Lecture Script

SHOCK
CPT Gretchen Hinson, MD, USAF
United States Air Force Academy
Colorado Springs

Definition: inadequate tissue perfusion occurring secondary to circulatory failure

1: a reduction of blood flow by diminished cardiac output or maldistributed output such that potential irreversible tissue damage occurs...

Shock occurs when acute circulatory dysfunction is marked by progressive impairment of blood flow to the skin, muscles, kidneys, mesentery, lungs, heart, and brain.


Catecholamine release (initial compensatory mechanism) in response to hypoperfusion state; this response is to maintain cardiac output and preserve critical organ blood flow during acute stage of shock

Increase heart rate, preload, cardiac output - catecholamines act as positive inotropes as well as positive chronotropes to augment CO (CO = stroke volume x heart rate)

Increase tone in venous capacitance vessels, arteriolar pre and post-capillary sphincters: by enhancing venous tone, preload is increased and the "pump is primed" thus increasing cardiac output due to larger stroke volume; also blood is shunted away from noncritical organs such as skin, GI tract, and skeletal muscle and redistributed to the central circulation (increased systemic vascular resistance = SVR )

Neuroendocrine response

Hypothalamic mediated

Glucocorticoid, growth hormone, and aldosterone - act in conjunction with glucagon and insulin to maintain glucose levels

Renal mediated

Antidiuretic hormone (ADH), renin, and angiotensin release - aid in maintaining blood pressure and blood volume in response to stress

Compensatory mechanism failure

Relax pre-capillary sphincters, maintain tone of post-capillary sphincters

Blood flow stagnation, sludging, altered laminar flow, rouleaux formation

Decreased microcirculatory flow is net effect

Cell swelling, mitochondrial disruption, and eventual cell death

The cell membrane is unable to maintain sodium outside the cell when the sodium-potassium pump fails due to lack of cellular energy (ATP).

The cell begins to accumulate sodium and water, which causes cellular swelling. This process is reversible at the cellular level until mitochondria swell and begin to break down. (This may correlate clinically to a sudden decrease in oxygen consumption in your patient.)

Switch from aerobic to anaerobic metabolism - at the cellular level this is very inefficient and energy substrates are used up quickly with minimal energy produced

Lactic acid formation - byproduct of anaerobic metabolism

Systemic acidosis - result of lactate buildup

Decreased myocardial contractility (acidosis is a "negative inotrope")

Decreased vascular smooth muscle tone (thus a decrease in BP, SVR, and venous return - unable to "prime pump")

Decrease blood pressure, preload, cardiac output (net results of the above)

Clinical presentation (assessment parameters)

Vital signs (normal adult parameters)

Blood pressure - systolic 90-140mmHg (hypotension is also defined as a decrease of 80 mmHg in the SBP in a normally hypertensive patient)

Pulse - 60-100/min

Respiratory rate - 12-20/min

Temperature - 35-38 degrees Centigrade (rectal temps most accurate)

Mental status - at patient baseline

Urine output - 1cc/kg per hour

Orthostatic changes - much debate over the use, significance, and clinical relevance; probably most clinically accurate in setting of moderate to severe hypovolemic shock, however the clinician should have other clues to the severity of the shock state with this degree of hypovolemia and orthostatics are redundant

Shock syndromes

Hypovolemic shock - Blood VOLUME problem

Etiologies

Severe dehydration secondary to :

Decreased fluid intake

Excessive fluid losses - diarrhea, vomiting, sweating

Blood loss secondary to :

Trauma - penetrating and blunt mechanisms

Intraabdominal bleeding - ruptured/dissecting aneurysms, GI bleeding (upper and lower), ruptured ectopic pregnancy, hemorrhagic ovarian cyst, retroperitoneal hemorrhage

Obvious external hemorrhage - massive hemoptysis/hematemesis/hematochezia/melena/vaginal bleeding or external trauma with active bleeding

Clinical presentation - initial presentation is representative of compensatory mechanisms produced by catecholamine response to hypoperfusion

Tachycardia and tachypnea - increase depth and rate of respirations

Decreased blood pressure and pulse pressure - narrowing of the pulse pressure is one of the earliest signs of shock

Delayed capillary refill; cool, clammy, pale skin

Mental status changes - range from anxious to agitation to lethargy

Decreased urine output - important parameter to assess in children

Management

Control obvious hemorrhage; recognize possibility of non- visualized hemorrhage and notify appropriate surgeon EARLY; in severe dehydration, volume replacement with attention to electrolyte abnormalities that may occur and careful observation for fluid overload in the patient at risk for congestive heart failure should be the initial management - blood component therapy is not usually necessary

Restore circulating blood volume crystalloid resuscitation, usually begin with 20cc/kg fluid boluses of normal saline or Ringer's lactate solution (warmed, if possible, and especially in trauma); if after 2 such boluses the patient remains in a hypoperfused state (and blood loss is significant or ongoing) transfuse cross matched blood,
in case of exsanguinating hemorrhage, type-specific blood ASAP(in conjunction with fluid resuscitation),
if patient is on death's doorstep give type O blood immediately (use Rh negative blood in child-bearing age females if possible), if autologous transfusion device is available, use it!

Optimize oxygen delivery - provide appropriate airway management and give supplemental O2 to maximize hemoglobin oxygen saturation

Cardiogenic shock - Blood PUMP problem

Etiologies

Inflow problems

pericardial tamponade (may develop secondary to ventricular wall rupture with subsequent tamponade)

tension pneumothorax

mitral/tricuspid stenosis

IHSS with filling defect

Pump problems

acute myocardial infarction - about 40% LV damage before signs of shock develop; apical akinesis/ hypokinesis poor prognostic indicator; majority of patients have severe LAD involvement

myocarditis

cardiomyopathy (dilated, hypertrophic, restrictive types)
myocardial contusion

Outflow problems

pulmonary embolism

aortic/pulmonic stenosis

mitral insufficiency (may be secondary to acute papillary muscle rupture or dysfunction in setting of acute MI)

ventricular septal defect (may have interventricular septum rupture in acute MI)

air embolism

Clinical presentation as discussed for hypovolemic shock

Heart murmurs

mitral stenosis - listen over apex or in left lateral decub position for low pitched diastolic rumble

mitral insufficiency - listen over apex and into left axilla for blowing high pitched pansystolic murmur

aortic stenosis- listen over aortic area for medium pitched, harsh midsystolic ejection murmur that radiates to neck, LSB,apex

pulmonic stenosis- listen over pulmonic area and left
third intercostal space for medium pitched, harsh
midsystolic ejection murmur that radiates to left neck
and shoulder (associated with widely split S2 and
diminished P2)

ventricular septal defect(VSD)- listen at left sternal
border and left third, fourth, and fifth interspace for
high pitched harsh pansystolic murmur that radiates
over precordium but not into axilla

ECG abnormalities associated with specific etiologies - low voltage and electrical alternans with pericardial tamponade; ST segment elevation, new bundle branch blocks, pathologic Q waves with acute MI; dysrhythmias

JVD, tracheal deviation, chest hyperresonance or decreased breath sounds with tension pneumothorax may not present with tachycardia in setting of acute MI because of heart block or bradycardic response to inadequate blood flow to nodal tissue or vagal response to posterior wall MI (Bezold-Jarish reflex)

S3 heart sounds representative of increased left ventricular diastolic pressure and may correlate clinically with congestive heart failure;S4 represents "stiff" ventricle associated with acute MI, hypertension, or cardiomyopathy
decrease in blood pressure below critical level if mean arterial pressure is below 70mmHg, coronary perfusion is inadequate and myocardial ischemia is worsened(MAP = 1/3PP + DBP)

Management

Treat reversible causes

relieve tamponade, pneumothorax with needle/catheter decompression and obtain definitive treatment

Optimize pump function (intervene to stop vicious cycle)
THE PROBLEM:

patient in cardiogenic shock secondary to acute MI with a critical level of damaged muscle (40%) cannot maintain adequate arterial blood pressure -> catecholamine response ->increase peripheral vascular resistance thus increased preload and afterload plus tachycardia -> increased myocardial oxygen demand -> increased ischemia and worsened myocardial pump performance

THE SOLUTION:

ideally, the patient is monitored with intraarterial and Swan-Ganz catheters, and treatment interventions are guided by these measurements in the intensive care unit; however, the unstable patient in the ED usually must be managed using the aforementioned clinical parameters

as always, aggressive airway management to optimize oxygen
delivery - intubate early for inadequate oxygenation,
fatigue, clinical signs of hypoxemia such as mental status
changes, cyanosis, or changes in respiratory pattern - use
serial blood gases to evaluate for hypoxemia, hypercarbia, and acidosis in response to interventions

maintain blood pressure with attempt at small fluid bolus of crystalloid first (200 cc) as 1/4 of patients in cardiogenic
shock may have relative fluid deficit, thus inadequate filling
pressure; also look for right ventricular infarction and thus
inadequate LV filling as etiology of shock

if patient has no response to fluids or if fluids worsen failure (rales, JVD, decrease in blood pressure) stop immediately and add pressor agents

DOPAMINE (alpha+beta) DOBUTAMINE(beta1)
BP ^ ^
HR ^ minimal ^
SVR ^ decrease PRELOAD ^ no change AFTERLOAD ^ decrease
O2 DEMAND ^ minimal ^

(Both drugs are positive inotropes and will increase myocardial
contractility. In setting of acute MI with a tachycardic patient who
is "clamped down peripherally", dobutamine is the better drug to start with and add dopamine to augment blood pressure as needed.)

consider morphine for pain relief, anxiolysis, and some preload and afterload reduction

diuretics may be needed if severe CHF, but use with caution as
they may decrease filling pressure further

vasodilators may be needed if additional afterload reduction is
required, however these too can drop blood pressure even
lower so they are best used in conjunction with invasive
monitoring

consider short acting beta blocker, esmolol, for refractory
tachycardia

Myocardial salvage - decrease myocardial oxygen demand to save

ischemic muscle from progressing to infarction

Consider thrombolytics, angioplasty, aortic balloon counterpulsation in specific cases

Vasogenic shock - Blood VESSEL problem

Etiologies

Septic shock - perfusion embarrassment secondary to blood widely distributed over dilated vascular bed in response to bacteria and their products circulating in the blood

Gram negative rods are the most common cause of
septic shock (shock occurs in approximately 40%
of Gram negative bacteremia) although all bacteria
can be etiologic agents.

Predisposing factors for septic shock include: immunocompromised host, manipulation of GU or respiratory tracts, asplenia, chronic disease, extremes of age, major burns, hospitalization, and abdominal surgery

The pathophysiology of bacteremia producing shock centers around the physiologic effects of endotoxin, a lipopolysaccharide in the cell wall of bacteria (gram- negative rods). Multiple mechanisms have been demonstrated that explain some of the changes seen, such as fever, hypotension, leaky capillaries, disseminated intravascular coagulation (DIC), complement activation, leukocytosis, and leukopenia.

Cardiovascular changes in septic shock include a hyperdynamic but depressed myocardium probably secondary to a direct endotoxin effect. This, in addition to the vascular bed dilatation in response to endotoxin, causes the hypotension and subsequent hypoperfusion that is seen clinically.

Anaphylactic shock -hypotension as part of the immune system response to an antigen that the body has developed a Type I hypersensitivity (IgE mediated)

Antigen (allergen) stimulates the body to produce IgE antibodies through B, T, and plasma cell interactions upon repeat exposure to the antigen

IgE binds to specific receptors on mast cells and basophils;
antigen binds to the IgE antigen specific antibody thus stimulating these cells to release mediators that result in vasodilation, increased vascular permeability, bronchoconstriction, increased mucus production, and increased inflammatory mediator recruitment

Neurogenic shock - hypotension is a result of the loss of sympathetic vascular tone below the level of spinal cord injury; the patient with spinal cord injury may also lose sympathetic tone to the heart resulting in bradycardia and thus loss of compensatory tachycardia in response to vascular bed dilatation. This is usually a transient (3-7 days) response, then sympathetic tone is restored.

Pharmacologic shock - hypotension secondary to medication effects from any drug category capable of decreasing blood pressure.
Examples include opiates, sedative-hypnotics, beta blockers, anticholinergics, antidepressants, nitrates, and antihypertensives.

Clinical presentation dependent on etiology of shock

Septic shock usually has a biphasic presentation:
-"Warm" shock is the first phase in which the body has a hyperdynamic response and the patient is vasodilated, warm, flushed, and has a normal or elevated cardiac output.
The patient exhibits mental status changes (usually agitation) and may have poikilothermia and increased
respiratory rate. Despite an increased cardiac output, the
patient may still be hypotensive in this stage of septic shock.
- "Cold" shock is the later phase in which the patient further decompensates; peripheral vasoconstriction and critical organ function impairment become evident. The patient's
mental status declines as well as the blood pressure and CO.

Atypical presentations of shock may also be seen: mental status change, fever, respiratory alkalosis, metabolic acidosis, or hypotension that is unexplained are possible presentations
of septic shock

Anaphylactic shock usually occurs almost immediately after contact with the inciting antigen. Cutaneous manifestations with urticaria, pruritis, and erythema may progress to airway compromise - stridor, wheezing, respiratory distress - and generalized circulatory collapse with tachycardia and hypotension

Neurogenic shock usually manifests as moderate hypotension with a relative bradycardia. The patient has warm, dry skin secondary to vasodilatation.

Pharmacologic shock may present with the physical findings of any toxidrome associated with the specific drug overdose.

Management dependent on etiology of shock - see discussion
a. Septic shock must be treated aggressively with parenteral antibiotics that are appropriate for the given source of the sepsis (after obtaining blood cultures) I. identification and definitive treatment (ie. find and drain the abscess) of the inciting infection ii. ABC support (as previously described, ie. crystalloid resuscitation, pressor drugs if no response to adequate fluid {dopamine is usually first choice as it spares renal perfusion and is an effective vasoconstrictor}, and optimal oxygenation.)

Anaphylactic shock must be recognized early in its course and treated aggressively to intercept the immune system hypersensitivity response

Airway management using high-flow O2, bronchodilators, and epinephrine - IV epi dose 0.3 - 0.5 mg of 1:10,000 solution (if circulatory collapse is not eminent, epi can be given subcutaneously)

Intubation may be necessary early in course; due to severe laryngospasm or soft tissue swelling, emergency surgical airway may be needed

Antihistamines, such as diphenhydramine, are useful if given via parenteral route, 50 mg IV or IM depending on severity of reaction

Corticosteroids may not be effective in acute anaphylaxis, however they should be given as soon as possible to prevent delayed or "rebound" reactions

Crystalloids should be administered with close attention to the lung and neck vein exam as the patient may develop pulmonary edema due to the increased capillary permeability seen in anaphylaxis

Pressors may be necessary to maintain adequate vital organ perfusion - dopamine, at alpha and beta effect dosing, or epi injections/drip may be used

Neurogenic shock can be considered the etiology of hypotension in the trauma patient ONLY after thorough evaluation of the patient to rule out hypovolemic/hemorrhagic shock.

Place patient in Trendelenberg position only if head injury has been excluded

Crystalloid boluses

Use alpha agonist to augment tone if above measures do not adequately restore perfusion (dopamine at alpha doses or ephedrine)

Bradycardia may be treated with atropine in usual doses, and external or transvenous pacing may be necessary

Pharmacologic shock management includes:

Specific reversal agents if available, ie. naloxone for narcotics and flumazenil for benzodiazepines (if no history of seizure disorder or chronic benzodiazepine use)

Removal of drug; in overdose, consider gastric lavage, charcoal adsorption, enhanced elimination (renal and GI) Supportive care with crystalloids and pressors as needed

Summary

Management goals

Identify etiology and begin appropriate interventions EARLY

Optimize oxygen delivery - remember ABC's

Follow serial clinical parameters and adjust your interventions based on evolving presentation