Management of Hypovolemic Shock - DOC

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Management of Hypovolemic Shock - DOC Powered By Docstoc
					Cardiac Physiology – Shock
PAACS 2009

Case: A 50 year old taxi driver is brought to casualty after a traffic accident. He is awake, in
moderate distress, and clutching his chest saying it is hard to breathe. He was alone in the vehicle
at the time of the accident, but witnesses say his car left the road on a curve and hit a large tree.
He has a history of high blood pressure and diabetes, his family history is unknown, and he does
report smoking about ½ pack of cigarettes daily. He cannot recall the names of his medications,
but he does not take them regularly. On examination he appears his stated age, is mildly
overweight, and appears unsteady and lightheaded when he attempts to stand. HEENT exam
shows equally round and reactive pupils, cut and bleeding lips, and bruises on the forehead.
Chest exam shows an irregular heart rhythm, wet crackles on ausculatation, and bruises on the
anterior chest. Abdominal exam shows diffuse tenderness with palpation. What is this patient’s
clinical syndrome? What could be the underlying diagnoses? What should be done?

I. Overview

Shock occurs when there is insufficient circulation of blood carrying oxygen to meet the
metabolic demands of the body’s tissues. Shock can be broadly classified into four types of
shock states: hypovolemic, cardiogenic, obstructive, and distributive. (1) (2) (See Table A)
Appropriate management of the patient in shock requires understanding of normal cardiac
physiology, determination of the shock state, and accurate assessment of the underlying

II. Normal Cardiac Function

In normal function, the cardiac cycle begins with depolarization of the sinoatrial (SA) node. This
depolarization causes contraction of the atria, and is conducted to the atrioventricular (AV) in the
septal wall of the right atrium. After a brief pause in the AV node, the depolarization impulse is
conducted via the right and left branches of the His-Purkinje system to the right and left
ventricles, causing systolic ventricular contraction. (3)

Stroke volume (SV) is the amount of blood pumped per cardiac cycle (70 cc in the average 70kg
male). Cardiac output (CO) is the product of heart rate (70 cycles/minute in the average 70 kg
male) and stroke volume. Thus, cardiac output in the average adult male is 4900 cc per minute.
Stroke volume is determined by preload, afterload, and inotropy. Preload, or ventricular volume
at the end of diastole, is determined primarily by returning venous inflow to the heart. Venous
flow, in turn, is determined by circulating blood volume, and venous tone. Afterload is the result
of systemic vascular resistance (SVR) to ventricular ejection, which is in turn due to arterial
tone. Inotropy, or contractility, is the ability of the heart muscle to contract and produce a
systolic ejection. Inotropy is primarily influenced by sympathetic or adrenergic tone, and by the
metabolic state of the heart (eg, acidosis, ischemia, etc). (3)
The interaction of preload, afterload, and inotropy is also affected by the Frank-Starling law,
which states that the energy of myocardial proportional to the initial length of the muscle fibers.
Thus, the greater the preload from venous return, the greater the stroke volume of systole, up to
the maximum ability of the myocardium to respond to preload. In a healthy heart, preload rarely
exceeds the contractile ability of the ventricle. However, cardiac decompensation may occur if
venous return is excessive (due to fluid overload) or if myocardial inotropy is impaired (due to
diseased or impaired heart muscle). (3)

Systemic and central blood pressures also play a key role in determining cardiac output. Right
ventricular preload is determined by the central venous pressure. Left ventricular filling is
determined by the pulmonary artery occlusion pressure, or the pressure obtained when a
pulmonary artery catheter is used to occlude the pulmonary artery, and the local pressure is
measured. Left ventricular outflow is determined by mean arterial pressure (MAP), which also
provides an approximation of tissue perfusion. Mean arterial pressure is estimated by adding the
diastolic pressure to one-third the value of the pulse pressure. The mean arterial pressure is the
result of cardiac output and systemic vascular resistance. Given these relationships, it is easy to
see how a drop in central venous pressure, cardiac output, or vascular resistance will decrease
mean arterial pressure and therefore decrease tissue perfusion. (3)

III. Hypovolemic Shock

In hypovolemic shock due to anemia, hemorrhage or dehydration, reduced preload and CVP lead
to reductions in stroke volume and cardiac output. Cardiogenic shock is generally caused by
acute dysfunction of the myocardium due to ischemia, infarction, or cardiomyopathy.
Dysrhythmias that lead to ineffective heart rates (brady- or tachy-cardias) can also cause
cardiogenic shock. Cardiogenic shock is associated with reduced cardiac output due to reduced
stroke volume, due to inadequate inotropy or excessively fast or slow heart rates. In obstructive
shock, such as decompensated aortic stenosis, high resistance reduces cardiac output and thus
mean arterial pressure. Distributive shock is due to a drop in systemic vascular resistance and
mean arterial pressure (eg, due to sepsis, shunt syndromes, or hypermetabolic states) beyond the
point at which the heart can compensate by increasing stroke volume or heart rate.

Management of acute shock can be guided using the principles of standard Advanced Cardiac
Life Support (ACLS) care. (Table B) After acute assessment and stabilization of the “ABC’s” of
airway, breathing, and circulation, the fifth “quadrad” of ACLS management includes
assessment of:
    • Volume (circulating blood volume)
    • Resistance (excessive or inadequate systemic vascular resistance)
    • Pump (pumping abiliyt or inotropic state of the heart)
    • Rate (hemodynamically significant brady- or tachycardia)
The algorithm (see below) provides a simplified overview of the active assessment and
management of acute shock using this approach. (4)

Hypovolemic shock is typically the result of dehydration or hemorrhage. Dehydration may occur
with significant vomitting and diarrhea, or with substantial environmental blood losses.
Hemorrhagic shock may be due to trauma, including lacerations or penetrating injuries, or due to
rupture of major vessels as in a major pelvic fracture. Gastrointestinal bleeding is another
important cause of hemorrhagic shock, due to malignancy, ulcers, esophageal varices.
Gynecologic or obstetric hemorrhage due to a ruptured ovarian cyst, a ruptured ectopic
pregnancy, or post-partum hemorrhage, can also be clinically significant. Rupture of a major-
vessel aneurysm or pulmonary hemorrhage, due to embolism or bleeding into a cavitary lesion,
are less common but important diagnostic considerations. (5)

Hemorrhage may be classified by symptoms and signs that are generally associated with
corresponding degrees of blood loss. Class I represents a normal health state, while class IV
hemorrhage is pre-terminal and requires immediate intervention. (Table C)

Loss of circulating blood volume leads to hemodynamic instability, decreased perfusion, organ
damage, and can ultimately lead to death. Reduction in circulating blood volume leads to
reduced venous return and reduced preload. With reduced preload, stroke volume is reduced
leading to lower mean arterial pressure and reduced peripheral perfusion. The body responds to
hemorrhagic shock and reduced cardiac output but increasing catecholamine and anti-diuretic
hormone levels. This leads to peripheral vasoconstriction which can boost venous return and
stroke volume, and to tachycardia, which can improve cardiac output. (5)

Management of hemorrhagic shock has 2 simultaneous priorities: identify and stop the source of
blood loss, and restore circulating blood volume. Appropriate clinical evaluation, including a
concise history and physical, is vital to identifying possible sources of blood loss and guiding
intervention. At the same time, fluid or blood product resuscitation should be initiated for patient
with, or at risk for, symptomatic shock. Initial fluid resuscitation is usually with intravenous
crystalloid (normal saline or Ringer’s Lactate), but in patients who do not improve after 2 liters
of crystalloid or who have lost 30% of blood volume (class III shock) blood product transfusion
is needed. If it is not possible to type and cross-match patients for transfusion, then O-positive
blood may be given if the patient is male, and O-negative blood may be given if the patient is

IV. Cardiogenic Shock

Cardiogenic shock arises from inadequate pumping function of the heart muscle itself. Common
causes of cardiogenic shock include: 1) an acute coronary syndrome (ACS), 2) acute myocarditis
with a recent history of acute viral infection, 3) acute valve dysfunction with a history of valve
disease or surgery, bacterial endocarditis, or chest trauma, 4) pulmonary embolism, 5) pericardial
tamponade, 6) dysrhythmia. The Killip classification provides a useful guide to clinical severity
of cardiogenic shock and heart failure. (6) (Table D)

Manifestations of forward heart failure with reduced perfusion include weakness, confusion, and
hypotension. drowsiness, paleness with peripheral cyanosis, cold clammy skin, low blood
pressure, filliform pulse, and oliguria, culminating in the full blown presentation of cardiogenic
shock. Acute management includes vasodilating agents, fluid replacement for optimal pre-load,
and inotropic support. Left-heart backward due to left ventricular dysfunction leads to exertional
dyspnoea, pulmonary oedema, and normal or elevated blood pressure. Acute management
includes vasodilation, diuretics, bronchodilators and narcotics. Respiratory support with
continuous positive airway pressure (CPAP) endotracheal intubation may be needed. Acute right
heart failure results from pulmonary and right heart dysfunction, chronic lung disease with
pulmonary hypertension, or right ventricular infarction. Symptoms may include peripheral
edema, dyspnea, and ascites. Severe left heart disease can also lead to right-sided failure. Acute
management includes diuretics for fluid overload, although in the setting of acute right
ventricular infarction careful administration of fluids may be needed to sufficiently augment
preload to support stroke volume and cardiac output. (6)

Pulmonary artery catheterization to measure PAOP is generally NOT needed for diagnosis of
heart failure or shock. However, a pulmonary artery catheter (PAC) may be helpful in
differentiating cardiogenic and non-cardiogenic shock mechanisms in patients with both cardiac
and pulmonary disease. PCOP does not give accurate estimations of LVEDP if there is valvular
disease such as mitral stenosis or aortic regurgitation, ventricular shunting, or a stiff left ventricle
due to hypertrophy , fibrosis, use of inotropic agents, obesity, or ischemia. A PAC is currently
only recommended in unstable patients not responding to standard interventions, or in patients
with both fluid overload and hypoperfusion. Due to the risk of complications, a PAC should only
be inserted if necessary, and removed as soon as it is no longer needed. (6)

V. Distributive Shock

Distributive shock may be associated with high-output heart failure in hypermetabolic conditions
such as thyrotoxicosis, or with systemic attempts to compensate for reduced oxygen carrying
capacity in the blood in acute anemia. Distributive shock may also result from severe
hypotension in septic shock, leading to reduced MAP, and decreased peripheral perfusion.
“Third-spacing” of plasma volume in septic shock can also reduce effective circulating blood
volume, leading to a dramatic decrease in venous return and preload. AV malformations or
intracardiac shunting may also lead to drops in MAP and thus drops in peripheral perfusion,
leading to distributive shock. Important steps in the management of distributive shock include
appropriate acute management of airway, breathing, and circulation (the “ABCs”), appropriate
support of blood pressure with fluids or vasopressors as needed, and prompt diagnosis of the
underlying cause. (6)

VI. Obstructive shock

Obstructive shock typically results from resistance to cardiac outflow, such as occurs with
decompensated aortic stenosis. In aortic stenosis, cardiac afterload is increased, despite the
presence of normal or decreased systemic vascular resistance and MAP. Typical symptoms of
aortic stenosis (AS) include angina, exertional syncope, and dyspnea. Physical examination
usually reveals a systolic ejection murmur radiating to carotids. As stenosis progressively
increases, the peak of the murmur may move later in systole, then soften if stenosis becomes
critical and the ejection fraction falls. Aortic stenosis typically has a long asymptomatic period as
mild stenosis develops. However, once a patient with AS develops symptoms of angina,
syncope, or heart failure, survival without intervention is only about 2-3 years.
Echocardiography is critical in evaluating suspected AS to determine both valve morphology and
the pressure gradient and jet velocity of blood flowing across the stenotic valve, as well as to
evaluate the ejection fraction and assess for ventricular hypertrophy. While a normal aortic valve
area is 3-4 cm2, stenosis is graded as mild, moderate, or severe. (7)

VII. Summary
Essential points to remember in managing a patient with shock include;
   1. Use a systematic approach to integrate rapid assessment and management (such as the
       ACLS “5 Quadrads”).
   2. Remember to consider possible contributions of all four classes of shock in any given
   3. Remember that cardiac output relies on a combination of factors, including venous return,
       stroke volume, heart rate, and systemic vascular resistance
   4. Remember to continually ensure that the basic “ABCs” (airway, breathing and
       circulation) are being addressed as management progresses
Table A: Shock states and precipitating factors
    Hemorrhage
    Aortic dissection
    Anemia
    Aortic valve stenosis
    Cardiac tamponade
    Sepsis
    Thyrotoxicosis
    Shunt syndromes
    Decompensated CHF
    Acute coronary syndrome
    Dysrhythmia
           o Bradycardia
           o Tachycardia
           o Atrial or ventricular fibrillation
    Valvular regurgitation
    Myocarditis,
    Post-partum cardiomyopathy

Adapted from references (1) and (6)

Table B: Five “Quadrads” of ACLS
Quadrad 1: Primary BLS
           – A, B, C’s
           – Defibrillation
Quadrad 2: Secondary BLS
           – A, B, C’s
           – Diagnosis
Quadrad 3:
           – Oxygen, IV, Monitor, Fluids
Quadrad 4:
           – Temperature , HR, BP, Respirations
Quadrad 5:
           – Tank (volume)
           – Tank (resistance)
           – Pump (inotropy)
           – Rate

Adapted from reference (4)
Table C: Classification of Shock
Parameter                        I        II         III         IV

Blood loss (ml)                  <750     750–1500 1500–2000 >2000
Blood loss (%)                   <15%     15–30%     30–40%      >40%
Pulse rate (beats/min)           <100     >100       >120        >140
Blood pressure                   Normal Decreased Decreased Decreased
Respiratory rate (breaths/min) 14–20 20–30           30–40       >35
Urine output (ml/hour)           >30      20–30      5–15        Negligible
Mental status                    Normal Anxious      Confused Lethargic

Adapted from Reference (8)

Table D: Killip stages of heart failure
            I.   No heart failure, no signs of decompensation
          II.    Heart failure, rales, S3 gallop, pulmonary venous hypertension
         III.    Severe heart failure, frank pulmonary edema, rales throughout lung fields
         IV.     Cardiogenic shock, hypotension (SBP <90mmHg), peripheral vasoconstriction
                  with as oliguria, cyanosis and diaphoresis

Adapted from reference (6)

(1) Elbers PW, Ince C. Mechanisms of critical illness--classifying microcirculatory flow
abnormalities in distributive shock. Crit Care. 2006;10(4):221. PMID: 16879732
( (accessed 8 December 2008)

(2) Weil MH, Shubin H. Proposed reclassification of shock states with special reference to
distributive defects. Adv Exp Med Biol. 1971 Oct;23(0):13-23. PMID: 5164840

(3) Rogers J. Cardiovascular Physiology. Updated in Anaesthesia. 1999 (Issue 10): 1-4.
( (accessed 8 December 2008)

(4) Advanced Cardiac Life Support Resource Text. Dallas, TX: American Heart Association,

(5) Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care.
2004 Oct;8(5):373-81. Epub 2004 Apr 2. PMID: 15469601

(6) Executive summary of the guidelines on the diagnosis and treatment of acute heart failure:
the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J. 2005
Feb;26(4):384-416. PMID: 15681577
( (accessed 8 December 2008)

(7) Bonow, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart
disease: a report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines. J Am Coll Cardiol. 2006 Aug 1;48(3):e1-148.
(, accessed 22 December 2008)

(8) Committee on Trauma. Advanced Trauma Life Support Manual. Chicago. American College
of Surgeons, 1997: 103 – 112.

Bill Cayley MD
Associate Professor
Department of Family Medicine
University of Wisconsin School of Medicine and Public Health
Figure 1: Simplified overview of shock management. Adapted from reference (4)

                                       Acute shock

     Volume                  Pump                  Resistance                   Rate

 Fluids?                                                              Bradycardia?
 Transfusion?                                                         Tachycardia?


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