IVMS-CV -Pathophysiology Pharmacology a

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: Autonomic pharmacology Formatives: Practice Question Set #1 Clinical: E-Medicine Articles Shock, Cardiogenic Shock, Hypovolemic 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 Compromised microcirculation 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) Vasodilatative 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: hypovolemic, cardiogenic, distributive and 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 Cardiogenic Myopathic, Mechanical, Arrhythmic Distributive Septic, etc. Obstructive 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: Septic shock Anaphylactic shock 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. Cardiac tamponade Tension pneumothorax pulmonary embolism 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 acidosis Decreased myocardial contraction Inracellular fluid loss Decreased 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 - Trauma - Gastrointestinal - Retroperitoneal • Fluid depletion (nonhemorrhagic) External fluid loss Dehydration Vomiting Diarrhea Polyuria Interstitial fluid redistribution Thermal injury Trauma Anaphylaxis • Increased vascular capacitance (venodilatation) - Sepsis - Anaphylaxis - 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) -Myocarditis -Cardiomyopathy -Post ischemic myocardial stunning -Septic myocardial depression -Pharmacologic Anthracycline cardiotoxicity Calcium channel blockers

CARDIOGENIC (2) : 

10/17/2009 19 Mechanical -Valvular failure Regurgitant Obstructive -Hypertropic cardiomyopathy -Ventricular septal defect Arrhythmic -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 Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic Adrenal crisis 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 Tachycardia, hypotension Restlessnes Disphoria Decreased urine output Anxiety Cool, clammy skin Obtundation Dyspnea Unconsciousness

Treatment of shock : 

10/17/2009 23 Treatment of shock Generalities: Positioning, avoiding hypothermia Maintaining adequate oxygenization Fluid resuscitation 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 angiotensin Increased vasopressin

Maximize Cardiac Performance : 

10/17/2009 27 Maximize Cardiac Performance Increased contractility Sympathetic stimulation 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 Dextrane Hydroethylstrach Gelatine Small volume resuscitation Rate, amount General conditions 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% Elimination: metabolic 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%) Elimination: kidney 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.