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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
98 T. Jones, R. McIntyre and E. Peltz
• Cardiac output is dependent on heart rate and stroke volume (CO = HR × SV).
• Stroke volume is dependent on rate, rhythm, preload, afterload and contractility.
{ Oxygen content consists primarily of hemoglobin bound oxygen. Goal
SaO2 and hemoglobin levels are necessary to optimize oxygen content.
{ Anemia has a much greater influence on arterial oxygenation than hypoxemia.
{ Oxygen uptake/consumption is difficult to measure without specialized
equipment (indirect calorimetry). Surrogates for oxygen uptake are mixed
venous hemoglobin oxygen saturation (SvO2) and central venous
hemoglobin oxygen saturation (ScvO2).
{ SvO
{ Oxygen extraction is measured via invasive methods but can assess the
or ScvO2 are dependent on SaO2, hemoglobin, CO and VO2.
2
relative adequacy of oxygen delivery and impaired oxygen extraction.
{ States that increased metabolic demand and oxygen consumption include
sepsis, fever, shivering, seizures or excess work of breathing.
{ Beyond maximizing VO
, there are few interventions to correct mito-
2
chondria oxidative dysfunction in both septic and trauma patients.
Background
A fundamental element of aerobic life is a combustion reaction utilizing oxygen
to release stored energy in foods while carbon dioxide (CO2) is produced as a
byproduct. In healthy individuals, oxygen is often in excess and aerobic metabolism is possible even with moderate amounts of stress.
However, the critically ill oxygen delivery can be the rate limiting step creating a delicate balance of sufficient DO2 to meet the patients increased metabolic
requirements and cellular VO2.
An imbalance in adequate oxygen supply to meet cellular metabolic demand
leads to anaerobic metabolism for energy production and is commonly referred
to as SHOCK (inadequate tissue perfusion with oxygen). This anaerobic metabolism becomes clinically apparent with increased lactate levels and metabolic
acidosis.
Thus a fundamental goal of resuscitation in the critically ill or injured patient
must be directed at the restoration of this balance between DO2, oxygen demand
(metabolic state of the patient) and VO
DO2 is the most readily modifiable factor in this process while altering
patient metabolic state or VO2 are more difficult to achieve.
.
2
Fundamentals of Oxygen Transport and Cellular Metabolism 99
Main Body
Cellular metabolism
Cellular respiration — combustion of nutrient fuels to produce energy in the form
of ATP occurs by two principle means:
{ Aerobic metabolism — When adequate oxygen is present for the com-
plete oxidation of glucose the result is the production of 36 moles of ATP
(673 Kcal).
{ Anaerobic metabolism — With inadequate oxygen delivery to tissues or
inadequate oxygen uptake by cells the result is a precipitous decline in the
production of ATP (2 moles ATP/glucose via anaerobic glycolysis) and an
associated production of pyruvate which is converted to lactate as a
byproduct (1 glucose molecule produces 2 lactate molecules).
{ This production of lactate leads to an anion gap metabolic acidosis and is
often followed clinically to assess adequacy of resuscitation.
{ In both septic and trauma patients, there can be defects in O
utilization
2
in mitochondria, limiting metabolism despite adequate DO2.
Assessment of cellular metabolism
{ Lactate is an end product of anaerobic glycolysis.
{ The normal serum lactate concentration is <2 mM/L.
{ Serum lactate production increases with tissue hypoxia (shock, organ
ischemia) aka type A lactic acidosis and with conditions unrelated to
hypoxia, aka type B, i.e. increased protein catabolism, decreased hepatic
clearance, and hematologic malignancy.
{ Serum lactate clearance is decreased with liver failure and shock.
{ In sepsis, defects in O
utilization in mitochondria increases serum
2
lactate. Components of the bacterial cell wall including endotoxin have
been implicated.
{ Base deficit is determined by arterial blood gas and is defined as
the amount of base that must be added to one liter of blood to raise pH
to 7.4.
{ The normal base deficit is <2 mmol/L.
{ Elevation in base deficit is a non-specific marker for impaired tissue
oxygenation and is a surrogate for serum lactate.
100 T. Jones, R. McIntyre and E. Peltz
Oxygen delivery
• Oxygen delivery (DO2) is described by two clinical parameters; the amount
of oxygen within the blood [ arterial oxygen content (CaO2)] and the flow
which delivers this to tissues [ cardiac output (CO)].
DO2 = CO × CaO2 Normal DO2 ≈ 1000 ml/min
Normalizing for patient size/habitus
Often more important than the absolute amount of blood pumped per minute
(CO) is the amount of blood pumped per minute in relation to the patient’s overall size which can be approximated by total body surface area.
In clinical practice, our patients vary significantly in body habitus and to
assess the adequacy of cardiac output providing blood flow in relation to the
smaller or larger total tissue beds for a given patient (i.e. normal weight vs.
morbidly obese patients), the CO in relation to total body surface area in m
calculated as the cardiac index (CI).
2
is
CI = CO/m2 total body surface area Normal CO = 4–8 L/min/m
Normal CI = 2.4–4 L/min/m
2
2
Similarly using CI in place of cardiac output (CO) to determine DO2 will provide
the oxygen delivery index (DO2I) in relation to total body surface area.
DO2I = CI × CaO2 in ml/min/m
2
Normal DO2I = 520–570 ml /min
We will now evaluate specific factors contributing to CaO2 and CO/CI which in
turn determine DO2/DO2I.
1) Arterial oxygen content (CaO2) is composed of hemoglobin (Hgb) bound
O2 and dissolved O2.
(CaO2) = (Hgb × SaO2 × 1.34) + PaO2 × 0.003 Normal CaO2 = 20 ml /dl
Hemoglobin bound oxygen is the predominate portion of blood oxygen
{ Hgb bound O
SO2 = % of hemoglobin molecules that are saturated with O
= 1.34 (ml/g) × Hgb (g/dL) × SO2 = ml’s O2/100 mL
2
2
Provided as a percent = Oxygenated Hgb/Total Hgb.
Fundamentals of Oxygen Transport and Cellular Metabolism 101
{ Example:
Trauma patient with Hgb of 7 g/dL and SO2 95%
Ö 1.34 × 7 × 0.95 = 8.9 ml O2/100 mL
Dissolved oxygen is a minor portion of blood oxygen content
Dissolved O2 = 0.003 mL/100 mL /mm Hg × PaO2 mm Hg
Oxygen does NOT dissolve readily in blood, thus need Hgb (i.e. PaO
= 100, 1L of blood only contains 3 mL of dissolved O2)
{ Example:
Trauma patient with PaO2 100 mm Hg on ABG
Ö 0.003 (mL/100 mL/mm Hg) × 100 mm Hg = 0.3 mL O2/100 mL
of dissolved O2 in pt’s blood
{ Given the relatively small contribution of dissolved oxygen, clinically
CaO2 content can be simplified to CaO2 = 1.34 × Hgb × SaO
{ Example:
2
Trauma patient with Hgb 7 g/dL, SO2 95% and PaO2 100
Ö (1.34 × 7 × 0.95) + (0.003 × 100) = 9.21 ml O2/100 mL
Increasing Hgb by 2 g /dl (Hbg 9, SO2 95% and PaO2 100)
Ö (1.34 × 9 × 0.95) + (0.003 × 100) = 11.76 O2/100 mL
Ö 22% increase in blood oxygen content
While increasing PaO2 to 300 mm Hg (Hgb 7 g/dL, SO2 95% and PaO2
300)
Ö (1.34 × 7 × 0.95) + (0.003 × 300) = 10.1 ml O2/100 mL
Ö Only 9.6% increase in blood oxygen content.
2
Assessment of Oxygen Content
{ SaO
{ Hgb — Hematology
{ PaO
2) Cardiac Output
As previously described oxygen delivery is dependent on CaO
optimize DO2, we have previously evaluated and augmented arterial oxygen content. We must now assess and optimize the rate oxygen is carried to the vital
organs by CO to deliver the oxygen to tissues.
— Pulse oximetry
2
— ABG
2
and CO. To
2
102 T. Jones, R. McIntyre and E. Peltz
Cardiac output = Heart Rate × Stroke Volume
{ CO is dependent on rate, rhythm, preload, afterload and contractility
Rate:
Ö Tachycardia decreases diastolic ventricular filling time resulting
in a decrement in ventricular preload and sub-optimal FrankStarling forces impairing both stroke volume (SV) and contractile
force.
— slow the rate
Ö Bradycardia: If SV is relatively fixed secondary to age (pediatric
physiology) or in certain cardiomyopathies then bradycardia may
be the limiting factor in cardiac output.
— increase the rate
Rhythm:
Ö Ineffective rhythm: (i.e. atrial fibrillation) this can result in
impaired preload. Up to 20% of ventricular filling, and supplemental preload and ventricular wall tension are, in part, reliant on
atrial contraction [Chapter 5-(vi)].
Treat the specific rhythm disturbance
Ö Tachy-dysrrythmias adversely impact as above under rate.
— Treat the specific rhythm disturbance
Pre-load: The goal is to optimize the cardiac myocyte overlap and the
Starling curve [Chapters 5-(iii) and 5-(iv)].
Ö Hypovolemia: In addition to impaired preload secondary to tachy-
cardia and dysrhythmias inadequate central venous pressure from
hypovolemia or distributive shock (i.e. sepsis/adrenal insufficiency) impairs ventricular filling and preload.
— Treatment in this setting is directed towards fluid resuscitation
followed by reassessment [Chapter 5-(iv)].
Ö Hypervolemia: Over distension of the ventricle as can occur with
congestive heart failure, myocardial infarction, cardiac contusion
can lead to impaired stroke volume and cardiac output.
— Treatment goals are aimed at reducing circulating volume, or
the addition of inotropic agents to augment contractile force
and stroke volume. Treatment may include diuretics, dialysis
[Chapter 7-(iv)] or inotropic agents.
Fundamentals of Oxygen Transport and Cellular Metabolism 103
Afterload:
Ö Increased afterload in the setting of myocardial strain from severe
illness or injury can precipitate heart failure and impair CO. This
is analogous to a strained heart attempting to pump against a
relatively closed circuit.
— Treatment directed at afterload reduction (vasodilators, diuretics).
Ö Low afterload may have less direct impact on cardiac — maintaining
mean arterial pressure such that forward flow continues to the
peripheral tissue beds is essential for delivery of oxygen (i.e.
distributive shock associated with sepsis, burns, adrenal insufficiency may require agents with α-adrenergic activity for support
of MAP and oxygen delivery).
— Treatment directed at the underlying cause and hemodynamic
support with volume resuscitation and vasopressors.
Contractility:
Ö Impaired by pre-existing cardiac defects (i.e. wall motion abnor-
malities, history of MI, CHF, etc.), cardiac injury, medication side
effect (i.e. anesthetics/sedation), electrolyte abnormalities (i.e.
hypocalcemia) and by acidosis.
— Treatment directed at the underlying cause or precipitating
factor and hemodynamic support of the patient with inotropes
and vasopressors.
{ Rate, rhythm, preload, afterload and contractility are patient specific. As
an example; a 75-year-old patient with history of MI and pre-injury/illness
ejection fraction of 40% may be significantly more sensitive to diminished
preload due to atrial fibrillation or SVT. This patient may also require a
significantly increased central venous pressure/preload to develop adequate contractility and SV as compared with a healthy 30-year-old patient.
{ In healthy patients without pre-existing CV comorbidities, the approach
can often be to clinically challenge the patient with resuscitation and
increased preload while this may require invasive monitoring in the
patient with previous CV dysfunction.
Assessment of CO
{ Severe blood loss affects both oxygen content (via Hgb) and cardiac
output (via stroke volume).
104 T. Jones, R. McIntyre and E. Peltz
{ Rate/Rhythm: telemetry, EKG.
{ Preload: Central venous pressure via central venous catheter, ultrasound
evaluation of respiratory variability in the infra-hepatic vena cava diameter, stroke volume variability via continuous arterial catheter cardiac
output monitoring or approximated by “delta-down” (systolic pulse pressure variability) in the arterial line tracing.
{ Contractility/Stroke Volume: echocardiography, pulmonary artery catheter.
{ Cardiac Index/Cardiac Output: pulmonary artery catheter. Other
devices are available to indirectly estimate cardiac output by assessing
thoracic bio-electric impedance or pulse volume waveform associated
with arterial lines.
Assessing oxygen balance and cellular metabolism
After optimizing oxygen content and cardiac output, it becomes necessary to
assess overall oxygen balance and effect on metabolism. Oxygen uptake is the
rate at which oxygen dissociates from hemoglobin and moves into tissues — it
can be thought of as VO2.
{ When VO
oxygen uptake or increased cellular metabolism.
{ When VO
producing lactate.
{ VO
itself is difficult to assess.
2
is low, it means there is either inadequate DO2, inadequate
2I
is less than the metabolic rate, anaerobic metabolism occurs,
2
Assessments of VO2
{ Calculated uptake VO
This reverse Fick method of calculating VO2 does not include the O2
consumption of the lung, which can be highly variable in septic/
trauma patients.
{ Indirect Calorimetry: assessment of the rate of oxygen disappearance and
carbon dioxide production by monitoring of gas exchange during respiration through a ventilator circuit or “metabolic hood” placed over the
patients head. This requires specialized personnel and equipment and is
often not clinically applicable during acute resuscitation but may help to
provide a measure of metabolic rate and oxygen consumption after initial
stabilization.
= Q × (CaO2−CvO2) × 10 (mL/Min)
2
Fundamentals of Oxygen Transport and Cellular Metabolism 105
{ Oxygen uptake (VO
) is also proportional to the oxygen extraction ratio
2
(O2ER), the ratio of oxygen consumption to oxygen delivery, and can be
estimated by the difference between arterial and venous oxygen content
(O2ER ≈ (CaO2 – CvO2)/CaO2). Normal O2ER = 20–30%
VO2 = DO2 × O2ER and O2ER ≈ (CaO2 – CvO2)/CaO
2
VO2 = DO2 × (CaO2 − CvO2)
{ CaO
and CvO2 share the equation for hemoglobin binding (1.34 × Hb)
2
and subsequently the equation can be isolated as such:
VO2 = DO2 × 1.34 × Hgb × (SaO2 – SvO2)
{ Like CI and DO
I, VO2 is often calculated using DO2I to provide oxygen
2
uptake in relation to body surface area in m2 as VO2I.
Normal VO2 = 180–280 ml/min
Normal VO2I = 110–160 ml/min/m
Central and Mixed Venous Oxygen Saturations (ScvO2 and SvO2)
{ As stated above, oxygen uptake can be estimated by the difference
between arterial and venous oxygen content and a normal Oxygen
Extraction Ratio is 20–30% of the oxygen delivered to peripheral tissues.
Estimation of adequate oxygen delivery can then be made by evaluating
the saturation of venous blood returned to the heart.
Arterial oxygen saturation in blood delivered peripherally is normally
90–100% (SaO2).
If O2ER = 20–30% then saturation of blood returning to the heart
should be approximately 60–80%.
Mixed venous and central venous saturations are followed clinically to assess
efficacy of resuscitation and adequacy of oxygen delivery
2
Assessment of SvO2 and ScvO
{ Mixed venous saturation: SvO
drawn from the distal channel of a pulmonary artery catheter and represents a true mixed venous O2 from all peripheral blood return to the heart.
{ SvO
can also be continuously monitored with fiberoptic venous oximetry
2
available with pulmonary artery catheters.
2
can be measured via venous blood gas
2
Normal SvO2 is 60–80%
106 T. Jones, R. McIntyre and E. Peltz
{ Central venous saturation: ScvO
is assessed by venous blood gas drawn
2
from central venous catheters and represents O2 saturation in the superior
vena cava. Assessment of oxygenation at this location will not reflect
lower body oxygen extraction and on average can be 10–15% higher than
SvO2 in critically ill patients. One must consider this “over-estimation” of
mixed venous saturation (SvO2) during evaluation and assessment of
ScvO2.
{ ScvO
can additionally be followed continuously with fiberoptic venous
2
oximetry available with some specialized central venous catheters.
Normal SvO2 is 65–85%
A decrease in SvO2 (< 70%) can be due to:
{ Hypoxemia (overall decrease in SaO
leading to decrease oxygen
2
delivery)
{ Anemia (decrease Hgb leading to decrease oxygen delivery)
{ Decreased cardiac output
{ Increased VO
(increased oxygen consumption)
2
Unfortunately, an increase in SvO2 (>75%) may indicate defect in oxygen
utilization at a mitochondria (decreased oxygen uptake) which may indicate
septic shock, as opposed to improvement in clinical condition.
Practical Algorithm(s)/Diagrams
Fig. 1. Factors affecting SvO2 and ScvO2.
*Changes in SvO
while they are inversely proportional to changes in VO
and ScvO2 are directly proportional to changes SaO2, Hgb, and CO
2
.
2
Fundamentals of Oxygen Transport and Cellular Metabolism 107
Fig. 2. Protocol for evaluation and management of tissue oxygenation.
Review of Current Literature with References
• McKinley et al. found there was no difference in outcomes between trauma
patients who were resuscitated to a DO2I of 500 vs 600. DO2I was increased
via a computerized protocol of volume resuscitation and inotropes. Less volume and transfusion requirements were required for similar outcomes. (J
Trauma 2002; 53: 825–832).
• To determine the value of early goal-directed therapy in the resuscitation of
critically ill patients, Rivers et al. randomized 263 patients diagnosed with
sepsis to standard resuscitation vs. early goal directed therapy. Therapy was
directed at optimizing the balance between systemic oxygen delivery and
oxygen demand in this critically ill population. Clinical endpoints for early
goal directed therapy included CVP, MAP and ScvO
directed group received crystalloid to achieve central venous pressure of
8–12 mm HG. If MAP remained <65 mmHG vasopressors were started. As a
. This early goal-
s