CV Pharmacology-

Pathophysiology and Treatment of Shock

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Autonomic Nervous System
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Clinical: e-Medicine articles
Shock, Cardiogenic
Shock, Hypovolemic
Shock, Septic

Prepared and presented by:

Marc Imhotep Cray, M.D.
BMS / CK-CS Teacher
http://www.imhotepvirtualmedsch.com/

Shock (circulatory)
Effects of inadequate perfusion on cell function

Click to expand

See: Shock (circulatory. pdf)

Shock, Circulatory Defined

Circulatory shock, commonly known as just shock, is a

serious, life-threatening medical condition where
insufficient blood flow reaches body tissues
As blood carries oxygen and nutrients around body,
reduced flow hinders delivery of these components to
tissues, and can stop tissues from functioning properly
The process of blood entering tissues is called perfusion,
so when perfusion is not occurring properly this is called a
hypoperfusional (hypo = below) state
Shock: An Overview PDF by Michael L. Cheatham, MD, Ernest F.J. Block, MD,
Howard G. Smith, MD, John T. Promes, MD, Surgical Critical Care Service,
Department of Surgical Education, Orlando Regional Medical Center Orlando,
Florida

The problem in shock

Altered circulatory parameters

Compromised microcirculation

Persistent severe hypoxia

Multiple organ failure

From: http://www.cvpharmacology.com/clinical
topics/hypotension.htm

Main types of Shock

Vasoconstrictive

Trauma, bleeding, burning, ileus (volumen loss)

Pulmonary embolism (impaired cardiac filling)

Myocardial infarction (impaired cardiac contraction)

Vasodilatative

Anaphylaxis, sepsis (maldistribution of blood flow)

Spinal medullary injury (venous pooling)

Hypothermia
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Classification

1.
2.
3.
4.

In 1972 Hinshaw and Cox suggested

the following classification which is
still used today
It uses four types of shock:
hypovolemic,
cardiogenic,
distributive and
obstructive shock
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Classification

(based on cardiovascular characteristics, which was

initially proposed in 1972 by Hinshaw and Cox)

Hypovolaemic

Hemorrhagic, Fluid
depletion, Increased
vascular capacitance

Cardiogenic

Myopathic,
Mechanical,
Arrhythmic

Distributive

Septic, etc.

Obstructive

PE, pericarditis,
pnumothorax etc.

Hypovolemic shock
Hypovolemic shock
This is the most common type of shock and
based on insufficient circulating volume.
Its primary cause is loss of fluid from the
circulation from either an internal or external
source.
An internal source may be haemorrhage.
External causes may include extensive
bleeding, high output fistulae or severe
burns.
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Cardiogenic shock
Cardiogenic shock
This type of shock is caused by the failure of
the heart to pump effectively.
This can be due to damage to the heart
muscle, most often from a large myocardial
infarction.
Other causes of cardiogenic shock include
arrhythmias, cardiomyopathy, congestive
heart failure (CHF), and cardiac valve
problems.
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Distributive shock

Distributive shock

As in hypovolemic shock there is an insufficient

intravascular volume of blood

This form of "relative" hypovolemia is the

result of dilation of blood vessels which
diminishes systemic vascular resistance
Examples of this form of shock are:
1.
Septic shock
2.
Anaphylactic shock
3.
Neurogenic shock

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Obstructive shock
Obstructive shock

In this situation the flow of blood is obstructed

which impedes circulation and can result in
circulatory arrest.

Several conditions result in this form of shock,

including:
1.
Cardiac tamponade
2.
Tension pneumothorax
3.
pulmonary embolism
4.
Aortic stenosis
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Endocrine shock

Recently a fifth form of shock has been introduced:

based on endocrine disturbances.
Causes:

Hypothyroidism, in critically ill patients, reduces cardiac output

and can lead to hypotension and respiratory insufficiency

Thyrotoxicosis may induce a reversible cardiomyopathy

Acute adrenal insufficiency is frequently the result of

discontinuing corticosteroid treatment without tapering the
dosage
However, surgery and intercurrent disease in patients on
corticosteroid therapy without adjusting the dosage to
accommodate for increased requirements may also result in this
condition
Relative adrenal insufficiency in critically ill patients where
present hormone levels are insufficient to meet the higher
demands
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Comparison of types of shock

(Early stage)

Vasoconstrictive
Hypovolamic

Cardiogenic

Vasodilatative
Circulatory

Septic

Cardiac
index

Cardiac
index

Peripheral
resistance

Peripheral
resistance

Blood
Volume

Blood
Volume

Malperfusion and organ dysfunction are the ultimate end point of any shock stage
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Pathophysiology Concept Map

Decreased
venous return

Decreased cardiac output

Decreased myocardial function

Decreased
myocardial
contraction

Decreased coronary perfusion

Decreased blood pressure

Inracellular
fluid
loss

BP = CO x SVR
Metabolic
acidosis
Cell hypoxia

Decreased tissue perfusion

Microcirculatory
obstruction

Microcirculatory demage
Cellular aggregation

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Hypovolemic Shock
loss in circulatory volume

Decreased venous return

Decreased filling of the cardiac chambers

Decreased cardiac output

increase in the systemic vascular resistance (SVR).

low central venous pressure (CVP), a low pulmonary capillary wedge pressure (PCWP), low
cardiac output (CO) and cardiac index (CI), and high SVR. The arterial blood pressure may be
normal or low.
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HYPOVOLEMIC (oligemic)
SHOCK

Hemorrhagic

Interstitial fluid redistribution

- Trauma

Thermal injury

- Gastrointestinal

Trauma

- Retroperitoneal

Anaphylaxis

Fluid depletion (nonhemorrhagic)

Increased vascular
capacitance (venodilatation)

External fluid loss

- Sepsis

- Anaphylaxis

- Toxins/Drugs

Dehydration
Vomiting

Diarrhea

Polyuria

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Cardiogenic Shock

dependent on poor pump function

acute catastrophic failure of left

ventricular pump function

high PCWP, low CO and CI, and generally a high SVR

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CARDIOGENIC

Myopathic

-Myocardial infarction (Left

ventricle, Right ventricle)
-Myocardial contusion
(trauma)
-Myocarditis

-Cardiomyopathy
-Post ischemic
myocardial stunning
-Septic myocardial
depression
-Pharmacologic
Anthracycline
cardiotoxicity Calcium
channel blockers
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CARDIOGENIC (2)

Mechanical
-Valvular failure Regurgitant Obstructive
-Hypertropic cardiomyopathy
-Ventricular septal defect
Arrhythmic
-Bradycardia Sinus (e.g.,vagal
syncope)Atrioventricular blocks
-Tachycardia SupraventricularVentricular
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DISTRIBUTIVE

Septic (bacterial, fungal, viral, rickettsial)

Toxic shock syndrome

Anaphylactic, anaphylactoid

Neurogenic (spinal shock)

Endocrinologic

Adrenal crisis

Toxic (e.g., nitroprusside, bretyllium)

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Extracardiac obstructive shock

Impaired diastolic filling (decreased
ventricular preload)

a physical impairment to adequate forward circulatory flow involving

mechanisms (different than primary myocardial or valvular dysfunction)
Frank decrease in filling pressures (as in mediastinal compressions of
great veins) or
trends towards equalization of pressures in the case of cardiac
tamponade or
markedly increased right ventricular filling pressures
High CVP, low PCWP Cardiac output is usually decreased with increased SVR.

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Symptoms

Narrowing of
pulse pressure

Tachycardia,
hypotension

Anxiety

Cool, clammy skin

Obtundation

Dyspnea

Unconsciousness

Restlessnes
Disphoria

Decreased urine
output

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Treatment of
shock
Generalities:
Positioning, avoiding
hypothermia
Maintaining adequate
oxygenization
Fluid resuscitation
Pain relief ?
(inotropic treatment?)
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Enhance compensatory phase

of the shock

Maintenance of mean circulatory pressure

Maximizing cardiac function

Redistributing perfusion to vital organs

Optimizing unloading of oxygen at tissues

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Maintain Volume

-Fluid redistribution to
vascular space

From interstitium
(Starling effect)
From intracellular
space (Osmotic
effect)

-Decreased renal fluid

losses

Decreased
glomerular filtration
rate (GFR) Increased
aldosterone
Increased
vasopressin
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Mintain Pressure

Decreased venous capacitance

Increased sympathetic activity

Increased circulating (adrenal) epinephrine

Increased angiotensin

Increased vasopressin
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Maximize Cardiac Performance

Increased contractility

Sympathetic stimulation
Adrenal stimulation

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Early mechanical ventilation

allows blood flow to be redistributed

tends to reverse lactic acidosis

supports the patient until other

therapeutic measures can be effective

Tidal volumes in the order of 7-10 mlkg-1 of lean body mass, an O2

concentration that results in arterial saturation not less than 92%, adequate
ventilator rate and sedation to minimize the work of breathing.
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Fluid resuscitation

IV line

Colloids

Large bore cannula

Dextrane

More iv line

Hydroethylstrach

Choice of infusion

Gelatine

Lactated Ringer's
solution (initial
bolus: 10-25 ml/kg
/ 10 min.)

Small volume resuscitation

Rate, amount

General conditions
parameters ( BP, Pulse,
CVP, SatO2 etc)

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Dextrane

Molecular weight: 40K - 60/70K Dalton

Concentration: 10% (40K)*; 6% (60/70K)**

Water binding: 25 ml/g -- 4 - 6 h

Plasma expanding effect: * 180-200; ** 150%

Elimination:

metabolic

kidney
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Hydroxyethylstrach

Molecular weight: 450K - 200K - 40K Dalton

Substitution: 0,5 - 0,62 - 0,7

Water binding: 15 - 20 ml/g -- 3 - 6 h

6% HES (200K/0,5) -- plasma substitution (100%)

10%HES (200K/0,5) -- plasma expanding (140%)

Elimination:

kidney

12 - 24 h (65 - 70 %) --- 168 h

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Inotropic drugs
Inotropie

Heart rate

SVR

Epinephrin

++

Norepinephrin

++

++

Dopamin

++

Dobutamin

+++

Isoproterenol

++

Amrinon

+++

Cardiac
Output

Dose

10-30
mcg/min

--

2-8
mcg/min

++

++

2-5
mcg/min/kg

(+)

--

++

5-15
mcg/min/kg

++

++

5 mcg/mi

++

Bolus 0.5 1.5 mg/kg

Cont.: 2 to
10
mcg/kg/min

--

Kidney
Cornarry
Blood flow Blood flow

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Further Study:
Joynt, Gavin (April 2003). "Introduction to
management of shock for junior ICU trainees and
medical students". The Chinese University of
Hong Kong. Retrieved on 9 October, 2014.

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