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.
3Causes
- 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
5Pathophysiology diagram of cardiogenic shock
6Hemodynamic changes in chock states
7Clinical 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
8Workup
- 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
9Workup
- 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.
10Echocardiogram image
11Workup
- 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
12Coronary angiogram Pre
13Coronary angiogram Post
14Treatment
- 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.
17Site 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
194 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
21Diagnosis
- 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
23Tests 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
24Treatment
- 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
30Septic 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).
31Etiology
- 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.
32Symptoms 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.
35WORKUP
- 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
36Treatment
- 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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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.)