Pathophysiology and Pharmacologic Treatment of Shock

CV Pharmacology-

Pathophysiology and Treatment of Shock Reading: Autonomic Nervous System Notes 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

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See: Shock (circulatory. pdf)

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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

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The problem in shock 

Altered circulatory parameters



Compromised microcirculation

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Persistent severe hypoxia



Multiple organ failure

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

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Main types of Shock 



Vasoconstrictive 

Trauma, bleeding, burning, ileus (volumen loss)



Pulmonary embolism (impaired cardiac filling)

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Myocardial infarction (impaired cardiac contraction)

Vasodilatative 

Anaphylaxis, sepsis (maldistribution of blood flow)

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Spinal medullary injury (venous pooling)

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Hypothermia 5

Classification ď Ž

ď Ž 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 6

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

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Distributive 



Septic, etc.

Obstructive 

PE, pericarditis, pnumothorax etc.

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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 11

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

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

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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 12

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 13

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 

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Hemorrhagic

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Interstitial fluid redistribution

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- Trauma

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Thermal injury

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- Gastrointestinal



Trauma



- Retroperitoneal

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Anaphylaxis

• Fluid depletion (nonhemorrhagic) 







• Increased vascular capacitance (venodilatation)

External fluid loss 

- Sepsis



- Anaphylaxis

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- Toxins/Drugs

Dehydration Vomiting



Diarrhea



Polyuria

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Cardiogenic Shock ď Ž

ď Ž

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 

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

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



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-Cardiomyopathy -Post ischemic myocardial stunning -Septic myocardial depression -Pharmacologic Anthracycline cardiotoxicity Calcium channel blockers 18

CARDIOGENIC (2) 

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Mechanical  -Valvular failure Regurgitant Obstructive  -Hypertropic cardiomyopathy  -Ventricular septal defect Arrhythmic  -Bradycardia Sinus (e.g.,vagal syncope)Atrioventricular blocks  -Tachycardia SupraventricularVentricular 19

DISTRIBUTIVE 

Septic (bacterial, fungal, viral, rickettsial)



Toxic shock syndrome

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Anaphylactic, anaphylactoid

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Neurogenic (spinal shock)

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Endocrinologic

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Adrenal crisis

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Toxic (e.g., nitroprusside, bretyllium) 20

Extracardiac obstructive shock Impaired diastolic filling (decreased ventricular preload) 

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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 

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Narrowing of pulse pressure

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Tachycardia, hypotension

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Anxiety

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Cool, clammy skin

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Obtundation

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Dyspnea

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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

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Maximizing cardiac function

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Redistributing perfusion to vital organs

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Optimizing unloading of oxygen at tissues 24

Maintain Volume 

-Fluid redistribution to vascular space 

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

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-Decreased renal fluid losses 

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Decreased glomerular filtration rate (GFR) Increased aldosterone Increased vasopressin 25

Mintain Pressure 

Decreased venous capacitance 

Increased sympathetic activity

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Increased circulating (adrenal) epinephrine

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Increased angiotensin

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Increased vasopressin 26

Maximize Cardiac Performance 

Increased contractility  

Sympathetic stimulation Adrenal stimulation

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Early mechanical ventilation ď Ž

allows blood flow to be redistributed

ď Ž

tends to reverse lactic acidosis

ď Ž

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 

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IV line

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Colloids

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Large bore cannula

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Dextrane

More iv line

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

Hydroethylstrach

Choice of infusion

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Gelatine

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

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

Small volume resuscitation

Rate, amount 

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

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Dextrane 

Molecular weight: 40K - 60/70K Dalton

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

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

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

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Elimination: 

metabolic

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kidney 30

Hydroxyethylstrach 

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

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

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

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

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

Elimination: 

kidney

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12 - 24 h (65 - 70 %) --- 168 h 31

Inotropic drugs Inotropie

Heart rate

SVR

Epinephrin

++

+

+

-

Norepinephrin

++

0

++

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

0

--

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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