibrillation

http://www.aafp.org/afp/2002/0715/p249.html


emedicine: http://emedicine.medscape.com/article/151066-treatment#aw2aab6b6b3

HyperTAG

• The serum triglyceride concentration can be stratified in terms of population percentiles and/or coronary risk (see 'Definitions, epidemiology, and detection' above):

• Normal <150 mg/dL (1.7 mmol/L)
• Borderline high — 150 to 199 mg/dL (1.7 to 2.2 mmol/L)
• High — 200 to 499 mg/dL (2.3 to 5.6 mmol/L)
• Very high — ≥500 mg/dL (≥5.7 mmol/L)

• Although the contribution of triglycerides to cardiovascular risk has been debated in the past, it now seems clear that elevated triglyceride levels are independently associated with cardiovascular risk, particularly coronary risk. It remains uncertain, however, whether this association is causal, such that hypertriglyceridemia, independent of associated lipoprotein, inflammatory and hemostatic abnormalities, causes atherosclerosis. It is also uncertain whether lowering triglyceride levels reduces risk. (See 'Triglycerides and atherosclerosis' above.)
• There are only limited data regarding which patients with hypertriglyceridemia require treatment and on the choice of therapies. (See 'Management' above.)
• Nonpharmacologic interventions such as weight loss in obese patients, aerobic exercise, avoidance of concentrated sugars and medications that raise serum triglyceride levels, and strict glycemic control in diabetics should be first-line therapy in patients with mild-to-moderate hypertriglyceridemia. Other risk factors for cardiovascular disease, such as hypertension and smoking, should also be addressed. (See 'Nonpharmacologic therapy' above.)
  
  In patients with severe hypertriglyceridemia (fasting triglyceride levels above 1000 mg/dL [11.3 mmol/L]), we suggest a very low fat diet (Grade 2C). (See 'Nonpharmacologic therapy' above.)
• Options for pharmacologic therapy directed at reducing triglycerides include fibrates, nicotinic acid, and fish oil. (See 'Pharmacologic therapy (including fish oil)' above.)
• For patients with mild to moderate hypertriglyceridemia (150 to 500 mg/dL [1.7 to 5.7 mmol/L]), and even in patients with triglyceride levels as high as 1000 mg/dL (11.3 mmol/L), the main indication for therapy is reduction of cardiovascular (CV) risk. In patients where the goal of therapy is CV risk reduction:

• Decisions about initiating pharmacologic therapy should be based on global cardiovascular risk. Nearly all patients with known coronary heart disease (CHD) or a CHD risk equivalent (table 4) will require therapy. (See "Treatment of lipids (including hypercholesterolemia) in primary prevention", section on 'Deciding whom to treat' and "Treatment of lipids (including hypercholesterolemia) in secondary prevention", section on 'Identification of patients at risk'.)
• For patients with a triglyceride level below 500 mg/dL (5.7 mmol/L) in whom pharmacologic therapy is indicated, we suggest treatment with a statin rather than an agent targeted at reduction of triglycerides (Grade 2B). Given the lack of high quality evidence directly comparing statin therapy with other treatment options, a reasonable alternative in such patients would be to treat them with fibrates, nicotinic acid, or fish oil. (See 'Mild to moderate hypertriglyceridemia' above.)
• In patients with CHD or a CHD risk equivalent (table 4) who have moderate hypertriglyceridemia (200 to 500 mg/dL [2.3 to 5.7 mmol/L]) and are intolerant of statin therapy, we suggest treatment with nicotinic acid or a fibrate (Grade 2C). Treatment with fish oil is a reasonable alternative. (See 'Mild to moderate hypertriglyceridemia' above.)
• For patients with a triglyceride level above 500 mg/dL (5.7 mmol/L) in whom pharmacologic therapy is indicated, we suggest treatment with a fibrate (such as fenofibrate), followed by the addition of a statin once the triglyceride levels are brought down (Grade 2C). Fish oil therapy is also an option. A reasonable alternative would be to treat lower-risk patients with a statin alone and to only add triglyceride-directed therapy in patients with CHD or a CHD risk equivalent (table 4). (See 'Severe hypertriglyceridemia' above.)

• In patients without a prior episode of pancreatitis, we suggest initiating pharmacologic therapy to reduce triglycerides with a goal of preventing pancreatitis when the level exceeds 1000 mg/dL (11.3 mmol/L) (Grade 2C). Even at this level of triglyceride elevation, the risk of pancreatitis appears to be quite small. Patients being treated for prevention of pancreatitis will often require combinations of triglyceride-lowering medications (ie, a fibrate, fish oil, nicotinic acid) to reduce the triglyceride level below 1000 mg/dL (11.3 mmol/L). (See 'Severe hypertriglyceridemia' above.)
• The management of patients with hypertriglyceridemia and acute pancreatitis and/or a prior episode of pancreatitis is discussed separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)

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HyperTAg causing Pancreatitis

Proposed approach to hypertriglyceridemic pancreatitis

Apheresis — Apheresis should be considered to remove triglycerides from serum if the patient does not have concurrent hyperglycemia and there are no contraindications, such as unstable vital signs or inability to tolerate central venous access.

Many case reports and series have described apheresis for HTGP [28-40]. One series of seven patients with an average level of 1406 mg/dL reported a 41 percent decrease in triglyceride levels after one plasma exchange session [35]. In another case report, triglycerides were lowered from 2410 to 138 mg/dL after three days of apheresis [40]. Neither report described the use of adjunctive therapy such as intravenous insulin, intravenous heparin, or oral statins.
The most common anticoagulant used during apheresis is heparin, but there are no data to recommend the appropriate apheresis replacement fluid (albumin versus fresh frozen plasma). When plasma exchange is compared with double membrane filtration apheresis, rates of removal of serum lipids have been lower with double membrane filtration apheresis [41].
The main concerns surrounding apheresis include cost and availability. After one cycle, serum triglyceride levels are re-checked and, if less than 500 mg/dL, apheresis is stopped. If the triglyceride rises (above 500 mg/dL), we generally re-treat with apheresis.
Early initiation of apheresis is likely to be beneficial. We generally proceed with apheresis as soon as possible. In a review of 10 patients with HTGP, nine patients received apheresis with IV heparin and insulin within 48 hours of the diagnosis of HTGP with successful outcomes [42].

Insulin — If apheresis is unavailable, if the patient cannot tolerate apheresis, or if the patient's serum glucose level is >500 mg/dL, we use intravenous insulin. Insulin decreases serum triglyceride levels by enhancing lipoprotein lipase activity, an enzyme that accelerates chylomicron metabolism to glycerol and fatty free acids [43,44]. Because HTGP often presents in patients with uncontrolled diabetes, insulin can decrease both triglyceride and glucose levels.

Intravenous insulin may be more effective than subcutaneous insulin in severe cases of HTGP [25,26]. Many regimens have been reported to lower triglyceride levels to less than 500 mg/dL over 3.5 to 4 days [25-27]. We typically initiate an intravenous infusion of regular insulin in 5 percent dextrose at a rate of 0.1 to 0.3 units/kg/hour to maintain blood sugar levels between 150 and 200 mg/dL.
Fingerstick glucose levels every four hours are suggested to ensure glucose control, and triglyceride levels should be monitored every 12 to 24 hours with adjustment of the insulin dosage as needed. Intravenous insulin should be stopped when triglyceride levels are <500 mg/dL, which typically occurs within several days.

Insulin and heparin — The role of heparin is controversial. Heparin stimulates the release of endothelial lipoprotein lipase into the circulation [45] and has been used without insulin to manage HTG [42,46,47]. Multiple case reports and series have described the use of heparin and insulin to lower HTG [21-24,48].

Studies have used varying doses of insulin and heparin administered by various routes [21,22,48]. As an example, in two reports subcutaneous heparin at 5000 units twice daily was used with intravenous insulin [22,48]. In both healthy volunteers and dialysis patients, low molecular weight heparin has been found to deplete lipoprotein lipase stores as efficiently as heparin and to retard the metabolism of triglyceride [49,50].
Despite the reported success of intravenous heparin in combination with insulin in HTG management, the use of heparin to treat HTGP has come under greater scrutiny. Heparin causes an initial rise in circulating lipoprotein lipase levels that is quickly followed by increased hepatic degradation of heparin [51]. This degradation contributes to further depletion of plasma stores of lipoprotein lipase and results in an increase of levels of chylomicrons [52]. The transient nature of the benefit seen with heparin raises question as to its use as monotherapy or in combination with insulin.

Antihyperlipidemic therapy — Antihyperlipidemic agents (eg, oral gemfibrozil 600 mg twice daily) should be initiated as adjuvant therapy in patients with HTGP. (See "Lipid lowering with fibric acid derivatives" and "Lipid lowering with diet or dietary supplements" and "Treatment of lipids (including hypercholesterolemia) in secondary prevention".)

Long-term therapy — Oral antihyperlipidemic agents and dietary fat restriction may be needed long-term to prevent recurrences of AP and prevent other complications of HTG. Periodic apheresis has been used with some success as continuing therapy after patients have recovered from their initial episode of AP, and particularly in patients who are noncompliant with diet and oral drug therapy [53]. (See "Lipid lowering with fibric acid derivatives" and "Lipid lowering with diet or dietary supplements" and "Treatment of lipids (including hypercholesterolemia) in secondary prevention".)

Pregnancy — The treatment of HTGP does not differ in pregnancy. Several case reports of gestational HTGP have described the use of apheresis [54,55], intravenous insulin and glucose with enteral restriction of triglyceride [56], intravenous heparin [42,46], low fat diet [57], and gemfibrozil. All resulted in the successful control of HTG and delivery of a healthy neonate

heart blog

http://blogs.theheart.org/private-practice/2011/8/24/adopting-dabigatran-pradaxa-the-pros-and-the-cons

Statin comparision

There are very good reasons to use rosuvastatin over atorvastatin.  Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor actitive metabolites (Lipitor has several very active metabolites), and Crestor is hydrophilic whereas Lipitor is not; hydrophilicity appears to minimize entry into muscles and minimizes muscle pain complaints.

Lipitor differs from simvastatin only in efficacy.  If you don't like simva you shouldn't like Lipitor.  Pravastatin, although the least potent, is not a 3A4 suThere are very good reasons to use rosuvastatin over atorvastatin.  Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor acbstrate and is hydrophilic.  It is a good first choice for many.

 with all the publicity over rhabdomyolysis at the 80 mg dose, the fact that simvastatin is markedly inferior to atorvastatin (both in hard endpoint trials like IDEAL and in 'softer' surrogate marker studies), and that simvastatin is by far and away the most prone to drug interactions through CYP3A4 of all the statins (witness the labelling revisions for amiodarone, verapamil, diltiazem on top of the previous litany of azole antifungals, antivirals, etc). Quite simply, this statin sucks! It is also the most myopathic of all the statins and the dose-response curve and renal clearance are worrisome. More than 40% of patients in SHARP discontinued it.

CO calculation usng Fick principle

http://www.josephsunny.com/medsoft/cardiology.html


Cardiac Output (Fick) in L/min = (135 ml O2/min/M2*BSA)/(13*Hgb*(SaO2-SvO2))

A commonly-used value for O₂ consumption at rest is 125 or 135 ml O₂ per minute per square meter of body surface area.

The calculation of the arterial and venous oxygen concentration of the blood is a straightforward process. Almost all oxygen in the blood is bound to hemoglobin molecules in the red blood cells. Measuring the content of hemoglobin in the blood and the percentage of saturation of hemoglobin (the oxygen saturation of the blood) is a simple process and is readily available to physicians. Using the fact that each gram of hemoglobin can carry 1.36 ml of O₂, the oxygen content of the blood (either arterial or venous) can be estimated by the following formula:

Assuming a hemoglobin concentration of 15g/dl and an oxygen saturation of 99%, the oxygen concentration of arterial blood is approximately 200ml of O₂ per litre.

The saturation of mixed venous blood is approximately 75% in health. Using this value in the above equation, the oxygen concentration of mixed venous blood is approximately 150ml of O₂ per litre.

management of Heart failure guidelines

http://content.onlinejacc.org/cgi/content/full/j.jacc.2008.11.009#SEC6c

T wave Abnormality

Diuretic resistance and its management

http://www.medscape.com/viewarticle/713934_3

Hypertensive emergency

Case: we had one patient presented with epistaxis from left nose and blood pressure of 210/130--------pt had nasal septum surgery 1 week back.....pt dint have any altered consciousness nor pappiloedema...U/a was normal...
Dx: As there is vascular injury but no end organ damage..so he has hypertensive urgency...
Rx: he was give hydralazin...bp came down to 160/100..... was given anterior nasal packing and Abx for nasal packing: ampi+sulbactam....
after 2 days he improved and was discharged...


A sudden rise in blood pressure to >180/120 mm Hg that is associated with end-organ damage is termed a hypertensive emergency

• Accelerated HTN is a sudden, marked elevation in blood pressure associated with end-organ damage but no papilledema (although retinal hemorrhage and exudates are often present).
• Malignant hypertension is a sudden, marked elevation in blood pressure accompanied by end-organ damage including papilledema.
• Hypertensive encephalopathy is a malignant HTN accompanied by cerebral edema, which presents with headache, nausea, vomiting, restlessness, and confusion.
  
  Hypertensive encephalopathy versus stroke: Onset is usually sudden in ischemic or hemorrhagic stroke but insidious in hypertensive encephalopathy..
  
  
  What is the difference between urgency and emergency?
  Urgency denotes severe hypertension (HTN), typically with diastolic blood pressure (DBP) > 130 mmHg, without symptoms or evidence of end-organ damage. The term accelerated hypertension falls in this category, where retinal exudates and hemorrhages are often present.
  Emergency is an acute, life-threatening elevation in BP with evidence of vascular injury + end-organ damage. The term malignant hypertension falls in this category, typified by papilledema.
  
  
  What causes the end-organ damage?Failure of autoregulation to regulate pressure in the arterioles and capillaries with increasing HTN results in disruption of the vascular endothelium. Fibrinoid necrosis results from deposition of plasma elements in the vascular wall, causing narrowing of the vascular lumen. Tissue ischemia as well as leakage of blood and plasma from affected vessels then results, causing end-organ damage.
  
  
  
  What is the treatment for specific hypertensive emergencies?
  

  Goal is the rapid lowering of mean arterial pressure by approximately 20-25% or to a DBP of 100-110 mmHg over 2-6 hours. However, in aortic dissection, the goal is to lower SBP to 100-120 mmHg and MAP below 80 mmHg ASAP, while patients with acute ischemic stroke or hypertensive encephalopathy may require slightly higher BP initially due to cerebral autoregulation.

  
  

  Malignant hypertension with retinal changes and/or hypertensive encephalopathy - Treatment of choice is a rapid, short-acting IV agent, such as nitroprusside (dose: 0.25-0.5 m g/kg/min to a max of 8-10 m g/kg/min; acts within seconds and lasts only a few minutes). Acts as both a veno- and vasodilator. Limited by cyanide or thiocyanate toxicity, especially with prolonged use or in renal insufficiency; do not use for more than 48 hours if possible (antidote is sodium thiosulfate). Other rapid-acting IV agents include labetolol (20mg IV bolus, 0.5-2 mg/min IV gtt), which is both an alpha- and beta-adrenergic blocker; and nicardipine (5-15 mg/hr IV gtt), which is a peripherally-acting calcium-channel antagonist. A newer medication, fenoldopam (0.1-1.6 m g/kg/min IV gtt), which is a pure dopamine agonist, has the advantage increasing renal blood flow and sodium excretion.

  What about hypertensive urgency?
  
  

  The goal is a reduction in blood pressure to 160/110 over several hours with conventional oral therapy. The oral medication used may vary with the clinical scenario - for example, beta-blockers and nitrates would be preferred in patients with coronary disease, while ACE-inhibitors might be useful in patients with a history of diabetes, scleroderma, or congestive heart failure. Loop diuretics are often very helpful initially in asymptomatic patients who are not volume-depleted. Nifedipine is generally not recommended due to rapid hypotension and possible precipitation of ischemic events, while clonidine often causes sedation and dry mouth as well as orthostatic hypotension and may require careful monitoring. There is no proven benefit in the rapid reduction of blood pressure in asymptomatic patients with severe HTN.

  
  

  
  

  check out this link for info: http://intmedweb.wfubmc.edu/blurbs/cards/hypertensive.html

Pericarditis vs STEMI

So what is a STEMI?
STEMI criteria:
The ST segment of an EKG will be elevated by more than 3 mm in the precordial leads and by more than 1 mm in the limb leads. Further, in the precordial leads, the shape should be convex up (like a tombstone). The shape matters more than the amount of elevation in some cases. You may have minimal elevation, but the shape is convex up, that could be considered a STEMI.
In the limb leads, the shape does not matter, just the elevation. Anything more than one small box, and you have a STEMI! Pretty straight forward. Unless, of course, it is an early repol!

So why do people get confused? And what is Early Repolarization?
There is an entity known as normal variant early repolarization that can give you ST segment elevation. But this is not a STEMI. It is a normal finding.
So how can you tell the difference? Look at the shape of the ST segment take off (the J point), it will usually be a notch and does not take off flat across. See the example below.

Above you see the first example on the right. The notch on the J point gives it away as early repol. In the far left example, you see the notch again in one of the precordial leads, usually V2 or V3. This is early repol, not a STEMI.
Here is an Early Repol EKG:


So what about pericarditis?
Pericarditis ST elevations look like the concave upwards ST elevations of early repol, but do not have the notch. Further, you may have PR segment depression in lead II. There will be no reciprocal changes or ST depressions anywhere.
 Good example of pericarditis EKG:
 
Notice the ST elevations all over the place with no reciprocal changes.
 Below is a good example of an Inferior STEMI.
 
Notice the reciprocal changes in the anterior leads. You see depressions. While it is not necessary to have reciprocal changes, they can happen, and it helps clinch your diagnosis.
Below is an anterior STEMI, without reciprocal changes.

 Below is another Anterior STEMI with the perfect tombstone pattern. No reciprocal changes.

 Here is a nice table comparing the various EKG findings in STEMI, early repol, and pericarditis.

Comparison of ECG Changes Associated with Acute Pericarditis, Myocardial Infarction and Early Repolarization
ECG finding	Acute pericarditis	Myocardial infarction	Early repolarization
ST-segment shape	Concave upward	Convex upward	Concave upward
Q waves	Absent	Sometimes Present	Absent
Reciprocal ST-segment changes	Absent	Sometimes Present	Absent
Location of ST-segment elevation	Limb and precordial leads	Area of involved artery	Limb and Precordial leads
ST/T ratio in lead V6*	>0.25	N/A	<0.25
Loss of R-wave voltage	Absent	Present	Absent
PR-segment depression	Sometimes in Lead II	Absent	Absent

If you are unsure if it is a STEMI or not, KEEP GETTING EKGs! PLASTER THE WALLS WITH EKG PAPER! STEMIs evolve! They don't look the same. If you have 10 EKGs in the last hour, and they all look the same.... it's not a STEMI!