This presentation is about shock and its treatment.

1. SHOCK

2. ‫بسم‬‫الرحیم‬ ‫الرحمن‬ ‫هللا‬

3. SHOCK
• Shock (acute circulatory failure; low-output state) is defined as a state in which
severe reduction in tissue perfusion leads first to reversible, and then, if
prolonged, to irreversible cellular injury. The cellular injury caused by
inadequate delivery of oxygen and substrates also induces production of
inflammatory mediators that further compromise perfusion.
• Basic derangement in shock is inadequate cardiac output with compensatory
vasoconstriction and tissue hypo perfusion.

4. • Cardiogenic shock is a clinical condition of inadequate tissue perfusion due to
cardiac dysfunction. The definition of cardiogenic shock includes haemo-
dynamic parameters: Persistent hypotension (systolic blood pressure <90 mmHg
or mean arterial pressure 30 mmHg lower than baseline) with severe reduction
in cardiac index ( < 1.8 L/minute/m2 without support or <2.0-2.2 L/minute/m2
with support), and adequate or elevated filling pressure (e.g. left ventricular
end-diastolic pressure> 18 mmHg or right ventricular end-diastolic pressure> 10-
15 mmHg).

5. CLASSIFICATION AND CAUSES
Type of shock Causes
Hypovolemic shock Hemorrhage, severe vomiting and diarrhea,
plasma loss in burns and acute
pancreatitis, diabetic ketoacidosis
Cardiogenic shock Acute myocardial infarction (when more than
40% of myocardium is
damaged), acute aortic regurgitation, acute
mitral regurgitation, rupture
of interventricular septum, myocarditis, rupture
of papillary muscle, right
ventricular infarction with excessive diuretic
therapy, acute massive pulmonary
embolism, cardiac arrhythmias, dilated
cardiomyopathy, pericardia! tamponade,
cardiac tumours, takotsubo cardiomyopathy

6. CLASSIFICATION AND CAUSES
Septic shock Gram-positive and gram-negative
bacterial infections, other infections
Anaphylactic shock Drugs, insect stings
Neurogenic shock High cervical cord injury, severe head
injury

7. TERMS USED IN RELATION TO CONDITIONS WITH
SYSTEMIC INFLAMMATION
Infection An inflammatory response to micro-organisms
or invasion of normally sterile host tissue by
micro-organisms
Bacteremia Presence of viable bacteria in the blood
Systemic inflammatory
response syndrome (SIRS)
Systemic inflammatory response to a variety of
insults manifested by two or more of the
following:
• Temperature >38°C or <36°C
• Heart rate >90 beats/minute
• Respiratory rate >20/minute or PaC02 <32
mmHg
• TLC count >12,000/mm3 or <4000/mm3 or
>10% immature cells

8. Sepsis SIRS due to infection
Severe sepsis Sepsis associated with organ
dysfunction, hypo-perfusion or
hypotension
(may manifest as lactic acidosis,
oliguria, acute alteration in mental
status)
Septic shock Sepsis-induced hypotension despite
adequate fluid resuscitation along
with perfusion abnormalities (including
lactic acidosis, oliguria and acute
alteration in mental status). Patients
whose blood pressure is supported on
inotropics are also considered to be in
septic shock

9. Multiple organ dysfunction
syndrome (MODS)
Presence of altered organ function in
an acutely ill patient such that
homeostasis cannot be maintained
Acute respiratory distress
syndrome (ARDS)

10. PATHOPHYSIOLOGY
• Sympathoadrenal and Neuroendocrine Responses
• Stimulation of baroreceptors and chemoreceptors by hypotension leads to increased sympathetic activity.
• This is augmented by release of catecholamines from the adrenals.
• These changes produce increased myocardial contractility, tachycardia and vasoconstriction resulting in partial
restoration of blood pressure.
• Reduction in blood flow to kidneys stimulates release of renin that ultimately results in enhanced production of
aldosterone (via angiotensin I and II). This causes sodium and water retention.
• During shock there is increased release of antidiuretic hormone and cortisol that helps in retaining fluid and sodium.
• All these effects try to restore blood pressure but at the expense of reduced perfusion to vital organs such as kidneys.
If shock is not treated in the early stage, these responses can no longer maintain the blood pressure and a stage of
irreversible shock develops.

11. INFLAMMATORY REACTION
• This occurs in patients with all types of shock but is more apparent in sepsis.
• There is activation of leucocytes and release of a variety of potentialy damaging mediators.
• Endotoxin (a lipopolysaccharide) released by gram-negative bacteria is a potent trigger of inflammatory
response.
• There is a release of cytokines (important being tumor necrosis factor-a, interleukin-1 and interleukin- I
0), activation of complement components, release of platelet activating factors, prostaglandins and
leukotrienes. TNF-a and IL-6 have myocardial depressant action. TNF-a also induces coronary
endothelial dysfunction, which may further diminish coronary flow in patients with cardiogenic shock.
• Endothelial cells also play a role in sepsis-induced shock as they produce increased amount of nitric
oxide synthase.
• This enzyme increases the production of nitric oxide, a potent vasodilator that may contribute to
prolonged shock and reduced reactivity to adrenergic agents.

12. NEUROGENIC SHOCK
• Neurogenic shock is caused by the loss of sympathetic control of resistance
vessels resulting in massive dilatation of arterioles and venules. Pooling of
blood in venous system leads to reduced venous return to heart, which
produces fall in stroke volume, cardiac output and blood pressure. Arteriolar
dilatation reduces blood pressure further.

13. CARDINAL FEATURES OF SHOCK
• Hypotension with a systolic blood pressure <90 mmHg
• Tachycardia(> 100/minute) with thready pulse
• Cold, clammy skin
• Peripheral cyanosis often present
• Tachypnoea, Cheyne-Stokes breathing
• Altered mental status
• Urine output <30 mL/hour
• Hyperlactatemia indicating abnormal cellular oxygen metabolism (lactate > 1.5 mmol/L)

14. NOTE
• Some patients with septic shock may initially present with warm
hyperperfused extremities ("warm shock") due to abnormal peripheral
vasodilatation.
• Specific clinical manifestations of the underlying cause of shock are usually
present.
• In neurogenic shock the extremities are often warm due to arteriolar
dilatation.

16. MANAGEMENT OF SHOCK
• Management of shock can be discussed under three headings:
• Patient monitoring
• General measures
• Vasopressors and inotropes (sympathomimetic amines and
vasopressin)
• Note that these measures are applicable to all shock syndromes. Special considerations in specific shock
syndromes willbe discussed later.

17. PATIENT MONITORING
• Clinical monitoring of pulse, blood pressure and respiration.
• Electrocardiographic monitoring for cardiac rate, rhythm and arrhythmias.
• Arterial blood gases and pH for correction of acidosis and hypoxia.
• Central venous pressure monitoring for knowing the absolute and relative
blood volume, and for guiding fluid replacement. This is particularly useful in the
management of hypovolemic shock.
• Pulmonary capillary wedge pressure monitoring with a Swan-Ganz catheter in
the management of cardiogenic shock.
• Urinary catheterization to monitor hourly urinary output.
• Arterial catheterization for monitoring arterial pressure.

18. GENERAL MEASURES
• Care of the skin, airway, bowel and bladder, and nutrition.
• Pain and anxiety should be alleviated by re-assurance .
• Patient should be put in a horizontal position with legs slightly elevated, unless this position is
uncomfortable or causes shortness of breath. In that case, he should be allowed the most
comfortable position (e.g. propped up).
• Correction of hypovolemia.
• Correction is based on the amount and nature of fluid lost, clinical state of the patient and
central venous pressure or pulmonary artery wedge pressure (PAWP).
• Hypovolemia is corrected by blood, Ringer's lactate solution, isotonic saline solution, dextran,
albumin or plasma, depending on the situation.
• Prevention and treatment of renal complications.

19. • In the initial stages of shock there is renal vasoconstriction that if prolonged
can lead to acute tubular necrosis and renal failure. Protection of the kidneys
from vasoconstriction can be achieved by one of the following measures, after a
rapid and adequate correction of hypovolemia:
• Inducing diuresis with furosemide
• Inducing diuresis with mannitol
• Intravenous low-dose (2-4 μg/kg/minute) dopamine has a vasodilator effect
on renal vessels.
• Note: None of these methods have been found to be of much use; however,
most physicians still use them.
• • Once acute tubular necrosis and renal failure have set in the patient, should
be managed as for acute renal failure.

20. • Correction of hypoxia with oxygen by face masks or nasal prongs, and if
necessary, by intubation and mechanical ventilation.
• Correction of acidosis with intravenous sodium bicarbonate (if acidosis is
severe).
• Treatment of cardiac arrhythmias with drugs, electrical cardioversion or
pacing.
• Treatment of sepsis (especially in septic shock) with antibiotics and drainage of
any abscesses.
• Low-dose corticosteroids are recommended in early stages of septic shock.

21. VASOPRESSORS AND INOTROPIC AGENTS
Sympathomimetic Amines
• These agents must be used only after correcting volume deficit.
• Sympathomimetic amines act by increasing the cardiac output (by increasing myocardial contractility and heart rate)
and selective vasoconstriction.
• By these two effects they raise the arterial pressure allowing better perfusion of ischemic regions. This is accomplished
by redistribution of blood flow to vital organs like kidneys, heart and brain, but away from skin and skeletal muscle.
• Main guidelines while using sympathomimetic amines should be elevation of arterial systolic blood pressure to levels
between 110 and 120 mmHg, and maintaining a urinary output of more than 30 mL/hour.
• Dobutarnine is primarily an inotropic agent as it mainly increases the myocardial contractility.
• For a better understanding of the actions of sympathomimetic amines one should be familiar with the adrenergic
receptors
and the pharmacokinetics of the drugs.

22. ADRENERGIC RECEPTORS
Receptors Site Action
α (vascular) Arterioles
Venules
Veins
Vasoconstriction
β-1 (cardiac) Myocardium
Sinoatrial node
AV node
Increase contraction
Increase heart rate
Increase AV conduction
β-2 (vascular) Arterioles
Lungs
Vasodilatation
Bronchial dilatation

23. COMMONLY USED SYMPATHOMIMETIC AMINES
Amine (dose) Receptor
activated
Actions
• Dopamine
• 3 μg/kg/minute
• 3-10 μg/kg/minute
• > 10 μg/kg/minute
Dopaminergic
β-1
Α
Vasodilator action on renal, mesenteric, cerebral and
coronary vessels
Increase myocardial contractility, heart rate and
cardiac output
Vasoconstriction
• Dobutamine
• 1-10 μg/kg/minute
β-1 Marked increase in myocardial contractility with
minimal increase in heart rate and minimal
vasodilatation of peripheral Vessels
• Noradrenaline
• 2-8 μg/minute
β-1
α
β-2
Increased myocardial contractility, heart rate and
cardiac output
Vasoconstriction in skin, muscle and splanchnic beds
Coronary vasodilatation

24. Amine (dose) Receptor
activated
Actions
• lsoproterenol
• 1-4 μg/minute
β-1
β-2
Increased myocardial contractility, heart rate and
cardiac output
Vasodilatation predominantly in skeletal muscles
• Phenylephrine
• 20-200 μg/minute
α Vasoconstriction
• In general, noradrenaline is the first vasopressor of choice. If an additional agent is required, adrenaline or
dopamine
is added. Dobutamine alone is useful to augment cardiac output if arterial pressure is near-normal.
Otherwise, noradrenaline or a combination of dopamine and dobutamine is preferred as initial
sympathomimetic agents in cardiogenic
shock.

25. VASOPRESSIN
• Vasopressin is a hormone synthesized in hypothalamus and then transported
to and stored in pituitary gland.
• It is released in response to decreased blood volume, decreased intravascular
volume and increased plasma osmolality.
• Vasopressin constricts vascular smooth muscle directly via V I receptors, and
also increases responsiveness of the vasculature to catechol-amines.
• Vasopressin may also increase blood pressure by inhibition of vascular smooth
muscle nitric oxide production.
• Addition of a low dose of vasopressin (0.01 to 0.04 U/minute) to
sympathomimetic catechol-amines can raise blood pressure in patients with
pressor-refractory septic shock.

26. SPECIAL CONSIDERATIONS IN SPECIFIC SHOCK
SYNDROMES
Cardiogenic Shock
• Establish large bore peripheral intravenous access.
• Correct any brady-arrhythmia (with atropine/temporary pacing) or tachyarrhythmia (with
cardioversion), which may be contributing to hypotension.
• Insert a peripheral arterial line to monitor blood pressure and a urinary catheter.
• If clinical signs or hemodynamic monitoring indicates that the left ventricle is under filled
(PCWP <15 mmHg), infuse 100-200 ml boluses of intravenous fluid to optimize left ventricular
filling pressures (aiming for PCWP of approximately 15 mmHg).
• If PCWP > 18 mmHg, do not infuse intravenous fluid.

27. • Give diuretics in conjunction with inotropes (to prevent further hypotension).
• Commonly used vasopressors are dobutarnine and dopamine. Less commonly
used are noradrenaline, milrinone and enoximone.
• Antithrombotic therapy with aspirin and heparin should be given in patients
with acute MI. Clopidogrel may be deferred until after emergency angiography,
because on the basis of angiographic findings, coronary artery bypass grafting
may be performed immediately.
• Vasodilator therapy (in selected cases).
• Venodilatation reduces central venous pressure and right ventricular output,
and slows the accumulation of pulmonary edema.

28. • Arteriolar dilatation improves left ventricular function by reducing the
afterload.
• Commonly used agents are nitroglycerine and nitroprusside.
• Circulatory assist devices
• Circulatory assist devices may be beneficial in selected cases of cardiogenic
shock. The various modalities include:
Intra-aortic balloon counter pulsation (use of an IABP improves coronary and
peripheral perfusion via diastolic
balloon inflation and augments left ventricle performance via systolic balloon
deflation with an acute decrease in afterload).
Partial cardiac bypass (left ventricle assist devices)
Extracorporeal membrane oxygenator (ECMO)

29. • Percutaneous coronary interventions (PCI) and thrombolytic therapy in selected cases of acute
myocardial infarction (see "acute ST-elevation myocardial infarction"). Thrombolytic therapy is
less effective but is indicated when PCI is impossible or if a delay has occurred in transport for
PCI, and when MI and cardiogenic shock onset is within 3 hours.
• Surgical therapy
• Role of surgical therapy in cardiogenic shock is mainly aimed at correction of underlying cause.
It is indicated in
selected cases of cardiogenic shock resulting from the following:
Ruptured papillary muscle and acute mitral regurgitation
Rupture of the interventricular septum
Selected cases of acute aortic regurgitation, aortic dissection and acute massive pulmonary
embolism
Myocardial infarction (where re-vascularisation is done by either PCI or coronary artery bypass
surgery)

30. NEUROGENIC SHOCK
• Horizontal positioning of the patient.
• Maintain an adequate fluid balance. Large amount of fluids may be
required.
• Noradrenaline may be required in some cases.