Cardiogenic Shock

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• Cardiogenic Shock
• By Fritzanella Lafond

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• 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 lt90mmHg for at least 30
  min) and a reduced cardiac index (lt2.2 L/min/m2)
  in the presence of elevated pulmonary capillary
  occlusion pressure (gt15mm 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.

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Causes

• 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.

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• 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

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Pathophysiology diagram of cardiogenic shock
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Hemodynamic changes in chock states
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Clinical presentation

• 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 (lt30mL/h)
• Hyperventilation due to sympathetic nervous
  system stimulation and acidosis
• Altered mental status due to decrease cerebral
  perfusion and subsequent hypoxia

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Workup

• 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

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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.

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Echocardiogram image
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Workup

• 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 gt15mm Hg and a cardiac index of
  lt2.2L/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

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Coronary angiogram Pre
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Coronary angiogram Post
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Treatment

• 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.

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• Hypovolemic Shock
• By Fatima Hussain

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• 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.

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Site of fluid loss Mechanism of loss
Skin 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
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• 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

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4 Stages of Hypovolemic shock

• 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 anxiety
• Stage 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

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• Stage 3 30-40 blood volume loss (1500 -
  2000mls)
• Systolic BP falls to 100mmHg or less
• Classic signs of hypovolemic shock
• Marked tachycardia gt120 bpm
• Marked tachypnea gt30 bpm
• Decreased systolic pressure
• Alteration in mental status (Anxiety, Agitation)
• Sweating with cool, pale skin
• Stage 4 Loss greater than 40 (gt2000mls)
• 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

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Diagnosis

• 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

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• 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

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Tests that may be done include

• 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

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Treatment

• 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 23 L of salt solution over 2030
  min should restore normal hemodynamic parameters.
  

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• 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.

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• 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

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• 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

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• 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.

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• Septic Shock
• By Ruby Bhullar

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Septic shock

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

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Etiology

• 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.

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Symptoms and Signs

• 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 (lt 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.

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• 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.

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• 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 lt 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.

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WORKUP

• 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

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Treatment

• 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

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• 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 HR120,
  BP82/45, and RR8. 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.

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• 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?

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• 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.)