Kardiogenik Hypovolemic Shock

7/28/2019 Kardiogenik Hypovolemic Shock

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King saud university

faculty of nursing

Cardiogenic Shock

DEFINITION

A life-threatening condition characterized by insufficient delivery of oxygenatedblood to cells and tissues secondary to decreased contractility, thus resulting in

decreased cardiac output.

ETIOLOGY

Cardiogenic shock occurs primarily as a result of severe left and/or right

ventricular dysfunction that results in inadequate cardiac pumping. The most

common cause is myocardial infarction; other causes include cardiomyopathy,

ventricular rupture, and congenital heart defects.

PATHOGENESIS

Decreased contractility results in decreased cardiac output, which causes decreased

tissue perfusion that is inadequate to meet basal metabolic requirements.

The sympathetic nervous system and renin-angiotensin system are stimulated as

compensatory mechanisms to increase cardiac output. The net result of the activation

of compensatory mechanisms is to increase myocardial oxygen demand. This mayprecipitate further myocardial damage, resulting in a progressive decline in cardiac

output.

CLINICAL MANIFESTATIONS Early signs include increased heart rate with maintenance of blood pressure even

though cardiac output has decreased. As compensatory mechanisms fail, the systolic

blood pressure falls and the diastolic pressure increases, causing a narrowed pulsepressure.

Other signs include increased tachycardia; cool, clammy skin; rapid, deep

respirations; pulmonary edema (crackles); an S3 gallop; decreased urine output; andimpaired level of consciousness.

TREATMENT IMPLICATIONS

Therapy is aimed at improving cardiac output and myocardial oxygen delivery while

reducing cardiac workload.

Medications often include inotropic agents (dopamine, dobutamine,), afterload-

reducing agents (vasodilators), and preload-reducing agents (venodilators, diuretics).

Intraaortic balloon counterpulsation may be used to reduce afterload and improve

coronary artery perfusion.

Ventricular-assist devices may be used for long-term circulatory support, whereas

heart transplant provides definitive treatment.


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Hypovolemic Shock -

Lectures Objectives

Upon completion of this course the student will be able to: Define Hypovolemic Shock Describe the difference between compensated, uncompensated and

irreversible Hypovolemic Shock Discuss the classes of hemorrhage List two fluid based treatment options Explain the role that vasopressors play in treatment of Hypovolemic

ShockHypovolemic ShockHypovolemic shock refers to a medical or surgical condition in which rapidfluid loss results in multiple organ failure due to inadequate perfusion. Mostoften, hypovolemic shock is secondary to rapid blood loss (hemorrhagicshock). It is defined as approximately 1 Liter or 1/5 loss of circulating volume).The following is the sequence of events that under perfused tissue goesthrough:

Profound ischemia for unperfused tissue causes a switch to anaerobicmetabolism >

Which leads to Lactic Acid waste >

This causes decreased ATP to be available for cell work >

The cell membrane cannot function and it dies >

This causes release of intracellular enzymes and inflammatory mediators >

This inflammatory process wrecks havoc on the Lungs, Kidneys, DigestiveTract, Capillary Lining and Coagulation. Whew!

There are 3 Stages in Hypovolemic Shock: Compensated,Uncompensated and Irreversible:

Compensated The body is still able to compensate for the decrease inperfusion. Cardiac Output and systolic blood pressure are maintained.

Uncompensated The bodys compensation mechanisms are starting to fail.Blood pressure begins to decrease and patient condition worsens.

Irreversible Cell and tissue ischemia leads to organ death due to lack ofperfusion. This process may begin on day one and continue to occur for up tothree weeks after the initial insult. Under such circumstances, the patientshould be re-evaluated to determine whether some reversible causes of the

persistent shock may have been overlooked.

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Treatable Causes of Hypovolemic Shock:

Hemorrhage Laceration of a vein or artery Open wounds Fractured pelvis (may be associated with 1500cc blood loss) Fractured femur (may be associated with 500-1000cc blood loss) Upper/Lower GI Bleed Pnuemo/Hemothorax

Saline or Combined Saline/Water Loss Gastrointestinal losses (vomiting, diarrhea)

High Fever Excessive sweating Diuretics

Third Spacing (Fluid shifts): Soft tissue trauma Sepsis Peritonitis (intestinal obstruction) Ascites Burn injuries

Other causes of hypovolemic shock include: Inadequate fluid administration (even if the patient clinically appears

to be overloaded with fluid) Inadequate ventilation or oxygenation Adrenal insufficiency Hypothermia Hypocalcemia

Classes of Hemorrhage:

Classes of hemorrhage have been defined, based on the percentage of bloodvolume loss. However, the distinction between these classes in the

hypovolemic patient often is less apparent. Treatment should be aggressiveand directed more by response to therapy than by initial classification.

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, delayedcapillary refill, and slight anxiety.

The decrease in pulse pressure is a result of increased catecholaminelevels, which causes increase in peripheral vascular resistance and asubsequent increase in the diastolic BP.

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 mentalstatus, such as confusion or agitation.

In patients without other injuries or fluid losses, 30-40% is the smallestamount of blood loss that consistently causes a decrease in systolic BP.

Most of these patients require blood transfusions, but the decision toadminister blood should be based on the initial response to fluids.

Class IV hemorrhage (loss of >40%)

Symptoms include the following: marked tachycardia decreasedsystolic BP, narrowed pulse pressure (or immeasurable diastolicpressure), and markedly decreased (or no) urinary output, depressedmental status (or loss of consciousness), and cold and pale skin.

This amount of hemorrhage is immediately life threatening.

Note: In the patient with trauma, hemorrhage usually is the presumedcause of shock.

Treatment

The initial resuscitative effort is to attempt to correct the absolute and relativehypovolemia by refilling the vascular tree. There is good evidence that earlygoal directed aggressive volume resuscitation improves outcomes in

hypovolemic shock. Because resuscitation efforts are not always black andwhite, treatment must be individualized for patient condition and need. Thefollowing are broad guidelines for the treatment of hypovolemic shock:

Targeting O2 delivery to vital organs rather then a specific B/P or heartrate

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.

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Fluid Replacement Choices:

Conventional crystalloids (see through) include both balanced salt solutions(BSS) and hypotonic salt solutions. Balanced salt solutions include such fluidsas 0.9% NaCl (normal saline), and Ringer's Lactate solutions. These solutionsare characterized by having an electrolyte composition or calculatedosmolality approximating that of plasma (isotonic). Balanced salt solutionsdistribute approximately or their volume to the extravascular space with

of the volume remaining in the intravascular space.

Colloid solutions are solutions of proteins, starches, dextrans, and gelatinscontaining molecules sufficiently large enough so that they do not normallycross capillary membranes. Under normal conditions most of theadministered volume remains in the intravascular space (unless tissue isdamaged and then it can cross membranes). Once colloids have leaked intothe interstitium, they must be removed by the lymphatic system or they willexert a reverse pressure gradient, drawing water from the vascular space. Theremoval of colloids from the interstitium is typically much slower than that ofcrystalloids.

Blood Component Therapy:

Packed Red Blood Cells - Red cell transfusions initially may be achievedwith uncross-matched type O red cells. If a patients blood type hasbeen determined, ABO and Rh specific red cells can be used. Everyeffort should be made to establish the blood type of a patient prior totransfusion to preserve type O red cell availability and accuratelydetermine the patients blood type.

Platelets - Platelet transfusion therapy after massive transfusion is anaccepted intervention in the presence of micro-vascular bleeding priorto documentation of thrombocytopenia. The platelet transfusion doserecommended is 1 unit per 10 kg body weight for platelet counts1.5normal range.

Cryoprecipitate - Cryoprecipitate therapy should be instituted for thecorrection of laboratory evidence of hypo-fibrinogenemia (fibrinogen


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fibrinogen levels between 50-100 mg/dl and 12-unit pool for fibrinogenlevels


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dopaminergic receptors, alpha and beta adrenoceptors, and it indirectlycauses the release of endogenous norepinephrine. At low doses (l to5mcg/kg/minute), dopamine directly stimulates dopaminergic receptors onarteries 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 andchronotropic effects, which increases myocardial contractility, and heart rate,

which results in, enhanced cardiac output. At higher doses (greater than 10mcg/kg/min), dopamine exerts effects primarily alpha-receptors, andextensive vasoconstriction causes blood pressure to increase.

Vasopressin:

Vasopressin is a unique vasopressor for two reasons. First, its principal use isfor a condition unrelated to its vasopressor properties. Vasopressin is an

antidiuretic hormone indicated to inhibit diuresis in patients with diabetesinsipidus. 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 epinephrinefor the treatment of adult shock-refractory ventricular fibrillation duringadvanced cardiac life support. Vasopressin is a distinctive vasopressor also

because its vasoconstrictive effects do not result from its interaction withadrenoceptors; rather, vasoconstriction arises from vasopressin's actions on

vasopressin receptors. Vasopressin receptors are classified as V-1 and V-2receptors. V-1 receptors are located on arterial smooth muscle, and V-2receptors are found in renal tubules. It is Vasopressin's interaction with V-1

receptors that is responsible for its potent vasopressor effects.

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Kardiogenik Hypovolemic Shock