1. Shock is the failure to meet the metabolic needs of cells due to decreased tissue perfusion. The four main types of shock are hypovolemic, vasogenic, neurogenic, and cardiogenic shock.
2. Shock progresses through compensatory, decompensatory, and irreversible phases. In the compensatory phase, the body tries to maintain hemodynamics through neuroendocrine responses to the initial loss of blood volume. In the decompensatory phase, ongoing cellular injury and microcirculatory dysfunction can perpetuate hypoperfusion.
3. Core principles in managing critically ill patients include securing the airway, controlling active hemorrhage through pressure or surgery, and volume resuscitation with
1. Shock is the failure to meet the metabolic needs of cells due to decreased tissue perfusion. The four main types of shock are hypovolemic, vasogenic, neurogenic, and cardiogenic shock.
2. Shock progresses through compensatory, decompensatory, and irreversible phases. In the compensatory phase, the body tries to maintain hemodynamics through neuroendocrine responses to the initial loss of blood volume. In the decompensatory phase, ongoing cellular injury and microcirculatory dysfunction can perpetuate hypoperfusion.
3. Core principles in managing critically ill patients include securing the airway, controlling active hemorrhage through pressure or surgery, and volume resuscitation with
1. Shock is the failure to meet the metabolic needs of cells due to decreased tissue perfusion. The four main types of shock are hypovolemic, vasogenic, neurogenic, and cardiogenic shock.
2. Shock progresses through compensatory, decompensatory, and irreversible phases. In the compensatory phase, the body tries to maintain hemodynamics through neuroendocrine responses to the initial loss of blood volume. In the decompensatory phase, ongoing cellular injury and microcirculatory dysfunction can perpetuate hypoperfusion.
3. Core principles in managing critically ill patients include securing the airway, controlling active hemorrhage through pressure or surgery, and volume resuscitation with
1. Shock is the failure to meet the metabolic needs of cells due to decreased tissue perfusion. The four main types of shock are hypovolemic, vasogenic, neurogenic, and cardiogenic shock.
2. Shock progresses through compensatory, decompensatory, and irreversible phases. In the compensatory phase, the body tries to maintain hemodynamics through neuroendocrine responses to the initial loss of blood volume. In the decompensatory phase, ongoing cellular injury and microcirculatory dysfunction can perpetuate hypoperfusion.
3. Core principles in managing critically ill patients include securing the airway, controlling active hemorrhage through pressure or surgery, and volume resuscitation with
SHOCK – SURGERY A - What does plasma have that is disadvantage to the recipient?
Dagani, MD Antibody, Waste product
References: Dany Targ trans, PPT 2019, 2B recording - Instead of giving WB, we give pRBC for volume HISTORICAL BACKGROUND D. Unrecognized or inadequately corrected hypoperfusion Alfred Blalock increases morbidity and mortality - Stated that shock in hemorrhage was associated with reduced • Patient optimization for faster recovery cardiac output due to volume loss and not by a toxic factor E. Excessive fluid resuscitation may exacerbate bleeding Shock • Related to principles of damage control surgery - The failure to meet the metabolic needs of the cell and the consequences that ensues PRIMARY SURVEY - Basically, if there will be a problem with the circulation the oxygen A – Airway and nutrition would not reach the cell or tissue for homeostasis to • Control the airway, if not breathing secure and intubate the patient ensue B – Breathing - Decreased tissue perfusion - is the central component of shock - Look if there is any obstruction C – Circulation Four categories of shock (by Alfred Blalock) - Check for blood pressure, use fluids 1. Hypovolemic Shock D – Deficit / Disability (Neurologic) - Most common type - Glasgow coma scale (highest-15, lowest-3) - Results from loss of circulating blood volume E – Exposure - Result of bleeding leading to hypotension • Hemorrhagic / Whole blood loss (trauma, gunshot wound), Non hemorrhagic / Plasma loss (due to third space loss like dehydration or PATHOPHYSIOLOGY OF SHOCK diarrhea), Interstitial fluid (bowel obstruction), or a combination PHASES: 2. Vasogenic (Septic) Shock Compensatory Phase - Results from decreased resistance (increase vasodilation and - The body compensate for the initial loss of blood volume through space) within a capacitance vessel, seen in sepsis hence at the neuroendocrine response to maintain hemodynamics (such the end insufficient circulation. as in hemorrhagic shock) 3. Neurogenic Shock - The body will try to compensate so that the blood pressure will - Form of vasogenic shock normalize due to the initial blood loss - Spinal cord injury or spinal anesthesia causes vasodilation due to acute loss of sympathetic vascular tone 4. Cardiogenic Shock - Results from failure of the heart as a pump, seen in arrythmias (uncoordinated contraction hence no effective cardiac output or ejection) or acute myocardial infarction (the myocardial cells are dead)
Overtime, 2 additional shocks were added
5. Obstructive Shock - Form of cardiogenic shock - Results from mechanical impediment to circulation leading to depressed cardiac output rather than primary cardiac failure (pulmonary embolism or tension pneumothorax) - In reality the heart has no problem it is the expansion of the heart Decompensatory Phase - Physiology: in preload the volume of blood coming from the - Continued hypoperfusion, which may be unrecognized, ongoing venous return will go to the heart hence more blood going to the cellular death and injury heart the better the pump BUT in cases such as tension - Microcirculatory dysfunction, parenchymal tissue damage and pneumothorax or cardiac tamponade the heart cannot expand inflammatory cell activation can perpetuate hypoperfusion thus lower blood amount going to the heart. - Ischemia or reperfusion injury often exacerbates the initial result 6. Traumatic Shock o If it is an anaerobic condition and you give oxygenated - Soft tissue and bony injury leads to the activation of inflammatory blood the patient will have free radicals, thus there will cells and the release of circulating factors (cytokines & be a compromise of the function of the organ. (Tissue intracellular molecules that modulate the immune response. cycle of shock) - The effects of tissue injury are combined with the effects of - Vicious cycle of shock: compromise function at the organ system hemorrhage creating a more complex and amplified deviation level due to untreated damage at the cellular level from homeostasis. - Core Principles in the Management of the Critically ill / Injured patient A. Definitive control of the airway must be secured B. Control of active hemorrhage - Paramount priority especially for hemorrhagic shock - WHY? If for example there was a patient with blood loss (neck wound) in the emergency room and you took his BP and the result was hypotensive or palpatory (can’t detect BP)- Management: give electrolytes and fluid (replace) - However, even if you infuse fluid to normalize the bp that would not happen until the patient is bleeding, so what is important is to control the bleeding by pressing or any other mechanical ways - If in another part like the abdomen or stomach which is hard to control a different type of management is used. C. Volume resuscitation with blood products with limited volume of Irreversible Phase crystalloid must occur while operative control of bleeding is - Persistent hypoperfusion results in further hemodynamic achieved. derangements and cardiovascular collapse - There are different types of blood products: WB, pRBC, platelet - Develop quite insidiously and may only be obvious in retrospect conc. FFP - Expensive parenchymal and microvasculature injury that volume - What does WB have that pRBC doesn't have? Plasma resuscitation fails to reverse process and will eventually lead to death Modified Wiggers model in animals representing the phases of Efferent Signals compensation, decompensation and irreversible phases of 1. Cardiovascular Response hemorrhagic shock: - Results from neuroendocrine and ANS response to shock and • 0% - 100% recovery constitute a prominent feature of the body’s adaptive response • 50% - death mechanism and clinical signs and symptoms of the patient in shock How many blood volume - Hemorrhage results in diminished venous return and decreased does a person have? 5L cardiac output (B1 adrenergic) o Compensated by (tachycardia) increase cardiac heart rate and contractility and venous and arterial vasoconstriction (via a1-adrenergic) Neuroendocrine and Organ - Specific Response to Hemorrhage o Increased myocardial O2 consumption occurs due to - Goal: maintain perfusion to the heart and brain, even at increased workload, thus O2 supply must be the expense of the other organs systems (EXCEPT: coronary maintained to prevent development of myocardial artery and circle of willis) dysfunction - Peripheral vasoconstriction occurs and fluid excretion is - Increased sympathetic output induces catecholamine release inhibited. from the adrenal medulla and peaks within 24-48 hours of o Hence those with prolonged hypovolemia or injury then return to baseline hypotension it will lead to acute renal failure because o Stimulate of hepatic glycogenolysis and it isn't the priority. gluconeogenesis - Mechanisms: o Increase skeletal muscle glycogenolysis 1. Autonomic control of peripheral vascular tone and o Suppression of insulin release cardiac contractility o Increased glucagon release 2. Hormonal response to stress and volume depletion 2. Hormonal Response 3. Local microcirculatory mechanism - activation of the ANS and the hypothalamic-pituitary- o organ specific adrenocorticotropic-axis o regulate regional blood flow ACTH and Cortisol - Initial stimulus: loss of circulating blood - Shock stimulates the hypothalamus to release corticotrophin - Magnitude of the response is based on: releasing hormone resulting to the release of ACTH by the o the volume of blood lost pituitary o rate at which it is lost (hemorrhagic) - ACTH stimulates the adrenal cortex to release cortisol (primary stress hormone) Afferent Signals - Functions of Cortisol: - Impulses transmitted from the periphery and processed o Acts synergistically with epinephrine and glucagon to within the CNS and activates reflexive efferent impulses induce catabolic state - Role of Effector: o Stimulates gluconeogenesis and insulin resistance 1. Expand plasma volume resulting in hyperglycemia as well as muscle cell 2. Maintain peripheral perfusion, and tissue O2 deliver protein breakdown (proteolysis) and lipolysis to 3. Restore homeostasis provide substrates for hepatic gluconeogenesis - Other stimuli: pain, hypoxemia, hypercarbia, acidosis, o Retention of sodium and water by the nephrons of the infection, change in temperature, emotional arousal or kidney hypoglycemia RAAS A. Spinothalamic Tracts - Renin is released from the juxtaglomerular cells and the release - Transmits the sensation of pain is caused by: - Resulting in activation of the hypothalamic – pituitary - o Decreased renal artery perfusion adrenal axis and autonomic nervous system including o Beta adrenergic stimulation direct sympathetic stimulation of the adrenal medulla to o Increased renal tubular sodium concentration release catecholamines (epinephrine and norepinephrine) - Renin catalyzes the conversion of angiotensinogen (from the B. Baroreceptors liver) to angiotensin I which is then converted to angiotensin II - Volume receptors sensitives to changes in both chamber by ACE (produced by the lungs) pressure and wall stretch present within the atria of the - Angiotensin I: NO significant functional activity heart, activated with low volume hemorrhage or mild - Angiotensin II: potent vasoconstrictor of both splanchnic and reductions in right atrial pressure peripheral vascular beds. - Receptors in the aortic arch and carotid bodies respond to - It also stimulates secretion of aldosterone, ACTH and ADH alterations in pressure or stretch of the arterial wall - Aldosterone: a mineralcorticoid that acts on nephron to responding to larger reductions in intravascular promote reabsorption of sodium and (as a consequence) water volume or pressure o Potassium and hydrogen ions are lost in the urine in - Normally inhibits induction of the ANS, but when activated exchange for sodium these receptors diminish their output, disinhibiting the ADH or Arginine Vasopressin ANS, increasing output via sympathetic activation at the - Released by the pituitary in response to: vasomotor centers producing centrally mediated o Hypovolemia constriction of peripheral vessels o Changes in circulating blood volume sensed by C. Chemoreceptors baroreceptors and left atrial stretch receptors - Found in the aorta and carotid bodies o Increased plasma osmolality detected by hypothalamic - Sensitive to changes in O2 tension, H+ ion concentration osmoreceptors and CO2 levels - Epinephrine, angiotensin II, pain and hypergylcemia increases - Stimulation -> production of ADH 1. Coronary Vasodilation - Acts on distal tubule and collecting duct of the nephrons to 2. Bradycardia o Increase water permeability 3. Splanchnic & skeletal circulation vasoconstriction o Decreased water and sodium losses D. Variety of protein and nonprotein mediators o Preserve intravascular volume - Histamine, cytokines, eicosanoids and endothelins - In hypovolemic state, acts as a potent mesenteric - Produced at the site of injury as part of the inflammatory vasoconstrictor, shunting circulating blood away from response, acts as afferent impulse to induce a host response splanchnic organs - In shock state, may contribute to intestinal ischemia and predispose to intestinal mucosal barrier dysfunction - Increases hepatic gluconeogenesis and increases hepatic glycolysis - In septic states, endotoxin directly stimulates arginine - Acidosis leads to changes in calcium metabolism and vasopressin (independent of blood pressure, osmotic or signaling intravascular volume changes) - - Proinflammatory cytokines also contribute to release of Effects of Catecholamines: vasopressin - Processes increased by catecholamines: Circulatory Homeostasis o Hepatic glycogenolysis A. Preload o Gluconeogenesis B. Ventricular Contraction o Ketogenesis - Franks Starlings Curve: strength of force of ventricular o Skeletal muscle protein breakdown contraction as a function of preload. o Adipose tissue lipolysis - If there are a lot of preload - the heart stretches more- - Cortisol, glucagon and ADH also contribute to the catabolism stronger contraction of ventricles during shock C. Afterload - Epinephrine induces further release of glucagon and - Force that resists myocardial work during contraction inhibits release of insulin resulting to: - Arterial pressure is a major component and influences the o Catabolic state with glucose mobilization ejection fraction o Hyperglycemia D. Microcirculation o Protein breakdown - Microvasculature bed is innervated by the sympathetic o Negative nitrogen balance nervous system and has a profound effect on the larger o Lipolysis arterioles o Insulin resistance during shock and injury - In hemorrhage, this vessel constricts but on septic or - The underuse of glucose by peripheral tissue preserve it for neurogenic, they dilate the glucose-dependent organs such as heart and brain - Other vasoconstrictors: vasopressin, angiotensin II and endothelin 1 Cellular Hypoperfusion - Pathophysiologic response of microcirculation in shock: - Crowell, 1961- hypoperfused cells and tissue experience o Failure of integrity of the endothelium of the what has been termed “oxygen debt” microcirculation - due to dysfunction of energy- - O2 debt - deficit in tissue oxygenation over time dependent mechanisms o normal circumstances cells can “repay” the O2 o Intracellular swelling - multifactorial debt during reperfusion o Recruitment of segmenters and platelet - higher - Magnitude of the O2 debt correlates with the severity and resistance of microcirculation duration of hypoperfusion o Extracellular fluid deficit - due to decreased o The more severe the hypoperfusion and longer the capillary hydrostatic pressure secondary to changes condition the more O2 debt will happen hence more in blood flow and increased cellular uptake of fluid compensation. It is a need for the oxygen demand o Capillary leak - dysfunction in secondary to to catch up in order for homeostasis to happen activation of endothelial cells by circulating - Changes in Cellular Gene Expression inflammatory mediators generated in septic or o The DNA binding activity of a number of nuclear traumatic shock transcription factors is altered by hypoxia and - Lead to diminished capillary perfusion: production of O2 or nitrogen radicals which are o Endothelial cell swelling produced by shock ((+) ROS, RNS) o Dysfunction o Other gene products increased by shock o Recruitment of PMN and platelets § Heat shock proteins Metabolic Effects § Vascular endothelial growth factor - Cellular metabolism is based on the hydrolysis of ATP (VEGF) o Splitting of the phosphoanhydride bond of the § inducible Nitric Oxide Synthase (iNOS) terminal or gamma-phosphate from ATP is the § Cytokines source of energy for most processes Immune and Inflammatory Response o Majority of ATP is generated in our bodies through Danger Signaling aerobic metabolism in the process of oxidative - Damage-associated molecular patterns (DAMPs) phosphorylation in the mitochondria o endogenous molecules are capable of signaling the o Process is dependent on O2 availability which serves presence of danger to surrounding cells and tissues as final electron acceptor in the ETC (proposed by Matzinger) - As O2 tension decreased, oxidative phosphorylation decreases, o recognized by cells surface receptors to effect and generation of ATP is slowed down intracellular signaling that primes and amplifies the o (+) anaerobic metabolism & glycolysis immune response (2 effects good or bad) - Glycolysis (is not an efficient process) only 2 mol of ATP is produced from 1 mol of glucose - Complete oxidation produces 38 mol of ATP per 1 mol of glucose - Under hypoxic conditions, in anaerobic metabolism, pyruvate is converted to lactate leading to intracellular metabolic acidosis (if it is in a local area: spasm, pain)
Consequences that are secondary to Metabolic Changes:
- Depletion of ATP potentially influence all ATP-dependent cellular processes: o Maintenance of cellular membrane potential (no traveling of impulse) o Synthesis of enzymes and proteins o Cell signaling o DNA repair mechanisms (paracrine function) - Decreased intracellular pH influences vital cellular functions Cytokines / Chemokines - Changes will lead to changes in gene expression within the - Substances released very early during changes in the body cell specifically inflammation (innate immune response) o Normal enzyme activity - Innate immune response can help restore homeostasis, or if o Cell membrane ion exchange excessive, it can promote cellular organ dysfunction o Cellular metabolic signaling 4. IL-6 - Elevated levels correspond with mortality in shock states - Contributes to lung, liver, and gut injury after hemorrhagic shock - Play a role in development of diffuse alveolar damage and ARDS (acute respiratory distress syndrome) - Along with IL-1, they are: o Mediators of hepatic acute phase response to injury o Enhance the expression and activity of complement,C-reactive protein, fibrinogen, 1. Tumor Necrosis Factor Alpha (THF-alpha) haptoglobin, amyloid A and a1-antitrypsin - One of the earliest potent proinflammatory cytokines o Promote neutrophil activation released in response to injurious stimuli 5. IL-10 - Released by: - Anti-inflammatory cytokine that may have o Monocytes immunosuppressive properties o Macrophages - Associated with depressed immune function and o T-cells increased susceptibility to infections - Peaks within 90 minutes of stimulation and returns to - Secreted by T-cells, monocytes and macrophages baseline by 4 hours - IL-10 inhibits: - Induced by: o Pro-inflammatory cytokine secretion o Bacteria or endotoxin and leads to development o O2 radical production by phagocytes of shock and hypoperfusion (most commonly o Adhesion molecule expression observed in septic shock) o Lymphocyte activation o Hemorrhage 6. Chemokines o Ischemia - Specific set of cytokines that have the ability to induce - Functions of TNF-a: chemotaxis of leukocytes o Produce peripheral vasodilation - Chemotaxis- is the property to let the immune cells migrate o Activate release of other cytokines to the sight of injury o Induce procoagulant activity - Involved in: o Stimulate a wide array of cellular metabolic o Immune system development changes o Immune surveillance - TNF-a (deadly!) levels correlate with mortality in models of o Immune priming hemorrhage o Effector response - Increase in serum TNF-a levels in trauma patients is less o Immune regulation than in septic patients - During stress response, it contributes to muscle protein Complement breakdown and cachexia (Cancer patient have increase - Marker of severity and injury TNF-alpha) - Activated complement factors (C3a, C4a, C5a) are potent mediators of 2. Interleukin - 1 (IL-1) o Increased vascular permeability - Actions similar to TNF-a o Smooth muscle contraction - Short half life of 6 minutes o Histamine and arachidonic acid by product release - Primarily acts in paracrine fashion to modulate local cellular o Adherence of neutrophils to vascular endothelium responses vs TNF which is more generalized - Acts synergistically with endotoxin top induce the release of - Produces a febrile response to injury by activating the TNF-a and IL-1 prostaglandins and causes anorexia by activating the - Development of ARDS and MODS in trauma patients satiety center correlates with intensity of complement activation - Augments the secretion of: o ACTH (related to stress) Neutrophils o Glucocorticoids - First cells to be recruited at the site of injury o B-endorphins - PMNs remove infectious agents, foreign substance and - Stimulate the release of other cytokines (together with TNF- nonviable tissue through phagocytosis alpha): - Activated PMNs and their products may produce cell injury o IL-2 and organ dysfunction o IL-4 - Generate and release a number of substances that may o IL-6 induce cell or tissue injury, such as: o IL-8 o Reactive O2 species o Granulocyte-macrophage colony stimulating o Lipid peroxidation products factor (increase macrophage) o Proteolytic enzymes (lysosome) o Interferon-y o Vasoactive mediators 3. Interleukin – 2 (IL-2) - Oxygen free radicals induce lipid peroxidation, inactivate - Produced by activated T-cells in response to variety of enzymes and consume antioxidants stimuli and activates other lymphocytes subpopulations and natural killer cells. Cell Signaling - Role is still not confirmed in shock, current postulates - Signaling pathways are altered by changes in: include: - Intracellular calcium (Ca2+) concentrations regulate many o Increased IL-2 secretion promotes shock- aspects of cellular metabolism and changes of Ca2+ levels induced tissue injury and the development of and Ca2+ transport is seen in shock shock - Alteration of Ca2+ regulation to: o Depressed IL-2 contributes to depression in o Direct cellular injury immune function after hemorrhage that o Changes in transcription factor activation increased the susceptibility of patients who o Alteration in the expression of genes important develop shock to suffer infections in homeostasis o Overly exuberant pro-inflammatory activation, o Modulation of the activation of cells by shock- promotes tissue injury, organ dysfunction, & induced hormones or mediators immune suppression Effects of Oxygen Radicals on the Intracellular Signaling Cascade - Direct pressure must be applied and sustained to minimize - Intracellular signaling cascade consists of a series of kinase ongoing blood loss that transmit and amplify the signal through phosphorylation TREATMENT: Control ongoing hemorrhage of target proteins o Treatment instituted concurrently with diagnostic - The O2 radicals produced during shock and intracellular evaluation redox state are known to influence the activity of components o Patients who fail to respond to initial of the intracellular cascade, such as: resuscitation should be assumed to have o Protein tyrosine kinase ongoing active hemorrhage from large o Mitogen activated kinase vessels and require prompt operative o Protein kinase C intervention → bring patient to OR immediately - Appropriate priorities in patients: FORMS OF SHOCK o Secure the airway HYPOVOLEMIC / HEMORRHAGIC SHOCK o Control the source of blood loss - Most common cause of shock is loss of circulating o Intravenous volume resuscitation volume from hemorrhage (due to surgery/trauma) - Active bleeding patient cannot be resuscitated until control - Response of the body to acute blood loss → decreased of ongoing hemorrhage is achieved baroreceptor stimulation → decreased inhibition of TREAMTMENT: Damage control resuscitation vasoconstrictor centers, increased chemoreceptor - begins in the emergency department and continues into stimulation of vasomotor centers, diminished output from the OR up to the ICU atrial stretch receptors → increases vasoconstriction and o Initial resuscitation: limit systolic BP (SBP) peripheral arterial resistance around 80-90 mmHg - Hypovolemia induces sympathetic stimulation leading to: o Prevent renewed bleeding from recently clotting o Epinephrine and Norepinephrine release vessels o Activation of the renin-angiotensin cascade o Warm the patient & prevent coagulopathy o Increased vasopressin release § Development of hypothermia in the - Peripheral vasoconstriction + lack of sympathetic effects bleeding patient is associated with on cerebral and coronary vessels + local autoregulation → acidosis, hypotension and maintenance of cardiac and CNS blood flow coagulopathy § Hypothermia is an independent risk factor for bleeding and death 2° to impaired platelet function and impairments in coagulation cascades o Resuscitation and intravascular volume resuscitation are accomplished with blood products (RBC, FFP, PLTs in equal numbers) and limited crystalloids - For patients with blunt injury (car crash, usually head - Initially, treatment is empiric (ABCDE) trauma), an SBP of 110 mmHg is more appropriate o Secure airway - For patients with penetrating injury (stab wound, gunshot o Volume infusion initiated while the search for the wound), a goal of SBP 80-90 mmHg may be adequate cause TREATMENT: Irreversible Shock o Shock in trauma or post-op patients is presumed - Patients who fail to respond to resuscitative efforts but with to be due to hemorrhage until proven otherwise control of hemorrhage have deteriorated to decompensate or - Clinical signs of shock: irreversible shock with peripheral vasodilation and resistance o Agitation to vasopressor infusion o Cool clammy extremities - Ongoing fluid requirements despite adequate control of o Tachycardia hemorrhage o Week or absent peripheral pulses - Persistent hypotension despite restoration of intravascular o Hypotension (atleast 25% of blood loss) volume necessitating vasopressor support - Elderly not very tolerant to hemorrhage: - Exhibit of futile cycle of acidosis, hypotension, and o Maintenance meds promote bleeding (aspirin, coagulopathy clopidogrel) - Fluid resuscitation → major adjunct to hemorrhage control o Atherosclerotic vascular disease o Crystalloids: mainstay of fluid of choice o Diminishing cardiac compliance o Increased risk of death treated with colloid vs o Inability to elevate HR or cardiac contractility in crystalloid (Colloid → requires crossmatch and response to hemorrhage blood products that are not readily available) o Overall decline in physiologic reserve o Severe hemorrhage: restoration of intravascular - Sites of blood loss sufficient to cause shock: volume should be achieved with blood products o External: carotid TREATMENT: Fluid resuscitation o Intrathoracic: pulmonary vessels - Hypertonic saline is evaluated as a resuscitative adjunct in o Intraabdominal: mesenteric vessels bleeding patients, & as the benefit of being immunomodulatory, o Retroperitoneal: renal vein/artery and may contribute to the decreases of incidence of perfusion- o Long bone fractures: femur mediated injury, less impairment of immune function, less brain - Each pleural cavity can hold 2-3L of blood and can be a swelling in multi-injured patients, contribute to decrease ARDS site of significant blood loss (HEMOTHORAX) and MOF (multiple organ failure) o Unstable patients - tube thoracostomy o PRBC: target Hgb of 7-9 g/dL § to drain the blood, because when lung o Damage control resuscitation: transfuse with pRBC, expands, it may cause cardiac FFP, platelet concentrate given in equal number tamponade o Increased platelet: appears to improve outcome o Stable patients- chest radiograph § Most pronounced in trauma patients with - Pelvic fracture: major retroperitoneal hemorrhage brain injury - Intraperitoneal hemorrhage: most common source § Maintain counts above 50x109 /L (<50, inducing shock spontaneous bleeding) - Non-trauma: GIT must always be considered o Minimization of heat loss and maintaining o Upper or Lower GIT bleeding normothermia --- Hypothermia → acidosis, o With hematemesis or bleeding hypotension, and coagulopathy → give warmers o Hx & PE is important § Independent risk factor for bleeding and death TRAUMATIC SHOCK - Starch-based colloid solutions should be avoided - Systemic response after trauma, combining the effects of soft - Antibiotics should be tailored to cover the responsible tissue injury, long bone fractures, and blood loss organism (give broad-spectrum, empiric even if you have not - MOF, including ARDS develop often in trauma patient, rarely yet isolated bacteria) in pure hemorrhagic shock patient - Role of surgery - source control - Hypoperfusion deficit is magnified by the pro-inflammatory - Catecholamines are used more often with norepinephrine activation that occurs following the induction of shock being the first line agent followed by epinephrine - At the cellular level, releases of DAMPs (RNA, Uric acid) → - Arginine vasopressin is often added with norepinephrine for (+) Pattern recognition receptors (PRRs) & TLR family of patients that develop resistance to catecholamines proteins - Dobutamine therapy is recommended for patients with - Examples of traumatic shock include: cardiac dysfunction as evidenced by high filling pressures and o Small-volume hemorrhage with by soft tissue low CO injury CARDIOGENIC SHOCK o Any combination of hypovolemic, neurogenic, - Circulatory pump failure leading to diminished forward flow cardiogenic, and obstructive shock that and subsequent tissue hypoxia, in the setting of adequate precipitates rapidly progressive intravascular volume proinflammatory action - Hemodynamic criteria: TREATMENT: o Sustained hypotension (SBP <90 mmHg for at least - Focused on correction of the individual elements to 30 mins) diminish the cascade of pro-inflammatory activation o Reduced cardiac index (<2.2L/min per square meter) - Prompt control of hemorrhage, adequate volume o Elevated pulmonary artery wedge pressure (>15 resuscitation to correct O2 debt mmHg) - Debridement of non-viable tissue - Mortality rate: 50-80% (ex. massive MI) - Stabilization of bone injures o Left anterior descending coronary art. supplies a big - Appropriate treatment of soft tissue injuries part of the heart, if this is obstructed, 2/3 of heart will be infarcted SEPTIC / VASODILATORY SHOCK - Acute, extensive MI is the most common cause and a - Result of the dysfunction of the endothelium and smaller infarction in a patient with existing left ventricular vasculature dysfunction also may precipitate this type of shock - Secondary to circulating inflammatory mediators and cells o Develops signs of cardiogenic shock within 24h after or as a response to prolonged and severe hypoperfusion onset of infarction, average within 7h - Hypotension and resistant to treatment with vasopressors DIAGNOSIS: result from failure of the vascular smooth muscle to - Cardiac exam: dysrhythmia, precordial heave, distal heart constrict appropriately tones - Catecholamine and RAAS are activated - Confirmation requires ECG and urgent echocardiography - Septic shock: Most frequently encountered vasodilatory - Blood chemistry- Troponins, CK-MB shock - Vasodilatory shock: final common pathway for profound TREATMENT: and prolonged shock of any etiology - Intubation and mechanical ventilation often are required, to o Other vasodilatory shock: decrease work of breathing and facilitate sedation of the ü Hypoxic lactic acidosis patient ü Carbon monoxide poisoning - Treatment of cardiac dysfunction: ü Decompensated & irreversible o Maintenance of adequate oxygenation hemorrhagic shock o Judicious fluid administration to avoid fluid overload ü Terminal cardiogenic shock and development of cardiogenic pulmonary edema ü Post-cardiotomy shock - Correct electrolyte abnormalities DIAGNOSIS: - Pain is treated with IV morphine sulfate or fentanyl Septic shock is a by-product of the body’s response to disruption - Dysrhythmias and heart block must be treated with anti- of the host-microbe equilibrium, resulting in invasive or severe arrhythmic drugs (amiodarone), pacing or cardioversion localized infection (shock) - Manifestation of sepsis (host response) - If profound cardiac dysfunction exists, inotropic support may o Fever be indicated to improve cardiac contractility and cardiac o Leukocytosis output o Hyperglycemia o Dobutamine: stimulates cardiac β1 receptors to o Enhanced cardiac output increase CO, but may: o Peripheral vasoconstriction § Vasodilate peripheral vascular beds o Tachycardia § Lower total peripheral resistance - Diagnostic criteria: manifestation of host response + § Lower systemic blood pressure through identification of offending organism effects of β2 receptors o Identify offending organism through blood § Adequate preload (measure via CVP culture: extract from at least 3 sites N=8-10 cmH20) is essential prior to ü (+) isolated in at least 2 giving dobutamine - Patients with sepsis have evidence of an infection, as well o Dopamine stimulates vasoconstriction, β1 as signs of systemic inflammation receptors (cardiac stimulation) and β2 receptors - Severe sepsis is hypoperfusion with signs of organ (vasodilation) at low doses dysfunction § Preferred treatment for cardiac - Septic shock requires presence of severe sepsis, dysfunction in hypotensive patients associated with more significant hypoperfusion and § Tachycardia and increased peripheral systemic hypotension (circulatory failure) resistance from dopamine infusion may worsen myocardial ischemia TREATMENT: o Epinephrine stimulates α and β receptors and may - Beings with the assessment of airway and ventilation increase cardiac contractility & HR, may also have - Severely obtunded patients require intubation and ventilation intense peripheral vasoconstrictor effects that can to prevent respiratory collapse impair cardiac performance - Fluid resuscitation and restoration of circulatory volume with o Phosphodiesterase inhibitors (amrinone and balanced salt solutions is essential (at least 30 mL/kg with the milrinone) may be required on occasion in patients first 4-6 hrs) with resistant cardiogenic shock - Intra-aortic balloon pump: mechanical circulatory for those NEUROGENIC SHOCK with resistant cardiotonic and increased CO and improved - Diminished tissue perfusion as a result of loss of vasomotor coronary blood flow tone to peripheral arterial beds → increase vascular - Percutaneous transluminal coronary angiography is capacitance → decreased venous return → decreased recommended for patients with: (treatment of choice) cardiac output o Cardiogenic shock - Usually secondary to spinal injuries (cervical or high thoracic o ST elevation region) o Left bundle branch block o Disrupt sympathetic regulation of peripheral vascular o Less than 75 years old tone - Coronary artery bypass grafting (CABG) seems to be more - Causes: spinal cord trauma, neoplasm, spinal / epidural appropriate for patients with multiple vessel diseases or left anesthesia main coronary artery diseases - Acute spinal cord injury results in activation of multiple secondary injury mechanisms: OBSTRUCTIVE SHOCK o Vascular compromise to the spinal cord with loss - Heart cannot pump or expand effectively of autoregulation, vasospasm and thrombosis - Most commonly due to presence of tension pneumothorax o Loss of cellular membrane integrity and impaired o Increased intrapleural pressure secondary to air energy metabolism accumulation, pushes mediastinum to side and o Neurotransmitter accumulation and release of free affects the heart radicals - Cardiac tamponade occurs when sufficient fluid has DIAGNOSIS: accumulated in the pericardial sac to obstruct blood flow to - Classic description of neurogenic shock: the ventricles (limited ventricular filling in diastole) o Hypotension with bradycardia - Pericardial pressure is the major determinant of degree § Hypotension is usually with of hypotension tachycardia to compromise cardiac output (absence of reflexive DIAGNOSIS: tachycardia) - Diagnosis of tension pneumothorax should be made on o Warm extremities (loss of peripheral clinical examination vasoconstriction) - Findings include: o Motor and sensory deficits indicative of a spinal o Respiratory distress cord injury o Hypotension o Radiographic evidence of a vertebral column o Diminished breath sounds over one hemithorax fracture o Hyperresonance to percussion o Cardiac dysrhythmias, hypotension may occur o Jugular venous distention up to 14days after SC injury (monitoring is o X-ray: Shift of mediastinal structures to the required) unaffected side with tracheal deviation - FOR CARDIAC TAMPONADE TREATMENT: o CXR: provide trajectory information - Airway, ventilation, Fluid resuscitation o ECG: preferred test for diagnosis of cardiac o Often respond tamponade - Vasoconstrictor to improve peripheral vascular tone, o UTZ: detect myocardial status if there is fluid decrease vascular capacitance, and increase venous § Large volume of fluid, right atrial return collapse, distensibility of right ventricle o Should only be considered once hypovolemia is excluded TREATMENT: - Vasoconstrictors: - Needling: pleural space can be decompressed with a o 1st line of medication: Dopamine large caliber needle (gauge 14,15) at mid-clavicular line 2nd o Phenylephrine (α agonist) is used in patients ICS who are not responsive to dopamine - Chest tube thoracotomy (CTT) is the definitive treatment o Typically lasts 24 to 48 hours for tension pneumothorax placed at the 4th ICS at the o Cardiac dysrhythmias and hypotension may anterior axillary line occur up to 14 days after spinal cord injury - Pericardiocentesis to diagnose pericardial blood and potentially relieve tamponade may be used o Potential to produce cardiac injury o Mapoke yung heart <3 - Diagnostic pericardial window o Most direct method to determine the presence of blood within the pericardium, performed through either subxiphoid or transdiaphragmatic approach o Best performed at the operating room under GA - Diagnosis of cardiac tamponade o Beck’s triad - collection of signs associated with acute cardiac tamponade § Hypotension (low arterial BP) § Distant, Muffled heart sounds § Neck vein distention (NV: 6 - 8cm H2O) o Narrowed pulse pressure o Pulsus paradoxus § Heart sounds disappear when px inhales, heard only on exhalation (when lung pressure is released) § Cardiac rate varies during inhale/exhale ENDPOINT IN RESUSCITATION o Base deficit and volume of blood transfusion required in the first 24 hours – better predictors of mortality than Goal of treatment: to restore adequate organ perfusion plasma lactate - Resuscitation is complete when: o Base deficit: amount of base in millimoles required to o O2 debt is repaid titrate 1L of whole blood to a pH of 7.40 with the sample o Tissue acidosis is corrected fully saturated with O2 at 37oC (98.6oC) and a partial o Aerobic metabolism is restored pressure of CO2 of 40 mmHg - Optimizing outcome in bleeding patients – measure by ABG o Early control of hemorrhage o Base deficit in the first 24 hours: o Adequate volume resuscitation (RBC & crystalloid) § Mild (3-5 mmol/L) - Expedient operative resuscitation - mandatory § Moderate (6-14 mmol/L) - Attempts to stabilize an actively bleeding patient not in OR are § Severe (15mmol/L) – 70% mortality inappropriate ✓ Require 2x volume of fluid infusion & - Compensated shock: normal BP, HR, UO 6x more BT in 1st 24hrs o Inadequate tissue perfusion § Directly correlated with mortality, organ failure § Increase lactate or decrease mixed venous o Factors may compromise utility of base deficit O2 saturation § IV bicarbonate, hypothermia, hypocapnia, § 3x infection than normal lactate (12hr) heparin, ethanol, ketoacidosis § Mortality – 4x if with infection o Lactate and base deficit – indicate global tissue acidosis. § Injury severity score, occult hypotension Focus on systemic endpoints. (lactic acidosis) >12 hrs are independent o Gastric tonometry – focus on tissue specific endpoints predictors of infection § Assess GIT perfusion - Divisions: § CO2 in gastric mucosa sampled via NGT o Systemic or global parameters: § Assume gastric HCO3 = serum level § Vital signs § pHi (gastric intramucosal pH) § Cardiac output ✓ should be > 7.3 § Pulmonary artery wedge pressure ✓ good prognostic indicator § O2 delivery and consumption o NIR – Near Infrared Spectroscopy § Lactate and base deficit § Measure tissue O2 o Tissue-specific parameters § Measure redox state of cytochrome A, A3 § Gastric tonometry § Tissue pH, O2, CO2 levels ✓ Correlated with tissue lactate § Near infrared spectrometry elevation o Cellular parameters o Decoupled oxyhemoglobin and cytochrome A, A3 = § Membrane potential redox dysfunction = higher organ failure § ATP o Tissue pH, O2, and CO2 concentration - Assessment of Endpoints in Resuscitation § Subcutaneous sites, muscle, and bladder o Inability to repay O2 debt o Right Ventricular End – Diastolic Volume (RVEDVI) § Predictor of mortality and organ failure § Accurate prediction of preload for cardiac § Directly correlated to probability of death index than does pulmonary artery wedge § Direct measurement is difficult pressure o Left Ventricular Power Output (LVP) • BP, HR, UO, CVP, Pulmonary § >320 mmHg L/min/m2 – with improved artery occlusion pressure – poor indicators clearance of base deficit § Serum lactate, base deficit – correlate with O2 debt o Lactate § Generated in insufficient O2 setting § Metabolized by liver (50%), kidneys (30%) § Admission lactate level, highest lactate level, & time to normalized – important prognostic indicators for survival § Survival normalization of lactate: 100% within 24H 78% between 24-48H 14% > 48H