KNOWLEDGE IS EVERYTHING (doctor blog)

 LEFT AXIS DEVIATION SIMPLE CONCEPT:  QRS-COMPLEX : (LEAD-1) AND (LEAD aVL) - [POSITIVE]                                                                   : (LEAD- 2, 3, aVF) - [NEGATIVE] RIGHT AXIS DEVIATION SIMPLE CONCEPT:  QES COMPLEX : (LEAD-1) AND (LEAD aVL) - [NEGATIVE] {S-WAVE GREATER THAN R-WAVE}.                                                                 : (LEAD- 2, 3, aVF) - [POSITIVE] CAUSES OF AXIS DEVIATION:  RIGHT AXIS DEVIATION: 1) NORMAL VARIANT-TALL THIN PEOPLE. 2) RIGHT VENTRICULAR HYPERTROPHY. 3) LATERAL MYOCARDIAL INFARCTION ( PERI-INFARCTION BLOCK). 4) WPW SYNDROME. 5) LEFT POSTERIOR FASCICULAR BLOCK. LEFT AXIS DEVIATION: 1) LEFT ANTERIOR HEMIBLOCK. 2) WPW SYNDROME. 3) INF. MI (PERI-INFARCTION BLOCK) 4) VENTRICULAR TACHYCARDIA.                             

 WOLFF-PARKINSON-WHITE SYNDROME (WPW) BASICS SIMPLE CONCEPT:  PR-INTERVAL (SHORT).                                    DELTA WAVE.                                    QRS COMPLEX (LONG) OVERVIEW: THE ONLY NORMAL ELECTRICAL CONNECTION BETWEEN THE ATRIA AND VENTRICLES IS THE HIS BUNDLE  . SOME PEOPLE, HOWEVER, HAVE AN EXTRA (OR) "ACCESSORY" CONDUCTING BUNDLE, A CONDITION KNOWN AS THE WPW SYNDROME. THE ACCESSORY BUNDLES FORM A DIRECT CONNECTION BETWEEN THE ATRIUM AND THE VENTRICLE, USUALLY ON THE LEFT SIDE OF THE HEART, AND IN THESE BUNDLES THERE IS NO (AV-NODE) TO DELAY CONDUCTION. A DEPOLARIZATION WAVE THEREFORE  REACHES THE VENTRICLE EARLY AND PRE-EXCITATION OCCURS. PR-INTERVAL SHORT, AND THE QRS COMPLEX SHOWS AN EARLY SLURRED UPSTROKE CALLED A "DELTA WAVE". THE SECOND PART OF QRS IS NORMAL, AS CONDUCTION THROUGH THE HIS BUNDLE CATCHES UP WITH THE PRE-EXCITATION. NOTE:  SINUS RHYTHM, RIGHT AXIS DEVIATION, SHORT PR-INTERVAL.              SLURRED UPSTROKE OF THE QRS COM

RIGHT VENTRICULAR HYPERTROPHY BASICS ECG CHANGES IN RIGHT VENTRICULAR HYPERTROPHY (RVH) SIMPLE CONCEPT: 1. RIGHT AXIS DEVIATION. 2. TALL R-WAVE IN RIGHT VENTRICLE LEADS. 3. DEEP S-WAVE IN LEFT VENTRICLE LEADS. OVERVIEW: RVH IS BEST SEEN IN THE RIGHT VENTRICULAR LEADS (ESPECIALLY V1). SINCE, THE LEFT VENTRICLE DOES NOT HAVE ITS USUAL DOMINANT EFFECT ON THE QRS SHAPE, THE COMPLEX IN LEAD V1 BECOMES UPRIGHT ( i.e. THE HEIGHT OF THE R-WAVE EXCEEDS THE DEPTH OF THE S-WAVE) . THIS IS NEARLY ALWAYS ABNORMAL.  THERE WILL BE A DEEP S-WAVE IN LEAD V6.  RIGHT VENTRICULAR HYPERTROPHY IS USUALLY ACCOMPANIED BY RIGHT AXIS DEVIATION, BY A PEAK P-WAVE ( RIGHT ATRIAL HYPERTROPHY), AND IN SEVERE CASES BY INVERSION OF THE T-WAVES IN LEADS V1-V4 AND LEADS 2,3 AND aVf. NOTE:  1) SINUS RHYTHM , RIGHT AXIS DEVIATION .              2) DOMINANT R-WAVES IN LEAD V1.              3) DEEP S-WAVES IN LEAD V6.              4) INVERTED T-WAVES IN LEADS 2,3 aVf, AND V1-V3              5) FLAT T-WAVES IN LEADS V4-V5.  

 LEFT VENTRICULAR HYPERTROPHY (LVH) BASICS ECG CHANGES IN LVH SIMPLE CONCEPT:  IN LEAD AVL - TALL (R-WAVE) -  > 11 mm (greater than 11mm, it's consider LVH) TALL (R-WAVE) IN V5-V6 AND DEEP (S-WAVE) IN V1  (some of this greater than 35mm, then the patient has LVH) E.G:  COUNT (R-WAVE) IN V5 = 25mm  AND COUNT (S-WAVE) IN V1 = 20mm  (together we have 45mm)  [ANYTHING GREATER THAN 35 mm, it's consider LVH] NOTE:  1) SINUS RHYTHM, RATE 83/MIN AND NORMAL AXIS.              2) TALL R-WAVE IN LEADS V5-V6 (R-wave in lead v5, 40mm) AND DEEP S- WAVES IN                      LEADS V1-V2.              3) INVERTED T-WAVES IN LEADS 1,VL AND V5-V6. OVERVIEW: LEFT VENTRICULAR HYPERTROPHY CAUSES A TALL R-WAVE (GREATER THAN 25mm) IN LEAD V5 (OR) V6 AND DEEP S-WAVE IN V1 (OR) V2, BUT IN PRACTICE SUCH "VOLTAGE" CHANGES ALONE ARE UNHELPFUL IN DIAGNOSING LVH.  WITH SIGNIFICANT HYPERTROPHY, THERE ARE ALSO INVERTED T-WAVE IN LEADS [1, AVL, V5-V6] AND THERE MAY BE LEFT AXIS DEVIATION. IT IS

 DIGOXIN - CARDIAC GLYCOSIDES ( BASICS ) HELPS,THE HEART TO PUMP MORE EFFICIENTLY, INHIBITS NORMAL FUNCTION OF Na+/K+ PUMP. HOW DOES IT AFFECTS THE HEART[ POSITIVE AND NEGATIVE EFFECTS] POSITIVE: INOTROPIC EFFECT ON THE HEART: SQEEZES/CONTRACTS HARDER. NEGATIVE:  CHRONOTROPIC EFFECT ON THE HEART: BEATS SLOWER. NEGATIVE:  DROMOTROPIC EFFECT ON THE HEART; SLOWS IMPULSES SENT THROUGH                          AV NODE RESULTS;   HEART SQEEZES MORE BLOOD OUT = INCREASED STROKE VOLUME = INCREASED CARDIAC OUTPUT DRUG USED FOR: HEART FAILURE, CARDIOGENIC SHOCK, A.FIB, A.FLUTTER. EFFECT ON ECG: THE ADMINISTRATION OF DIGOXIN CAUSES (T-WAVE) INVERSION - CHARACTERISTICALLY WITH SLOPING DEPRESSION OF THE ST SEGMENT. IT IS HELPFUL TO RECORD AN ECG BEFORE GIVING DIGOXIN, TO SAVE LATER CONFUSION ABOUT THE SIGNIFICANCE OF T-WAVE CHANGES. THERAPEUTIC: 0.5 - 2 ng/ml (ANYTHING GREATER THAN  2ng  IT'S CONSIDER TOXIC) ANTIDOTE : DIGIBIND

  PULMONARY EMBOLISM PULMONARY EMBOLISM IS A BLOCKAGE IN ONE OF THE PULMONARY  ARTERIES IN YOUR LUNG. OFTEN PRESENT AS A COMBINATION OF CHEST PAIN AND BREATHLESSNESS. ALTHOUGH THE CHEST PAIN IS  CHARACTERISTICALLY ONE-SIDED AND PLEURITIC, A MAJOR EMBOLUS AFFECTING THE MAIN PULMONARY ARTERIES MAY CAUSE PAIN RESEMBLING THAT OF MYOCARDIAL INFARCTION. PATIENT WITH PULMONARY HYPERTENSION USUALLY COMPLAIN OF BREATHLESSNESS BUT NOT PAIN. WITH PULMONARY EMBOLISM THE MOST COMMON ECG FINDING IS SINUS TACHYCARDIA WITH NO OTHER ABNORMALITY. SO, THE ECG IS NOT A VERY USEFUL DIAGNOSTIC TOOL, HOWEVER THE APPEARANCE OF RIGHT BUNDLE BRANCH BLOCK (OR) THE CHANGES ASSOCIATED WITH RIGHT VENTRICULAR HYPERTROPHY [ RIGHT AXIS DEVIATION, A DOMINANT R WAVE IN LEAD V1, AND T WAVE INVERSION IN LEADS V1-V3] WOULD STRONGLY SUPPORT THE DIAGNOSIS. WHEN PULMONARY EMBOLISM SUSPECTED, LOOK FOR ANY OF THE FOLLOWING: 1. PEAKED P WAVES. 2.RIGHT AXIS DEVIATION (S WAVES IN LEAD 1). 3. TALL R WAVES IN LEAD V1. 4. RIGHT BUNDL

ATRIAL FIBRILLATION   WHEN THE ATRIAL MUSCLE FIBRES CONTRACT INDEPENDENTLY THERE ARE NO (P WAVES) ON THE ECG, ONLY AN IRREGULAR LINE. AT TIMES THERE MAY BE FLUTTER- LIKE WAVES FOR 2-3 SEC. THE AV NODE IS CONTINUOUSLY BOMBARDED WITH DEPOLARIZATION WAVES OF VARYING STRENGTH  AND DEPOLARIZATION SPREADS AT IRREGULAR INTERVALS DOWN THE HIS BUNDLE. THE AV NODE CONDUCTS IN AN "ALL (OR) NONE" FORMATION, SO THAT THE DEPOLARIZATION WAVES PASSING INTO THE HIS BUNDLE ARE CONSTANT INTENSITY. HOWEVER, THESE WAVES ARE IRREGULAR  AND THE VENTRICLES THEREFORE CONTRACT IRREGULARLY. BECAUSE CONDUCTION INTO AND THROUGH THE VENTRICLES IS BY THE NORMAL ROUTE, EACH QRS COMPLEX IS OF NORMAL SHAPE. FIBRILLATION WAVES CAN AFTER BE SEEN MUCH BETTER IN SOME LEADS [ 2ND AND V1  ] NOTE:  NO P WAVES.              IRREGULAR BASELINE.               IRREGULAR QRS COMPLEXES, RATE VARYING BETWEEN 75/MIN AND 190/MIN.              NARROW QRS COMPLEXES OF NORMAL SHAPE.              DEPRESSED ST-SEGMENTS IN LEADS V

 SVT (ATRIAL TACHYCARDIA) BASICS [ABNORMAL FOCUS IN THE ATRIUM]  ATRIA DEPOLARIZE FASTER THAN 150/MIN. THE AV NODE CANNOT CONDUCT ATRAIL RATES OF DISCHARGE GREATER THAN 200/MIN, IF THE ATRIAL  RATE IS FASTER THAN THIS, " ATRIVENTRICULAR BLOCK  "OCCURS, WITH SOME P WAVES NOT FOLLOWED BY QRS COMPLEXES.  THE DIFFERENCE BETWEEN THIS SORT OF ATRIOVENTICULAR BLOCK AND SECOND DEGREE HEART BLOCK IS THAT ATRIOVENTRICULAR BLOCK ASSOCIATED WITH TACHYCARDIA THE AV NODE IS FUNCTIONING PROPERLY - IT IS PREVENTING THE VENTRICLES FROM BEING ACTIVATED AT A FAST RATE. IN FIRST, SECOND (OR) THIRD DEGREE HEART BLOCK ASSOCIATED WITH SINUS RHYTHM, THE AV NODE ( OR ) THE HIS BUNDLE ARE NOT CONDUCTING NORMALLY. NOTE:  AFTER 3 SINUS BEATS, ATRIAL TACHYCARDIA DEVELOPS AT A RATE OF 150/MIN.             P WAVES CAN BE SEEN SUPER IMPOSED ON THE T WAVES OF THE PRECEDING BEATS.             THE QRS COMPLEXES HAVE THE SAME SHAPE  AS THOSE OF THE SINUS BEATS. SIMPLE CONCEPT:   ABSENT P WAVE  - REGULAR  - SVT