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What are the common signs and symptoms of CO toxicity?
Headache nausea, confusion, flushing, vomiting, malaise, syncope, chest pain, etc.
Identify risk factors associated with CO poisoning
Infants, young children, and adults 65+ years at higher risk
People w/ chronic heart disease, anemia, breathing problems, and lung disease are more likely to be affected
High altitude living
Smoking: smokers have elevated levels of CO in their blood
Alcohol use
Combustion engines/fire occupations
Malfunctioning appliances (e.g., water heaters, furnaces, or gas clothes dryers)
Using unvented space heaters, wood-burning fireplaces
Gas or fuel-burning appliances
Vehicles left running inside garages
Is PaCO2 elevated or depressed in CO poisoning? Why?
Increased respiratory rate leads to excessive CO2 elimination (low PaCO2)
Why is Tropnonin 1 elevated in patients with CO poisoning?
Elevated Troponin I
CO causes myocardial injury through:
Direct cellular toxicity to cardiac myocytes
Myocardial hypoxia due to reduced oxygen delivery
Increased cardiac workload from compensatory tachycardia
Relate elevated COHb to the patient's inability to provide consent to treatment.
High COHb levels directly affect cognitive abilities
CO binds to Hb more strongly than O2, thus reduced O2 delivery to brain and other tissues
CO exposure can cause confusion, disorientation, and impaired judgment
As COHb levels increase, pts may experience progressively worsening mental status changes including progression to loss of consciousness
Explain why hemoglobin and hematocrit were normal in this patient with CO poisoning.
CO does not destroy RBCs thus total hemoglobin content remains unchanged even though a portion is bound to CO
State whether oxyhemoglobin causes a left or right shift dissociation curve and explain how this occurs.
Left shift
Reduced O2-carrying capacity
Impaired O2 unloading at tissue level (very severe factor)
What is COHb? Why it is increased or decreased in CO poisoning
Hallmark finding in CO poisoning
CO binds to Hb with an affinity 220-270x greater than oxygen; results in:
Reduced O2-carrying capacity of blood
Left shift of oxyhemoglobin dissociation curve; further impairing O2 delivery to tissues
Levels > 20% in adults indicate significant poisoning
Explain how respiratory alkalosis can occur in patients with CO poisoning.
Tachypnea occurs as the body attempts to increase oxygen delivery → respiratory alkalosis
What is PaO2 and why is it normal in CO poisoning?
Standard pulse oximetry cannot differentiate COHb from oxyhemoglobin
Dissolved oxygen in plasma is not affected by CO
Explain why there is a lack of oxygen saturation changes on the pulse oximeter reading in the patient experiencing CO poisoning.
Pulse oximeters use light absorption at two specific wavelengths to estimate O2 saturation
COHb has optical absorbance characteristics very similar to O2Hb thus difficult to distinguish both
Pulse oximeters tend to overestimate actual O2 saturation in the presence of elevated COHb levels
“Pulse oximetry gap” in CO poisoning aka difference b/w the pulse oximetry reading and actual O2Hb saturation
Gap tends to increase linearly w/ rising COHb levels
Limitations highlight the importance of using more accurate methods, such as co-oximetry or arterial blood gas analysis with direct measurement of COHb levels, for proper diagnosis and management of CO poisoning
1) What is the most common arrhythmia associated with CO poisoning?
2) Occlusions in the RCA and LDA would be associated with ST changes in what leads? What locations?
1) Most common = sinus tachycardia
2) Leads II, III, and aVF (RCA), V1-V4 (LAD); Inferior and anteroseptal
Outline the differences between hypoxia and ischemia, including their effects on nutrient metabolism.
Hypoxia = lack of O2 supply to myocardium
Can occur due to low blood O2 levels, anemia, or CO poisoning even w/ normal blood flow
Anaerobic glycolysis can continue as substrates are still delivered via blood flow
Primarily affects oxidative phosphorylation
May resolve quickly once oxygen levels are restored
Ischemia = reduction in blood flow to myocardium which leads to inadequate O2 supply
Usually due to coronary artery obstruction or spasm
Both aerobic metabolism and anaerobic glycolysis are compromised due to lack of substrate delivery and metabolite removal
Usually causes more severe injury than hypoxia alone as it affects both O2 and nutrient delivery
Can have prolonged effects even after blood flow is restored, due to reperfusion injury
Discuss preventative measures for CO poisoning (Minimum 3).
Installation of CO detectors
Annual professional inspections for all fuel-burning appliances
Regular inspection and cleaning of vents, chimneys, etc. to ensure proper ventilation
Recognize symptoms of CO poisoning (dizziness, headache, and nausea)
Discuss the role of a 100% O2 non-rebreather (NRB) mask in CO poisoning. Also, state one limitation to this treatment.
High O2 delivery: can deliver up to 60-91% inspired O2 concentration
Contains one-way valves to prevent rebreathing of exhaled air
Does not require pt effort to operate
Limitations:
Requires good seal on face for maximum effectiveness
Not suitable for pts unable to breathe on their own
Safety considerations:
Flow rates must be sufficient to prevent reservoir bag collapse
One valve is typically removed to prevent suffocation if oxygen supply fails
Relate these findings to CO poisoning:
LV dilation: CO poisoning can cause myocardial injury and stunning leading to mild dilation of LV from:
Reduced O2 delivery to heart muscle
Direct toxic effects of CO on cardiac myocytes
Increased workload of heart as it tries compensation for reduced O2-carrying capacity of blood
Moderate systolic dysfunction: impaired ability of LV to contract effectively b/c:
Myocardial hypoxia from CO interference w/ O2 transport and utilization
Direct toxic effects of CO on cardiac myocytes
Potential ischemia-reperfusion injury as oxygen levels are restored
Ejection fraction 45%: compromised cardiac function
The degree of reduction correlates with the severity of CO poisoning and its impact on cardiac function
High affinity for hemoglobin: CO crosses the alveolar-capillary membrane, and it is rapidly bound to Hb, maintaining a low partial pressure of CO in the blood
Maintained concentration gradient: rapid binding of CO to Hb keeps partial pressure of CO in blood low, maintaining steep conc gradient b/w alveoli and blood
Constant gradient allows for continuous diffusion of CO across the membrane
Rate of CO transfer is primarily limited by properties of the alveolar-capillary membrane (thickness, surface area) rather than blood flow
Outline the mechanism(s) by which HBOT treats CO poisoning, include protocol for treatment.
Accelerated CO elimination: HBOT dramatically increases CO rate elimination from body → helps restore normal O2 delivery to tissues more quickly
Allows more O2 to be dissolved directly in blood plasma, bypassing Hb bound to Co; helps oxygenate tissues even when Hb is impaired by CO
Reduce inflammatory response and oxidative stress caused by CO poisoning
Protocol:
Treatment as soon as possible after CO exposure, typically within 24 hours
Patients are typically treated at 2.5 to 3.0 atmospheres absolute (ATA)
Three 90-minute sessions at pressure, with 5-minute air breaks every 30 minutes to reduce the risk of oxygen toxicity.
During HBOT, pts exposed to high atmospheric pressures
Myringotomy helps equalize pressure b/w middle ear and external environment which prevents barotrauma to eardrum
Can also relieve otic pressure that may occur with severe CO poisoning
A medical student exercises each day by cycling on a stationary bicycle for an hour. As blood passes through the capillaries of her working leg muscles, the release of oxygen from hemoglobin is increased by the local decrease in:
A) 2,3-biphosphoglyceric acid
B) PCO2
C) H+ concentration
D) PO2
E) tissue temperature
D) PO2
The saturation of hemoglobin for oxygen decreases when the PO2 decreases. Other factors that decrease the affinity of hemoglobin for O2 are increases in temperature, PCO2 or 2,3 biphosphoglycerate, or decreases in pH.
A 62-year old female is picked up EMS after she was found by her husband confused in her car. She complains of a headache but only mumbles when asked anything else. Vital signs reveal: BP 135/85 mmHg, HR 105/min, RR 18/min, O2 saturation: 98% on room air
On physical examination, she is confused but there are no signs of trauma or bleeding. Blood drawn from vein is red in color. Lab studies and arterial blood gas reveals:
Bicarbonate: 10 mEq/L (22-29 mEq/L)
Arterial pH: 7.25 (7.35-7.45)
PO2: 84 mmHg (83-108 mmHg)
PCO2: 37 mmHg (32-45 mmHg)
The most likely underlying cause of this patient's symptoms is:
A) Accumulation of CO2 in the blood
B) Competitive inhibition of the heme-binding site
C) Increased levels of oxalic acid in the bloodstream
D) Inhibition of acetylcholinesterase
E) Predominance of oxidized iron in hemoglobin
B) Competitive inhibition of the heme-binding site
Patient most likely suffering from CO toxicity. CO displaces O2 from heme, leading to hypoxemia. O2 saturation will often be normal due to inability to distinguish between CoHb and oxyhemoglobin on pulse oximetry.
Outline the Glasgow Coma Scale, including the three specific criteria and the assigned point ranges for each criterion.
The GCS is used to assess the level of consciousness:
Eye opening (1-4 points)
Verbal response (1-5 points)
Motor response (1-6 points)
In CO poisoning:
Mild poisoning: GCS 14-15
Moderate poisoning: GCS 9-13
Severe poisoning: GCS ≤8
Lower GCS scores indicate more severe CNS effects and correlate with worse outcomes
A 61-year old male is brought to the hospital by his son for nausea and vomiting during the last three days. He is confused and is only able to state his name and birth date. He also complains of chest pain and a headache. He lives alone in an apartment that he has been heating with a kerosene heater. Vital signs reveal a BP of 140/90 mmHg, HR 95/min, RR 12/min, O2 saturation: 99% on room air.
Arterial blood gas reveals:
PaCO2 = 37mmHg (32-45mmHg)
PaO2 = 85mmHg (83-108mmHg)
Blood pH = 7.20 (7.35-7.45)
The best treatment for this patient's most likely diagnosis is:
A) Amyl nitrate administration
B) Bicarbonate administration
C) Cyproheptadine administration
D) Dimercaprol administration
E) High-flow oxygen provided via a nonbreathing mask
Correct answer: E
The patient is most likely suffering from CO toxicity. Treatment is with 100% oxygen and hyperbaric oxygen if available.
Explain how the following occur in patients w/ CO poisoning:
Tachycardia
Tachypnea
Elevated BP
Combativeness and confusion
Rales/crackles
Tachycardia: body tries to compensate for reduced O2 delivery by increasing CO
Tachypnea: respiratory compensation for metabolic acidosis and attempt to increase O2 intake
BP: elevated initially b/c CO binding Hb in RBCs to form COHb prevents RBCs from carrying O2
Combative and confusion due to decreased O2 to brain and other organ tissue
Rales/crackles: indicative of developing pulmonary edema
A 15-year old male is rescued from a house fire and brought to the ED in an unconscious state. Vitals reveal a HR of 110/min, RR of 40/min, and BP of 145/90 mmHg. He is presently coughing and expectorating black mucus. PE reveals bilateral rales, injected conjunctiva, bright red lips, and cherry red skin. Which of these findings on arterial blood is most likely to be associated with this patient's condition?
A) decreased carboxyhemoglobin saturation and increased bicarbonate
B) decreased oxygen saturation via pulse oximetry
C) decreased oxyhemoglobin saturation and decreased bicarbonate
D) decreased partial pressure of oxygen
E) increased carboxyhemoglobin saturation and increased bicarbonate
C) decreased oxyhemoglobin saturation and decreased bicarbonate
CO binds to Hb with a much greater affinity than O2, decreasing oxyhemoglobin levels. in severe CO poisoning, lactic acidosis can cause a decrease in bicarbonate buffering levels due to enhanced aerobic respiration.