Pathology and Pathophysiology of Shock

Pathology and Pathophysiology of Shock

Marc Imhotep Cray M.D.

Learning Objectives By the end of this lecture the learner should be able to: 1. Discuss the general concepts associated with shock states, including physiologic response to shock, and shock progression.

2. Describe cardiogenic shock, including pathophysiology, clinical manifestations, diagnosis, and management.

3. Discuss hypovolemic shock, including pathophysiology, clinical manifestations, diagnosis, and management.

4. Explain the septic type of distributive shock, including pathophysiology, clinical manifestations, diagnosis, and management.

Marc Imhotep Cray, M.D.

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Learning Objectives By the end of this lecture the learner should be able to: 5. Discuss the neurologic and anaphylactic types of distributive shock, including the pathophysiology, clinical manifestations, diagnosis, and management of each type.

6. Describe the major causes of obstructive shock, including the pathophysiology, clinical manifestations, diagnosis, and management of each cause 7. Discuss use of pharmacotherapy in the management of shock states.

Marc Imhotep Cray, M.D.

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Shock Capsule  Shock is a clinical condition characterized by a fast pulse rate (usually > 100 beats/min) and a low blood pressure (systolic blood pressure usually < 100 mmHg)  Common types of shock are  hypovolemic (low blood volume, e.g. in hemorrhage),  cardiogenic (heart pump failure, e.g. in myocardial infarction)  septic (severe infection)  Less common types are  anaphylactic (type I hypersensitivity reaction, e.g. penicillin allergy)  neurogenic (loss of sympathetic vasomotor tone, e.g. in a spinal cord injury) Marc Imhotep Cray, M.D.

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Shock, Pathology of Different Types, Animation_Alila Medical Media

Online Version Marc Imhotep Cray, M.D.

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Stages of Shock As stated above Shock is a progressive disorder that leads to death if underlying causes are not corrected  Exact mechanisms of sepsis-related death are still unclear; aside from increased lymphocyte and enterocyte apoptosis, cellular necrosis is minimal • Death typically follows the failure of multiple organs usually offer no morphological clues to explain their dysfunction

 For hypovolemic and cardiogenic shock pathways leading to a patient’s demise are reasonably well understood tissue ischemia, acute tubular necrosis, lactic acidosis severe cellular and tissue injury cardiopulmonary arrest  Unless insult is massive and rapidly lethal (e.g., exsanguination from a ruptured aortic aneurysm), shock tends to evolve through three general (albeit somewhat artificial) stages…

Marc Imhotep Cray, M.D.

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The 3 Stages of Shock These stages have been documented most clearly in hypovolemic shock but are common to other forms as well: ď&#x201A;§ Stage 1 An initial nonprogressive stage during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained ď&#x201A;§ Stage 2 A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis ď&#x201A;§ Stage 3 An irreversible stage in which cellular and tissue injury is so severe that even if hemodynamic defects are corrected, survival is not possible Marc Imhotep Cray, M.D.

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Shock, Circulatory Defined Circulatory shock, commonly known as just shock, is a serious, lifethreatening 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

Marc Imhotep Cray, M.D.

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Shock (circulatory) Effects of inadequate perfusion on cell function

Learn more from Dr. Najeebâ&#x20AC;&#x2122;s Video Series on Circulatory shock Marc Imhotep Cray, M.D.

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The problem in shock • Altered circulatory parameters • Compromised microcirculation • Persistent severe hypoxia • Multiple organ failure

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

Marc Imhotep Cray, M.D.

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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

Marc Imhotep Cray, M.D.

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Classification of Shock â&#x20AC;˘ In 1972 Hinshaw and Cox suggested following classification which is still used today

â&#x20AC;˘ It uses four types of shock: 1.

2.

3.

4.

hypovolemic cardiogenic distributive and obstructive shock

Marc Imhotep Cray, M.D.

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Classification (Based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox.)

Hypovolemic

Distributive

Hemorrhagic

Septic, etc.

Fluid depletion

Obstructive

Increased vascular capacitance

PE, pericarditis, pnumothorax etc.

Cardiogenic Myopathic

Mechanical Arrhythmic

Marc Imhotep Cray, M.D.

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Hypovolemic shock Hypovolemic shock This is most common type of shock and based on insufficient circulating volume = circulating shock • Its primary cause is loss of fluid from circulation from either an internal or external source • An internal source may be hemorrhage • External causes may include extensive bleeding, high output fistulae (greater than 500 ml per day)or severe burns

Marc Imhotep Cray, M.D.

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Hypovolemic Shock Loss in circulatory volume • • • •

Decreased venous return Decreased filling of cardiac chambers Decreased cardiac output increase in systemic vascular resistance (SVR)

Low central venous pressure (CVP), Low pulmonary capillary wedge pressure (PCWP), Low cardiac output (CO) and cardiac index (CI), and high SVR arterial blood pressure may be normal or low

Marc Imhotep Cray, M.D.

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Hypovolemic Shock (2) Causes Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal

Interstitial fluid redistribution • Thermal injury • Trauma • Anaphylaxis

Fluid depletion (nonhemorrhagic) • External fluid loss • Dehydration • Vomiting • Diarrhea • Polyuria

Increased vascular capacitance (venodilation) • Sepsis • Anaphylaxis • Toxins/Drugs

Marc Imhotep Cray, M.D.

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Cardiogenic shock Cardiogenic shock This type of shock is caused by failure of heart to pump effectively â&#x20AC;˘ This can be due to damage to heart muscle, most often from a large myocardial infarction â&#x20AC;˘ Other causes of cardiogenic shock include o arrhythmias, o cardiomyopathy, o congestive heart failure (CHF), and o cardiac valve problems

Marc Imhotep Cray, M.D.

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Cardiogenic Shock (2) • dependent on poor pump function • acute catastrophic failure of LV pump function High PCWP, low CO and CI, and generally a high SVR

Marc Imhotep Cray, M.D.

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Cardiogenic (3) Myopathic • Myocardial infarction (left ventricle, right ventricle) • Elevations in CK-MB and Troponin I enzymes

• • • • • •

Myocardial contusion (trauma) Myocarditis Cardiomyopathy Post ischemic myocardial stunning Septic myocardial depression Pharmacologic o Anthracycline cardiotoxicity o Calcium channel blockers

Marc Imhotep Cray, M.D.

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Cardiogenic (4) • Mechanical • -Valvular failure Regurgitant Obstructive • -Hypertropic cardiomyopathy • -Ventricular septal defect

• Arrhythmic • -Bradycardia Sinus (e.g.,vagal syncope), Atrioventricular blocks • -Tachycardia SupraventricularVentricular

Marc Imhotep Cray, M.D.

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Distributive shock  Distributive shock results from excessive vasodilation and impaired distribution of blood flow • Septic shock is the most common form of distributive shock and is characterized by considerable mortality (treated, around 30%; untreated, probably >80%) • In United States, this is leading cause of noncardiac death in intensive care units (ICUs)

Marc Imhotep Cray, M.D.

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Distributive shock (2) ď&#x201A;§ Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions such as burns and pancreatitis; toxic shock syndrome (TSS); anaphylaxis; reactions to drugs or toxins, including insect bites, transfusion reaction, and heavy metal poisoning; addisonian crisis; hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury

Marc Imhotep Cray, M.D.

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Distributive (3) • • • • • • •

Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic Adrenal crisis Toxic (e.g., nitroprusside, bretyllium)

Marc Imhotep Cray, M.D.

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Major pathogenic pathways in septic shock Microbial products activate endothelial cells and cellular and humoral elements of the innate immune system, initiating a cascade of events that lead to end-stage multiorgan failure.

DIC, Disseminated intravascular coagulation; HMGBI, high-mobility group box I protein; NO, nitric oxide; PAF, platelet-activating factor; PAI-I, plasminogen activator inhibitor- I ; PAMP, pathogen- associated molecular pattern; STNFR, soluble tumor necrosis factor receptor; TF, tissue factor; TFPI, tissue factor pathway inhibitor.

Robbins Basic Pathology 10e, Elsevier, 2018. Fig. 4.19, Pg. 117.

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Distributive shock (4) Capsule Distributive shock • As in hypovolemic shock, there is an insufficient intravascular volume of blood • This form of "relative" hypovolemia is 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 Marc Imhotep Cray, M.D.

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Obstructive shock Obstructive shock â&#x20AC;˘ In this situation flow of blood is obstructed which impedes circulation and can result in circulatory arrest â&#x20AC;˘

Several conditions result in this form of shock, including: 1. Cardiac tamponade 2. Tension pneumothorax 3. pulmonary embolism 4. Aortic stenosis

Marc Imhotep Cray, M.D.

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Extracardiac obstructive shock Impaired diastolic filling (decreased preload) â&#x20AC;˘ A physical impairment to adequate forward circulatory flow involving mechanisms different than primary myocardial or valvular dysfunction â&#x20AC;˘ Frank decrease in filling pressures (as in mediastinal compressions of great veins) or trends towards equalization of pressures in case of cardiac tamponade or markedly increased right ventricular filling pressures (Pulmonary arterial hypertension [PAH])

High CVP, Low PCWP, Cardiac Output is usually decreased w increased SVR Marc Imhotep Cray, M.D.

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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 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

Marc Imhotep Cray, M.D.

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Compensated vs. decompensated shock With compensated shock, body is experiencing a state of low blood volume but is still able to maintain blood pressure and organ perfusion by increasing heart rate and constricting blood vessels Symptoms of compensated shock include:          

Agitation, restlessness and anxiety Altered mental status Tachycardia or tachypnea Change in pallor, cyanosis around the lips, or clammy skin Nausea or vomiting Thirst Weak, thready or absent pulse Narrowing pulse pressure Shallow, rapid breathing Mental status may be normal, in the early stages

Marc Imhotep Cray, M.D.

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Compensated vs. decompensated shock (2) With compensated shock, body is able to take measures to maintain blood pressure, however as shock worsens (decompensates), body becomes unable to keep up perfusion of vital organs is no longer maintained Lactic acidosis Symptoms of decompensated shock include:         

Falling blood pressure (systolic of 90 mm Hg or lower with adults) Tachycardia and tachypnea Low urine output Labored and irregular breathing Weak, thready or absent peripheral pulses Ashy or cyanotic pallor Reduced body temperature Decreased mental status Dilated pupils

Marc Imhotep Cray, M.D.

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Decompensated shock  With decompensated shock, it may be necessary to request advanced life support measures for patient  Priority should be given to management of airway and treatment of the underlying cause of shock  A decrease in blood pressure is often an indication of latestage shock and treatment should start well before this is detected  If condition remains untreated will progress into irreversible shock ultimately leads to death Marc Imhotep Cray, M.D.

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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

NB: Malperfusion and organ dysfunction are ultimate end point of any shock stage

Marc Imhotep Cray, M.D.

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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 damage Cellular aggregation

Marc Imhotep Cray, M.D.

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Treating Shock Capsule  The key toward successfully treating shock is a rapid response

 If it can be treated before reaching decompensated phase, that is best  In many major life-threatening situations development of shock should be anticipated  EM providers refer to a ‘golden hour’ or ‘golden period’ in which care should be delivered as quickly as possible and if it is, patient will not suffer any lasting damage  requires a speedy assessment of patient and rapid transport to a advance care facility Marc Imhotep Cray, M.D.

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Treatment of shock Generalities: ABCs Positioning, avoiding hypothermia Maintaining adequate oxygenization Fluid resuscitation Pain relief ? inotropic treatment?

Marc Imhotep Cray, M.D.

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Enhance compensatory phase of shock • Maintenance of mean circulatory pressure • Maximizing cardiac function • Redistributing perfusion to vital organs • Optimizing unloading of oxygen at tissues

Marc Imhotep Cray, M.D.

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Maintain Blood Volume • Fluid redistribution to vascular space • From interstitium (Starling effect) • From intracellular space (osmotic effect)

Marc Imhotep Cray, M.D.

• Decreased renal fluid losses • Decreased glomerular filtration rate (GFR) • Increased aldosterone • Increased vasopressin

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Mintain Blood Pressure • Decreased venous capacitance • Increased sympathetic activity

• Increased circulating (adrenal) epinephrine • Increased angiotensin

• Increased vasopressin

Marc Imhotep Cray, M.D.

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Maximize Cardiac Performance • Increased contractility • Sympathetic stimulation • Adrenal stimulation

Marc Imhotep Cray, M.D.

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Early mechanical ventilation â&#x20AC;˘ allows blood flow to be redistributed â&#x20AC;˘ tends to reverse lactic acidosis â&#x20AC;˘ supports patient until other therapeutic measures can be effective Tidal volumes in order of 7-10 ml/kg 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.

Marc Imhotep Cray, M.D.

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Fluid resuscitation IV line c Large bore cannula Choice of infusion Sm. volume resuscitation (hypertonic NaCl solution) General conditions: parameters ( BP, Pulse, CVP, SatO2 etc.)

Lactated Ringer's solution Colloids Dextrane Hydroethylstrach Gelatine

Marc Imhotep Cray, M.D.

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Inotropic drugs Inotropie

Heart rate

SVR

Epinephrin

++

+

+

-

Norepinephrin

++

0

++

Dopamin

++

+

Dobutamin

+++

Isoproterenol

++

Amrinon

+++

Marc Imhotep Cray, M.D.

Kidney Cornarry Blood flow Blood flow

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

--

+

+

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Summary of Shock  Shock is defined as a state of systemic tissue hypoperfusion resulting from reduced cardiac output and/or reduced effective circulating blood volume.  The major types of shock are cardiogenic (e.g., myocardial infarction), hypovolemic (e.g., blood loss), and septic (e.g., infections).  Shock of any form can lead to hypoxic tissue injury if not corrected.  Septic shock is caused by the host response to bacterial or fungal infections; it is characterized by endothelial cell activation, vasodilation, edema, disseminated intravascular coagulation, and metabolic derangements.

Marc Imhotep Cray, M.D.

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THE END

Marc Imhotep Cray, M.D.

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Further Study: Reading: Robbins Basic Pathology 10e, Elsevier, 2018 ;Pgs. 115-118.

Sethi, AK et al. Shock-A Short Review. Indian J. Anaesth.

2003; 47 (5) : 345-359 Video Lectures: Circulatory Shock_Dr. Najeeb

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