Shock Flashcards

• Is a condition during which the cardiovascular system fails to perfuse the tissues adequately --> results in cellular hypoxia
• Causes general and widespread impairment of cellular metabolism

Types

• Cardiogenic (caused by heart failure)
• Hypovolemic (caused by insufficient intravascular fluid volume)
• Obstructive Shock
• Distributive Shock
  • Neurogenic or vasogenic (caused by alterations in vascular smooth muscle tone)
  • Anaphylactic (caused by hypersensitivity)
  • Septic (caused by infection)

• Impairment of cellular metabolism
• Shift from aerobic to anaerobic metabolism
• Loss of the ability to maintain an electrochemical gradient
  • Accumulation of sodium and chloride in the cell
  • Water follows, thus reducing the extracellular volume
  • K exits cell
  • Activation of coagulation pathway
• Impaired oxygen use, regardless of cause
• Impaired glucose delivery and use
• Impaired delivery or uptake
• Cells shifting to glycogenolysis, gluconeogenesis, lipolysis
• Gluconeogenesis causes proteins to be used for fuel, thus no longer available for maintaining cellular structure, function, repair, and replication
• Toxic ammonia and urea production
• Metabolic acidosis
• Glycogenolysis and lipolysis contribute to cellular failure

Clinical manifestations

• Weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath, and generally “feeling sick”
• Decreased blood pressure, cardiac output, and urinary output
• Increased respiratory rate

Treatment

• Oxygenation: Absolute necessity in all shock states
• Correct or remove underlying cause
• Provide supportive therapy

• "heart fails to pump blood"
• Inability of the heart to pump adequate blood to tissues and end organs from any cause

• Patients with cardiogenic shock have decreased
  
  • hypotension
  • hypoperfusion
  • cardiac output

Cardiogenic shock may occur due to:

• Myocardial infarction (most common)
• Myocardial Ischemia
• Acute mitral valve regurgitation due to papillary muscle rupture
• Sustained arrhythmias/dysthymias
• Severe dilated cardiomyopathy
• Cardiac surgery

1. cardiomyopathy, sepsis, myocarditis, pericarditis, aneurysm, dysrhythmias, contusion, metabolic abnormalities, and papillary muscle rupture

2. impaired diastolic filling related to dysrhythmias

3. obstruction attributable to pulmonary embolism, cardiac tamponade, valvular
disorders, tumors, and wall rupture or defects.

Dysrhythmias or conditions related to post–cardiopulmonary resuscitation reduce
cardiac function and output

• Chest pain
• Dyspnea
• Faintness
• along with feelings of impending doom
• Classic hallmarks:
  • Tachycardia
  • Tachypnea
  • Hypotension
  • Jugular venous distention
  • Dysrhythmia
  • Low measured cardiac output

• cyanotic lips, nail beds, and skin
• Hypotension, oliguria, and cool skin Cyanosis; skin mottling
• rapid, faint, or irregular pulses; low urine output; and occasional
  peripheral edema are additional signs and symptoms of end-organ
  hypo perfusion
• Pulmonary edema increases as volume accumulates and expands from the heart into the lungs as crackles wheezes

• Medications
  • Fluids
  • Cardio supportive drug
  • Fibrinolytic therapies: To disintegrate coronary thrombus
• Assist the pump
  
  • Pacemakers
  • Internal defibrillator devices
  • Implantable VADS
  • Intra-aortic balloon pump (IABP) or percutaneous or ventricular assist devices (VADS)

• Percutaneous interventions
  • Balloon angioplasty
  • Stent placement
  • Thrombectomies
• Surgery:
  • Coronary artery bypass
  • ventriculoplasty
  • heart transplantation

• Insufficient intravascular fluid volume

• loss of whole blood
  • Hemorrhage
• plasma loss
  • burns: increase in capillary permeability due to heat effect and damage causes plasma to leak out from capillaries to interstitial spaces

• interstitial fluid loss
  
  • emesis
  • diuresis
  • diaphoresis
  • diabetes mellitus /insipidus

"CHART"

• C: cool extremities, cyanosis. pale
• H: hypotension, High SVR (SVR increases due to the body’s attempt to compensate for the loss in volume)
• A: Altered LOC
• R: rapid/weak HR, reduced urine output
• T: thirst increased, tachycardia
• low systemic and pulmonary preloads

• Compensatory vasoconstriction, increased systemic vascular resistance (SVR), and afterload
• To improve blood pressure and perfusion to core organs

SNS

• Heart rate and vasoconstriction increase as a result of catecholamine release by the adrenals

Liver and Spleen

• The liver and spleen add to blood volume by disgorging stored red blood cells and plasma

Kidney- RAAS

• In the kidneys, renin (through several intermediaries) stimulates aldosterone release and the retention of sodium (and hence water)
  • Antidiuretic hormone (ADH, or vasopressin) from the posterior pituitary gland increases water retention.

Treatment

• Prompt control of hemorrhage
• Fluid replacement

aka vasodilatory shock

• distributive shock is a form of shock in which severe vasodilation despite normal blood volume results in improper distribution of blood flow
• Characterized by
  • loss of blood vessel tone
  • enlargement of the peripheral vascular compartment (large diameter blood vessels)
  • displacement of the vascular volume away from the heart and central circulation
• In distributive shock, the capacity of the vascular compartment expands.

• Neurogenic shock
  • caused by decreased sympathetic
    control of blood vessel tone due to a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels (e.g. spinal cord injury)
• Anaphylactic shock
  • caused by a severe systemic allergic reaction.
  • it is an immunologically mediated reaction
    in which vasodilator substances such as histamine are
    released into the blood
• Septic shock
  • systemic immune response to severe
    infection. It is the most common type of distributive shock
• Patients with Distributive shock have blood vessel dilation and warm skin in contrast to other shock types

widespread and massive vasodilation that results from an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle

• Trauma to the spinal cord
• Trauma to the medulla (Lack of food and O2)
  • conditions that interrupt the supply of oxygen to the medulla
  • conditions that deprive the medulla of glucose (e.g., insulin reactions) can cause neurogenic shock
    by interrupting sympathetic activity.
• Depressive drugs, anesthetic agents
• severe emotional stress and pain are other causes of
  neurogenic shock

Clinical hallmark of neurogenic shock is a very low SVR, bradycardia, fainting

outcome of a widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis.

• caused by a severe systemic allergic reaction. It is an immunologically
  mediated reaction in which vasodilator substances such as histamine are released into the blood.
• Production of mast cells, immunoglobulin E (IgE), and
  low-affinity IgE receptor (FceRI) is induced by cellular response to the
  antigen
• Physiologic alterations related to the inflammatory and immune response, similar to neurogenic shock, are massive; vasodilation, peripheral pooling, and relative hypovolemia lead to decreased tissue perfusion and impaired cellular metabolism

Anaphylactic shock is often severe and has immediate symptoms:

• itchy rash
• throat swelling
• low blood pressure: related to the massive vasodilation and systemic
  inflammation

Symptoms often affect multiple organ systems, including

• gastrointestinal (e.g., nausea, abdominal pain, vomiting, diarrhea)
• cutaneous (e.g., erythema, pruritus, urticaria, or angioedema),
• respiratory (e.g., shortness of breath, cough, rhinorrhea, tightening of
  throat, difficulty swallowing, wheezing)
• cardiovascular (e.g., diaphoresis, pallor, hypotension), or hematologic (e.g., fever, hemolysis).

• Treatment begins with removal of the antigen (if possible).
• Epinephrine is administered to decrease mast
  cell and basophil degranulation, cause vasoconstriction, and reverse
  airway constriction
• Volume expanders (e.g., lactated Ringer solution) are given intravenously to reverse the relative hypovolemia
• antihistamines and corticosteroids are given to stop the
  inflammatory reaction

disease process begins with infection entering the bloodstream and causing bacteremia.

• SIRS has 4 criteria: -Temp > 38 or Temp < 36
  -Heart rate > 90
  -RR > 20 or PaCO2 < 32
  -WBC >12,000 or WBC < 4,000 or >10% Bands
• The patient must have a suspected/proven infection and fulfill at least 2 of the SIRS criteria to be defined as septic.

Two main mechanisms contribute to lactic acid accumulation in sepsis:

• tissue hypoxia
• epinephrine-induced stimulation of aerobic glycolysis.
• The patient with sepsis is at risk of developing shock through the loss of systemic vascular resistance
• A patient has severe sepsis if they fulfill sepsis criteria and have organ dysfunction, hypotension, lactic acidosis, oliguria, or mental status changes.
• Elevated procalcitonin (PCT) level indicates a nonspecific
  proinflammatory response seen in bacterial infection
• C-reactive protein (CRP) is an acute
  phase reactant protein produced by the liver, mainly in response to
  interleukin-6 produced by inflammation of any type. CRP is most
  sensitive to acute phase reactants; consequently, its level rises rapidly
  during inflammation. Similarly to PCT, CRP is nonspecific to types of
  inflammation, but may be used to trend severity of infection and
  response to treatment, especially in occult and resistant infections,
  such as osteomyelitis.

• Pharmacologic hemodynamic support and adjunctive therapy to
  maintain tissue perfusion include vasoactive agents.
• Norepinephrine is now considered the initial vasopressor of choice
• Dopamine, epinephrine, phenylephrine, and vasopressin are alternatives;
  however, these are less preferred because of potential tachycardia,
  dysrhythmias, or reduction in splanchnic blood flow.
• Pharmacologic hemodynamic support and adjunctive therapy to maintain tissue perfusion include vasoactive agents.
• Norepinephrine is now considered the initial vasopressor of choice
• Dopamine, epinephrine, phenylephrine, and vasopressin are alternatives; however, these are less preferred because of potential tachycardia, dysrhythmias, or reduction in splanchnic blood flow

• Acute lung injury/acute respiratory distress syndrome (ALI/ARDS)
  • Rapid and profound onset of dyspnea that can be caused by shock.
• Acute kidney injury (AKI)
  • Impaired renal perfusion that occurs in response to decreased intravascular volume.
• Gastrointestinal complications
  • Patients may develop gastrointestinal ulcers and bleeding.
• Disseminated intravascular coagulation
  • Widespread activation of the coagulation system with resulting clots and thrombotic occlusion of vessels as well as bleeding.
  • More commonly occurs as a consequence of gram-negative (bacteria) sepsis
• Multiple organ dysfunction syndrome
  • Malfunctioning of multiple organ systems as a consequence of shock

organ injury is directly associated with a
specific insult, most often ischemia or impaired perfusion from an
episode of shock or trauma, thermal injury, soft tissue necrosis, or
invasive infection

• Obstructive shock occurs due to mechanical obstruction of the blood flow through the circulation

• Obstructive shock can be due to:
  
  • Pulmonary embolism (most common)
  • Cardiac tamponade
  • Pneumothorax
  • Dissecting aortic aneurysm