Shock Management and Clinical Signs Quiz

Shock

• Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen delivery to meet cellular metabolic needs. It results in cellular and tissue hypoxia.
• Shock is defined as a state of cellular and tissue hypoxia caused by reduced oxygen delivery, increased oxygen consumption, or inadequate oxygen utilization. It commonly presents as hypotension (reduced tissue perfusion), but can also present as hypertensive or normotensive.
• Shock is initially reversible, but must be recognized and treated immediately to prevent irreversible organ damage.
• "Undifferentiated shock" is when the cause of shock is unknown.

Relevant Physiology

• Cardiac output (CO) is calculated as stroke volume (SV) multiplied by heart rate (HR).
• Preload is the myocardial sarcomere length just before contraction.
• Afterload is the resistance to ventricular ejection, the load the heart must eject blood against.
• Contractility is the change in peak isometric force at a given initial fiber length (end-diastolic volume).

Determinants of Preload

• Factors affecting ventricular filling include intrathoracic pressure, atrial pressure, right atrial pressure, mean systemic filling pressure, total venous blood volume, resistance to venous return, and venous vascular compliance.

Determinants of Afterload

• Wall stress is defined by Laplace's Law (P × r/T), where P is ventricular transmural pressure, r is ventricular radius, and T is ventricular wall thickness.
• Input impedance, during systole, depends on arterial compliance, blood column inertia, and ventricular outflow resistance and the length of the arterial tree, blood viscosity, and vessel radius.

Determinants of Contractility

• Increased preload increases the force of contraction.
• Increased afterload - increases end-systolic volume and sarcomere length = increased force of contraction.
• Heart rate affects contractility (Bowditch effect). Higher heart rates reduce intracellular calcium, leading to increased force of contraction.
• Other determinants include catecholamines, ATP availability, temperature, and hormones (e.g., thyroid, glucagon). Calcium plays a crucial role.

Clinical Diagnosis of Shock

• Neurologic: altered mental status (agitation, bradypsychic, bradylalia, coma).
• Pulmonary: tachypnea.
• Cardiac: hypotension (MAP < 65 mmHg or significant drop from baseline), bradycardia, tachycardia (>120 bpm associated with profound bleeding in hemorrhagic shock).
• Renal: shock index (HR / BP) > 0.8 is suggestive of hemodynamic instability, low urine output (<0.5 ml/kg/h).
• Peripheral perfusion/temperature: decreased temperature in shock; warm peripheral skin temperature predicts septic shock. Skin mottling is a poor prognostic sign; capillary refill time is prolonged in shock

Types of Shock

• Cardiogenic shock: pump problem, including myocardial infarction, cardiomyopathy arrhythmias, myocarditis, valvular dysfunction, post-cardiopulmonary bypass, intrinsic depression (SIRS related).
• Obstructive shock: pipes problem: pulmonary hypertension, pulmonary/air embolism, tension pneumothorax, cardiac tamponade, positive pressure ventilation, mediastinal tumors, high spinal anesthesia.
• Distributive shock: tank problem. Hypovolemic: hemorrhage, trauma, surgery, obstetric. Examples: traumatic, gastric ulcers, post-partum bleedings, non-hemorrhagic (e.g., intestinal losses, renal losses, burns). Septic (including anaphylactic): sepsis, sepsis coupled with high mean arterial pressure and blood lactate level > 2 mm/L.

Cardiogenic Shock: Definition

• Cardiogenic shock is the final common pathway in which cardiovascular disease causes circulatory failure, hypoperfusion, and eventual end-organ dysfunction.

Cardiogenic Shock: Classification

• SCAI Shock classification stages (E, D, C, B, A) outline the severity of cardiogenic shock based on hypoperfusion and hemodynamic instability.

Cardiogenic Shock: Phenotypes & Severity

• Different patterns of ventricular function, filling pressures, peripheral vascular tone, and congestion are important to consider.
• The end stage of cardiogenic shock includes severe lactic acidosis, RV congestion, greater shock severity, and multiple organ failure.
• Hemodynamic profiles, laboratory biomarkers, and clustering of "omics" data help evaluate the severity and phenotype of cardiogenic shock.

Cardiogenic Shock: Monitoring

• Vital signs (blood pressure, heart rate, respiratory rate, pulse oximetry), urine output, laboratory values (ureaa, creatinine, liver function tests, lactate), and basic echocardiography are essential
• Advanced monitoring, including cardiac ultrasound (e.g., using apical 4-chamber, 2-chamber, 5-chamber, and long-axis views), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), and superior vena cava (SVC) and inferior vena cava (IVC) assessment are crucial.

Cardiogenic Shock: Management

• Treat the underlying cause of the shock acutely, including oxygen supplementation, using high-flow oxygen therapy, non-invasive or invasive mechanical ventilation, inotropic support (e.g., dobutamine, Milrinone, Levosimendan), volume optimization (administration, reduction).
• Consider mechanical circulatory support (e.g., intra-aortic balloon pump [IABP], venoarterial ECMO [VA-ECMO]) as a bridge to recovery, heart transplant, or other definitive treatment.

Obstructive Shock: Cardiac Tamponade

• Cardiac tamponade results from pericardial pressure exceeding cardiac filling pressures, leading to reduced venous return, cardiac chamber shrinkage, stroke volume decrease, and blood pressure drop.
• Causes include idiopathic (viral inflammation), infectious (viral, bacterial, fungal, parasitic), non-infectious (autoimmune or autoinflammatory, neoplasms (metastatic, or primary), cardiac (early infarction pericarditis, myocarditis, dissecting aortic aneurysm), trauma, iatrogenic complications.
• Diagnosis relies on physical examination (tachycardia, hypotension, elevated jugular venous pressure, pulsus paradoxus), together with echocardiography, which typically displays pericardial effusion and chamber collapse.
• Management involves urgent pericardial fluid drainage, commonly through percutaneous pericardiocentesis, and/or surgical drainage if percutaneous access is not possible.

Obstructive Shock: Pulmonary Embolism

• Increased RV afterload results from pulmonary artery obstruction, leading to RV dilation, TV insufficiency, RV wall tension, neurohormonal activation, myocardial inflammation, and intrapulmonary A-V shunting; and RV ischemia and hypoxic injury.
• Diagnosis relies on physical examination (tachycardia, hypotension, low respiratory rate, respiratory distress, or cyanosis) alongside echocardiography assessment (e.g., enlarged right ventricle, dilated RV with basal RV/LV ratio > 1.0, flattened intraventricular septum, distended inferior vena cava with diminished inspiratory collapsibility, and abnormal tricuspid annular plane systolic excursion).
• Management includes anticoagulation, thrombolytic therapy, surgical embolectomy, and possibly catheter-directed treatment.

Obstructive Shock: Tension Pneumothorax

• Tension pneumothorax results from the increased pressure within the pleural cavity when air continuously enters but cannot escape. It causes the lung to collapse; the mediastinum shifts from the affected side; and subsequently, blood flow is negatively compromised, cardiac output is reduced, and blood pressure falls.
• Diagnosis involves detection of a tracheal deviation in an upright chest radiograph. Treatment involves insertion of a needle or thoracostomy tube to release the air from the pleural space.

Distributive Shock: Septic Shock

• Sepsis is defined as widespread host inflammatory responses to infection. Septic shock is a subset of sepsis with abnormalities in cellular and metabolic function that increases mortality risk.
• Sepsis involves suspected or documented infection coupled with a SOFA score >2. Septic shock involves this along with vasopressor requirement to maintain MAP of 65 mm Hg, and blood lactate > 2 mmol/L without hypovolemia.

Distributive Shock: Anaphylactic Shock

• It is characterized by profound reduction in venous tone, with features of hypovolemic shock (including fluid extravasation), causing depressed myocardial function. It also typically involves rapid onset of the illness (minutes to hours), and simultaneous involvement of the skin (hives, flushing, urticaria) and mucosal tissues, or both (lips, tongue, and uvula swelling) alongside respiratory compromise (dyspnea, wheeze, stridor, reduced peak flow, and hypoxia). Circulatory compromise comprises reduced blood pressure with associated end-organ dysfunction (e.g., hypotension, collapse, syncope, incontinence) or gastrointestinal symptoms (severe crampy abdominal pain, severe repetitive vomiting).
• Cardiac effects can include myocardial ischemia (often due to coronary vasospasm) which can lead to myocardial infarction. Additionally, conduction defects can arise and include atrial and ventricular arrhythmias. Post-menopausal women are particularly vulnerable to stress cardiomyopathy (Takotsubo syndrome) during anaphylaxis. Also, there are pulmonary effects, including upper airway symptoms (sneezing, rhinorrhea, dysphonia, laryngeal edema, laryngeal obstruction, and oropharyngeal angioedema) and lower airway symptoms (cough, wheeze, pulmonary hyperinflation, edema, hemorrhage, respiratory failure, respiratory arrest).

Hypovolemic Shock (Hemorrhagic Shock)

• A person dies from injury approximately every 3 minutes, and 40% of these deaths are due to major hemorrhage or consequences. Death from hemorrhage is early, with 60% of deaths occurring within the first 3 hours.
• Classified into four classes (I, II, III, and IV) based on blood loss percentage and clinical presentation (e.g., varying degrees of hypotension, tachycardia, decreased capillary refill time).
• Causes include trauma, surgery, obstetrical issues (antepartum, postpartum), and medical issues (e.g., bleeding peptic ulcer disease, gastritis, esophagitis, esophageal varices, and anticoagulants).
• Management prioritizes controlling bleeding and quickly mobilizing resources to address hypovolemia rapidly (e.g., surgery, anesthesia, blood bank, and transfer to a trauma center). It is essential to avoid coagulopathy and hypothermia.
• Management includes using intravenous fluids judiciously, and if necessary, promptly administering blood products (red blood cells, plasma, and platelets) in a 1:1:1 ratio, using thromboelastography or similar testing to guide resuscitation.

Test your knowledge on the clinical features and management of shock. This quiz covers various types of shock, diagnostic indicators, and treatment protocols. Prepare to enhance your understanding of this critical medical condition.