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Normal Capnogram - At first there is a rapid rise as the dead space gas comes out of the major airways. Then there is a plateau, which is allowed to have a slow rise. Finally there is a rapid decline as the next breath enters the patient.
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Poor Plateau – This can be do to a kinked ET Tube, herniation of the cuff, bronchospasm or and other obstruction that limits expiration.
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Curare Cleft – This waveform is usually seen with high CO2 levels.
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Cardiogenic Oscillations – The beating heart against the lungs usually causes this waveform. (Because the heart takes up more space, this is more commonly seen in children).
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Camel Capnogram – This waveform can be seen if there is unequal emptying of the lungs, when patient is placed in a lateral position, or if the ET tube is touching the carina.
Abnormal Findings:
Slow decrease in ETCO2 :
· Hyperventilation
· Fall in Body Temperature
· Decreasing Lung or Body Perfusion
A Sudden Drop in ETCO2 to zero:
· Kinked ET tube/Capnometer
· Patient Extubated
· Ventilator Circuit Disconnect/Failure
A Sudden Drop in ETCO2 but not to zero:
· Leak in Circuit (Deflated Cuff)
· Obstruction (Bronchospasm)
· Leak in Capnomete
An Exponential Decrease in ETCO2:
· Circulatory Arrest (Cardiac or Hypovolemic)
· Pulmonary Embolism
· Sudden Severe Hypertension
A Sudden Rise in Baseline:
· Stuck Valve in Circle Absorber System
· Exhausted Capnometer/Calibration Error
Gradual Increase in ETCO2:
· Hypoventilation
· Absorption of ETCO2 in the peritoneal cavity
· Rapidly Rising Body Temperature
Sudden increase in ETCO2:
· Injection of Sodium Bicarbonate
· Sudden Increase in Blood Pressure
Sepsis:
Statistics:
· There are more than 750,000 cases of sepsis annually in North America
· The number of deaths from sepsis is equal to that of acute myocardial
infarction.
· Sepsis occurs in 2 of every 100-hospital admissions. It is caused by
bacterial infection that can originate anywhere in the body.
· The death rate can be as high as 60% for people with underlying medical
problems.
· Mortality is less (but still significant) in individuals without other medical
problems.
Defining Sepsis:
Severe sepsis is characterized by stimulation of a series of inflammatory cascades leading to extensive cardiovascular derangement, the most overt signs of which are hypotension relative hypovolemia, and widespread dysfunction of the microvasculature (capillary leak). Simultaneously, there is activation of the coagulation cascades, the formation of intravascular thrombus, and subsequent tissue injury and multi-organ dysfunction.
Focus of Treatment:
The two major priorities in management of septic patients are to first; maintain delivery of oxygen to the tissues by way of optimization of cardiac output and peripheral resistance and second, modulate the pro-coagulation response.
Oxygen Delivery and Consumption in relation to the” Starling Curve”, can be calculated:
CaO2 = (1.34 x hemoglobin concentration x SaO2) + (0.0031 x PaO2)
where:
• PaO2 is the partial pressure of oxygen in the arterial blood
• SaO2 is the arterial oxyhemoglobin saturation
Each gram of fully saturated hemoglobin carries 1.34 mL of oxygen. Oxygen dissolves in plasma proportionally to the PaO2, with 0.0031 mL dissolved per deciliter of blood per mmHg PaO2. Normal CaO2 is approximately 20 mL O2/dL (1000ml/min), depending upon the site from which the blood is sampled.
Similarly, the mixed venous blood oxygen content (CvO2) can be determined by adding the amount of oxygen dissolved in the venous blood to the amount of oxygen remaining bound to hemoglobin:
CvO2 = (1.34 x hemoglobin concentration x SvO2) + (0.0031 x PvO2)
where:
• PvO2 is the partial pressure of oxygen in the mixed venous blood
• SvO2 is the mixed venous oxyhemoglobin saturation
“Normal” extraction ratio is usually 25%-30/% to calculate this:
(CaO2 – CvO2)/CaO2
Causes of Increased O2 Consumption:
Causes of Decreased O2 Consumption:
Re-establishing Circulation:
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Fluid - Hypotension is caused by myocardial depression, pathological vasodilatation and extravasations of circulating volume due to widespread capillary leak. The initial resuscitative effort is to attempt to correct the absolute and relative hypovolemia by refilling the vascular tree. There is good evidence that early goal directed aggressive volume resuscitation improves outcomes in sepsis. Use of previously discussed crystalloids or colloids are the treatment option to restore circulation.
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Vasopressors - Current pharmacological management of sepsis is to maintain blood pressure and tissue perfusion, while minimizing unwanted systemic/metabolic effects. As a result it may be necessary to combine multiple agents with differing pharmacologic profiles. Vasopressors are agents that cause constriction of blood vessels, leading to an increase in blood pressure. Some vasopressors are also positive inotropes (capable of increasing contractility of the heart) and/or positive chronotropes (capable of increasing heart rate). The hemodynamic effects of most vasopressors occur secondary to their interactions with receptors in the heart and vascular system. The following Vasopressors should be considered in cases of severe sepsis:
Norepinephrine:
Norepinephrine is one of the principal neurotransmitters chemical substances involved in the transmission of nerve impulses in the sympathetic nervous system. It is released from nerve cells, and is indicated for the treatment of acute hypotension resulting from conditions such as spinal anesthesia, myocardial infarction, septicemia, blood transfusions, and drug reactions. This agent is also used adjunctively in the treatment of cardiac arrest and profound hypotension. Norepinephrine is a potent alpha adrenoceptor agonist and is therefore a strong vasoconstrictor, increasing systolic and diastolic blood pressures. In addition, Norepinephrine stimulates beta 1 cells so it increases both heart rate and contractility.
Epinephrine:
Epinephrine is another neurotransmitter in the sympathetic nervous system, but it is not released from nerve cells; rather, epinephrine is a hormone secreted by the adrenal medulla. Epinephrine is used intravenously during advanced cardiac life support and may also be used to treat other conditions, including anaphylactic shock and acute, severe asthma unresponsive to normal treatment. Because Epinephrine is a potent alpha and beta adrenoceptor agonist, it is also a powerful vasoconstrictor with both positive inotrope, and chronotrope effects. Epinephrine causes increased heart rate, increased force of contraction, an increase in cardiac output, and increased systolic blood pressure. The vasoconstrictive effects of epinephrine become more apparent as the dose is increased.
Dopamine:
Dopamine, a precursor of norepinephrine and epinephrine, is also a neurotransmitter. Dopamine is found in both the central and peripheral nervous systems and is released from nerve cells. Dopamine is indicated in the treatment of shock due to myocardial infarction, trauma, septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation. The effects of dopamine are complex and dose dependent. Dopamine directly stimulates dopaminergic receptors, alpha and beta adrenoceptors, and it indirectly causes the release of endogenous norepinephrine. At low doses (l to 5mcg/kg/minute), dopamine directly stimulates dopaminergic receptors on arteries in the kidneys, abdomen, heart, and brain and causes vasodilatation. At these doses, urine output may increase, but blood pressure and heart rate are usually not affected. As the dose is increased (5 to 10 mcg/kg/min), dopamine stimulates beta 1 adrenoceptors, resulting in positive inotropic and chronotropic effects, which increases myocardial contractility, and heart rat which results in, enhanced cardiac output. At higher doses (greater than 10 mcg/kg/min), dopamine exerts effects primarily alpha-receptors, and extensive vasoconstriction causes blood pressure to increase.
Phenylephrine (Neosynephrine):
Phenylephrine is chemically related to epinephrine and used to treat hypotension resulting from shock, shock like states, anesthesia, or hypersensitivity reactions to drugs.
Phenylephrine is a powerful vasoconstrictor that strongly stimulates alpha adrenoceptors but has little effect on the beta adrenoceptors of the heart. Its vasoconstrictive properties are similar to those of norepinephrine. Phenylephrine increases systolic and diastolic blood pressures in a dose dependent manner, but because it has minimal effects on beta-receptors, heart rate and contractility are generally not affected.
Vasopressin:
Vasopressin is a unique vasopressor for two reasons. First, its principal use is for a condition unrelated to its vasopressor properties. Vasopressin is an antidiuretic hormone indicated to inhibit diuresis in patients with diabetes insipidus. However, at higher doses, vasopressin causes vasoconstriction. Because there is a fair amount of evidence to support its effectiveness as a vasopressor, vasopressin is now considered as an alternative to epinephrine for the treatment of adult shock-refractory ventricular fibrillation during advanced cardiac life support. Vasopressin is a distinctive vasopressor also because its vasoconstrictive effects do not result from its interaction with adrenoceptors; rather, vasoconstriction arises from vasopressin's actions on vasopressin receptors. Vasopressin receptors are classified as V-1 and V-2 receptors. V-1 receptors are located on arterial smooth muscle, and V-2 receptors are found in renal tubules. It is Vasopressin's interaction with V-1 receptors that is responsible for its potent vasopressor effects.
Dobutamine:
Dobutamine is indicated for short-term inotropic support in patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgery. Classifying the drugs that have been discussed so far as vasopressors has been fairly straightforward. Including Dobutamine in this class of drugs is more difficult. Although Dobutamine is an inotrope, and considered by some to be a vasopressor, others consider it a vasodilator. Dobutamine is generally considered a relatively selective beta adrenoceptor agonist because the net effect of Dobutamine administration is an increased cardiac contractility, decreased after load and improved cardiac output.
Note: If your patient is DRY forget about it…….
Fluid Resuscitation and Acid-Base Imbalances:
Blood Transports gases, brings oxygen to the cells and takes carbon dioxide back to the lungs. Blood also transports nutrients and waste products. The protection property of blood carries antibodies and WBC’s. The regulatory property of blood transports regulatory hormones and chemicals. Blood volumes average 4.5 to 5 Liters and equals 7% of today body weight in males and 6.5% of total body weight in females.
Hypovolemic Shock (defined as approximately 1 Liter or 1/5 loss of circulating volume). The following is the sequence of events that under perfused tissue goes through:
Profound ischemia for unperfused tissue causes a switch to anaerobic metabolism >
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Which leads to Lactic Acid waste >
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This causes decreased ATP to be available for cell work >
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The cell membrane cannot function and it dies >
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This causes release of intracellular enzymes and inflammatory mediators >
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This inflammatory process wrecks havoc on the Lungs, Kidneys,
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Digestive Tract, Capillary Lining and Coagulation. Whew!
There are 3 Stages in Hypovolemic Shock: Compensated, Uncompensated and Irreversible:
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Compensated – The body is still able to compensate for the decrease in perfusion. Cardiac Output and systolic blood pressure are maintained.
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Uncompensated – The bodies compensation mechanisms are starting to fail. Blood pressure begins to decrease and patient condition worsens.
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Irreversible – Cell and tissue ischemia lead to organ death due to lack of perfusion. This process may begin on day one and continue to occur for up to three weeks after the initial insult. Under such circumstances, the patient should be re-evaluated to determine whether some reversible causes of the persistent shock may have been overlooked.
The following are some of the more frequent, treatable causes of persistent shock:
· Inadequate fluid administration (even if the patient clinically appears to be overloaded with fluid)
· Inadequate ventilation or oxygenation
· Pneumothorax
· Pulmonary emboli
· Pericardial tamponade
· Inadequately treated sepsis
· Adrenal insufficiency
· Hypothermia
· Hypocalcemia
Classes of Hemorrhage:
Classes of hemorrhage have been defined, based on the percentage of blood volume loss. However, the distinction between these classes in the hypovolemic patient often is less apparent. Treatment should be aggressive and directed more by response to therapy than by initial classification.
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Class I hemorrhage (loss of 0-15%)
· In the absence of complications, only minimal tachycardia is seen.
· Usually, no changes in BP, pulse pressure, or respiratory rate occur.
· A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately 10%.
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Class II hemorrhage (loss of 15-30%)
· Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.
· The decrease in pulse pressure is a result of increased catecholamine levels, which causes increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.
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Class III hemorrhage (loss of 30-40%)
· By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP, oliguria, and significant changes in mental status, such as confusion or agitation.
· In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.
· Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids.
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Class IV hemorrhage (loss of >40%)
· Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness), and cold and pale skin.
· This amount of hemorrhage is immediately life threatening.
In the patient with trauma, hemorrhage usually is the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits)
The 4 areas in which life-threatening hemorrhage can occur are as follows: chest, abdomen, thighs, and outside the body.
· The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration.
· The abdomen should be examined for tenderness or distension, which may indicate intra-abdominal injury.
· The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh).
· The patient’s entire body should then be checked for other external bleeding.
Lab Values:
Monitoring Lab Values and ABG’s is a crucial part of evaluating patient condition and expected outcome. The following list of labs (with normal values listed) should be monitored frequently:
· Hemoglobin – Male 14-18 g/dl, Female 11-16 g/dl
· Hematocrit – Male 39-54%, Female 34-47%
· Prothrombin Time (PT) – 10-14 seconds
· Partial Prothrombin Time (PTT) – 32-45 seconds
· Fibrinogen – 160-450mg/dl
· BUN – 6-23 mg/dl
· Creatinine – Male 0.2-0.6 mg/dl, Female 0.6-1.0 mg/dl
· Sodium – 135-148 mEq/L
· Potassium – 3.5-5.5 mEq/L
· Glucose – 70-110 mg/dl
· Lactic Acid – 0.3-2.3 mEq/L
· ABG’s:
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pH 7.35 - 7.45
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PaCO2 35 - 45 mm Hg
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HCO3 22 - 26 mEq/L
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O2 sat 96 - 100%
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PaO2 85 - 100 mm Hg
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BE -2 to +2 mmol/L
When evaluating ABG’s, note that persistent metabolic acidosis, as reflected by a continuing lactic acidosis or base deficit of > 10 mEq/L, is usually due to inadequate resuscitation or ongoing blood loss and should be treated with fluids, blood, and consideration of operative intervention for control of hemorrhage. In general, a metabolic acidosis persisting for more than 12 hours is associated with an increased incidence of multiple organ failure.
Note: All electrolyte levels should be frequently sent and replaced as appropriate
Goals of Fluid Resuscitation:
Resuscitation Goals are not black and white, and should be focused on individual patient condition and need. Broad guidelines that can be followed include:
· Targeting O2 delivery to vital organs rather then a specific B/P or heart rate
· This usually requires MAP of 60-70 mmHg
· Monitor mental status, skin color, blood gases, hemoglobin, urine output, electrolytes and Lactic Acid levels
· PA catheter is not necessarily a mainstay but can offer a more detailed view of patient condition. If PA catheter not available, try using CVP monitoring for baseline.
· PiCCO catheter, this is a catheter that is placed in the femoral artery that provides information about hemodynamic stability by measuring heart and lung volumes rather then pressure.
Fluid Replacement Choices:
Conventional “crystal”loids (see through):
Include both balanced salt solutions (BSS) and hypotonic salt solutions. Balanced salt solutions include such fluids as 0.9% NaCl (normal saline), and Ringer's Lactate solutions. These solutions are characterized by having an electrolyte composition or calculated osmolality approximating that of plasma. Balanced salt solutions distribute approximately ¾ or their volume to the extravascular space with ¼ of the volume remaining in the vascular space.
Colloid solutions:
These are solutions of proteins, starches, dextrans, and gelatins containing molecules sufficiently large enough so that they do not normally cross capillary membranes. Under normal conditions most of the administered volume remains in the intravascular space (unless tissue is damaged and then it can cross membranes). Once colloids have leaked into the interstitium, they must be removed by the lymphatic system or they will exert a reverse pressure gradient, drawing water from the vascular space. The removal of colloids from the interstitium is typically much slower than that of crystalloids.
Blood Component Therapy:
· Packed Red Blood Cells - Red cell transfusions initially may be achieved with uncross-matched type O red cells. If a patient’s blood type has been determined, ABO and Rh specific red cells can be used. Every effort should be made to establish the blood type of a patient prior to transfusion to preserve type O red cell availability and accurately determine the patient’s blood type.
· Platelets - Platelet transfusion therapy after massive transfusion is an accepted intervention in the presence of micro-vascular bleeding prior to documentation of thrombocytopenia. The platelet transfusion dose recommended is 1 unit per 10 kg body weight for platelet counts <50,000 or when platelet dysfunction is suspected.
· Plasma – Plasma (FFP) transfusion therapy should be instituted after laboratory confirmation of coagulation factor deficiencies. The recommended dose is 10-15 mL/kg body weight for PT/PTT>1.5 normal range.
· Cryoprecipitate - Cryoprecipitate therapy should be instituted for the correction of laboratory evidence of hypo-fibrinogenemia (fibrinogen <100 mg/dl). Dosing will depend on the degree of hypo-fibrinogenemia and the patient’s weight. For an average size adult, 6-unit pool for fibrinogen levels between 50-100 mg/dl and 12-unit pool for fibrinogen levels <50 mg/dl.
Acid-Base Imbalance:
Tight controls of the bodies Hydrogen [H+] ion concentration must be maintained so the body can function normally. Even slight changes can significantly alter the biologic processes of the cells and tissue. Pathophysiologic changes in the concentration of hydrogen ion in the blood, lead to what is commonly referred to as acid-base imbalance. Acid-base imbalance can occur in one of four ways, metabolic acidosis or alkalosis and respiratory acidosis or alkalosis. The pH can either be high (alkalosis) or low (acidosis). This condition can be caused by a metabolic or respiratory problem. Monitoring ABG’s is the most effective way to determine the degree of acid-base imbalance.
Respiratory Acidosis:
This occurs when ventilation is depressed and carbon dioxide is retained (hypercapnia) increasing hydrogen and producing acidosis. Common causes of respiratory acidosis include:
· Depression of the Respiratory Center (brain stem, trauma, over sedation)
· Respiratory Muscle Paralysis
· Disorders of the Chest Wall (kyphoscoliosis, pickwickian syndrome, flail chest)
· Disorders of Lung Parenchyma (pulmonary edema, pneumonia, asthma, bronchitis)
Respiratory Alkalosis:
This occurs when there is alveolar hyperventilation and excessive reduction of carbon dioxide (hypocapnia). Stimulation of ventilation is often caused by hypoxemia, which in turn may be caused by any of the following:
· Pulmonary Disease
· Congestive Heart Failure
· High Altitude
· Hypermetabolic States (anemia, fever)
· Salicylate Intoxication
· Hysteria
· Cirrhosis
· Gram Negative Sepsis
Metabolic Acidosis:
This occurs when there is an increase in noncarbonic acid or a decrease (loss) of bicarbonate. This can occur quickly in such cases of lactic acidosis or more slowly in cases of Diabetic Ketoacidosis. Other causes of Metabolic Acidosis include:
· Vomiting (bicarb loss)
· Diarrhea (bicarb loss)
· Renal Failure (bicarb loss)
· Ingestions (ammonia, chloride, salicylates) – (Increased Noncarbonic Acid)
Metabolic Alkalosis:
This occurs when bicarbonate is increased but more commonly occurs when there is an excessive loss of metabolic acid. Causes of Metabolic Alkalosis include:
· Prolonged Vomiting
· Gastrointestinal Suctioning
· Excessive Bicarbonate Intake
· Hyperaldosteronism
· Diuretic Therapy
Maintenance of Acid-Base Balance:
Normally pH remains relatively constant both outside and inside the cells. Alterations in the acid-base balance are resisted by extracellular and intracellular chemical buffers and by respiratory and renal regulation. While the kidneys and blood buffers attempt to correct metabolic disorders, the lungs attempt to correct respiratory disorders.
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