When “Science of Medicine” Kneeling for the respect of “Art of medicine”

ژمانیکه “علم طب” به حرمت “هنرطب” زانو می زند !!!Image
در تطبیقات روزانه عملی طبی ، کتاب های غربی هم دورغگو هستند ، عمل ، عمل و عمل باید کرد تا پخته شود ، خامی !!!
دوستان علاقمند میتوانند به بیان یک واقعه جالب حمله قلبی که در کابل واقع شد ، زیر نظر من ، و آنرا در صفحه طبی ذیل شریک ساختم مستفید شوند .البته به زبان انگریزی است و بحث به کلی تخصصی !!!
Explanation of Case # 5 !( please see the two days back question about ECG strip case # 5)
Thanks to all Dear Participant Responses 
Written by :
Dr.Nabil Paktin, MD.FACC.
when the “Sciences of Medicine” Kneeling for 

respect of “Art of Medicine”
How its possible HTN in RVWMI , ??? Crazy concepts in Medicine, that is why we must Practice Practice and Practice!!! Books Are great liars sometimes in daily Practice. !!! Because two patient of the same disease have not the same clinic , due to that experience based medicine is favored and we should not treat the “Book” but we should treat the patient . 
Diagnosis : RVWMI ( Extensive RVWMI) , First degree AV block , HTN urgency . 
Severe persistent HTN+RVWMI ???????
General Concept about RWMI: 
1) Right ventricular infarction occurs in approximately 20% of patients with an inferior wall ST-elevation myocardial infarction (STEMI). Although ischemia of the right ventricle may occur in a high percentage of patients with inferior ST-elevation myocardial infarction (STEMI), only 10% to 15% develop right ventricular myocardial infarction with hemodynamic abnormalities. These patients have a significantly higher in-hospital mortality rate (25%-30%) compared with patients with inferior STEMI without right ventricular infarction, and thus these patients should receive reperfusion therapy. 
2) If the initial ECG confirms the diagnosis of acute Inferior MI , right-sided Precordial leads should be recorded immediately . this is a class I indication according to the 2004 ACC/AHA guidelines on ST elevation MI . If right sided Precordial leads are not Immediately recorded , ST elevation in the right Precordial leads may disappear within 10 hours after symptom onset in approximately half of patient with RVMI . 
3) Right sided Precordial leads are recorded by repositioning the Precordial leads V3,V4,V5, and v6 to the right side of the chest in the same standard location as that on the left . Right sided Precordial leads are not routinely recorded if there is no evidence of Acute inferior wall MI . Any ST elevation ≥ 1mm in any of the right sided Precordial leads V3R to V6R is consistent with RVMI . these leads , especially V4R , are the most SENSITIVE and most SPECIFIC for the diagnosis of RVMI . very often , right sided Precordial leads are not recorded at the time of entry . these leads are special leads and are not routine in a regular 12 leads ECG. Even if they wer recorded , they may be recorded much later and not within the limited time window in which RVMI can be diagnosed . RVMI can be suspected if the initial standard 12 lead ECG will show he following changes . 
– ST elevation in leads III is greater than lead II: this suggests that the RCA ( and not the LCx ) , is the cause of the inferior MI . 
– ST elevation is present in V1 : although V1 is not very sensitive lead for the diagnosis of RVWMI when compared with V4R, v1 is also a right-sided Precordial leads . thus , ST elevation in V1 during acute inferior MI may be the only indication that an RVMI is present if right –sided Precordial leads were not recorded in the ECG . the ST elevation may extend to V3 resembling anterior MI . RVMI is predominantly a complication of inferior myocardial infarction. In patients with anterior left ventricular infarction, ST segment elevation was the lowest in lead V1, increasing in amplitude toward lead V5. On the other hand, patients with an occluded RCA and RV infarction displayed the greatest amplitude of ST segment elevation in lead V1, which progressively decreased toward lead V5. The right ventricle is a unique chamber of the heart . It is the anterior most chamber and triangular in shape. Even though the walls of RV are not clearly demarcated , it does have anterior , posterior, and lateral free surfaces . Anatomically it has a inflow body, apex and outflow portions . The apex of right ventricle , blends with the lower IVS at an acute angle.
What happens in RVMI ?
Unfortunately, when we refer to RVMI , we generally do not make any efforts to locate or estimate it’s size. Since RV has , anterior , lateral and posterior surface , the site and the extent of the mI will have a major impact on the ECG features . Most often the RVMI occur as a part of infero posterior MI .Hence , it is uncommon for the anterior surface of RV to get involved. But , it can be involved if RCA gives of a large RV branch that reach the anterior surface of RV.Anterior RVMI can occur as a part of LAD MI , if a large conal branch cross the RV surface.
What prevents the lead V1 from showing the ST elevation of RVMI ?
• Most of the RVMI do not involve the anterior surface of the RV so , less chances for ST elevation 
• Further , if a true posterior wall MI occur as a part of RVMI (Which is often the case !) V1 can never show ST elevation as the posterior MI tend to have a ST depressing effect in the V1, V2 leads.
• Extensive IWMI , can have reciprocal ST depression in V1-V2.This again , prevents V1 lead to show the ST elevation. So many times , even though V1 lead is just sitting over the chamber RV it fails to pick the ST elevation forces of RVMI.
• When can V1 show ST elevation in RVMI ?
• If the RV anterior wall is predominantly involved (Ie Anterior RVMI ) ST elevation can occur in V 1 like a anteroseptal MI.
RVMI is possible only when the proximal RCA is occluded . It does not occur when the distal RCA or LCx coronary artery is involved . this is important prognostically because occlusion of the proximal RCA usually implies the presence of a larger infarct and is associated with a high incidence of AV nodal block when compared to occlusion of a nondominant LCx or distal RCA . 
ST – elevation and T-wave configuration in lead V4R in Inferoposterior AMI will bring variable changes with variable meaning , proximal occlusion of the RCA produces ST-elevation >1mm and a Positive T wave . Distal occlusion is characterized by a positive T –wave but no ST-elevation . occlusion of the LCx artery produces a negative T-wave and ST-depression if at least 1mm. 
4) RVWMI have a traditional triad of hypotension , JVD and clear lung . this is highly specific and poorly sensitive . Inferior wall MI’s commonly lead to two types of heart block (via mechanism of damage to autonomic fibers in the atrial septum giving increased vagal tone impairing AV node conduction ) First degree AV block and Mobitz Type I (Wenckebach) second degree AV block. Sinus bradycardia can also occur. Progression to complete AV block is not common. Conduction disturbances are more common in patient with RVWMI . if hemodynamic stability is maintained , patients with these conduction disturbances do not require pacemaker and they often respond to the administration of atropine (0.5mg) IV.if hemodynamic compromise occurs in association with either Wenckebach block or junctional rhythm , however or if any arrhythmia requires treatment with more than one dose of atropine , a transvenous pacemaker is warranted . large initial or total doses of atropine can lead to tachycardia with exacerbation of ischemia and at times VT or VF . for patients with RVMI and hemodynamic compromise associated with the loss of atrial kick , and AV sequential pacemaker is recommended . in general , Hemodynamically significant conduction disturbances occur in patients with inferior infarction early during the evolution of infarction , late conduction disturbances are usually well tolerated . some of these conduction respond to an IV infusion of 250mg of aminophyline . 13
Inferior wall MI is notorious to be associate with hypotension and this hypotension is caused by sever right ventricular infarction , bradyarrhythmia , acute sever MR , prior MI , left ventricular septal wall rupture , bezold-jarish reflex . 12
Volume expansion is the primary supportive treatment for the hemodynamic abnormalities of a right ventricular myocardial infarction. Although ischemia of the right ventricle may occur in a high percentage of patients with inferior ST-elevation myocardial infarction (STEMI), only 10% to 15% develop right ventricular myocardial infarction with hemodynamic abnormalities. In the setting of right ventricular myocardial infarction, right ventricular contractility is reduced, resulting in higher right ventricular diastolic pressure, lower right ventricular systolic pressure, and reduced preload or filling of the left ventricle. Volume expansion improves the hemodynamic abnormalities of right ventricular myocardial infarction because the gradient of pressure from the right atrium to the left atrium maintains filling of the left ventricle. In addition to reperfusion therapy for STEMI, the acute treatment of right ventricular myocardial infarction is supportive. Inotropic support, specifically using intravenous dobutamine, is appropriate treatment in patients with right ventricular myocardial infarction whose hypotension is not corrected after 1 L of saline infusion. However, volume expansion should be tried before giving inotropic agents. Bradycardia, potentially caused by increased vagal activity or sinoatrial node ischemia, exacerbates the hemodynamic abnormalities of right ventricular myocardial infarction, so β-blocker therapy is contraindicated in this patient. Nitroglycerin is contraindicated in patients with right ventricular myocardial infarction because of the potential for venodilation and hypotension. 1
this patient came with chest pain and HTN urgency , after taking ECG , we found Inf wall STEMI and then recommended for right Precordial leads , and we found the Proximal occlusion of RCA that causes RVMI , and V1 st elevation is also due to RCA occlusion and infarction of anterior wall of Right ventricle otherwise should give st depression due to reciprocal change of Inferior wall stemi or separated Inferoposterior wall infarction , first hours the Biomarkers was normal , after two hours rechecking of Biomarkers , were elevated . and Echocardiography shown RV regional wall abnormalities . but still the traditional triad of hypotension , JVD and clear lung were negative however its poorly sensitive . In physical examination just there was sings of right sided S3 and AV block . In contrast to traditional ECG criteria that the Q wave is the sign of old or evolved phase MI , from clinical standpoints and management guideline indications never ever presence of Q wave by itself is avoiding us to withhold reperfusion and PCI, because patient has severe high risk chest pain together with HTN. So how ever with RVMI the HTN is not mentioned in literatures, as a fact that we are all witness in contrast of traditional protocols we managed it with Na nitroprusside cautiously plus morphine, ACE inhibitor however it he had resistant HTN we gradually lowered it and then start reperfusion therapy, after stabilizing the patient and seeing result patient well controlled by our management and we got decision to find the secondary cause of HTN., and referred for more infestations.

About Dr.Nabil Paktin

Cardiologist , M.D.,F.A.C.C.

Posted on November 15, 2012, in Uncategorized. Bookmark the permalink. Leave a comment.

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