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.
 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
 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
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
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.
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
 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.
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 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 Increased capillary
extravascular space permeability secondary to
inflammation or traumatic
 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 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
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
 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
 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.
 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
 issevere 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).
 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.
 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.
 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
 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
CASES
38
39
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.)