Hematology Review

1. What are the stages of hemorrhagic shock?
Trauma - 5th Ed. (2004),



The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss. Loss of up to 15% of the circulating volume (700 to 750 mL for a 70-kg patient) may produce little in terms of obvious symptoms while loss of up to 30% of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety. Hypotension, marked tachycardia (pulse > 110 to 120 beats/min) and confusion may not be evident until more than 30% of the blood volume has been lost, while loss of 40% of circulating volume (2 L) is immediately life-threatening. Young healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs despite significant peripheral hypoperfusion being present. These patients may maintain a near-normal blood pressure until a precipitous cardiovascular collapse occurs. Elderly patients may be taking medications that either promote bleeding (warfarin, aspirin) or mask the compensatory response to hypovolemia (beta blockers). In addition, atherosclerotic vascular disease, diminished cardiac compliance with age, inability to elevate heart rate or cardiac contractility in response to hemorrhage, and overall decline in physiologic reserve decrease the elderly patient's ability to tolerate hemorrhage.



2. What are the hemodynamic changes associated with septic shock?
Current Critical Care Diagnosis & Treatment - 2nd Ed. (2003)

The distinguishing hemodynamic features of septic shock are elevated cardiac output, decreased systemic vascular resistance, and decreased blood pressure. Tachycardia is partially responsible for maintaining the blood pressure. [NB the ventricles become dilated so as to increase output according to the Frank-starling curve, this is how the heart compensates for the myocardial depression that septic mediators often cause]. More recent investigations have shown that cardiac output remains elevated until decreased output develops as a preterminal event. A normal or elevated mixed venous oxygen saturation and decreased arterial-venous oxygen content difference is present.

3. What are the hemodynamic changes associated with cardiogenic shock?
Schwartz's Principles of Surgery - 8th Ed. (2005)
Emergency Medicine: A Comprehensive Study Guide - 6th Ed.

Hemodynamic criteria include sustained hypotension, reduced cardiac index (< 2.2 L/min per square meter), and elevated pulmonary artery wedge pressure (> 15 mm Hg). Clinical signs of cardiogenic shock include evidence of poor CO with tissue hypoperfusion (hypotension, mental status changes, cool mottled skin) and evidence of volume overload (jugular venous distention, rales, and an S3 gallop).

4. What are the hemodynamic changes associated with hypovolemic shock?
Harrison's Principles of Internal Medicine - 16th Ed. (2005)

Reduced cardiac output and a compensatory sympathetic mediated response characterized by tachycardia and elevated systemic vascular resistance.

5. A 30 y.o. pt. arrives s/p fall from a tree. He is noted to be hypotensive on arrival. Invasive hemodynamic monitoring shows him to have a CVP of 1 mm Hg (nl 2-8 mm Hg), a cardiac output of 3 L/min (nl 4-6 L/min), an SVR of 450 dyne/sec/cm-5 (nl 900-1200 dyne/sec/cm-5), and a mixed venous oxygen saturation of 55% (nl 70-80%). Characterize his shock state.
Schwartz's Principles of Surgery - 8th Ed. (2005)

Neurogenic Shock - Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone. Rarely, a spinal cord injury without bony fracture, such as an epidural hematoma impinging on the spinal cord, can produce neurogenic shock. Sympathetic input to the heart, which normally increases heart rate and cardiac contractility, and input to the adrenal medulla, which increases catecholamine release, may also be disrupted, preventing the typical reflex tachycardia that occurs with hypovolemia. Acute spinal cord injury results in activation of multiple secondary injury mechanisms: (1) vascular compromise to the spinal cord with loss of autoregulation, vasospasm, and thrombosis, (2) loss of cellular membrane integrity and impaired energy metabolism, and (3) neurotransmitter accumulation and release of free radicals. Importantly, hypotension contributes to the worsening of acute spinal cord injury as the result of further reduction in blood flow to the spinal cord. Management of acute spinal cord injury with attention to blood pressure control, oxygenation, and hemodynamics, essentially optimizing perfusion of an already ischemic spinal cord, seems to result in improved neurologic outcome. Patients with hypotension from spinal cord injury are best monitored in an intensive care unit, and carefully followed for evidence of cardiac or respiratory dysfunction.

6. When should a pulmonary artery wedge pressure be recorded? Is it any different in a ventilated versus a non-ventilated patient?
Emedicine

The timing of PCWP measurement is critical because intrathoracic pressures can vary widely with inspiration and expiration and are transmitted to the pulmonary vasculature. During spontaneous inspiration, the intrathoracic pressures decrease (more negative); during expiration, intrathoracic pressures increase (more positive). Positive pressure ventilation (eg, in an intubated patient) reverses this situation. To minimize the effect of the respiratory cycle on intrathoracic pressures, measurements are obtained at end-expiration, when intrathoracic pressure is closest to zero. [NB this is the same in ventilated and non-ventilated patients. The difference is how the pressure tracing looks].

7. What are some indications for placement of a pulmonary artery catheter?
Emedicine, Uptodate.com - Swan-Ganz catheterization: Indications and complications.
No study has definitively demonstrated improved outcome in critically ill patients managed using pulmonary artery catheters. Thus, the accepted indications for pulmonary artery catheterization have been generated largely on the basis of expert opinion. Fundamentally, the decision to place a Swan-Ganz catheter should be based on a specific question regarding a patient's hemodynamic status that cannot be satisfactorily answered by clinical or noninvasive assessment; if the answer could change management, then placement of the catheter is indicated [NB remember this principle for the ABSITE!] Common indications are listed
• Diagnosis of shock states
• Differentiation of high- versus low-pressure pulmonary edema
• Diagnosis of primary pulmonary hypertension (PPH)
• Diagnosis of valvular disease, intracardiac shunts, cardiac tamponade, and pulmonary embolus (PE)
• Monitoring and management of complicated AMI
• Assessing hemodynamic response to therapies
• Management of multiorgan system failure and/or severe burns
• Management of hemodynamic instability after cardiac surgery
• Assessment of response to treatment in patients with PPH (Primary pulmonary hypertension)

8. What are some indicators of endpoints of resuscitation? What are their benefits
and drawbacks?
Schwartz's Principles of Surgery - 8th Ed. (2005)

Lactate - Elevated serum lactate is an indirect measure of the oxygen debt, and therefore an approximation of the magnitude and duration of the severity of shock. The admission lactate level, highest lactate level, and time interval to normalize the serum lactate are important prognostic indicators for survival.
Base deficit - Base deficit can be stratified into mild (3 to 5), moderate (6 to 14) and severe (≥15) categories, with a trend toward higher mortality with worsening base deficit in patients with trauma. Both the magnitude of the perfusion deficit as indicated by the base deficit and the time required to correct it are major factors determining outcome in shock. [NB Both lactate and base deficit are global measures of perfusion, and thus may miss regional hypoperfusion. They may be confounded by underlying organ dysfunction as well, and may not fully reflect the oxygen debt of underlying tissue. Nevertheless, they are useful indetermining both response and mortality]
Gastric tonometry - Goal-directed human studies, with gastric mucosal pH (pHi) as an endpoint in resuscitation, have shown normalization of pHi to correlate with improved outcome in several studies, and with contradictory findings in other studies. Utility of pHi as a singular endpoint in the resuscitation of critically-ill patients remains controversial.
Tissue pH, oxygen, carbon dioxide levels - Tissue probes with optical sensors have been used to measure tissue pH and partial pressure of oxygen and carbon dioxide in subcutaneous sites, muscle, and the bladder. These probes may utilize transcutaneous methodology with Clark electrodes or direct percutaneous probes. The percutaneous probes can be inserted through an 18-gauge catheter and hold promise as continuous monitors of tissue perfusion.
Near infrared spectroscopy - Trauma patients with decoupled oxyhemoglobin and cytochrome a,a3 have redox dysfunction and have been shown to have a higher incidence of organ failure (89 vs. 13%). Not widely used in clinical practice

9. How do you calculate oxygen delivery? Systemic vascular resistance?
Current Critical Care Diagnosis & Treatment - 2nd Ed. (2003)

The delivery of oxygen is dependent upon the quantity of oxygen present in the blood and the cardiac output. The oxygen content, is calculated as follows:

. Multiply by cardiac output to get oxygen delivery. The last term is often negligible.





Systemic Vascular resistance is calculated as follows:



10. Where on the EKG tracing should the CVP be measured? Where should the pulmonary artery wedge pressure be measured?