2. Shock is the clinical syndrome that results from inadequate
tissue perfusion. Irrespective of cause, the hypoperfusion-
induced imbalance between the delivery of and
requirements for oxygen and substrate leads to cellular
dysfunction. The cellular injury created by the inadequate
delivery of oxygen and substrates also induces the
production and release of damage-associated molecular
patterns (DAMPs or “danger signals”) and inflammatory
mediators that further compromise perfusion through
functional and structural changes within the
microvasculature. This leads to a vicious cycle in which
impaired perfusion is responsible for cellular injury that
causes maldistribution of blood flow, further compromising
cellular perfusion; the latter ultimately causes multiple
organ failure (MOF) and, if the process is not interrupted,
leads to death. The clinical manifestations of shock are also
the result, in part, of autonomic neuroendocrine responses
to hypoperfusion as well as the breakdown in organ
function induced by severe cellular dysfunction
3. Clinical shock is usually accompanied by
hypotension (i.e., a mean
arterial pressure [MAP] <60 mmHg in
previously normotensive
persons). Multiple classification schemes have
been developed in an
attempt to synthesize the seemingly dissimilar
processes leading to
shock.
4. MICROCIRCULATION Normally when cardiac output falls,
systemic vascular resistance rises to maintain a level of
systemic pressure that is adequate for perfusion of the
heart and brain at the expense of other tissues such as
muscle, skin, and especially the gastrointestinal (GI)
tract. Systemic vascular resistance is determined
primarily by the luminal diameter of arterioles. The
metabolic rates of the heart and brain are high, and
their stores of energy substrate are low. These organs ar
continuous supply of oxygen and nutrients, and neither
tolerates severe ischemia for more than brief periods
(minutes). Autoregulation (i.e., the maintenance of
blood flow over a wide range of perfusion pressures) is
critical in sustaining cerebral and coronary perfusion
despite significant hypotension. However, when MAP
drops to ≤60 mmHg, blood flow to these organs falls,
and their function deteriorates.
5. Arteriolar vascular smooth muscle has both α- and β-
adrenergic receptors. The α1 receptors mediate
vasoconstriction, while the β2 receptors mediate
vasodilation. Efferent sympathetic fibers release
norepinephrine, which acts primarily on α1 receptors as
one of the most fundamental compensatory responses to
reduced perfusion pressure. Other constrictor substances
that are increased in most forms of shock include
angiotensin II, vasopressin, endothelin 1, and thromboxane
A2. Both norepinephrine and epinephrine are released by
the adrenal medulla, and the concentrations of these
catecholamines in the bloodstream rise. Circulating
vasodilators in shock include prostacyclin (prostaglandin
[PG] I2), nitric oxide (NO), and, importantly, products of
local metabolism such as adenosine that match flow to the
tissue’s metabolic needs. The balance between these
various vasoconstrictors and vasodilators influences the
microcirculation and determineslocal perfusion.
6. Transport to cells depends on microcirculatory flow; capillary
permeability; the diffusion of oxygen, carbon dioxide, nutrients,
and products of metabolism through the interstitium; and the
exchange of these products across cell membranes. Impairment
of the microcirculation that is central to the pathophysiologic
responses in the late stages of all forms of shock results in the
derangement of cellular metabolism that is ultimately
responsible for organ failure. The endogenous response to mild
or moderate hypovolemia is an attempt at restitution of
intravascular volume through alterations in hydrostatic pressure
and osmolarity. Constriction of arterioles leads to reductions in
both the capillary hydrostatic pressure and the number of
capillary beds perfused, thereby limiting the capillary surface
area across which filtration occurs. When filtration is reduced
while intravascular oncotic pressure remains constant or rises,
there is netreabsorption of fluid into the vascular bed, in accord
with Starling’s law of capillary interstitial liquid exchange.
Metabolic changes (including hyperglycemia and elevations in
the products of glycolysis, lipolysis, and proteolysis) raise
extracellular osmolarity, leading to an osmotic gradient that
increases interstitial and intravascular volume at the expense of
intracellular volume
7. CELLULAR RESPONSES Interstitial transport of nutrients is
impaired in shock, leading to a decline in intracellular
high- energy phosphate stores. Mitochondrial
dysfunction and uncoupling of oxidative phosphorylation
are the most likely causes for decreased amounts of
adenosine triphosphate (ATP). As a consequence, there is
an accumulation of hydrogen ions, lactate, reactive
oxygen species, and other products of anaerobic
metabolism. As shock progresses, these vasodilator
metabolites override vasomotor tone, causing further
hypotension and hypoperfusion. Dysfunction of cell
membranes is thought to represent a common end-stage
pathophysiologic pathway in the various forms of shock.
Normal cellular transmembrane potential falls, and there
is an associated increase in intracellular sodium and
water, leading to cell swelling that interferes further with
microvascular perfusion. In a preterminal event,
homeostasis of calcium via membrane channels is lost
8. NEUROENDOCRINE RESPONSE
Hypovolemia, hypotension,
and hypoxia are sensed by
baroreceptors and
chemoreceptors that
contribute to an autonomic
response that attempts to
restore blood volume,
maintain central perfusion,
and mobilize metabolic
substrates. Hypotension
disinhibits the vasomotor
center, resulting in
increased adrenergic output
and reduced vagal activity.
Release of norepinephrine
from adrenergic neurons
induces significant
peripheral and splanchnic
reduced vagal activity
increases the heart rate and
cardiac output. Loss of
vagal
activity is also recognized to
upregulate the innate
immune inflammatory
response. The effects of
circulating epinephrine
released by the adrenal
medulla in shock are largely
metabolic, causing
increased glycogenolysis
and gluconeogenesis and
reduced pancreatic insulin
release. However,
epinephrine also inhibits
production and release of
inflammatory mediators
9. Severe pain or other stresses cause the hypothalamic
release of adrenocorticotropic hormone (ACTH). This
stimulates cortisol secretion that contributes to
decreased peripheral uptake of glucose and amino acids,
enhances lipolysis, and increases gluconeogenesis.
Increased pancreatic secretion of glucagon during stress
accelerates hepatic gluconeogenesis and further elevates
blood glucose concentration. These hormonal actions act
synergistically to increase blood glucose for both
selective tissue metabolism and the maintenance of
blood volume. Many critically ill patients have recently
been shown to exhibit low plasma cortisol levels and an
impaired response to ACTH stimulation, which is linked
to a decrease in survival. The importance of the cortisol
response to stress is illustrated by the profound
circulatory collapse that occurs in patients with
adrenocortical insufficiency
10. Renin release is increased in response to adrenergic discharge and
reduced perfusion of the juxtaglomerular apparatus in the kidney.
Renin induces the formation of angiotensin I that is then converted
to angiotensin II by the angiotensin converting enzyme; angiotensin
II is an extremely potent vasoconstrictor and stimulator of
aldosterone
release by the adrenal cortex and of vasopressin by the posterior
pituitary. Aldosterone contributes to the maintenance of
intravascularvolume by enhancing renal tubular reabsorption of
sodium, resulting
in the excretion of a low-volume, concentrated, sodium-free urine.
Vasopressin has a direct action on vascular smooth muscle,
contributing
to vasoconstriction, and acts on the distal renal tubules to enhance
water reabsorption.
11. CARDIOVASCULAR RESPONSE Three
variables—ventricular filling
(preload), the resistance to
ventricular
ejection (afterload), and myocardial
contractility—are paramount in
controlling stroke volume. Cardiac
output, the major determinant of
tissue perfusion, is the product of
stroke volume and heart rate.
Hypovolemia leads to decreased
ventricular preload that, in turn,
reduces the stroke volume. An
increase in heart rate is a useful but
limited compensatory mechanism to
maintain cardiac output. A shock-
induced reduction in myocardial
compliance is frequent, reducing
ventricular end-diastolic volume
and, hence, stroke volume at any
given ventricular filling pressure.
Restoration of intravascular volume
may return stroke volume to normal
but only at elevated filling pressures.
Increased filling pressures stimulate
release of brain natriuretic peptide
(BNP) to secrete sodium and volume
to relieve the pressure on the heart.
Levels of BNP correlate with outcome
following severe stress. In addition,
sepsis, ischemia, myocardial
infarction (MI), severe tissue trauma,
hypothermia, general anesthesia,
prolonged hypotension, and
acidemia may all also impair
myocardial contractility and reduce
the stroke volume at any given
ventricular end-diastolic volume.
The resistance to ventricular ejection
is significantly influenced by the
systemic vascular resistance, which
is elevated in most forms of shock.
However, resistance is decreased in
the early hyperdynamic stage of
septic shock or neurogenic shock
thereby initially allowing the cardiac
output to be maintained or elevated.
12. PULMONARY RESPONSEThe
response of the pulmonary
vascular bed to shock
parallels that of the
systemic vascular bed, and
the relative increase in
pulmonary vascular
resistance, particularly in
septic shock, may exceed
that of the systemic vascular
resistance, leading to right
heart failure. Shockinduced
tachypnea reduces tidal
volume and increases both
dead space and minute
ventilation. Relative hypoxia
and the subsequent
tachypnea induce a
respiratory alkalosis. These
disorders are characterized
by noncardiogenic
pulmonary edema secondary
todiffuse pulmonary
capillary endothelial and
alveolar epithelial injury,
hypoxemia, and bilateral
diffuse pulmonary
infiltrates. Hypoxemia
results from perfusion of
underventilated and
nonventilated alveoli. Loss
of surfactant and lung
volume in combination with
increased interstitial and
alveolar edema reduces lung
compliance. The work of
breathing and the oxygen
requirements of respiratory
muscles increase.
13. RENAL RESPONSE Acute kidney injury, Acute tubular
necrosis is now more frequently seen as a result of the
interactions of shock, sepsis, the administration of
nephrotoxic agents (such as aminoglycosides and
angiographic contrast media), and rhabdomyolysis; the
latter may be particularly severe in skeletal muscle
trauma. The physiologic responseof the kidney to
hypoperfusion is to conserve salt and water. In addition
to decreased renal blood flow, increased afferent
arteriolar resistance accounts for diminished glomerular
filtration rate (GFR) that, together with increased
aldosterone and vasopressin, is responsible for reduced
urine formation. Toxic injury causes necrosis of tubular
epithelium and tubular obstruction by cellular debris
with back leak of filtrate. The depletion of renal ATP
stores that occurs with prolonged renal hypoperfusion
contributes to subsequent impairment of renal function.
14. METABOLIC DERANGEMENTS During shock, there is
disruption of the normal cycles of carbohydrate, lipid,
and protein metabolism. Through the citric acid cycle,
alanine in conjunction with lactate, which is converted
from pyruvate in the periphery in the presence of
oxygen deprivation, enhances the hepatic production of
glucose. With reduced availability of oxygen, the
breakdown of glucose to pyruvate, and ultimately
lactate, represents an inefficient cycling of substrate
with minimal net energy production. An elevated plasma
lactate/pyruvate ratio is preferable to lactate alone as a
measure of anaerobic metabolism and reflects
inadequate tissue perfusion. Decreased clearance of
exogenous triglycerides coupled with increased hepatic
lipogenesis causes a significant rise in serum
triglyceride concentrations. There is increased protein
catabolism as energy substrate, a negative nitrogen
balance, and, if the process is prolonged, severe muscle
wasting.
15. INFLAMMATORY RESPONSESActivation of an extensive
network of proinflammatory mediator pathways
by the innate immune system plays a significant role in
the progression
of shock and contributes importantly to the development
of
multiple organ injury, multiple organ dysfunction (MOD).
delayed MOF.
Multiple humoral mediators are activated during shock
and tissue
injury. The complement cascade, activated through both
the classic
and alternate pathways, generates the anaphylatoxins
C3a and C5aDirect complement fixation to injured
tissues can
progress to the C5-C9 attack complex, causing further
cell damage.
16. HYPOVOLEMIC SHOCKThis blood cell mass and plasma from
hemorrhage or from the lomost common form of shock
results either from the loss of red ss of plasma volume
alone due to extravascular fluid sequestration or GI,
urinary, and insensible losses. The signs and symptoms
of nonhemorrhagic hypovolemic shock are the same as
those of hemorrhagic shock, although they may have a
more insidious onset. The normal physiologic response to
hypovolemia is to maintain perfusion of the brain and
heart while attempting to restore an effective circulating
blood volume. There is an increase in sympathetic
activity, hyperventilation, collapse of venous capacitance
vessels, release of stress hormones, and an attempt to
replace the loss of intravascular volume through the
recruitment of interstitial and intracellular fluid and by
reduction of urine output. Mild hypovolemia (≤20% of the
blood volume) generates mild tachycardia but relatively
few external signs, especially in a supine young patient.
17. With moderate hypovolemia (~20–40% of the blood
volume), the patient becomes increasingly anxious
and tachycardic; although normal blood pressure may
be maintained in the supine position, there may be
significant postural hypotension and tachycardia. If
hypovolemia is severe (≥40% of the blood volume),
the classic signs of shock appear; the blood pressure
declines and becomes unstable even in the supine
position, and the patient develops marked
tachycardia, oliguria, and agitation or confusion.
Perfusion of the central nervous system is well
maintained until shock becomes severe. Hence,
mental obtundation is an ominous clinical sign. The
transition from mild to severe hypovolemic shock can
be insidious or extremely rapid. If severe shock is not
reversed rapidly, especially in elderly patients and
those with comorbid illnesses, death is imminent.
18. Diagnosis Hypovolemic shock is readily diagnosed when there
are signs of hemodynamic instability and the source of
volume loss is obvious. The diagnosis is more difficult when
the source of blood loss is occult, as into the GI tract, or
when plasma volume alone is depleted. Even after acute
hemorrhage, hemoglobin and hematocrit values do not
change until compensatory fluid shifts have occurred or
exogenous fluid is administered. It is essential to distinguish
between hypovolemic and cardiogenic shockbecause,
although both may respond to volume initially, 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 and
may cause further organ dysfunction.
19. Adults: A: 0.9% Sodium chloride given as the 1L
bolus infusion. Repeat bolus until blood pressure
is improved. Transfuse blood and plasma
expanders (-) in hemorrhagic shock Children: A:
0.9% Sodium chloride 20 mol/kg as a slow
infusion.
Do not administer calcium containing fluids, e.g.
Ringer Lactate, within 48 hours of administering
ceftriaxone Contra-indicated in neonatal
jaundice Annotate dose and route of
administration on referral letter
20. TRAUMATIC SHOCKShock following trauma is, in large measure,
due to hemorrhage. However, even when hemorrhage has been
controlled, patients can continue to suffer loss of plasma
volume into the interstitium of injured tissues. These fluid
losses are compounded by injury-induced inflammatory
responses, which contribute to the secondary microcirculatory
injury. Proinflammatory mediators are induced by DAMPs
released from injured tissue and are recognized by the highly
conserved membrane receptors of the TLR family (see
“Inflammatory Responses” above). These receptors on cells of
the innate immune system, particularly the circulating
monocyte, tissue-fixed macrophage, and dendritic cell, are
potent activators of an excessive proinflammatory phenotype in
response to cellular injury. This causes secondary tissue injury
and maldistribution of blood flow, intensifying tissue ischemia
and leading to multiple organ system failure. In addition, direct
structural injury to the heart, chest, or head can also contribute
to shock. For example, pericardial tamponade or tension
pneumothorax impairs ventricular filling, whereas myocardial
contusion depresses myocardial contractility.
21. Inability of the patient to maintain a systolic blood pressure ≥90
mmHg after trauma-induced hypovolemia is associated with a
mortality
rate up to ~50%. To prevent this decompensation of homeostatic
mechanisms, therapy must be promptly administered.
The initial management of the seriously injured patient requires
attention to the “ABCs” of resuscitation: assurance of an airway (A),
adequate ventilation (breathing, B), and establishment of an adequate
blood volume to support the circulation (C). Control of ongoing
hemorrhage requires immediate attention. Early stabilization of
fractures, debridement of devitalized or contaminated tissues, and
evacuation of hematomata all reduce the subsequent inflammatory
response to the initial insult and minimize damaged tissue release
of DAMPs and subsequent diffuse organ injury. Supplementation of
depleted endogenous antioxidants also reduces subsequent organ
failure and mortality.
22. NEUROGENIC SHOCK Interruption of sympathetic
vasomotor input after a high cervical spinal cord injury,
inadvertent cephalad migration of spinal anesthesia, or
devastating head injury may result in neurogenic
shock. In addition to arteriolar dilation, venodilation
causes pooling in the venous system, which decreases
venous return and cardiac output. The extremities are
often warm, in contrast to the usual sympathetic
vasoconstrictioninduced coolness in hypovolemic or
cardiogenic shock. Treatment involves a simultaneous
approach to the relative hypovolemia and to the loss of
vasomotor tone. Excessive volumes of fluid may be
required to restore normal hemodynamics if given
alone. Once hemorrhage has been ruled out,
norepinephrine or a pure α-adrenergic agent
(phenylephrine) may be necessary to augment vascular
resistance and maintain an adequate MAP.
23. Animals mount both local and systemic
responses to microbes that traverse their
epithelial barriers and enter underlying tissues.
Fever or hypothermia, leukocytosis or
leukopenia, tachypnea, and tachycardia are
cardinal signs of the systemic response. In
general, when an infectious etiology is proven
or strongly suspected and the response results
in hypofunction of uninfected organs, the term
sepsis (or severe sepsis) should be used. Septic
shock refers to sepsis accompanied by
hypotension that cannot be corrected by the
infusion of fluids.
24. BacteremiaPresence of bacteria in blood, as
evidenced by positive blood cultures
Signs of possibly harmful systemic responseTwo
or more of the following conditions: (1) fever
(oral temperature >38°C [>100.4°F]) or
hypothermia (<36°C [<96.8°F]); (2) tachypnea
(>24 breaths/min); (3) tachycardia (heart rate
>90 beats/min); (4) leukocytosis (>12,000/μL),
leukopenia (<4000/μL), or >10% bands
Sepsis (or severe sepsis) The harmful host
response to infection; systemic response to
proven or suspected infection plus some degree
of organ hypofunction, i.e.:
25. 1. Cardiovascular: Arterial systolic blood pressure
≤90 mmHg or mean arterial pressure ≤70 mmHg
that responds to administration of IV fluid
2. Renal: Urine output <0.5 mL/kg per hour for 1 h
despite adequate fluid
Resuscitation
3. Respiratory: Pao2/Fio2 ≤250 or, if the lung is the
only dysfunctional organ,
≤200
4. Hematologic: Platelet count <80,000/μL or 50%
decrease in platelet count from highest value
recorded over previous 3 days
5. Unexplained metabolic acidosis: A
pH ≤7.30 or a base deficit ≥5.0 mEq/L
and a plasma lactate level >1.5 times
upper limit of normal for reporting lab
26. Septic shockSepsis with hypotension (arterial
blood pressure <90 mmHg systolic,
or 40 mmHg less than patient’s normal
blood pressure) for at least 1 h
despite adequate fluid resuscitationa
Refractory septic shockSeptic shock that lasts for
>1 h and
does not respond to fluid or pressor
administration
27. The systemic response to any class of microorganism
can be
Harmful. Microbial invasion of the bloodstream is not
essential because local inflammation can also elicit
distant organ dysfunction and hypotension. In fact,
blood cultures yield bacteria or fungi in only ~20–
40% of cases of severe sepsis and 40–70% of cases of
septic shock. Respiratory infection was most
common (64%). Microbiologic results were positive in
70% of individuals considered infected; of the
isolates, 62% were gram-negative bacteria
(Pseudomonas species and Escherichia coli were
most common), 47% were grampositive bacteria
(Staphylococcus aureus was most common), and 19%
were fungi (Candida species).
28. The manifestations of the septic response are
superimposed on the symptoms and signs of the
patient’s underlying illness and primary infection. The
rate at which severe sepsis develops may differ from
patient to patient, and there are striking individual
variations in presentation. For example, some patients
with sepsis are normo- or hypothermic; the absence of
fever is most common in neonates, in elderly patients,
and in persons with uremia or alcoholism.
Hyperventilation, producing respiratory alkalosis, is
often an early sign of the septic response.
Disorientation, confusion, and other manifestations of
encephalopathy may also develop early on, particularly
in the elderly and in individuals with preexisting
neurologic impairment. Focal neurologic signs are
uncommon, although preexisting focal deficits may
become more prominent
29.
30. Renal ComplicationsOliguria, azotemia,
proteinuria, and nonspecific urinary casts are
frequently found. Many patients are
inappropriately polyuric; hyperglycemia may
exacerbate this tendency. Most renal failure is
due to acute tubular necrosis induced by
hypovolemia, arterial hypotension, or toxic
drugs,
ImmunosuppressionPatients with severe sepsis
often become profoundly immunosuppressed.
Manifestations include loss of delayedtype
hypersensitivity reactions to common
antigens, failure to control the primary
infection, and increased risk for secondary
infections
31. There is no specific diagnostic test for sepsis.
Diagnostically sensitive
findings in a patient with suspected or proven infection
include fever
or hypothermia, tachypnea, tachycardia, and leukocytosis
or leukopeniaacutely altered mental status,
thrombocytopenia,
an elevated blood lactate level, respiratory alkalosis, or
hypotension
also should suggest the diagnosis. Definitive etiologic
diagnosis requires identification of the causative
microorganism from blood or a local site of infection.
LABORATORY FINDINGS
Abnormalities that occur early in the septic response
may include leukocytosis
with a left shift, thrombocytopenia, hyperbilirubinemia,
andproteinuria. Leukopenia may develop.
32. Antimicrobial chemotherapy should be started
as soon as samples
of blood and other relevant sites have been
obtained for culture.
33. Cardiogenic shock and pulmonary edema are life-
threatening conditions that should be treated as
medical emergencies. The most common joint
etiology is severe left ventricular (LV)
dysfunction that leads to pulmonary congestion
and/or systemic hypoperfusion
CARDIOGENIC SHOCK Cardiogenic shock (CS) is
characterized by systemic hypoperfusion due to
severe depression of the cardiac index (<2.2
[L/min]/m2) and sustained systolic arterial
hypotension (<90 mmHg) despite an elevated
filling pressure (pulmonary capillary wedge
pressure [PCWP] >18 mmHg). It is associated
with in-hospital mortality rates >50%.
34. Pathophysiology CS is characterized by a vicious circle
in which depression of myocardial contractility,
usually due to ischemia, results in reduced cardiac
output and arterial blood pressure (BP), which result
in hypoperfusion of the myocardium and further
ischemia and depression of cardiac output. Systolic
myocardial dysfunction reduces stroke volume and,
together with diastolic dysfunction, leads to elevated
LV end-diastolic pressure and PCWP as well as to
pulmonary congestion. Reduced coronary perfusion
leads to worsening ischemia and progressive
myocardial dysfunction and a rapiddownward spiral,
which, if uninterrupted, is often fatal. A systemic
inflammatory response syndrome may accompany
large infarctions and shock. Inflammatory cytokines,
inducible nitric oxide synthase, and excess nitric
oxide and peroxynitrite may contribute to the genesis
of CS as they do to that of other forms of shock
35. Patient Profile Older age, female sex, prior MI, diabetes, anterior
MI
location, and extensive coronary artery stenoses are associated
with
an increased risk of CS complicating MI. Shock associated with a
first
inferior MI should prompt a search for a mechanical cause.
Timing Shock is present on admission in only one-quarter of
patients
who develop CS complicating MI; one-quarter develop it rapidly
thereafter, within 6 h of MI onset. Another quarter develop shock
later
on the first day.
Diagnosis Due to the unstable condition of these patients,
supportive
therapy must be initiated simultaneously with diagnostic
evaluationA focused history and physical examination should be
performed, blood specimens sent to the laboratory, and an
electrocardiogram
(ECG) and chest x-ray obtained.
36. Electrocardiogram In CS due to acute MI with LV failure, Q
waves and/or >2-mm ST elevation in multiple leads or left
bundle branch block are usually present.
Echocardiogram A two-dimensional echocardiogram with
color-flow Dopplershould be obtained promptly in patients
with suspected CS to help define its etiology.
PULMONARY ARTERY CATHETERIZATION
LEFT HEART CATHETERIZATION AND CORONARY
ANGIOGRAPHY
Clinical findings Most patients have dyspnea and appear pale,
apprehensive, and diaphoretic, and mental status may be
altered. The pulse is typically weak and rapid, often in the
range of 90–110 beats/min, or severe bradycardia due to
high-grade heart block may be present. Systolic BP is
reduced (<90 mmHg or ≥30 mmHg below baseline) with a
narrow pulse pressure (<30 mmHg), but occasionally BP
may be maintained by very high systemic vascular
resistance. Tachypnea, Cheyne-Stokes respirations, and
jugular venous distention may be present. There is typically
a weak apical pulse and soft S1, and an S3 gallop may be
audible.
37. Laboratory findings The white blood cell count
is typically elevated with a left shift. Renal
function is initially unchanged, but blood urea
nitrogen and creatinine rise progressively.
Hepatic transaminases may be markedly
elevated due to liver hypoperfusion. The lactic
acid level is elevated. Arterial blood gases
usually demonstrate hypoxemia and anion gap
metabolic acidosis, which may be
compensated by respiratory alkalosis. Cardiac
markers, creatine phosphokinase and its MB
fraction, and troponins I and T are typically
markedly elevated.
38. Acute myocardial infarction/ischemia
LV failure
Ventricular septal rupture
Papillary muscle/chordal rupture–severe MR
Ventricular free wall rupture with subacute tamponade
Other conditions complicating large Mis
Hemorrhage
Infection
Excess negative inotropic or vasodilator medications
Prior valvular heart disease
Hyperglycemia/ketoacidosis
Post-cardiac arrest
Post-cardiotomy
Refractory sustained tachyarrhythmias
Acute fulminant myocarditis
End-stage cardiomyopathy
LV apical ballooning
Takotsubo’s cardiomyopathy
Hypertrophic cardiomyopathy with severe outflow obstruction
Aortic dissection with aortic insufficiency or tamponade
Severe valvular heart disease
Critical aortic or mitral stenosis
Acute severe aortic regurgitation or mitral regurgitation
Toxic/metabolic
β blocker or calcium channel antagonist overdose
39. In addition to the usual treatment of acute MI initial
therapy is aimed at maintaining adequate systemic
and coronary perfusion by raising systemic BP with
vasopressors and adjusting volume status to a level
that ensures optimum LV filling pressure. There is
interpatient variability, but the values that generally
are associated with adequate perfusion are systolic
BP ~90 mmHg or mean BP >60 mmHg and PCWP
>20 mmHg. Hypoxemia and acidosis must be
corrected; most patients require ventilatory support
VASOPRESSORS Various IV drugs may be used to
augment BP and cardiac output in patients with CS.
All have important disadvantages, and none has
been shown to change the outcome in patients with
established shock. Norepinephrine is a potent
vasoconstrictor and inotropic stimulant that is
useful for patients with CS.
40. Sudden cardiac death (SCD) is defined as natural death
due to cardiac causes in a person who may or may not
have previously recognized heart disease but in whom
the time and mode of death are unexpected The term
“sudden,” in the context of SCD, is defined for most
clinical and epidemiologic purposes as 1 h or less
between a change in clinical status heralding the onset
of the terminal clinical event and the cardiac arrest
itself. Biological death may be delayed by
interventions, but the relevant pathophysiologic event
remains the sudden and unexpected cardiac arrest.
Accordingly, for statistical purposes, deaths that occur
during hospitalization or within 30 days after
resuscitated cardiac arrest are counted as sudden
deaths.
41. The majority of natural deaths are caused by cardiac disorders.
However, it is common for underlying heart diseases—often far
advanced—to go unrecognized before the fatal event. As a result,
up
to two-thirds of all SCDs occur as the first clinical expression of
previously
undiagnosed disease or in patients with known heart disease, the
extent of which suggests low individual risk.
Cardiovascular collapse is a general term connoting loss of
sufficient
cerebral blood flow to maintain consciousness due to acute
dysfunction
of the heart and/or peripheral vasculature. It may be caused by
vasodepressor syncope (vasovagal syncope, postural hypotension
with
syncope, neurocardiogenic syncope; , a transient severe
bradycardia, or cardiac arrest. The latter is distinguished from
the
42. PRODROME, ONSET, ARREST, DEATHSCD may be presaged by
days to months of increasing angina, dyspnea, palpitations,
easy fatigability, and other nonspecific complaints.
However, these prodromal symptoms are generally
predictive of any major cardiac event; they are not specific
for predicting SCD. The onset of the clinical transition,
leading to cardiac arrest, is defined as an acute change in
cardiovascular status preceding cardiac arrest by up to 1 h.
The probability of achieving successful resuscitation from
cardiac arrest is related to the interval from onset of loss of
circulation to return of spontaneous circulation (ROSC), the
setting in which the event occurs, the mechanism (VF, VT,
PEA, asystole), and the clinical status of the patient before
the cardiac arrest. The immediate outcome is good for
cardiac arrest occurring in the intensive care unit in the
presence of an acute cardiac event or transient metabolic
disturbance, but survival among patients with far-advanced
chronic cardiac disease or advanced noncardiac diseases
(e.g., renal failure, pneumonia, sepsis, diabetes, cancer) is
low and not much better in the in-hospital setting.
43. The probability of progression to biologic death is a function of
the mechanism of cardiac arrest and the length of the delay
before interventions. VF without CPR within the first 4–6 min
has a poor outcome even if defibrillation is successful because
of secondary brain damage; the prompt interposition of
bystander CPR (basic life support; see below) improves
outcome at any point along the time scale, especially when
followed by early successful defibrillation. However, there are
few survivors among patients who had no life support activities
for the first 8 min after onset. Evaluations of deployment of
automaticexternal defibrillators (AEDs) in communities (e.g.,
police vehicles, large buildings, airports, and stadiums) are
beginning to generate encouraging data, but the data for home
deployment has been have been less impressive. Death during
the hospitalization after a successfully resuscitated cardiac
arrest relates closely to the severity of central nervous system
injury. Anoxic encephalopathy and infections subsequent to
44. An individual who collapses suddenly is managed in five stages: (1)
initial evaluation and basic life support if cardiac arrest is confirmed,
(2) public access defibrillation (when available), (3) advanced life
support, (4) postresuscitation care, and (5) long-term management.
The initial response, including confirmation of loss of circulation,
followed by basic life support and public access defibrillation, can be
carried out by physicians, nurses, paramedical personnel, and trained
laypersons.
INITIAL EVALUATION AND BASIC LIFE SUPPORT Confirmation that a
sudden collapse with loss of consciousness (LOC) is due to a cardiac
arrest includes prompt observations of the state of consciousness,
respiratory movements, skin color, and the presence or absence of
pulses in the carotid or femoral arteries. For lay responders, the pulse
check is no longer recommended because it is unreliable. As soon as a
cardiac arrest is suspected, confirmed, or even considered to be
impending, calling an emergency rescue system (e.g., 911) is the
immediate priority. The third action during the initial response is to
clear the airway. The head is tilted back and the chin lifted so that the
oropharynx can be explored to clear the airway. Dentures or foreign
bodies are removed, and the Heimlich maneuver is performed if there
is reason to suspect that a foreign body is lodged in the oropharynx. If
45. Basic life support, more popularly known as CPR, is intended to
maintain organ perfusion until definitive interventions can be
instituted. The initial and primary element of CPR is maintenance
of perfusion until spontaneous circulation can be restored. Closed
chest cardiac compression maintains a pump function by
sequential filling and emptying of the chambers, with competent
valves maintaining forward direction of flow. The palm of one hand
is placed over the lower sternum, with the heel of the other resting
on the dorsum of the lower hand. The sternum is depressed, with
the arms remaining straight, at a rate of 100 per minute. Sufficient
force is applied to depress the sternum 4–5 cm, and relaxation is
abrupt. Until recently, providing ventilation of the lungs by mouth-
to- mouth respiration was used if no specific rescue equipment
was immediately available (e.g., plastic oropharyngeal airways,
esophageal obturators, masked Ambu bag). However, ventilatory
support during CPR has yielded to evidence that continuous chest
compressions (“hands only” CPR) results in better outcomes.
Compressions are interrupted only for single shocks from an AED
when available, with 2 min of CPR between each single shock.
46. AUTOMATED EXTERNAL DEFIBRILLATION (AED)
AEDs that are easily used by nonconventional responders, such
as nonparamedic firefighters, police officers, ambulance drivers,
trained security guards, and minimally trained or untrained
laypersons,
have been developed. This advance has inserted another level
of response into the cardiac arrest paradigm. A number of studies
have demonstrated that AED use by nonconventional responders
in strategic response systems and public access lay responders
can improve cardiac arrest survival rates. The rapidity with which
defibrillation/cardioversion is achieved is an important element for
successful resuscitation, both for ROSC and for protection of the
central nervous system. Chest compressions should be carried out
while the defibrillator is being charged.
