Shock
Definition of shock
 Severe tissue hypoperfusion resulting in low supply of oxygen to the organs
 Systemic hypotension (of various causes) is present
 P = Q  R
 Q ~ CO = SV  f
 CO depends on
a) cardiac function
b) venous return (→preload)
• R – systemic resistance (mostly arterioles) - afterload
Cardiac and venous function
Phases of shock
•Compensation of initiating cause
•Decompensation
•Refractory shock
Compensatory mechanisms and their limits
 Activation of sympathetic nervous system
(tens of seconds)
 Activation of RAAS (cca 1 hour)
 Vasoconstriction (if possible)
 Vasodilatation in some tissues
(esp. myocardium)
 Positively inotropic effect of SNS (if possible)
– but at cost of higher metabolic
requirements of the heart
Compensatory mechanisms and their limits
 Increased heart rate
– but CO decreases in high HR (>150 bpm)
 Keeping circulating volume by lower diuresis
– but at cost of acute renal failure
 Shift to anaerobic metabolism
– but at cost of ↓ ATP a ↑ lactate (acidosis)
 Shift of saturation curve of hemoglobin to right
(↑2,3-DPG)
 Hyperglycemia
– but decreased utilization of Glc in the periphery
Decompensated shock
•↓ BP
•↓ diuresis
•Brain hypoperfusion – involvment of mental functions
•Acrocyanosis (in peripheral hypoperfusion)
•Tachypnoe
•Treatment – colloid solutions, catecholamines
Shock at the cellular level
•Mitochondrial dysfunction (result of hypoxia)
– lower production of ATP
•↑ ROS production by dysfunctional mitochondria
•Failure of ion pumps
(e.g. Na/K ATP-ase →↑intracelular Ca2+)
•Lysosomal abnormalities
– release of lysosomal proteases
•↓ intracelular pH
Refractory shock – Vicious circles
1) Vasodilatation ↔ hypoperfusion
• Endothelial cells contain two isoforms of nitric oxid synthase – constitutive (eNOS) and inducible (iNOS)
• In lasting hypoxia of endothelial cells there is increased iNOS activity (primarily physiological mechanism)
• ↑NO increases vasodilation and hypoperfusion
2) Myocardial hypoxia ↔ lower contractility
• Lower myocardial perfusion leads into ↓CO, which further reduces coronary flow
• Myocardium does not benefit from the shift of Hb saturation curve
– efficiency of O2 extraction is already at its maximum
3) Brain hypoperfusion ↔ ↓SNS activity
• Lower perfusion of vasomotor centre leads first into SNS hyperactivity, which is then followed by its supression
• That leads into ↓brain perfusion
Other vicious circles in refractory shock
Forms of shock
a) Hypovolemic shock (i.e. absolute fluid loss)
– low preload
b) Distributive („warm“) shock
– low resistance, afterload, CO might be increased
c) Cardiogennic shock
– normovolemia, normodistribution, low CO in bad cardiac function
d) Obstructive shock
– low preload of one ventricle in normovolemia and subsequent lowering of CO
– pathophysiology similar to cardiogennic shock
Cardiac and venous function in shock
Hypovolemic shock
̶ compensation by the vasoconstriction
and cardiac mechanisms
Distributive shock
̶ compensation by cardiac mechanisms
(vasoconstriction is usually impossible)
Cardiogennic (and obstructive) shock
̶ compensation by vasoconstriction
Q [dm3.min-1]
P [mmHg] in right atrium
Hypovolemic shock - causes
• Acute bleeding
• Burns, trauma
• Rapid development of ascites
• Acute pancreatitis
• Severe dehydratation
o Vomiting, diarrhoea
o Excessive diuresis (e.g. in diabetes insipidus)
Distributive shock - causes
 Anafylactic shock
 Anafylactoid shock
◦ Mediators of mast cells, but without IgE
◦ E.g. snake venoms, radiocontrasts
 Septic shock
◦ Role of bacterial lipopolysaccharides
◦ Bacterial toxins
◦ IL-1, TNF-α – stimulate synthesis of PGE2 and NO
 Neurogennic shock
◦ Vasodilatation as a result of vasomotoric centre (or its efferent pahways) impairment
Cardiogennic shock - causes
 Myocardial infarction
 Arrhythmias
 Valvular disease (e.g. rupture of papillary muscles)
 Decompensation of heart failure in dilated/restrictive cardiomyopathy, amyloidosis
 Overload by catecholamines (“tako-tsubo cardiomyopathy“ – apical akinesia + basal hyperkinesia)
 Rupture of ventricular septum
 Obstructive shock
– e.g. cardiac tamponade, massive pulmonary
embolism, aortic dissection
Organ complications in shock
 Lungs
◦ ARDS
 Liver
◦ necrosis of hepatocytes
 GIT
◦ stress ulcer
◦ Damage of intestinal mucosa by ischemic necrosis → sepsis
 Kidneys
◦ Acute renal failure in vasoconstriction of a. afferens
◦ Acute tubular necrosis during ischemia
Disseminated intravascular coagulopathy (DIC)
 Systemic exposure to tissue factor
 Consequence of the vessel wall damage
 Moreover, slower blood flow contributes
to the extent of coagulation reactions
 Two phases:
1) Formation of microtrombi (with local ischemia)
2) Bleeding as a result of consummation of
coagulation factors
 DIC is especially frequent in septic shock
ttps://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/disseminated-intravascular-coagulation
https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/disseminated-intravascular-coagulation
Systemic Inflammatory Response Syndrome(SIRS)
• Systemic activation of immune mechanisms
• Causes:
̶ infections (sepsis)
̶ Shock caused by non-infectious causes (diffuse tissue damage in hypoxia)
̶ Non-compatible blood transfusions
̶ Radiation syndrome (esp. GIT form)
Acute Respiratory Distress Syndrome (ARDS – „shock lung“)
 Result of lung inflammation in SIRS, pulmonary
infections, aspiration of gastric juice, drowning
 Exsudative phase (hours): cytokine release,
leukocyte infiltration, pulmonary edema,
destruction of type I pneumocytes
 Proliferative phase: fibrosis, ↑ dead space,
proliferation of type II pneumocytes
 Reparative phase: ↓ inflammation, ↓ edema,
continuing fibrosis, in most cases permanent
restrictive diseases
Multiorgan dysfunction syndrome (MODS)
• Failure of more organs at once
(lungs, liver, GIT, kidneys, brain, heart)
• It can develop after initial insult
(days or weeks)
• Hypermetabolism, catabolic stress
• Can both preceed or result from SIRS
General principles of treatment
 Treatment of underlying cause
 Positively inotropic drugs, vasopressors
(e.g. catecholamines – but: they can worsen the situation in obstructive shock)
 Colloid solutions, crystaloid solutions (but: there is a risk of edema in cardiogennic shock)
 O2
 i.v. corticoids (anafylaxis, SIRS?)
 ATB (septic shock)
 Mechanic circulation support (cardiogennic shock)
 Anti-shock position
https://upload.wikimedia.org/wikipedia/commons/a/ad/Sepsis_Steps.png