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The Oswald Shot

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The Oswald shot from Ruby has always bothered me. JFK got it in the head and RFK got it in the head....but Oswald got it in the belly (or thereabouts) and was shot by a fairly pedestrian revolver (a .38). He was also shot within a couple miles from a hospital. Basically a gutshot will kill you (without surgery) in anywhere between some hours and a few days (depending on which blood vessels are hit) without surgery. A liver shot can be terminal in a few hours but LHO was obviously shot in the right side and turned that way..so a liver shot is out of the question...so he was basically gutshot middle-right..with a fairly small calibre revolver....one time.

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According to the Doctors at Parkland it was a fatal wound that there were few survivors of in 1963 due to the liver, kidney and spleen damage.

The more interesting question for me is, did the emergency procedures performed on him by the Dallas Police actual finish Lee Oswald off?

Indeed, Lee, and if not necessarily so, ensure his demise.

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It did do some fairly substantial damage. Are you saying it should have been non fatal?


You have asked an almost completely overlooked, yet poignant question.

When surgery was completed on LHO he was assumed to be in relatively stable and good condition.

And, he was being purportedly cared for as such.

Then, with absolutely no prior warning, his situation suddenly reversed and he immediately became critical and died shortly thereafter from loss of blood.

So! Highly suspicious or highly incompetent------take your choice.

P.S. Might want to check into exactly who was the "attending" on that one too.


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When surgery was completed on LHO he was assumed to be in relatively stable and good condition.

And, he was being purportedly cared for as such.

Then, with absolutely no prior warning, his situation suddenly reversed and he immediately became critical and died shortly thereafter from loss of blood.

So! Highly suspicious or highly incompetent------take your choice.

P.S. Might want to check into exactly who was the "attending" on that one too.

According to Dr. Charles Crenshaw, "Oswald did not die from damaged internal organs, he died from the chemical imbalances of hemorrhagic shock."

Crenshaw pointed out that "Parkland had superlative surgeons, state of the art equipment, and it was an early Mecca of medical research for trauma.

I'm convinced beyond any doubt that President Kennedy or Lee Harvey Oswald, in the same condition we received them at Parkland, would have died at

any hospital in the world."

For a detailed description of the efforts to save Oswald's life see Crenshaw's book:


If one believes Crenshaw's account, (and in absence of any conflicting evidence there is no reason not to) Oswald was never in "relatively stable and good condition."

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see page 135. For 30 odd minutes very little blood circulated in Oswald, this led to the hemmorhagic shock. He did not die from damaged internal organs.They thoroughly believed they could have saved him.

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oops hit the wrong key meant 20 odd. Thank you for your vigilance, Michael.

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Ok, I won't.

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I wasn't quoting, could is short for had a chance. And stick your insults where the sun don't shine.

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see page 135. For 30* odd minutes very little blood circulated in Oswald, this led to the hemmorhagic shock. He did not die from damaged internal organs.They thoroughly believed they could have saved him.

edit : correction: 20*

edit add *

Edited by John Dolva
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see page 135. For 30 odd minutes very little blood circulated in Oswald, this led to the hemmorhagic shock. He did not die from damaged internal organs.They thoroughly believed they could have saved him.

"hemmorhagic shock"




In hemorrhagic shock, an acute reduction in blood volume leads

to sympathetic compensation by peripheral vasoconstriction,

tachycardia, and increased myocardial contractility, which in

turn increases the myocardial demand for oxygen, to a level that

cannot be maintained.1 Simultaneously, tissue hypoperfusion

from precapillary vasoconstriction leads to anaerobic metabolism

and acidosis.11 Tissue hypoxia, acidosis, and the release of

various mediators lead to a systemic inflammatory response.5,11





SHIRES, G.T. and HOLMAN, J. "Dilutional Acidosis". Ann. Intern. Med. 28, 557; 1948. (Acidosis due to I.V. Fluids).






Clinical problems of pH are all related to pH of the plasma of whole blood. pH in extracellular fluid is always close to that of blood. pH inside cells differs from that of blood but it is not recognised as being an important clinical problem apart from blood pH changes.

In the clinical situation if the actual pH of the blood is lowered, one can usually assume that the primary disturbance has been the addition to the blood of acid or the removal of base and vice versa.


Blood pH may be changed if acids or bases are added to or removed from the blood. Secretion of an acid (e.g. gastric juice) implies that the acid involved (HCl in this case) is removed from the blood.

The acids which can cause changes in blood pH are: Metabolic





Lactic Acid


Drug Induced


Might be called "true" metabolic acidoses

Keto Acids




Sulphuric Acid

Inorganic acids, increase in renal failure

Phosphoric Acid

Hydrochloric Acid



Organic only

Carbonic Acid

A rise in concentration of any of these acids in the blood causes a fall in the pH of the blood. Loss of acid from the blood (e.g. into gastric juice) causes a rise in the pH. Only HCl and H2CO3 can be lost from the blood in appreciable quantities.

The bases which can cause changes in blood pH are:



Administration of base by mouth or parenterally may cause blood pH to rise if rate of excretion does not match rate of administration. Loss of alkaline fluid from bowel (diarrhoea, intestinal obstruction or intestinal fistulae), or urine (after acetoazolamide) will cause blood pH to fall.


Clinical states of pH disturbence (acid-base inbalance) can conveniently be divided into two groups, i.e. (a)respiratory and (b)metabolic or non-respiratory. The reasons for this division into respiratory and non-respiratory are that:

i) the compensatory mechanisms (Section 3.5.1) and treatments (Section 7) of the two types are different.;

ii) the recognition of non-respiratory disturbances is masked by compensatory alterations in PCO2 and the recognition of changes in pH caused by PCO2 changes are masked by renal compensation.

6.3.1 RESPIRATORY ACIDOSIS. This is synonymous with CO2 retention and is usually a sign of hypoventilation. Compensation is renal. There is renal loss HCl in the form of buffer or as NH4Cl. During recvovery chloride has to be supplied and retained. Causes of hypoventilation:

Central nervous system

Peripheral nervous system

Neuromuscular transmission

Muscle disorders

Chest wall abnormalities

Lung and airway disorders. Inhalational of CO2 This is another cause of respiratory acidosis, but it is only likely to occur under situations of re-breathing, e.g. under anaesthesia or during resuscitation with a Water's cannister circuit without the cannister, i.e. ward resuscitators or Type C anaesthetic systems. (Mapleson, 1954). Increased production of CO2. This very rarely causes a high PaCO2. In thyrotoxicosis and fever CO2 production is raised but the rise is well within the capacity of a normal respiratory system. In malignant hyperpyrexia high PaCO2s have been recorded due undoubtedly to increased production.

NaHCO2 therapy in non-respiratory acidosis causes a rise in PaCO2 until the CO2 generated by the neutralization of HCO3- has been excreted (Singer et al, 1956). This effect may be prolonged if CO2 excretion is impaired (Ostrea and Odell, 1972).

Acute respiratory acidosis is diagnosed by high PaCO2 and low actual pH associated with near normal non-respiratory pH, (standard HCO3-and base excess). (See Appendix 4.2).

Chronic respiratory acidosis is compensated by loss of H+Cl- by the kidney and generation (not reabsorption) of (Na+) HCO3-. (See Appendix 3.4). Compensation causes slightly lowered actual pH with a high non-respiratory pH (positive base excess and high standard HCO3-). Steroids and diuretics (except acetazolamide (Diamox) ) may produce a non-respiratory alkalosis which may cause a respiratory acidosis to appear to be "over compensated". There will then be a high (actual) pH.

In chronic respiratory failure ventilation is maintained by hypoxic drive and also by the acid pH of the blood. If the pH stimulus is removed by the actual pH being raised, some of the respiratory drive will be removed causing a diminution of respiratory effort and further CO2 retention.

When a chronic respiratory acidosis (with compensation, i.e. high non-respiratory pH, Base excess, and Standard HCO3-.) is improved by increasing alveolar ventilation the actual pH may rise above 7.4. The resulting chemical picture of high pH, high non-respiratory pH (positive base excess), and high PaCO2 is indistinguishable chemically from a primary metabolic alkalosis with compensatory CO2 retention. Clinical information is required to distinguish them. (Plot this and other examples on a standard Siggaard-Andersen nomogram as an exercise). ( See Footnote to table 4.2.2.)

N.B. The compensatory renal or respiratory changes which partially correct pH disturbances are chemically true pH changes in the opposite direction to the original disturbances. It is a semantic problem whether the compensatory renal change induced for example by primary chronic CO2 retention is called a metabolic alkalosis or not. This semantic muddle can be avoided if the term alkalosis is used only in a non-precise term.

6.3.2. RESPIRATORY ALKALOSIS. This is associated with hyperventilation. Usually these are acute so there is no time for renal compensation, but if prolonged, such as in acclimatization to high altitudes, there would probably be renal compensation. Deliberate induced hyperventilation during anaesthesia. Some causes of hypoxia associated with hyperventilation. This would include "air hunger" of hypovolaemia, severe ventilation-perfusion abnormalities and acclimatization to high altitudes. Critically ill patients without arterial hypoxaemia can have severe hypocapnia (Mazzara et al,1974). This may be explained by low cardiac output.

In asthma attacks, unless severe, the PaCO2 is usually lowered, i.e. the alveolar ventilation is increased (McFadden and Lyons, 1968). This is at least sometimes associated with hypoxaemia due to mismatching of ventilation and perfusion. Fever. This may cause hypocapnia due presumably to central stimulation of the respiratory control mechanisms (Chapot et al, 1974). Some types of C.N.S. damage. Hysterical hyperventilation.


This (non-respiratory acidosis) is due to increase in acids (i.e. H+ donating substances) other than H2CO2 or decrease in base (i.e. H+ acceptors) in the blood. Compensation is by hyperventilation. This lowers the PaCO2 thus deducing the any pH change. The causes of non-respiratory acidosis are:


Increased alimentary or parenteral intake of acid or alimentary loss of base. (Addition and subtraction).

Increased production of acid. (Accumulation).

Failure of excretion of acid or loss of base by the renal system.

Increased Intake of Acid or Loss of Base Increased alimentary or parenteral intake of acid or alimentary loss of base. Adding acid. The acid content of blood may be raised by ingestion or injection of ammonium chloride or dilute hydrochloric acid. The hydrochloric acid directly increases [H+]. The ammonium chloride produces hydrochloric acid by the NH3 being split off and converted to urea. Adding ammonium chloride directly to blood would not change the pH greatly until the NH4+ has been metabolised. Alimentary loss if Base. Loss of intestinal contents by diarrhoea, low small bowel obstruction or intestinal fistulae causes loss of fluid of high pH, i.e. containing an excess of base (Na+HCO3- or K+HCO3-). This results in the fluid left in the body having a lower base content than normal. The removal of base causes the blood pH to fall (Leading Article, 1966). A similar disturbance has been reported from loss of lymph. (Siegler et al, 1978). Intravenous infusions. These can cause an acidosis. Stored blood for transfusion. This has la ow pH. The anticoagulant contains citric acid. When mixed with the blood the pH drops. PCO2 rises because of the action of acid on bicarbonate ions. Most of the pH drop is due to this CO2 which does not escape from the stored blood. The non-respiratory pH of the stored blood is not as low as the actual pH. The pH of stored blood does not fall progressively if stored for up to three weeks at 4C (Gaudry, Joseph and Duffy, 1974).

The acidic salt of sodium citrate and "dilutional" acidosis are the main contributers to the non-respiratory pH of stored blood. There is a variable amount of lactic acid acid in stored blood This usually contributes less to the non-respiratory pH change. If stored concentrated red cells are washed there will be a considerable and even an increased non-respiratory acidosis in the product. If 27meq NaHCO2 is added to each litre of washing fluid this would not occur, but would introduce other problems.

Stored blood transfusion rarely causes a non-respiratory acidosis if the circulation and temperature are maintained normal. It is possible that if the circulation and temperature are not maintained, that metabolic acidosis could occur with massive transfusion. In a situation where a massive transfusion is given it will not usually be possible to distinguish the low pH due to blood, from that due to the condition for which the blood is being given. From personal observations the low base excess observed during liver transplantation appears to be mainly a combination of lactic acidosis from the transfused blood and released or generated in the new liver and dilutional acidosis. The sodium citrate in the anti-coagulant solution can cause a metabolic alkalosis after the citrate has been metabolised and replaced by bicarbonate ion.

Howlands et al (1965) have advocated routine use of sodium bicarbonate during massive blood transfusion to counteract the acidosis of the infused blood. This is usually unnecessary (Bookallil and Joseph, 1968), and will probably only aggravate post transfusion alkalosis (Miller et al, 1971).

If the temperature and circulation are not maintained as is common in when more than say 5 litres in 2 hours are transfused in trauma the composition of the circulating blood approaches that of the transfused blood. In liver transplantation 3 times the blood volume may be replaced in an hour and up to 30 times the blood volume during the operation. This can result in pH<6.9 and base excess <-20meq/litre. The cause is lactic and dilutional acidosis. There appars to be little circulatory effects and spontaneous recovery occurs without alkali therapy (Personal observation). "Dilution Acidosis" (Shires et al, 1948; Garella et al, 1973) is an acidosis due to the intravenous infusion of a neutral non-buffer solution.

Intravenous solutions which contain only non-acids or non-bases, e.g. sodium chloride, glucose and other carbohydrates usually have a pH slightly less than 7. This is usually due to pharmaceutical details in the preparation. In these non-buffer solutions this low pH represents a very small amount of acid. One would only have to add a fraction of a miliequivalent of strong base to a litre to make the solution alkaline.

If such a non-buffer solution (e.g. Saline or 5% glucose) is equilibrated with a gas mixture containing 40mmHg CO2 it has a pH of 4.9 (Gaudry et al, 1972). 24meq Na0H (or NaHC03) would have to be added to it to give a pH of 7.4, therefore a neutral solution plus 24meq NaHC03 will on infusion cause no change in pH in the blood. The original solution of saline or glucose will act in a similar fashion to an injection of 24meq HCl for each litre infused. This will only be importasnt if large volumes of intravenous fluid are given in a short time,e.g. in burns or cholera (see Diuretic Alkalosis,

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