Cardiogenic Shock By Fritzanella Lafond

Cardiongenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most commonly following acute MI. The Clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock are sustained hypotension (systolic blood pressure <90mmHg for at least 30 min) and a reduced cardiac index (<2.2 L/min/m2) in the presence of elevated pulmonary capillary occlusion pressure (>15mm Hg).

The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing hypotension and clinical signs of poor tissue perfusion, which include oliguria, cyanosis, cool extremities, and altered mental mentation. These signs usually persist after attempts have been made to correct hypovolemia, arrhythmia, hypoxia, and acidosis.

Based on the etiology and pathophysiology, cardiogenic shock can be divided into systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, coronary artery disease, and mechanical complications.

Systolic dysfunction: The primary abnormality in systolic dysfunction is decreased myocardial contractility. Acute MI or ischemia is the most common cause. The other causes of systolic failure leading to cardiogenic shock are severe myocarditis, end-stage cardiomyopathy (including valvular causes: i.e., MR/AR), myocardial depressant drugs (i.e., beta-blockers, calcium channel blockers) myocardial contusion, and prolonged cardiopulmonary bypass.

Causes

Cardiac arrhythmias: Tachyarrhythmias are often associated with cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock due to another etiology. Sinus tachycardia and atrial tachyarrhythmias contribute to hypoperfusion and aggravate shock.

Mechanical complications: Complication of acute MI, such as acute mitral regurgitation, large RV infarction, and rupture of the interventricular septum or left ventricular free wall, are other causes of cardiogenic shock

Pathophysiology diagram of cardiogenic shock

Hemodynamic changes in chock states

Cool, clammy, and mottled skin due to vasoconstriction and subsequent hypoperfusion of the skin.

Jugular venous distention and crackles in the lungs are usually present. Peripheral edema also may be present.

Hypotension due to decrease CO Rapid, weak, thready pulse due to decreased circulation

combined with tachycardia. Oliguria (<30mL/h) Hyperventilation due to sympathetic nervous system

stimulation and acidosis Altered mental status due to decrease cerebral perfusion

and subsequent hypoxia

Clinical presentation

Lab studies: Biochemical profile: Measurement of routine biochemistry

parameters, such as electrolytes, renal function (eg, urea and creatinine), and liver function tests.

CBC count: A CBC count is generally helpful to exclude anemia; a high WBC count may indicate an underlying infection, and the platelet count may be low because of coagulopathy related to sepsis

Cardiac enzymes: Check markers for CK-MB, LDH , and Troponin I and T (are most important enzyme test to order because of greater sensitivity and specificity than CK-MB for MI) . Measuring these markers can show whether the heart is damaged and the extent of the damage.

Arterial blood gases: Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation. A base deficit elevation correlates with the occurrence and severity of shock. A base deficit is also an important marker to follow during resuscitation of a patient from shock

Workup

Imaging Studies: Echocardiography should be performed early to establish the cause of

cardiogenic shock.Can diagnose a variety of mechanical causes of shock, such as

papillary muscle rupture causing acute myocardial regurgitation, acute ventricular septal defect, free myocardial wall rupture, and pericardial tamponade.

Also identify valve disease, estimate EF, and pericardial effusion, etc.

Chest radiography findings are useful for excluding other causes of shock or chest pain. A widened mediastinum may indicate aortic dissection. Tension pneumothorax detected on x-ray films may manifest as low-

output shock. Most patients with established cardiogenic shock exhibit findings of

left ventricular failure. The radiological features of left ventricular failure include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions.

Workup

Echocardiogram image

Other Tests: Electrocardiogram: Acute myocardial ischemia is

diagnosed based on the presence of ST-segment elevation, ST-segment depression, or Q waves. Therefore, it is imperative to perform electrocardiography immediately to help diagnose MI, myocardial ischemia, or both.

Hemodynamic monitoring with a Swan-Ganz catheter is very helpful for excluding other causes of shock: PCWP >15mm Hg and a cardiac index of <2.2L/min/m2.

Coronary artery angiography : Is urgently indicated in patients with myocardial ischemia

or MI who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries and the need for urgent revascularization

Workup

Coronary angiogram: Pre

Coronary angiogram: Post

ABCs: Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required.

Fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present

Pulmonary artery catheter (PAC) and percutaneous oximetry are routine

Electrolyte and acid-base abnormalities should be corrected Identify and treat underlying causes:( i.e., Acute MI, Cardiac

Tamponade, valvular abnormalities and cardiac arrhythmia) Hemodynamic support: -Dopamine, norepinephrine,

epinephrine, and dobutamine Intra-aortic balloon pump or left ventricular device can be

considered.

Treatment

Hypovolemic Shock

By Fatima Hussain

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.

Loss of approximately one-fifth or more of the normal blood volume produces hypovolemic shock.

Site of fluid loss Mechanism of lossSkin Thermal or chemical burn,

sweating from excessive heat exposure

GI tract Vomiting or diarrhea

Kidneys Diabetes mellitus or insipidus, adrenal insufficiency, “salt-losing” nephritis, polyuric phase after acute tubular damage, and use of potent diuretics

Intravascular fluid lost to the extravascular space

Increased capillary permeability secondary to inflammation or traumatic injury (e.g. crush), anoxia, cardiac arrest, sepsis, bowel ischemia, and acute pancreatitis

The normal physiologic response to hypovolemia is to maintain perfusion of the brain and heart, while restoring an effective circulating blood volume. This is accomplished by:

increase in sympathetic activity Hyperventilation collapse of venous capacitance vessels release of stress hormones and an attempt to limit the loss of intravascular

volume through the recruitment of interstitial and intracellular fluid and reduction of urine output

Stage 1 : Up to 15% blood volume loss (750mls) Compensation by constriction of vascular bed Blood pressure maintained Normal respiratory rate Pallor of the skin and slight anxietyStage 2: 15-30% blood volume loss (750 - 1500mls) Cardiac output cannot be maintained by arterial

constriction Tachycardia Increased respiratory rate Blood pressure maintained Increased diastolic pressure Narrow pulse pressure Sweating from sympathetic stimulation Mildly anxious/Restless

4 Stages of Hypovolemic shock

Stage 3: 30-40% blood volume loss (1500 - 2000mls)

Systolic BP falls to 100mmHg or less Classic signs of hypovolemic shock

◦Marked tachycardia >120 bpm◦Marked tachypnea >30 bpm◦Decreased systolic pressure◦Alteration in mental status (Anxiety, Agitation)◦Sweating with cool, pale skin

Stage 4: Loss greater than 40% (>2000mls) Extreme tachycardia with weak pulse Pronounced tachypnea Significantly decreased systolic blood pressure of 70

mmHg or less Decreased level of consciousness Skin is sweaty, cool, and extremely pale

Hypovolemic shock is readily diagnosed when there are signs of hemodynamic instability and the source of volume loss is obvious.

An examination will show signs of shock, including:

Low blood pressure Low body temperature Rapid pulse, which is often weak and

thready

Diagnosis

It is essential to distinguish between hypovolemic and cardiogenic because definitive therapy differs significantly.

Both forms are associated with a reduced cardiac output and a compensatory sympathetic mediated response characterized by tachycardia and elevated systemic vascular resistance.

However, the findings in cardiogenic shock of jugular venous distention, rales, and an S3 gallop distinguish it from hypovolemic shock and signify that ongoing volume expansion is undesirable

Blood chemistry, including kidney function tests

Complete blood count CT scan, ultrasound, or x-ray of suspected

areas Echocardiogram Endoscopy Swan-Ganz catheterization Urinary catheterization

Tests that may be done include:

Initial resuscitation requires rapid re-expansion of the circulating intravascular blood volume along with interventions to control ongoing losses.

Volume resuscitation is initiated with the rapid infusion of isotonic saline, or a balanced salt solution such as Ringer's lactate through large-bore intravenous lines

The infusion of 2–3 L of salt solution over 20–30 min should restore normal hemodynamic parameters.

Treatment

Successful resuscitation also requires support of respiratory function. Supplemental oxygen should be provided, and endotracheal intubation may be necessary to maintain arterial oxygenation.

Medicines such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and cardiac output.

Continued hemodynamic instability implies that shock has not been reversed and/or that there are significant ongoing blood or volume losses.

Continuing blood loss, with hemoglobin concentrations declining to 100 g/L (10 g/dL), should initiate blood transfusion, preferably as fully cross-matched blood.

In extreme emergencies, type-specific or O-negative packed red cells may be transfused

Prevention Preventing shock is easier than trying to treat it

once it happens. Quickly treating the cause will reduce the risk of developing severe shock. Early first aid can help control shock.

Possible Complications Kidney damage Brain damage Gangrene of arms or legs, sometimes leading to

amputation Heart attack

In general, patients with milder degrees of shock tend to do better than those with more severe shock.

In cases of severe hypovolemic shock, death is possible even with immediate medical attention. The elderly are more likely to have poor outcomes from shock.

Septic Shock

By Ruby Bhullar

is severe sepsis with organ hypoperfusion and hypotension (systolic < 90 mm Hg) that are poorly responsive to initial fluid resuscitation, so requires pharmacological intervention (vasopressors and/or inotropic agents).

Septic shock

Most cases of septic shock are caused by hospital-acquired gram-negative bacilli or gram-positive cocci and often occur in immunocompromised patients and those with chronic and debilitating diseases. Rarely, it is caused by Candida or other fungi.

Etiology

With sepsis, the patient typically has fever, tachycardia, and tachypnea; BP remains normal. Other signs of the causative infection are generally present.

As severe sepsis or septic shock develops, the first sign may be confusion or decreased alertness. BP generally falls, yet the skin is paradoxically warm.

Oliguria (< 0.5 mL/kg/h) is likely to be present. Later, extremities become cool and pale, with

peripheral cyanosis and mottling. Organ failure causes additional symptoms and

signs specific to the organ involved.

Symptoms and Signs

The physical examination should first involve assessment of the patient's general condition, including an assessment of airway, breathing, and circulation (ABCs) and mental status. Attention should be paid to skin color and temperature. Pallor, grayish, or mottled skin are signs of poor tissue perfusion seen in septic shock. Skin is often warm in early septic shock as peripheral dilation and increased cardiac output occur (warm shock). As septic shock progresses, depletion of intravascular volume and decreased cardiac output lead to cool, clammy extremities and delayed capillary refill. Petechiae or purpura can be associated with disseminated intravascular coagulation (DIC) sign.

Hyperventilation with respiratory alkalosis (low Paco 2 and increased arterial pH) occurs early, in part as compensation for lactic acidemia.

Serum HCO 3 is usually low, and serum and blood lactate increase. As shock progresses, metabolic acidosis worsens, and blood pH decreases.

Early respiratory failure leads to hypoxemia with PaO 2 < 70 mm Hg. Diffuse infiltrates may appear on the chest x-ray.

BUN and creatinine usually increase progressively as a result of renal insufficiency.

Bilirubin and transaminases may rise, although overt hepatic failure is uncommon.

CBC with Differentials Comprehensive Chemistry Panel- serum electrolyte

levels , lactate levels , renal and hepatic function Chest X-ray Coagulation status, as calculated by prothrombin time

(PT), activated partial thromboplastin time (aPTT or PTT), fibrinogen, FDP and D-dimer can reflect the potential for disseminated intravascular clotting (DIC).

Arterial blood gas (ABG)- measures the amount of oxygen, carbon dioxide, and acidity.

Urinalysis and culturing- to rule out the presence of UTIs.

Gram stain- to document bacterial infection and help determine the type of initial antibiotic therapy.

Blood cultures

WORKUP

Fluid resuscitation with 0.9% normal saline

O2 Broad-spectrum antibiotics (modified by culture results)

Abscesses drained, necrotic tissue excised

Blood glucose levels normalized Vasopressor therapy (norepinephrine or dopamine)

Administration of steriods

Treatment

CASES

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A 35 year old construction worker is brought in to the ER immediately following a 20-30 foot fall off a ladder. His past medical history is unknown. On exam, his vitals are: HR=120, BP=82/45, and RR=8. He is on a backboard and in a cervical collar. He withdraws from painful stimuli, but is otherwise non-responsive. Upon a quick superficial examination, he has an obvious fracture of his right femur and numerous mild lacerations.

What is the initial treatment of choice? If he fails to respond to the initial treatment, should a pressor be considered? If so, which one?

Fluids, fluids, and more fluids. Normal saline is the best initial fluid choice, though type O negative pRBCs could also be given as an adjunct, if massive hemorrhage was obvious.

No. Pressors are not effective in patients who are in hypovolemic shock, as the SVR is already severely elevated in response to the hypovolemia. Pressors, in this case, will probably worsen tissue perfusion, leading to lactic acidosis and end-organ damage. If a patient in hypovolemic shock fails to respond to initial fluids, they should receive more fluids and undergo more definitive treatment emergently (i.e. OR for traumatic injury, endoscopy for intraluminal lesions.)