Volume loading is required for the management of acute Right Ventricular infarction, specially in patients with arterial hypotension. More critical, RV infarction and failure is at the bottom of hemodynamic basis in myocardial infraction shock, when the severe depressed RV output explains the reversion of pulmonary congestion or edema as well the hypotension states.

•Patients suffering from RVMIappears to be verysensitivefor changes in volume status.

•In patients with RVMI and low cardiac output/hypotension, low CVP, and no pulmonary congestion it is prudent to administer boluses of normal saline (200 cc) reaching a maximal of 1.5 ltr. (voluvenis frequently administered in the cathlab)

•This group of patients may be simply suffering from a lowcirculating volumestatus.

•In case of no response on this initial “fluid challenge”, invasive monitoring of CVP should be considered.

•CVP 14mmHgmodest dose diuretics/±venodilators(beside dobuen LV unloading). ( See also the attached PDF file).

Let me update the physiology and hemodynamics in Acute Myocardial Infarction (AMI) Cardiogenic Shock (CS), as a Clinical research investigator

a) 1975-76: Our research at William Likoff Cardiovascular Institute (Hahnemann Medical College and Hospital of Philadelphia): First, prospective study of CS in Post-op of coronary bypass surgery, with evidence of intra-operatory evidence of RV-AMI, and post-op CS.

In brief, RV-AMI was involved in all episodes of CS, explaining the absence of pulmonary edema (RV-IAM), and RX-regression of pulmonary edema (RV and LV-AMI) simultaneously with the episode of hypotension. Improved survival 69%.  

Antonio Delgado Almeida. Deborah Young Investigator Award, Deborah Hospital Foundation, NJ, USA, 1976. 

b) 1978-1983: Founder and Director, Intensive Care Unit, Adolfo Prince Lara, MD Hospital, University of Carabobo Medical School. The same approach with some unexplained failures. We developed new method for RBC-K content, monitoring the large cell K fraction, and safety infusion of G-I-K (Sodi-Pallares solution), while new method for ionized calcium, sharply decreased in metabolic acidosis of CS, while reversion of ionized hypocalcemia rapidly improved LV C.O, and shock: Two novel points in the treatment of AMI and CS.

c) 1983-present: Discovery of an inherited defect in RBC-K content in hypertensives and 48% of their normotensive sibling and offspring, and the simultaneous RBC-K and O2 binding by human hemoglobin (2012) change the prevention, diagnosis and treatment of hypertension and related CVD. Since then, the improved of this genetic defect was associated to rapid BP control and ST-T alteration of ischemia.

In brief, treatment of hypertension and coronary heart disease with Amiloride HCl Dihydrate, have simply vanished complication of CHD as CS, hoping to be in the future worldwide!

Sorry, for this extensive response, I was simple immerse on the request from APS Living History Program, invitation for an interview videotape, received at Dec. 05, 2014.