LifeguardsForLife

To keep on living the dream baby....................

Stay alive, don't break my back, produce excellent student paramedics, blah, blah, so-forth and so-forth.......

In the coming year I would like to learn to play piano, and get "back" in shape.

I would like to continue learning about emergency medicine and hope everyone has a safe and happy new year(s)!

thank you vent and chbare for the information.

Chbare-I apologize, that should of read carbon monoxide poisoning not carbon dioxide. If the affinity between carbon monoxide and hemoglobin is roughly 200 times that of oxygen and hemoglobin, i figured that, carbon monoxide poisoning would result in a higher Pao2 and lower Sao2. Which seemed to conradict the refrenced passage.

I will go and review the oxyhemoglobin dissociation curve.

• Carbon Monoxide. Hemoglobin binds with carbon monoxide 240 times more readily than with oxygen, and therefore the presence of carbon monoxide can interfere with the hemoglobin's acquisition of oxygen. In addition to lowering the potential for hemoglobin to bind to oxygen, carbon monoxide also has the effect of shifting the curve to the left. With an increased level of carbon monoxide, a person can suffer from severe hypoxemia while maintaining a normal PO₂.

I think the above statements answers the question i was attempting to ask.

In simplest terms the Pa02 is the amount of oxygent that is not bound to HB, but is in the plasma.

The Sao2 is the percent of oxygen bound to the heme portion of hemoglobin.

Neither the amount of hemoglobin, nor the binding characteristics of hemoglobin, should affect the amount of dissolved oxygen, and hence should not affect the PaO₂). Stated another way, the number of dissolved oxygen molecules is independent of the amount of hemoglobin or what is bound to it. To repeat one more time (because it is so important), PaO₂ is not a function of hemoglobin content or of its characteristics, but only of the alveolar PO₂ and the lung architecture (alveolar-capillary interface). This explains why, for example, patients with severe anemia or carbon monoxide poisoning or methemoglobinemia can (and often do) have a normal PaO₂.

Thus hemoglobin is like an efficient sponge that soaks up oxygen so more can enter the blood. Hemoglobin continues to soak up oxygen molecules until it becomes saturated with the maximum amount it can hold - an amount that is largely determined by the PaO₂

Why wouldn't Pao2 and Sa02 vary inversly? It seems to me that if a low Sao2 existed(due to a deficiency of Hb, or inability of oxygen to bind to the Hb), one would find a higer Pa02, as no oxygen molecules are being removed from the plasma?

Would Co2 poisoning result in a low sa02, and a higher Pa02 as the heme bonding sites are occupied, thus preventing oxygen from bonding with hemeglobin?

Several sources seem to use Sp02 and Sa02 interchangebly. Spo2 and Sa02, while similiar, should represent 2 entirely differnet values, correct? If a patient has an Sp02/Sa02 level within an acceptable range, would that indicate that the Pa02 is also satisfactory?

Does the Ca02, simply combine the data gathered by the sa02 and the Pao2, in to a quantifiable amount?

If Cao2 is calculated with the following amount, would it stand to reason that a patient could be found to have an adequate Sa02 or Pao2 and still "not be oxygneating properly"?

CaO₂ = Hb (gm/dl) x 1.34 ml O₂/gm Hb x SaO₂ + PaO₂ x (.003 ml O₂/mm Hg/dl).

This is awesome and informative, guys, but I'm still interested mainly in the original question. I guess we've all agreed that there can be a strong placebo effect attached to any use of O2; that said, there will still be cases where it's also physiologically beneficial, and those where it's not.

My treatment for anemia is a bolus of definitive care

Oxygen is inexpensive, easily obtainable, ad widely utilized as to impede and prevent the effects of hypoxia. Since it's discovery in the late 1700's oxygen has remained one of the most effective therapeutic agents known to the medical world. However, currnent literature suggests this medication is all too commonly administered at extremely high doses, causing hyperoxia. But oxygen is harmless right? Hyperoxia induces bradycardia and a reduction in cardiac output, which partly offsets the otherwise increased oxygen delivery. below are several different articles or studies regarding potentila risks of high flow oxygen.

A publication in the October 2003 issue of Chest confirm that 100% oxygen can be harmful for asthmatics and support recommendations to use the minimum concentration required to maintain target O2 saturation.

. Results: The administration of 100% oxygen significantly increases Paco₂ (p = 0.03) and decreases PEFR (p = 0.001) as compared with administration of 28% oxygen. Paco₂ before and during oxygen administration correlated significantly (p = 0.001) in both groups. Patients breathing 28% oxygen experienced a Paco₂ fall; on the contrary, patients who received 100% oxygen showed an increase in Paco₂, particularly those with Paco₂ before oxygen treatment > 40 mm Hg.

Retinopathy of prematurity

ROP, first identified in 1942, occurs in about 3,500 premature infants each year in the United States. Estimates are that between 350 and 500 infants each year are blinded because of the condition. The remaining infants can suffer some long-lasting visual problems.

The problem occurs when an infant is given supplemental oxygen at birth to aid his or her underdeveloped lungs. At that time, the blood vessels in the child¹s retinas are still developing, and oxygen therapy can cause these blood vessels to grow abnormally. After the abnormal growth begins, vessels that are supposed to remain with the retina of the eye can actually grow into the center of the eye, causing retinal detachment. The only way to repair the problem is with invasive laser therapy, which can cause damage to healthy retinal tissue.

Dr. Bledsoe on "the oxygen myth"

Stroke: The brain is very vulnerable to the effects of oxidative stress. The brain has fewer antioxidants than other tissues. Thus, should we give oxygen to non-hypoxic stroke patients? Studies have shown that patients with mild-moderate strokes have improved mortality when they receive room air instead of high-concentration oxygen.

The data on patients with severe strokes is less clear.(5) Current research indicates that supplemental oxygen should not be routinely given to patients with stroke and can, in some cases, be detrimental.(6)

Acute Coronary Syndrome: The myocardium is highly oxygen dependent and vulnerable to the effects of oxidative stress. Thus far, there's no evidence that giving supplemental oxygen to acute coronary syndrome patients is helpful, but there's no evidence it's harmful.(7)

Post-Cardiac Arrest: Here, too, the evidence is too scant to tell. We do know that virtually all current therapies for cardiac arrest (drugs, airway) are of little, if any, benefit. The primary therapies remain CPR (often with limited ventilation initially) and defibrillation followed by induced hypothermia. The whole purpose of induced hypothermia is to prevent the detrimental effects of oxidative stress and the other harmful effects of reperfusion injury.

Trauma: What role should oxygen play in non-hypoxic trauma patients? Little research exists, but an interesting study out of New Orleans demonstrated that there was no survival benefit to the use of supplemental oxygen in the prehospital setting in traumatized patients who do not require mechanical ventilation or airway protection.(8)

Carbon Monoxide (CO) Poisoning: We have learned a lot about carbon monoxide poisoning in the past few years. We know that the mechanism of CO poisoning is a lot more complex than once thought. We also know that there's no reliable evidence that hyperbaric oxygen (HBO) therapy improves outcome (although it's still widely used).(9) But when you think about it, the goal of treatment in CO poisoning is to eliminate CO through ventilation -- not hyperoxygenation. Although oxygen can displace some CO from hemoglobin, the induction of free-radicals may be worse than the effects of CO. Again, the science here is in a state of flux.

Neonates: The science is clear in regard to supplemental oxygen in neonates. It should be used only when room air ventilation fails.

Again, this is a discussion of the changing science. Always continue to follow the direction of your medical director and local protocols. That said, it's clear that we need to use every tool possible to support, but not replace, our physical exam skills. We should use pulse oximetry and waveform capnography. Although, individually, each technology has its limitations, together they provide important information about the patient.

oh and, apparently concentrated oxygen is ineffective at harming or killing cancer cells(an interesting read) -http://www.cancer.org/docroot/eto/content/eto_5_3x_oxygen_therapy.asp

hope this provides some insight for you.

Thank you all for your much valued responses. For any other members interested, I think the following article also answered some of the other questions I had regarding negative pressure ventilations.

http://chestjournal..../2217.full.html

IMV is very effective treatment for respiratory failure but can be associated with many complications, especially in patients requiring prolonged intubation. Complications included laryngeal and tracheal trauma with potential long-term effects, such as stenosis. In addition, sinusitis and VAP can occur during IMV. The incidence of complications is closely related to the duration of invasive ventilation, particularly the acquisition of VAP.²¹

Difficult weaning is often a problem in patients with COPD who undergo invasive ventilation. To avoid these problems and reduce hospital stay, many ICUs perform tracheostomy precociously, leading to high human and social costs due to this artificial airway. In the last 10 years, many studies have reported positive results regarding NIMV treatment for exacerbation of CRF primarily in patients with COPD.

The iron lung is our first choice of treatment for several reasons. Patients with acute exacerbation of CRF often present inspiratory muscle weakness, rapid shallow breathing, and excessive CO₂ retention. The iron lung improves the performance of respiratory muscles and restores sufficient respiratory compensation.¹⁶ Furthermore, many patients in the early phase of ARF are restless and do not tolerate NPPV with nasal or full face mask, whereas with the iron lung these patients receive ventilation effectively. Tracheobronchial secretions are often a problem in patients treated with NIMV and require efficient cleaning of the airways (with catheter or fiberoptic bronchoscope). This is achieved more easily when the iron lung is used.²² Noncontrolled studies²³²⁴²⁵ indicate a better survival rate when patients with COPD and ARF are treated with the iron lung vs IMV. Using controlled ventilation via iron lung, patients with COPD in hypercapnic-induced coma can be safely treated.²⁶

... paging Ventmedic - Ventmedic to the forums please.....

haha Kaisu, I had also posted this over at another forum, though figured I had a better chance of getting valuable information over here.

Do any of you have any experience with negative pressure ventilators? Are they still in use, and what would indicate their use over positive pressure ventilators?

As others have probably noticed, there are several newer members joining up around the same time. I'm new here as well, just "following the flow" of the good information to better my knowledge base so I can better serve those that keep me employed. So HI!

'howdy FMA08,

nice to see all these familiar faces over here in the city.

be prepared to defend what you say with logic, reason and facts......

Hey, piranha, and welcome.

I too recently joined here after a recent turn of events.

Kaisu- are you sure, the forum i used to frequent didn't seem to support logic, reasoning or facts in defense of a statement

If you have a chance to attend one of Bob Pages seminars, jump on it. You will learn what you need to know.

You can check the website for dates. multileadmedic.com

I have heard his seminars are very good, however there are non scheduled in my state. do you have ant experience with his book?

I have had positive experiences with Dale Dubin's Rapid EKG Interpretation, and would recommend it to anyone who is just beginning to learn EKG interpretation.

below are some free sites you may wish to view:

http://library.med.utah.edu/kw/ecg/ecg_outline/index.html

http://www.ecglibrary.com/ecghome.html

http://www.monroecc.edu/depts/pstc/backup/prandekg.htm

http://library.med.utah.edu/kw/ecg/image_index/index.html