Shock

• 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
Definition
• 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%
 Etiology
• Causes of cardiogenic shock
 RV failure due to:
Acute myocardial infarction
Acute cor pulmonale
Refractory sustained bradyarrhythmias
Pericardial tamponade
Toxic/metabolic
Severe acidosis, severe hypoxemia
Etiology continued..
• Causes of both Cardiogenic shock or pulmonary edema
• Acute myocardial infarction/ischemia
• Hemorrhage
• Refractory sustained tachyarrhythmias
• Acute fulminant myocarditis
• End-stage cardiomyopathy
• Takotsubo’s cardiomyopathy
• Hypertrophic cardiomyopathy with severe outflow obstruction
• Aortic dissection with aortic insufficiency or tamponade
• Severe valvular heart disease
• Toxic/metabolic
• β blocker or calcium channel antagonist overdose
Incidence
• The rate of CS complicating acute MI was 20% in the 1960s,
stayed at ~8% for >20 years, but decreased to 5–7% in the
first decade of this millennium largely due to increasing use
of early reperfusion therapy for acute MI.
• Shock is more common with ST elevation MI
(STEMI) than with non-ST elevation MI
• LV failure accounts for ~80% of cases of CS complicating
acute MI.
• Acute severe mitral regurgitation (MR), ventricular septal
rupture (VSR), predominant right ventricular (RV) failure,
and free wall rupture or tamponade account for the
remainder
clinically
Risk factors
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.
CS may rarely occur in the absence of significant
stenosis, as seen in LV apical ballooning/Takotsubo’s
cardiomyopathy.
Clinically
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.
Subsequent onset of CS may be due to reinfarction,
marked infarct expansion, or a mechanical complication.
Clinically
Presentation
 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.
 Acute, severe MR and VSR usually are associated
with characteristic systolic murmurs
 Rales are audible in most patients with LV failure.
 Oliguria is common.
Investigations
Laboratory findings
 WBCis typically elevated with a left shift.
 Renal function is initially unchanged, but BUN & 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.
• CXR:
 The chest x-ray typically shows pulmonary vascular congestion and
often pulmonary edema, but these findings may be absent in up to
a third of patients.
 The heart size is usually normal when CS results from a first MI but
is enlarged when it occurs in a patient with a previous MI.
Investigations
• Echocardiography: invaluable
• ECG:
 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.
More than one-half of all infarcts associated
with shock are anterior.
 Global ischemia due to severe left main stenosis usually
is accompanied by severe (e.g., >3 mm) ST depressions
in multiple leads.
Investigations …..
 PULMONARY ARTERY CATHETERIZATION
• Its use with established or suspected CS is controversial
• Generally recommended for measurement of filling pressures and cardiac
output to confirm the diagnosis and to optimize the use of IV fluids, inotropic
agents, and vasopressors in persistent shock
• O2 saturation measurement from right atrial, RV, and pulmonary arterial blood
samples can rule out a left-to-right shunt.
• In CS, low mixed venous O2 saturations and elevated arteriovenous (AV) O2
differences reflect low cardiac index and high fractional O2 extraction.
• However, when sepsis accompanies CS, AV O2 differences may not be elevated
The PCWP is elevated.
• Use of sympathomimetic amines may return these measurements and the
systemic BP to normal. Systemic vascular resistance may be low, normal, or
elevated in CS.
• Equalization of right- and left-sided filling pressures (right atrial and PCWP)
suggests cardiac tamponade as the cause of CS.
Investigations….
• Left heart catheterization and coronary
angiography
• Measurement of LV pressure and definition of the
coronary anatomy provide useful information and are
indicated in most patients with CS complicating MI.
• Cardiac catheterization should be performed when there
is a plan and capability for immediate coronary
intervention (see below) or when a definitive diagnosis
has not been made by other tests.
Treament
• General principles
• 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 (see “Pulmonary Edema,” below). Negative
inotropic agents should be discontinued and the doses of renally
cleared medications adjusted.
• Hyperglycemia should be controlled with insulin. Bradyarrhythmias
may require transvenous pacing. Recurrent ventricular tachycardia
or rapid atrial fibrillation may require immediate treatment
• Vassopresors
• Norepinephrine is a potent vasoconstrictor and inotropic
stimulant that is useful for patients with CS.
• As first line of therapy norepinephrine was associated with
fewer adverse events, including arrhythmias, compared to a
dopamine randomized trial of patients
• although it did not significantly improve survival compared to
dopamine, its relative safety suggests that norepinephrine is
reasonable as initial vasopressor therapy.
• Norepinephrine should be started at a dose of 2 to 4 μg/
min and titrated upward as necessary. If systemic perfusion or
systolic pressure cannot be maintained at >90 mmHg with a
dose of 15 μg/min, it is unlikely that a further increase will be
beneficial.
• Dopamine
• has varying hemodynamic effects based on the dose;
at low doses (≤ 2 μg/kg per min), it dilates the renal vascular bed,
although its outcome benefits at this low dose have not been
demonstrated conclusively;
• at moderate doses (2–10 μg/kg per min), it has positive chronotropic
and inotropic effects as a consequence of β-adrenergic receptor
stimulation.
• At higher doses, a vasoconstrictor effect results from α-receptor
stimulation. It is started at an infusion rate of 2–5 μg/kg per min, and
the dose is increased every 2–5 min to a maximum of 20–50 μg/kg per
min.
• Dobutamine
• is a synthetic sympathomimetic amine with positive inotropic action
and minimal positive chronotropic activity at low doses (2.5 μg/kg per
min) but moderate chronotropic activity at higher doses. Although
the usual dose is up to 10 μg/kg per min, its vasodilating activity
precludes its use when a vasoconstrictor effect is required.