Oxygen Supply and Demand Part 2

Module 2. Features: Gas exchange, Circulation

What are the key determinants of gas exchange?

Ventilation/Perfusion (V/Q) Matching and Diffusion

What is Ventilation/Perfusion Matching (V/Q Matching)?

It is the ratio of alveolar ventilation:alveolar perfusion

It is the distribution of air within the alveoli, and the blood flow to the alveoli

Why is Perfusion (Q) important in alveolar gas exchange? Decreased perfusion leads to what?

It is the measure of the ability to bring blood to the capillaries to receive the O2 at the alveolar-capillary interface. Decreased perfusion, or decreased Cardiac Output = decrease in amount of blood available to which O2 can diffuse.

What is the difference between Shunt/Shunt-like units vs. Dead-Space/Dead-Space-like units?

Shunt/Shunt-like units indicate ventilation issues. Blood passes by the alveoli without being oxygenated due to little O2 available for gas exchange.

Dead-Space/Dead-Space-like units indicate perfusion issues.

What are Shunt Units? Give examples.

Mucous plugs and atelectasis = total blockage of access to the alveoli.

What are Shunt-Like Units? Give examples.

Pulmonary edema, pneumonia = some O2 can pass through the fluid into the alveoli and participates in SOME gas exchange.

What are Dead Space Units? Give examples.

Pulmonary embolism = stops blood flow to the alveolus ENTIRELY. Total blockage.

What are Dead-Space-Like Units? Give examples.

Pulmonary vasoconstriction or decreased cardiac output = reduced blood flow to the alveolus, but SOME blood can pass.

What are 4 factors that affect diffusion?

1. A-C membrane thickness

2. Anatomical Surface Area of the alveoli

3. Diffusion Co-Efficient

4. Driving Pressure

True or False: A thicker A-C membrane leads to less O2 diffusion.

True

What is the Diffusion Co-Efficient?

It describes how readily a molecule moves through a solution of membrane.

Does CO2 or O2 diffuse faster across the a-c membrane?

CO2

Using your knowledge about the diffusion co-efficient, explain why a patient with lung disease will become hypoxemic faster than hypercapnic.

Since CO2 diffuses 20x faster than O2, diffusion blockages (like fluid in the lungs) cause low O2 levels (hypoxia) before they cause major CO2 retention (hypercapnia).

Define Driving Pressure and relate this to the law of diffusion.

Driving Pressure is the difference in concentrations of a gas. The greater driving pressure of a gas = faster rate of diffusion.

Law of diffusion: gases diffuse from high concentrations to lower concentrations, and also from areas of high pressures to lower pressures.

What intervention can be used to increase driving pressure?

O2 therapy

What are some interventions to increase gas exchange?

• O2 therapy

• DB+C

• Suctioning

• Repositioning for V/Q matching (High-Fowlers)

• BiPAP to keep alveoli open = increases surface area

Why is PaCO2 a better indicator of ventilation compared to PaO2?

CO2 elimination is directly tied to alveolar ventilation, whereas O2 levels can be influenced by other factors, like Hgb binding.

Why is SpO2 not a good measurement of overall end-organ perfusion?

SpO2 measures the % of binding sites occupied on Hgb. It does not account for Hgb amount. A person with an SpO2 of 98% with a Hgb of 76 (L) has an inadequate carrying capacity for end-organ perfusion.

Define O2 Affinity

Ability of O2 to combine to Hgb

Normal O2 Affinity

O2 binds to Hgb in the lungs and releases from Hgb at the tissues adequately.

Why is high O2 Affinity bad?

O2 stays bound to Hgb and does not release into the plasma for tissues appropriately = PaO2 decreased.

Why is low O2 Affinity bad?

Hgb has difficulty binding to O2 at the lungs.

Why is PaO2 decreased in the context of high O2 affinity?

PaO2 is a measurement of how much O2 is dissolved in the plasma. In high O2 affinity, O2 stays bound to Hgb and is not released into the plasma.

Why is SaO2 and SpO2 decreased in the context of low O2 affinity?

SaO2 and SpO2 measure the % of binding sites that are occupied on Hgb. In low O2 affinity, Hgb has difficulty binding to O2 = leading to a decrease in these measurements.

What are factors that influence O2 Affinity?

• pH

• PaCO2

• Temperature

• 2,3 Diphosphoglycerate (DPG)

What is 2,3 DPG?

It is an organic phosphate in RBC’s that decreases O2 affinity by facilitating the release of O2 into the tissues and cells.

What happens when 2,3 DPG is increased? What circumstances lead to an increase in value?

Increased 2,3 DPG leads to decreased O2 affinity.

• Exercise

• High altitude

• Hypoxemia

• COPD

• Heart Disease

What happens when 2,3 DPG is decreased? What circumstances lead to a decreased value?

Decreased 2,3 DPG leads to increased O2 affinity.

• Hypophosphatemia

• Septic shock

• Banked blood

Why does banked blood have less 2,3 DPG?

Because 2,3 DPG only lasts for 2 weeks outside of the body.

What is the most important factor influencing O2 affinity? Why?

PaO2. This is because higher PaO2 (partial pressure) drives O2 into the blood (Hgb) from the alveoli = increasing SaO2.

What causes a left shift of the Oxyhemoglobin Dissociation Curve (ODC)? What is the result?

A left shift occurs when 1+ of these factors is present:

• Decreased temperature

• Alkalosis (increased pH)

• Decreased PaCO2

• Decreased 2,3 DPG

It results in lower PaO2 = higher O2 affinity (more O2 molecules attach to Hgb and less O2 is released into the tissues). Demand for O2 in tissues is lower.

In a left shift of the ODC, SaO2 is ____ and PaO2 is _____.

SaO2 is higher and PaO2 is lower.

SaO2 is higher because of higher O2 affinity = O2 stays bound to Hgb in the blood.

Lower PaO2 = less “free” O2 in the blood as it is mostly bound to Hgb.

What causes a right shift in the ODC? What is the result?

It results in decreased O2 affinity due to greater O2 demand and metabolism.

Causes:

• Fever

• Increased PaCO2

• Increased 2,3 DPG

• Acidosis (decreased pH)

In a right shift in the DOC, SaO2 is ____ and PaO2 is _____.

SaO2 is decreased and PaO2 is increased.

SaO2 is decreased due to decreased O2 affinity because Hgb is releasing O2 into the tissues from the blood.

PaO2 is increased because there is more loose, floating O2 in the blood (not bound to Hgb).

Cardiac Output

The volume oof blood ejected from the heart per minute.

How is Cardiac Output (CO) calculated?

CO (L/min) = Stroke Volume x HR

Stroke Volume

The volume of blood ejected from the heart with each beat.

What determines Stroke Volume?

• Preload

• Afterload

• Contractility

How can tachycardia and bradycardia decrease CO?

Tachycardia: not enough time for ventricles to fill during diastole.

Bradycardia: cardiac output will decrease over one minute.

What is Preload? What influences Preload?

Volume of blood in the ventricle at the end of diastole. It is influenced by venous return to the heart and total circulating volume.

Why is preload important for contractility?

More volume into the heart stretches the muscle of the heart more = increased contractility = increased CO.

Total Circulating Volume

Amount of fluid within the heart, arteries, and blood vessels at any given time.

How does intrathoracic pressure influence venous return?

Intrathoracic pressure is pressure within the entire chest cavity. A higher intrathoracic pressure compresses the vena cava = less venous return of blood to the heart.

It can be caused by tension pneumothorax, CPAP, and BiPAP.

What are some patient assessment cues for preload?

• Daily weights/fluid balance

• Skin turgor

• Mucous membranes = moist? dry?

• Dehydration/fluid and blood loss = vomit, diarrhea, urination (DKA, HHS)

• Jugular vein pressure = distension?

• Central venous pressure monitoring (CVP)

What is CVP monitoring? Why is it important? What is the normal range?

Central venous pressure monitoring = measures blood flowing into the right side of the heart. It is a good assessment cue for judging preload, especially for patients with significant fluid alterations. Normal range = 2-6 mmHg.

Why is urine output not a good indicator of preload? (Kidney failure/Heart failure)

1. Kidney failure = decreased u/o is within the patient’s normal, but preload is actually increased since fluid is not removed from the body.

2. Heart failure = contractility issues where the heart is not pumping blood forward properly = preload becomes excessive. CO and organ perfusion decreases = kidneys not perfused = u/o decreases.

What is Afterload? What is its determinants?

The resistance/force the ventricles work against when ejecting blood during systole. It is determined by the 3 V’s:

• Vessel diameter

• Viscosity of blood: thicker blood = more force to pump out (ex: prolonged hyperglycemia)

• Valve dysfunction (stiffness)

How is vessel diameter measured?

It is measured by trends in Diastolic BP (DBP) and pulse pressure.

What is DBP? How does it measure vessel diameter?

DBP is the pressure in the arteries during diastole. It informs afterload.

High DBP = increased vasoconstriction = increased afterload.

What is pulse pressure? How does it measure vessel diameter?

Pulse pressure is the difference between systolic and diastolic BP.

A narrow pulse pressure indicates vasoconstriction (less than or equal to 25 mmHg).

A widening pulse pressure may indicate vasodilation.

What are the assessment findings of decreased afterload?

• Fever/flushed skin

• Bounding peripheral pulses

• Capillary refill less than 3 seconds + brisk

• Downward trend in DBP

• Widening pulse pressure

What are the assessment findings of increased afterload?

• Narrow pulse pressure less than or equal to 25 mmHg

• Increased DBP

• Cool/pale/dusky skin

• Prolonged capillary refill

• Weak or non-palpable pulses

How can increasing preload reduce afterload in some cases?

Because increased afterload/vasoconstriction could have been a compensatory mechanism for decreased preload.

What is Contractility? What is it determined by?

It is the contractile strength of the heart. It is determined by preload, because preload determines how much the heart fibres stretch for effective recoil and contraction of the ventricle.

Why can too much preload be bad for contractility?

Too much stretching can cause the myofibrils to stretch too much and lose recoil.

What are the assessment cues for Contractility?

• Preload

• Pre-existing heart conditions that has damaged the heart muscle (ex: MI)

• End-organ perfusion

• HR and rhythm

• SNS activation

• Calcium in the myocardial cell

• O2 supply to the heart

• Electrolyte imbalances

• Ejection fraction

• Inotropic drugs

What are inotropic drugs? What is the difference between positive and negative inotropic drugs?

They change the force of the heart’s contractions.

Positive = strengthens the force of the heartbeat

Negative = weakens

What is a normal ejection fraction?

55-75%

What are interventions to correct contractility?

• Correct preload

• Drugs to manage heart failure (ACE Inhibitors, ARBS, Beta Blockers)

• Correct electrolyte imbalances/dysrhythmias

• Antiarrhythmic drugs

• Inotropic drugs

What is MAP? How is it calculated?

The average pressure within the arterial vessels during one full cardiac cycle. It indicates the average perfusion measure to ensure organ and tissue perfusion (greater or equal to 65 mmHg).

MAP = 1(SBP) + 2(DBP) / 3

Explain why a high MAP is bad.

High MAP (above 100 mmHg) = causes stress on the heart, the heart must work harder than normal to push against the elevated pressure in the vessels.

Can lead to heart disease, blood clots, heart attack, and stroke.

Explain why a low MAP is bad.

Low MAP (below 65 mmHg) = organs in the body do not get enough perfusion.

Aortic Impedance

The resistance that blood pumped from the heart meets as it enters the aorta.

What are the 3 determinants of O2 demands?

1. Temperature: fever requires energy

2. Physical Activity

   1. Increase O2 demand for compensation (increased HR, RR, accessory muscle use)

   2. Restlessness, coughing, vomiting, agitation

   3. Nursing care - repositioning, washing, dressing changes

3. Stress

   1. Physiological

      1. Pain, shock, infection, injury

   2. Perceived

      1. Emotional/psychological = fear, anger, unfamiliar environment.

Interventions to decrease O2 demands

• Pain meds

• Anti-emetic

• Anti-anxiety

• Sleep medication

• Reducing noise/light

• Limiting visitors

• Balance between rest and activity

Explain how increased Lactic Acid is a sign of decreased cellular oxygenation.

When cellular O2 is decreased, cellular hypoxia occurs = cells then shift from aerobic metabolism to anaerobic metabolism. The end product is lactic acid.

Rising lactic acid is a sign that compensation is inadequate or failing.