ITLS Shock

Cardiac Output =

Heart Rate x Stroke Volume

■ Mechanical shock (cardiogenic or obstructive) is a "pump" problem either caused by

a damaged heart (myocardial contusion or myocardial infarction) or by conditions preventing the filling of the heart (pericardial tamponade, tension pneumothorax), or something obstructing blood flow through the lungs (massive pulmonary embolism).

Shifting of mediastinal structures also may lower venous return by impinging on the superior and inferior vena cava, also causing ? (rarely seen clinically).

a deviation of the trachea away from the affected side

Nonhemorrhagic Hypovolemic Shock The patient who has low-volume shock syndrome not due to hemorrhage can generally be managed in the same manner as a patient with shock due to bleeding that can be controlled. An example of this type of patient would be one with shock due to fluid loss from burns or severe diarrhea. Low-volume shock is a common cause of death in these patients. Because the loss of volume in this case is not from an injured vascular system, it is reasonable to treat such patients with

aggressive volume replacement to restore vital signs toward normal.

The midbrain responds to the progressive hypoxia and acidosis with

an increase in the respiratory rate.

The backup (?) processes may postpone cellular death for a time. However, the lack of oxygen is compounded by those toxic by-products because they can poison certain cellular functions, such as the ? Eventually, accumulating lactic acid in the blood and organs creates a systemic acidosis that further disrupts cellular activity. Respiratory muscle function also weakens, respiratory failure develops, and hypoxia worsens.

anaerobic production of energy by mitochondria.

Thus, if cardiac output falls (either due to falling heart rate or lowered stroke volume) or if peripheral vascular resistance falls (such as in the dilated arteries that occur in neurogenic shock), then

blood pressure will fall.

Calcium channel blocker or beta-blocker poisonings often produce ?, whereas nitroglycerin overdose might produce ? Be sure to get a good

bradycardia tachycardia. History.

The clinical presentation of neurogenic shock differs from hemorrhagic shock in that there is no

catecholamine release and thus no pallor (vasoconstriction), tachycardia, or sweating.

Acidosis can ultimately cause a loss of response to ?, worsening the drop in blood pressure. This is often the point at which the patient in "compensated" shock suddenly "crashes."

catecholamines

You also may see a lack of ? and only simple diaphragmatic movement when the patient is asked to take a deep breath.

chest wall movement

Patients in shock have decreased oxygen being supplied to their cells. This is either because they have lost blood through hemorrhage or the heart is not circulating it effectively. Thus, if you are monitoring a patient either in shock or at risk of going into shock, monitor the level of exhaled CO2 as part of your overall care. A level of exhaled CO2 that falls much under 35—especially if it falls into the 20s or below—may be an indication of ? and thus can be an additional warning sign of worsening shock.

circulatory collapse

Generally, the onset of the symptoms and signs of hypovolemic shock (including hemorrhagic shock) occur in the following order:

compensated shock and then decompensated shock.

Special Situations in Hypovolemic Shock Head Injury The patient with severe head injury (Glasgow Coma Scale score of 8 or less) and shock is a special situation. These patients do not tolerate hypotension. Therefore, if necessary, adults with suspected hemorrhagic shock in addition to head injury should be

fluid resuscitated to a blood pressure of 120 mm Hg systolic to maintain a cerebral perfusion pressure of at least 60 mm Hg.

Someone bleeding to death, literally, may not have enough

hemoglobin around to manifest cyanosis.

■ Low-volume shock (absolute hypovolemia) is caused by

hemorrhage or other major body fluid loss (diarrhea, vomiting, and "third spacing" due to burns, peritonitis, and other causes).

Although there are some similarities in the body's response to different kinds of shock, there also are some differences. For example, the stabbed and bleeding patient in hemorrhagic shock often shows many of the same signs as the burned or dehydrated patient with low blood volume not due to ?

hemorrhage.

Myocardial contusion often cannot be differentiated from cardiac tamponade in the field. Therefore, rapid transport, supportive care, and cardiac monitoring are the mainstays of therapy

hmm

Falling measured CO2 indicates either that the patient is ? or that the ?

hyperventilating (from anxiety or acidosis) amount of oxygen being supplied to the cells is falling.

■ Hypotension—caused by

hypovolemia, either absolute or relative (see later paragraphs for a discussion of relative hypovolemia), and/or by the diminished cardiac output seen in "obstructive" or "mechanical" shock

■ Decreased urinary output—caused by ■ Weakened peripheral pulses—

hypovolemia, hypoxia, and circulating catecholamines (important to remember in interfacility transfers) the "thready" pulse (meaning "threadlike"; arteries actually shrink in width as intravascular volume is lost); caused by vasoconstriction, tachycardia, and loss of blood volume

Deprived of oxygen, cells begin to use "backup" processes, which use energy less efficiently and produce toxic by-products such as

lactic acid.

Several processes cause this drop in perfusion. For example, the loss of red blood cells in hemorrhaging patients results in ? to the body tissues. Decreased circulating blood volume leads to ? fluid volume, and electrolytes to the cells. Those circulatory disturbances result in the cells of the body becoming "shocked," and grave changes in body tissue begin to occur.

less oxygen transport lowered glucose,

Finally, the part of shock that field personnel do not usually see occurs after the patient is admitted to the hospital. Days after hemorrhagic shock in the field, the patient may suffer ? in the ICU.

multisystem organ failure

Although several causes of high-space shock exist (such as sepsis syndrome and drug overdose), ?, commonly called spinal shock, is addressed here because it may be caused by trauma

neurogenic shock

Examples of drug overdoses and chemical exposures that may produce the relative hypovolemia syndrome include (3) ? cyanide, and even the ethyl alcohol found in legal alcoholic beverages.

nitroglycerin, calcium channel blockers, antihypertensive medications,

In neurogenic shock the patient will have a decreased blood pressure, but the heart rate will be ?, and the skin is usually ? The patient also may have accompanying ?

normal or slow warm, dry, and pink paralysis and/or sensory deficit corresponding to the spinal-cord injury.

There are ? in the appearance of patients with these conditions, and it is critical that you be aware of the signs and symptoms that accompany each one.

notable differences

The patient with shock may be .

pale, diaphoretic, and tachycardic

Males may present with

priapism.

An injury to the spinal cord in the neck can prevent the brain from being able to send out the sympathetic nervous system signals. Thus, a cervical spinal-cord injury can prevent the brain from (3)?

raising the pulse rate, from raising the strength of the heart's contraction, or from constricting the peripheral arterioles (the vessels that maintain blood pressure).

■ High-space shock (relative hypovolemia) is caused by

spinal injury, vasovagal syncope, sepsis, and certain drug overdoses that dilate the blood vessels and redistribute blood flow to a larger vascular volume.

Children are unable to increase their ?, so their cardiac output depends on their heart rate alone (cardiac output = ?). Children in decompensated shock may develop ?, which can have a devastating effect on their ability to maintain blood flow to their vital organs.

stroke volume stroke volume x heart rate bradycardia

■ Tension pneumothorax. This very high positive pressure collapses the low-pressure ?, preventing the return of ?

superior and inferior vena cava venous blood to the heart.

Inadequate oxygen delivery causes the body to respond with increased activity of the ?

sympathetic nervous system (increased sympathetic tone),

Hypovolemic shock victims usually have (3) ?. So, if you find a trauma victim with a fast heart rate, who is pale, with weak radial pulses and flat neck veins, this patient is probably bleeding from some injury.

tachycardia, are pale, and have flat neck veins

As many as 20% of patients with bleeding into the abdomen may not show ? Another point to consider is the injured patient's ?

tachycardia. medications.

The term thready pulse means that

the actual width of the artery shrinks, becoming barely wider than a thread.

Note: The signs and symptoms listed here are in the order of progressive "compensation," as the body attempts to deal with the cause of shock. Beginning with the next sign, hypotension, the body is no longer able to maintain perfusion, and the shock condition is now ?

"decompensated."

■ Early shock. This is the loss of approximately ? of the blood volume. That is enough to stimulate slight to moderate tachycardia, pallor, narrowed pulse pressure, thirst, weakness, and possibly delayed capillary refill. In "early shock," the body is "compensating" for the physical insult that iscausing the problem (hemorrhage, dehydration, tension pneumothorax, and so on).

15% to 25%

■ Late shock. Late shock is the loss of approximately ? of the blood volume. It is enough to cause hypotension as well as the other symptoms of hypovolemic shock listed earlier. When "late shock" occurs, it means the body's ability to compensate for the physical insult has failed. As mentioned earlier, hypotension is the first sign of "late shock." The hypotensive patient, then, is near death. Aggressive assessment and management must be provided to prevent the death of the patient.

30% to 45%

Pericardial tamponade may occur in more than ?

75% of cases of penetrating cardiac injury.

Blood Pressure =

Cardiac Output x Peripheral Vascular Resistance

■ Cardiac arrest—caused by

critical organ failure secondary to blood or fluid loss, hypoxia, and occasionally arrhythmia caused by catecholamine stimulation and/ or low perfusion

An important point to remember is that the positive pressure breaths you give when you ventilate someone actually can ?

decrease blood return to the heart, lowering cardiac output

■ Weakness and lightheadedness—caused by ? ■ Thirst—caused by ■ Pallor (pale, white color of the skin)—caused by

decreased blood volume hypovolemia (especially with relatively low fluid amounts in the blood vessels) catecholamine-induced vasoconstriction and/or loss of circulating red blood cells

■ Altered mental status (confusion, restlessness, combativeness, unconsciousness)— caused by

decreased cerebral perfusion, acidosis, hypoxia, and catecholamine stimulation

Mechanical shock is caused by a Thus, these patients usually have a different

diminished cardiac output rather than blood loss. appearance at the bedside than hemorrhagic shock patients.

Myocardial contusion can result in diminished cardiac output because the heart loses pumping strength due to ? and or ?

direct injury to the heart muscle and/or cardiac dysrhythmias

Because the cardiac output is diminished, the blood backs up into the venous system, resulting in ?. The lungs are not being perfused well, causing the patient to become ?. Because the patient is in shock with an intact spinal cord, ? are released, and the patient develops tachycardia and diaphoresis.

distended neck veins cyanotic catecholamines

"Beck's triad," consisting of

distended neck veins, mufflied heart tones, and pulsus paradoxus.

The resulting "backup" of blood presents as

distended neck veins.

resulting in the increased release of circulating catecholamines (? and ?). Those hormones increase both the rate and strength of the heart's contractions and constrict peripheral arterial blood vessels.

epinephrine and norepinephrine

To summarize, many of the symptoms of shock of any etiology including the classic hemorrhagic shock picture are caused by the release of catecholamines. When the brain senses that perfusion to the tissues is insufficient, chemical messages are sent down the spinal cord to the sympathetic nervous system and the adrenal glands, causing a release of catecholamines (epinephrine and norepinephrine) into the circulation. The circulating catecholamines cause the tachycardia, anxiety, diaphoresis, and vasoconstriction. This narrowing of the small arteries shunts blood away from the skin and intestines to the heart, lungs, and brain.

etc

Put another way, the level of exhaled CO2 indicates how brightly the ?

fire of metabolism is burning in the cells.

■ Tachycardia—caused by ■ Diaphoresis (sweating)—caused by ■ Tachypnea (elevated respiratory rate)—caused by

the effect of catecholamines on the heart as the brain increases the activity of the sympathetic nervous system the effects of catecholamines on sweat glands the brain elevating the respiratory rate under the influence of stress, catecholamines, acidosis, and hypoxia

Use of IV fluids in this situation should be during transport and only on

the order of medical direction.

The term shock describes a condition that occurs when ?

the perfusion of the body's tissues with oxygen, electrolytes, glucose, and fluid becomes inadequate to meet the body's needs.

The pulse pressure is the pressure driving blood through the vascular system. It is calculated by subtracting the diastolic blood pressure from the systolic. It is usually about 40 mm Hg (blood pressure of 120/80 equals pulse pressure of 40). There will almost always be an initial narrowing of the pulse pressure because ?

vasoconstriction raises the diastolic pressure more than the systolic.

High-Space Shock An argument can be made for the use of ? in patients with vasodilatory shock due to causes such as calcium channel blocker overdose or sepsis.

vasopressors

The normal perfusion of body tissues requires four intact components. They are as follows:

■ Adequate volume of fluid in the vascular system: red blood cells and plasma ■ Functioning pump: the heart ■ Intact vascular system to deliver oxygenated blood throughout the body: the blood vessels ■ Adequate air exchange in the lungs to allow oxygen to enter the blood: oxygenation

*Decompensated Shock* (3)

■ Hypotension—caused by hypovolemia, either absolute or relative (see later paragraphs for a discussion of relative hypovolemia), and/or by the diminished cardiac output seen in "obstructive" or "mechanical" shock ■ Altered mental status (confusion, restlessness, combativeness, unconsciousness)— caused by decreased cerebral perfusion, acidosis, hypoxia, and catecholamine stimulation ■ Cardiac arrest—caused by critical organ failure secondary to blood or fluid loss, hypoxia, and occasionally arrhythmia caused by catecholamine stimulation and/ or low perfusion

The three shock states can be categorized according to their causes as follows:

■ Low-volume shock (absolute hypovolemia) ■ High-space shock (relative hypovolemia) ■ Mechanical shock (cardiogenic or obstructive)

The preservation of these components can be related to the basic rules of shock management, which are: (4)

■ Maintain the airway. ■ Maintain oxygenation and ventilation. ■ Control bleeding where possible. ■ Maintain circulation through an adequate heart rate and intravascular volume.

The heart is a pump. Like any pump, it has a "power" stroke and a "filling" stroke, just like a piston moving up and down in the cylinder of a motor. In the normal adult's resting state, the heart pumps out about 5 liters of blood per minute. This means, of course, that the heart also must take in about 5 liters of blood per minute. Therefore, any traumatic or medical condition that slows or prevents the venous return of blood can cause shock by lowering cardiac output and thus oxygen delivery to the tissues. Likewise, anything that obstructs the flow of blood to or through the heart can cause shock. The following are traumatic conditions that can cause mechanical shock:

■ Tension pneumothorax. ■ Cardiac tamponade. ■ Myocardial contusion.

During compensated shock, the body is still able to maintain perfusion by compensatory mechanism and will present with the following signs and symptoms:

■ Weakness and lightheadedness ■ Thirst ■ Pallor ■ Tachycardia ■ Diaphoresis (sweating) ■ Tachypnea ■ Decreased urinary output ■ Weakened peripheral pulses