Shocks 2066dbe579bb4f7abdb7aed644236843

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📒
Shocks 
Dates
Type 📒 Lesson
Nombre Montoya Corral José Luis
Topic
Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen 
delivery to meet cellular metabolic needs and oxygen consumption requirements, 
producing cellular and tissue hypoxia.
Effects intitally reversible but rapidly irreversible 
Leads to multi organ failure (MOF)
State of cellular and tissue hypoxia due to either reduced oxygen delivery, increased 
oxygen consumption, inadequate oxygen utilization, or a combination of these 
processes
💡 it is crucial to recognize that a patient in shock can present hypertensive, 
normotensive, or hypotensive states 
Undifferentiated shock: situation where shock is recognized but the cause is unclear
Epidemiology
Septic shock (distributive) most common form among patients in the ICU 
1. Septic
2. Cardiogenic 
3. Hypovolemic 
@March 2, 2021
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4. Obstructive (rare) 
Classification and Etiology 
4 types: Distributive, cardiogenic, hypovolemic and obstructive 
💡 Many patients with circulatory failure have a combination of more than one 
form of shock (Multifactorial shock) 
Distributive: characterized by severe peripheral vasodilatation (vasodilatory shock)
Septic Shock: dysregulated host response to infection resulting in life-threatening 
organ dysfunction, is the most common cause of distributive shock. Subset of sepsis. 
Mortality in the 40 to 50 percent range. Can be identified by the use of vasopressor 
therapy and the presence of elevated lactate levels (>2 mmol/L) despite adequate fluid 
resuscitation. 
Neurogenic shock: common in patients with severe traumatic brain injury and spinal 
cord injury. Interruption of autonomic pathways, causing decreased vascular resistance 
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and altered vagal tone, is thought to be responsible for distributive shock in patients with 
spinal cord injury. However, hypovolemia from blood loss and myocardial depression 
may also contribute to shock in this population.
Anaphylactic shock: most commonly encountered in patients with severe, 
immunoglobulin-E (Ig-E) mediated, allergic reactions to insect stings, food, and drugs. 
Anaphylaxis also applies to acute systemic reactions caused by direct release of 
mediators from mast cells and basophils produced by various triggers
Drug and toxin-induced shock: include those associated with drug overdoses (eg, 
long-acting narcotics); snake bites; insect bites including scorpion envenomation and 
various spider bites; transfusion reactions; heavy-metal poisoning including arsenic, 
iron, and thallium; and infections associated with toxic shock syndrome (eg, 
Streptococcus and Escherichia spp)
Endocrine shock: Addisonian crisis (adrenal failure due to mineralocorticoid 
deficiency) and myxedema can be associated with hypotension and states of shock. 
Vasodilatation can occur due to altered vascular tone and aldosterone-deficiency-
mediated hypovolemia. The exact mechanism of vasodilation in patients with 
myxedema is unclear; concurrent myocardial depression or pericardial effusions likely 
contribute to hypotension and shock in this population
Cardiogenic: due to intracardiac causes of cardiac pump failure that result in 
reduced cardiac output (CO)
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Cardiomyopathic: Myocardial infarction involving greater than 40 percent of the left 
ventricular myocardium, myocardial infarction of any size if accompanied by severe 
extensive ischemia due to multivessel coronary artery disease, severe right 
ventricular infarction, acute exacerbation of heart failure in patients with severe 
underlying dilated cardiomyopathy, stunned myocardium following cardiac arrest, 
prolonged ischemia or cardiopulmonary bypass, myocardial depression due to 
advanced septic or neurogenic shock, and myocarditis
Arrhythmic: atrial and ventricular tachyarrhythmias and bradyarrhythmias may 
induce hypotension, often contributing to states of shock. When CO is severely 
compromised by significant rhythm disturbances, patients can present with 
cardiogenic shock
Mechanical: severe aortic or mitral valve insufficiency, and acute valvular defects 
due to rupture of a papillary muscle or chordae tendineae (mitral valve defect) or 
retrograde dissection of the ascending aorta into the aortic valve ring or an abscess 
of the aortic ring (aortic insufficiency). 
Hypovolemic: due to reduced intravascular volume (ie, reduced preload), 
which, in turn, reduces CO. Hypovolemic shock can be divided into two 
categories: hemorrhagic and nonhemorrhagic
Hemorrhagic: Reduced intravascular volume from blood loss can result in 
shock. Blunt or penetrating trauma is the most common, followed by upper or 
lower gastrointestinal bleeding
Nonhemorrhagic: Reduced intravascular volume from fluid loss other than 
blood can cause shock. Volume depletion from loss of sodium and water can 
occur from a number of anatomic sites
Obstructive: mostly due to extracardiac causes of cardiac pump failure and often 
associated with poor right ventricular output. Divided into pulmonary vascular and 
mechanical. 
Pulmonary vascular: Most cases of obstructive shock are due to right ventricular 
failure from hemodynamically significant pulmonary embolism (PE) or severe 
pulmonary hypertension (PH). The right ventricle fails because it is unable to 
generate enough pressure to overcome the high pulmonary vascular resistance 
associated with PE or PH. 
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Mechanical: present clinically as hypovolemic shock because their primary 
physiologic disturbance is decreased preload, rather than pump failure. Causes:
Tension pneumothorax 
Pericardial tamponade 
Constrictive pericarditis 
Restrictive cardiomyopathy 
Combined: Patients often present with combined forms of shock
Pathogenesis and pathophysiology 
Mechanisms of shock: Cellular hypoxia occurs as a result of reduced tissue 
perfusion/oxygen delivery and/or increased oxygen consumption or from inadequate 
oxygen utilization. Causes cell membrane ion pump dysfunction, intracellular edema, 
leakage of intracellular contents into the extracellular space, and inadequate regulation 
of intracellular pH. These processes progress to systemic level, cause acidosis, 
endothelial dysfunction and inflammatory and anti-inflammatory cascades. This reduces 
tissue perfussion 
Physiology: major physiologic determinants of tissue perfusion (and systemic blood 
pressure [BP]) are cardiac output (CO) and systemic vascular resistance (SVR)
BP = CO X SVR 
CO is the product of heart rate (HR) and stroke volume (SV):
CO = HR X SV
Stroke volume determined by:
Preload
Myocardial contractility
Afterload
SVR is governed by: 
Vessel length
Blood viscosity
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Vessel diameter (ie, vessel tone)
💡 Biologic processes that change any one of these physiologic parameters can 
result in hypotension and shock
💡 Some forms of shock have normal CO and SVR. patients with profound 
mitochondrial dysfunction have a shock state that occurs despite normal CO, 
SVR, and tissue perfusion because of inadequate oxygen utilization
Stages of shock: It begins with an inciting event, such as a focus of infectio, injury, 
triggering pathophysiological changes, which can profress through several stages.
Pre-shock: Compensated or cryptic shock. Characterized by compensatory responses 
to diminished tissue perfusion. With timely and appropriate management, deterioration 
can be prevented and signs of impending deterioration can be reversed
Shock: Compensatory mechanisms become overwhelmed, and signs and symptoms of 
organ dysfunction appear including symptomatic tachycardia, dyspnea, restlessness, 
diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin
End-organ dysfunction: irreversible organ damage, multiorgan failure (MOF), and 
death. Anuria and acute renal failure develop, acidemia further depresses CO, 
hypotension becomes severe and recalcitrant to therapy. Death is common
Summary
Shock is defined as a state of cellularand tissue hypoxia due to reduced oxygen 
delivery, increased oxygen consumption, inadequate oxygen utilization, or a 
combination of the three. "Undifferentiated shock" refers to the situation where shock is 
recognized but the cause is unclear
Four types of shock are recognized. However, many patients have a combination of 
more than one of the forms of shock
Distributive shock has many causes, including septic shock, systemic inflammatory 
response syndrome (SIRS; eg, pancreatitis), neurogenic shock, anaphylactic shock, 
toxin-related shock, and endocrine shock (eg, addisonian crisis).
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Cardiogenic shock may be cardiomyopathic (eg, myocardial infarction), or due to an 
arrhythmia (eg, sustained ventricular tachycardia) or a mechanical abnormality (eg, 
acute valvular rupture).
Hypovolemic shock may be due to hemorrhagic (eg, trauma) or nonhemorrhagic 
fluid losses (eg, diarrhea).
Obstructive shock may be pulmonary vascular related (eg, pulmonary embolism 
[PE]) or due to a mechanical cause of reduced preload (eg, tension pneumothorax, 
pericardial tamponade).
Cellular hypoxia results in cell membrane ion pump dysfunction, intracellular edema, 
leakage of intracellular contents into the extracellular space, and inadequate regulation 
of intracellular pH. Progress to acidosis, endothelial dysfunction, and further stimulation 
of inflammatory and anti-inflammatory cascades
Common to most forms of shock is diminished cardiac output (CO) and/or systemic 
vascular resistance (SVR). Severe hypovolemia, cardiogenic shock, and late-stage 
obstructive shock are characterized by a low CO and compensatory increase in the 
SVR that attempts to maintain perfusion to vital organs, whereas distributive shock is 
classically associated with reduced SVR and a compensatory increase in the CO. 
Shock due to disorders of mitochondrial function have normal CO and SVR but 
inadequate oxygen utilization.
Shock begins with an inciting event and may progress through several stages: pre-
shock, shock, and end-organ dysfunction. The progression can culminate in irreversible 
end-organ damage and death
Hemorrhagic Shock.pdf
SHOCKHYPOVCVSSEPSIS.ppt
📍 Shock → Condición en la cual el sistema cardiovascular no puede proveer 
de una perfusión adecuada a los tejidos 
https://www.notion.so/signed/https%3A%2F%2Fs3-us-west-2.amazonaws.com%2Fsecure.notion-static.com%2Ffa9789c4-0dc2-4939-bc48-8423aeb30098%2FHemorrhagic_Shock.pdf?table=block&id=4b5edbcd-55b4-4a0d-b4e4-d198da09d88c&spaceId=ac04ee24-8d79-490d-b963-b0e6c89efd2c&userId=7d76c91a-bfa3-4ba9-a277-9a11593f15da&cache=v2
https://www.notion.so/signed/https%3A%2F%2Fs3-us-west-2.amazonaws.com%2Fsecure.notion-static.com%2Fc3b30785-c180-4a13-b299-8a80d3f69162%2FSHOCKHYPOVCVSSEPSIS.ppt?table=block&id=b8958c31-f964-4bec-b1dc-fba2c7f0bdda&spaceId=ac04ee24-8d79-490d-b963-b0e6c89efd2c&userId=7d76c91a-bfa3-4ba9-a277-9a11593f15da&cache=v2
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Una perfusión inadecuada puede generar 
Hipoxia celular generalizada
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Cambios en el metabolismo celular 
Daño a tejidos y Órgano diana 
La muerte 
El shock se produce cuando hay un desbalance en el aporte/demanda de oxigeno por 
parte del organismo
Cambios en el Metabolismo (pasa de aerobeo a anaerobeo) 
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Mecanismos Compensatorios de un estado de Shock (son regulados por el sistema 
nervioso simpático) 
Neurohormonal response → Estimulado por los Baroreceptores (aumentan F.C., 
aumentan contractilidad, produce vasoconstricción, aumenta la precarga)
Hormonal response → S.R.A.A (disminución de la prefusión renal = aumento de 
producción de renina = conversión de angiotensina 1 en angiotensina 2 = 
vasoconstricción, retencion de sodio y agua y excreción de potasio) 
Hormonal response → Hormona Antidiuretica (Osmoreceptores son activados 
en el hipotalamo, los cuales mandan señales para realizar ADH en la neurohipofisis 
-parte posterior de la glándula pituitaria- lo cual genera una retención de agua en 
los tubulos renales con al finalidad de aumentar la presión arterial) Por medio de 
los receptores V2 de aquaporina
Hormonal response → Glándula Suprarenal (Se genera ACTH con al finalidad 
de estimular la glándula suprarrenal para generar glucocorticoides, con la finalidad 
de aumentar los niveles de glucosa para saciar las demandas metabólicas del 
organismo) 
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TIPOS DE SHOCK 
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SHOCK HIPOVOLEMICO → Problemas con el Volumen (principalmente el 
volumen sanguíneo) 
Perdida de sangre circulante (tienes un tanque vacío), lo que genera una 
hipoperfusión de los tejidos 
Etiologías → Perdida de fluidos internos o externos/compartimentos 
intracelulares y extracelulares
Causas mas comunes → 
 - HEMORRAGIA (Trauma, puede ser interna que no la ves o externa que si la 
ves) 
 - Deshidratación (Vomito, Diarrea, Diuresis masiva, Quemaduras extensas) 
Fisiopatología y Secuencia del Shock Hipovolemico 
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RAP → Right Atrial Pressure PAWP → Pulmonary Artery Wedge Pressure
Clinica de los Px con Shock Hipovolemico 
- Taquicardia y Taquipnea 
- Pulso debil 
- Hipotensión 
- Piel fría y húmeda 
- Hipoperfusión cerebral = Cambio en el status mental 
- Disminución de la producción de orina: oscura y concentrada
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SHOCK CARDIOGENICO → Problemas en el Corazón como Bomba (no puede 
bombear correctamente la sangre, INSUFICIENCIA CARDIACA) 
El corazón es incapaz de bombear correctamente la sangre y pues no llega a 
los tejidos = hipoperfusión tisular 
Causa mas común → IAM Anterior (esto cuando mas del 40% de la masa 
ventricular se ve afectada) 
Etiologias (son muchas) 
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Fisiopatología y Secuencia del Shock Cardiogénico 
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SHOCK DISTRIBUTIVO → Perfusión inadecuada de los tejidos debido a la mala 
distribución del flujo sanguíneo (vasodilatación y aumento de la permeabilidad 
vascular) 
La bomba y el volumen esta bien pero la sangre no llega a los tejidos 
Causas/Etiologias → Shock Septico, Neurogenico y Anafilactico 
ANAFILACTICO
Reacción alérgica sistémica generada por un antígeno (Hipersensibilidad 1)
Respuesta al antigeno: Vasodilatación, Aumento de la permeabilidad 
vascular, Broncoconstricción, Aumento de la producción de moco, Proceso 
Inflamatorio 
Clinica: 
NEUROGENICO (es la menos común) 
Perdida del tono simpático (Trauma Vertebomedular, OD, Envenenamiento) 
Predominio del parasimpático en Trauma Vertebromedular debido a que el 
vago no va a travez de la medula espinal ya que sale a travez del craneo 
directamente 
Provoca vasodilatación masiva en la vasculatura → disminuye el retorno 
venoso al corazón → disminuye el gasto cardíaco → Disminuye el 
suministro de oxígeno celular → Se altera la perfusión tisular y afecta el 
metabolismo 
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Gasto
Etiología mas común → Lesión Medular por encima de T6 
SEPTICO 
Respuesta Inflamatoria Sistémica a alguna infección manifestada por dos o 
> de los siguientes: 
Temperatura > 38ºC o < 36ºC
F.C. > 90
F.R. > 20 o PaCO2 < 32 
WBC > 12,000 / mm3 o > 10% (WBC inmaduras)
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2 fases 
 - Fase Temprana → Caliente (Respuesta Hiperdinámica - Vasodilatación) 
 - Fase Tardia → Frio (Respuesta Hipodinámica - Estado 
Descompensado) 
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SVR → Tono Vascular 
UOP → Urine Osmotic Pressure 
SHOCK OBSTRUCTIVO (Entra en Cardiogénico) 
Falla en precarga y/o poscarga 
Neumotorax a tensión → Ingreso de aire que ocupa espacio de mas en el 
pulmón, ocasionando una desviación del mediastino y no permite un correcto 
retorno venoso de las cavas y tambien afecta directamente la poscarga 
Taponamiento cardiaco (Triada de Beck) → Pericardio lleno de liquido, esto 
genera una compresión del corazón así que no permite que tenga una 
distensión correcta (falla en la precarga) y tampoco puede generar una 
contracción con la suficiente fuerza para sacar la sangre a la circulación (falla 
en la poscarga) 
1. Pletora yugular
2. Ruidos cardiacos disminuidos
3. Hipotensión 
Tromboembolismo Pulmonar→ Trombos ubicados en los pulmones 
comprometen la precarga del ventrículo izquierdo (no hay un correcto retorno 
de la sangre al V.I.) 
Hernia Diafragmática 
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Lo Visto en Clase 
"Una desarticulación brusca en la maquinaria de la vida"
"Un alto momentáneo en el acto de morir" 
Presión media adecuada >65 mmHg 
2(PD) + PS / 3 
Shock Definiciones
1. Estado médico extremadamente delicado que proviene de una reducción profunda 
de la perfusión tisular eficaz que lleva a disfunción celular e insuficiencia orgánica
2. Estado de hipoxia celular y tisular debida a la disminución de O2 entregado, 
aumento en el consumo del mismo o su inadecuada utilización 
3. Estado fisiopatológico agudo y complejo de disfunción circulatoria originado por un 
fracaso del organismo para aportar cantidades suficientes de O2 y otros nutrientes 
para satisfacer necesidades de los lechos hísticos y eliminar los productos de su 
catabolismo 
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El ciclo de krebs es la vía aeróbica de la generación de energía 
Sus principales metabolitos 
CO2
H2O
ATP
Sin oxígeno se bloquea el ciclo de krebs, por lo tanto aumenta el piruvato, si hay mucho 
piruvato entramos al ciclo anaerobio, generando lactato, por eso se genera la acidosis 
metabólica 
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Fases de la muerte celular 
1. Bloqueo del ciclo de krebs - Acidosis intracelular 
2. Cambio de pH intracelular - Afección de la NaKATPasa - Edema mitocondrial
3. Inhibición mitocondrial
4. Fase de no retorno - Aumento del calcio intracelular, activando las vías apoptóticas 
5. Calcificación mitocondrial - Depósitos mitocondriales de calcio 
6. Digestión de organelos, aumenta la permeabilidad de la membrana 
7. Muerte celular 
💡 A partir de la 4 es irreversible 
Componentes necesarios para la oxigenación del organismo 
Pulmón 
Sistema circulatorio y corazón 
Capacidad de liberar O2 
💡 Al paciente con metahemoglobinemia le doy azul de metileno 
Hipoxia + hipoperfusión = isquemia 
Corazón, cerebro y pulmones aguantan de 4 a 6 minutos en hipoxia 
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La fisiopatología depende de la etiología 
Sepsis
Quemadura
Embolias
Lesión medular
Anafilaxia
Mixedema 
TEP
Tapón cardíaco 
IAM 
Respuesta cardiovascular
Incremento de crono e inotropismo
Incremento de resistencias vasculares
Disminución de capacitancia venosa
Reclutamiento capilar 
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Disminución de demandas de O2 por el miocardio 
Depresión miocardica 
Compromiso coronario
Arritmias
Falla cardiaca aguda 
Respuesta pulmonar
Taquipnea 
Elevación del volumen/minuto 
Fatiga de músculos respiratorios, hipoxia, hipercapnia, acidosis 
Daño en la matriz del colágeno, elastina, fibronectina (leucocitos activados que 
liberan RL y proteasas)
Escape de líquido de los capilares y pérdidad de elasticidad pulmonar 
Microembolias 
Respuesta renal
Vasoconstricción de la arteriola eferente 
Disminuye perfusión de la corteza 
Incremento del SRAA 
Producción de eritropoyetina 
Necrosis tubular aguda 
Lesión renal con subsecuente falla renal, acidosis tubular renal, disminución de 
bicarbonato 
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Hay que aprenderse esa tabla 
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Choque anafilactico que afecte a 2 sistemas se da adrenalina
Todos los choques terminan en disminución de gasto cardiaco y presión arterial media, 
shock y disfunción multiorgánica 
Sx disfunción multiorgánica 
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💡 Todas las IL proinflamatorias afectan principalmente al miocardio 
Dx diferencial tienen que ser los otros choques 
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Airway - vía aerea permeable 
Breathing - respiración adecuada
Circulation - presión arterial media 
Disability - Glasgow
Exposure - sobretodo en pacientes lesionados