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Cardiogenic Shock

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Title: Cardiogenic Shock


1
  • Cardiogenic Shock
  • By Fritzanella Lafond

2
  • 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.

3
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.

4
  • 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

5
Pathophysiology diagram of cardiogenic shock
6
Hemodynamic changes in chock states
7
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

8
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

9
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.

10
Echocardiogram image
11
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

12
Coronary angiogram Pre
13
Coronary angiogram Post
14
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.

15
  • Hypovolemic Shock
  • By Fatima Hussain

16
  • 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.

17
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
18
  • 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

19
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

20
  • 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

21
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

22
  • 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

23
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

24
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.

25
  • 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.

26
  • 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

27
  • 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

28
  • 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.

29
  • Septic Shock
  • By Ruby Bhullar

30
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).

31
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.

32
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.

33
  • 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.

34
  • 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.

35
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

36
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

37
  • CASES

38
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40
  • 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.

41
  • 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?

42
  • 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.)
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