Decoding the OHDC
DECODING THE OXYHEMOGLOBIN DISSOCIATION CURVE
Introduction
Focus of the material is understanding the oxyhemoglobin dissociation curve in the context of nursing care (NUR 251).
LEARNING OBJECTIVES
Identify factors that cause shifts in the oxyhemoglobin dissociation curve.
Implement nursing care strategies for patients experiencing shifts in the curve.
Recognize patient manifestations impacting SpO2 monitoring and readings.
Compare and contrast patient presentations for shifts to the left or right of the curve.
OXYHEMOGLOBIN DISSOCIATION CURVE
Definition of Oxyhemoglobin
Amount of oxygen (4) that is bound to a hemoglobin molecule.
Definition of the Dissociation Curve
It is an indicator the relationship between the oxygen saturation of hemoglobin and the partial pressure of arterial oxygen (paO2).
PaO2 = Partial pressure of arterial blood oxygen
PaCO2 = Carbon dioxide
Thinking about the pressures exerted onto the arterial blood, paO2 and PaCO2, not always does the oxygen on the hemoglobin match the perfusion of organs.
Importance of the Curve
It is critical for oxygen to detach from hemoglobin in red blood cells as they reach body tissues, allowing for diffusion into cells for survival.
Staying alive hinges on adequate oxygen moving from lungs to body tissues and cells.
Of the 4 oxygen molecules bound to hemoglobin, in a normal patient, there is 1 oxygen being dropped off into the tissues (25%). Body keeps reserve of 75% in case of increased demand for oxygen.
BASIC PRINCIPLES
Effects of Partial Pressure of Oxygen (Po2):
Increase in Po2 leads to higher saturation and hemoglobin stores oxygen.
Oxygen saturation viewed with pulse ox (least invasive).
Decrease in Po2 leads to lower saturation and hemoglobin is released to the tissues.
Dropping off more oxygen to tissues.
Mechanism of autoregulation for oxygen delivery:
Inactive tissues have lower oxygen demands, while active tissues utilize oxygen more rapidly.
Inactive Tissue: Necrotic, gangrene, osteomyelitis.
Active tissues use oxygen at an accelerated rate.
Ex. Going on a run, tissues need more oxygen → body compensates by breathing heavier and faster to bring in more oxygen.
NORMAL TISSUE O2 SATURATION
Normal tissue PaO2 is approximately 40 mm Hg with 75% saturation.
In a normal state, about 25% of O2 is released from hemoglobin while 75% remains as a reserve, ensuring oxygen supply meets demand during emergencies.
Adjusting hemoglobin’s affinity for oxygen allows an increase or decrease in supply to the tissue.
Affinity = How tightly a substance is bound to something.
Ex. Increased affinity of oxygen to tissues, the tissues are holding onto more oxygen.
FACTORS AFFECTING HEMOGLOBIN'S AFFINITY FOR OXYGEN
Right Shift: (Requires more oxygen = more concerning)
Caused by acidosis (low pH), increased 2,3-DPG (increased CO2 as body need more oxygen), and elevated temperatures (fever).
Ex. Pt with an infection (metabolic processes).
Results in more and easier oxygen release to tissues from hemoglobin (drops off 3 oxygen molecules)
Decreased affinity for oxygen on hemoglobin (unloads oxygen) and increased affinity for tissues. More oxygen need for tissues.
If tissues are not oxygenated → necrosis, cyanosis, denaturing of proteins, increased lactic acid.
New infection = shift to the right
“Giving oxygen is the RIGHT thing to do”
Ex. Carbon monoxide poisoning → shift to the right → increased breathing.
Left Shift (Less oxygen demand):
Caused by alkalosis (high pH), decreased 2,3-DPG (decreased CO2), and hypothermia (low temperature). Cold pts don’t require as much oxygen.
Results in hemoglobin retaining oxygen more tightly, only releases 1 oxygen from 1 hemoglobin.
Increased affinity for oxygen on hemoglobin (keeps oxygen) and decreased affinity for tissues. Less oxygen need for tissues.
“They’re not dead until they’re warm and dead” → due to oxygen delivery to tissues
“Everything you own in a box to the left” that’s cold of Beyoncé.
PULSE OXIMETER
A pulse oximeter reading of 95% or higher is considered clinically acceptable.
A reading of 90% or lower is worrisome:
Corresponds to a paO2 of 60 mm Hg indicating = hypoxia at tissue level.
Acceptable in people with COPD, they normally sit lower.
Respiratory acidosis = increased CO2.
Pt reads at 60% → make sure hooked up to oxygen, make sure sensor is on, make sure not shaking, feel temperature of hands (least invasive to most invasive).
Push code blue button if pt is unresponsive and appears grey.
Limitations of Pulse Oximetry:
Does not provide hemoglobin levels or functionality (carboxyhemoglobin/methemoglobin).
Scenario: Pt has a hemoglobin of 4 but but SpO2 of 98%. Not enough oxygen is being delivered to the tissues since there isn’t enough hemoglobin to hold onto oxygen.
Causes of Non-Functional Hemoglobin:
Anemia (Sickle-Cell because it can’t hold onto enough oxygen, only holds 1)
Carbon monoxide poisoning: Carboxyhemoglobin and methemoglobin are more tightly bound to the hemoglobin, so oxygen is competing.
SpO2 only tells you that all the hemoglobin have something bound to them, not what is bound to them.
Does not account for ventilation status (breathing enough).
Patient and technical disruption
Dark nail polish (UV light)
Cold fingers (vasoocculsive disease, chronic smoker)
A-fib
Movement (Parkinson’s)
Other places to put pulse ox → earlobe, forehead, big toe
PATIENT MANIFESTATIONS
Clinical symptoms may include:
Slight tachycardia (trying to pump out more oxygen) and tachypnea (trying to take in more oxygen).
Alertness with possible restlessness.
Lethargic?
Normotension but may appear febrile.
When pulse oximetry shows decline, further assessments may be required:
Consideration of arterial blood gases (ABGs).
Review of hemoglobin and hematocrit (H&H) levels.
Assessment for existing or new infections.
New infection = shift to the right