CV Pharmacology-Pathophysiology and Treatment of Shock : CV Pharmacology-Pathophysiology and Treatment of Shock Prepared and Presented by:
Marc Imhotep Cray, M.D.
Professor Pharmacology Recommended Reading:
Practice Question Set #1
Shock, Septic Shock (circulatory)See: Shock (circulatory) : 10/17/2009 2 Shock (circulatory)See: Shock (circulatory) Effects of inadequate perfusion on cell function.
From:http://en.wikipedia.org/wiki/Shock_%28circulatory%29 Shock, Circulatory Defined : 10/17/2009 3 Shock, Circulatory Defined Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition where insufficient blood flow reaches the body tissues.
As blood carries oxygen and nutrients around the body, reduced flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly.
The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.
See: 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 : 10/17/2009 4 The problem in shock Altered circulatory parameters
Persistent severe hypoxia
Multiple organ failure From: http://www.cvpharmacology.com/clinical topics/hypotension.htm Main types of Shock : 10/17/2009 5 Main types of Shock Vasoconstrictive
Trauma, bleeding, burning, ileus (volumen loss)
Pulmonary embolism (impaired cardiac filling)
Myocardial infarction (impaired cardiac contraction)
Anaphylaxis, sepsis (maldistribution of blood flow)
Spinal medullary injury (venous pooling)
Hypothermia Classification : 10/17/2009 6 Classification In 1972 Hinshaw and Cox suggested the following classification which is still used today
It uses four types of shock:
obstructive shock Classification (based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox) : 10/17/2009 7 Classification (based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox) Hypovolaemic
Hemorrhagic, Fluid depletion, Increased vascular capacitance
Myopathic, Mechanical, Arrhythmic Distributive
PE, pericarditis, pnumothorax etc. Hypovolemic shock : 10/17/2009 8 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. Cardiogenic shock : 10/17/2009 9 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. Distributive shock : 10/17/2009 10 Distributive shock Distributive shock –
As in hypovolaemic shock there is an insufficient intravascular volume of blood.
This form of "relative" hypovolaemia is the result of dilation of blood vessels which diminishes systemic vascular resistance. Examples of this form of shock are:
Neurogenic shock Obstructive shock : 10/17/2009 11 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.
Aortic stenosis Endocrine shockbased on endocrine disturbances. : 10/17/2009 12 Endocrine shockbased on endocrine disturbances. Recently a fifth form of shock has been introduced:
* 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 Comparison of types of shock(Early stage) : 10/17/2009 13 Comparison of types of shock(Early stage) Malperfusion and organ dysfunction are the ultimate end point of any shock stage Slide 14: 10/17/2009 14 Decreased cardiac output Decreased blood pressure Decreased tissue perfusion Decreased coronary perfusion Decreased myocardial function Microcirculatory
obstruction Cellular aggregation Microcirculatory demage Cell hypoxia Metabolic
venous return BP = CO x SVR Pathophysiology Concept Map Hypovolemic Shock : 10/17/2009 15 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. HYPOVOLEMIC (oligemic) SHOCK : 10/17/2009 16 HYPOVOLEMIC (oligemic) SHOCK Hemorrhagic
• Fluid depletion (nonhemorrhagic)
External fluid loss
Polyuria Interstitial fluid redistribution
• Increased vascular capacitance (venodilatation)
- Toxins/Drugs Cardiogenic Shock : 10/17/2009 17 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 CARDIOGENIC : 10/17/2009 18 CARDIOGENIC Myopathic
-Myocardial infarction (Left ventricle, Right ventricle)
-Myocardial contusion (trauma)
-Post ischemic myocardial stunning
-Septic myocardial depression
-Pharmacologic Anthracycline cardiotoxicity Calcium channel blockers CARDIOGENIC (2) : 10/17/2009 19 Mechanical
-Valvular failure Regurgitant Obstructive
-Ventricular septal defect
-Bradycardia Sinus (e.g.,vagal syncope)Atrioventricular blocks
-Tachycardia SupraventricularVentricular CARDIOGENIC (2) DISTRIBUTIVE : 10/17/2009 20 DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Neurogenic (spinal shock)
Toxic (e.g., nitroprusside, bretyllium) Extracardiac obstructive shock Impaired diastolic filling (decreased ventricular preload) : 10/17/2009 21 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. Symptoms : 10/17/2009 22 Symptoms Narrowing of pulse pressure
Disphoria Decreased urine output
Cool, clammy skin
Unconsciousness Treatment of shock : 10/17/2009 23 Treatment of shock Generalities:
Positioning, avoiding hypothermia
Maintaining adequate oxygenization
Pain relief ?
(inotropic treatment?) Enhance compensatory phase of the shock : 10/17/2009 24 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 Maintain Volume : 10/17/2009 25 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 Mintain Pressure : 10/17/2009 26 Mintain Pressure Decreased venous capacitance
Increased sympathetic activity
Increased circulating (adrenal) epinephrine
Increased vasopressin Maximize Cardiac Performance : 10/17/2009 27 Maximize Cardiac Performance Increased contractility
Adrenal stimulation Early mechanical ventilation : 10/17/2009 28 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. Fluid resuscitation : 10/17/2009 29 Fluid resuscitation IV line
Large bore cannula
More iv line
Choice of infusion
Lactated Ringer's solution (initial bolus: 10-25 ml/kg / 10 min.) Colloids
Small volume resuscitation
parameters ( BP, Pulse, CVP, SatO2 etc) Dextrane : 10/17/2009 30 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%
kidney Hydroxyethylstrach : 10/17/2009 31 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%)
12 - 24 h (65 - 70 %) --- 168 h Inotropic drugs : 10/17/2009 32 Inotropic drugs Reference Resource : 10/17/2009 33 Reference Resource 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, 2006.