Leadership and Emotional Intelligence Quiz

Shock

• Shock is a syndrome of impaired tissue oxygenation and perfusion, resulting from one or more of the following mechanisms:
  • Inadequate cardiac output
  • Low blood oxygen content
  • Ineffective tissue perfusion (maldistribution of blood flow to tissues)
  • Impaired utilization of delivered oxygen (cellular or mitochondrial dysfunction)
• Essentially, shock occurs when oxygen demand exceeds supply.

Etiologies of Shock

• Reduced return to the heart (preload):
  • Intravascular volume loss (plasma loss)
  • Extravascular fluid loss (gastrointestinal, renal)
• Reduced total peripheral resistance (afterload):
  • Arterial vasodilation
  • Altered venous capacitance
  • Obstruction of filling
• Pump dysfunction:
  • Reduced contractility
  • Impaired relaxation
  • Abnormal rate or rhythm
  • Forward flow failure

Physiological Causes of Shock

• Decreased cardiac output:
  • Cardiac abnormalities decreasing heart's ability to pump blood (e.g., myocardial infarction, heart arrhythmias)
  • Factors decreasing venous return (e.g., obstruction to blood flow).
• Circulatory shock without diminished cardiac output:
  • Excessive metabolic rate
  • Abnormal tissue perfusion patterns

Tissue Oxygen Delivery

• Tissue oxygen delivery (DO2) is the process of delivering arterial oxygenated blood to tissues.
• Arterial oxygen content (CaO2) is calculated as: CaO2 = (1.34 x Hb x SaO2) + (0.0031 x PaO2) - Hb: Hemoglobin - SaO2: Hemoglobin oxygen saturation - PaO2: Partial pressure of oxygen in arterial blood
• Oxygen delivery to tissue (DO2) is the product of arterial oxygen content and cardiac output (CO): DO2 = CO x CaO2 = CO x [(1.34 x Hb x SaO2) + (0.0031 x PaO2)]

Tissue Oxygen Uptake

• Tissue oxygen uptake (VO2) is the amount of oxygen consumed by tissues.
• It is calculated by the difference between DO2 and the amount of oxygen in the returned venous blood (CvO2): VO2 = CO x (CaO2 - CvO2) = CO x 1.34 x Hb x (SaO2 - SvO2) - CO: Cardiac output - Hb: Hemoglobin - SaO2: Arterial oxygen saturation - SvO2: Venous oxygen saturation - CvO2: Venous oxygen content

Cardiac Output Determinants

• Heart rate (beats/min) x Stroke volume (mL/beat) = Cardiac output (L/min)
• Preload: Muscle length prior to contraction; influenced by ventricular end-diastolic volume, blood volume, posture, intrathoracic pressure, pericardial pressure, venous tone, rhythm, and heart rate. Venous return is the most important determinant of right ventricular preload.
• Afterload: Tension against which the muscle contracts; related to systemic vascular resistance. Right ventricular afterload is primarily determined by pulmonary vascular resistance (PVR).
• Contractility: Intrinsic property of the muscle related to the force of contraction, independent of preload and afterload. Increased by sympathetic nervous system activity. -Major factors affecting stroke volume include preload, afterload, contractility, wall motion abnormalities, and valvular dysfunction.

Pathophysiology of Shock

• Vascular Response:
  • Sympathetic nervous system increases heart rate and myocardial contractility, redistributing blood flow to vital organs.
  • Autoregulation of blood flow maintains cerebral and cardiac blood supply.
  • Release of vasoactive hormones (e.g., antidiuretic hormone) and renin-angiotensin system activation maintain intravascular volume.
• Microcirculatory Dysfunction:
  • Endothelial cell damage
  • Glycocalyx alteration
  • Coagulation activation
  • Microthrombi formation
  • Leukocyte and red blood cell alteration
• Cellular Injury:
  • Insufficient oxygen delivery prevents pyruvate from entering the TCA cycle.
  • Cellular energy stores are depleted, leading to impaired cellular systems and homeostasis.

Anaphylactic Reaction

• Anaphylaxis is a severe, rapid-onset, multi-systemic allergic reaction.
• It often involves IgE-mediated responses or IgE-independent events.
• Common triggers include antibiotics, food, and venom.

Cardiovascular/Metabolic Compensatory Responses to Shock

• Maintain mean circulatory pressure (venous pressure):
  • Fluid redistribution to vascular space from interstitium/intracellular space
  • Reduced renal fluid losses
  • Increased aldosterone and vasopressin
• Maximize cardiac performance: Increased contractility, sympathetic stimulation, and adrenal stimulation
• Redistribute perfusion: Extrinsic regulation of systemic arterial tone, optimization of oxygen unloading
• Cellular energy generation/utilization: Citric acid (Kreb) cycle, oxidative phosphorylation pathway, and other pathways

Stages of Shock

• Compensated/Nonprogressive:
  • Normal circulatory compensatory mechanisms restore function.
• Progressive:
  • Compensatory mechanisms fail; shock worsens.
• Irreversible:
  • All known therapies are inadequate to save life.

Nonprogressive Shock-Compensated Shock

• Baroreceptor reflexes
• Central nervous system ischemic response
• Reverse stress-relaxation of the circulatory system
• Increased renin secretion and angiotensin II formation
• Increased vasopressin secretion (antidiuretic hormone)

Classification of Hemorrhage

• Class I: Minor blood loss (e.g., 1 unit donation)
• Class II: Moderate blood loss (requiring crystalloid fluid resuscitation)
• Class III: Significant blood loss (requiring crystalloid and blood replacement)
• Class IV: Severe blood loss (often requiring massive transfusion)

Management of Hemorrhagic Shock

• Initial Step (1/2):
  • Establish airway and breathing
  • Control hemorrhage
  • Neurological assessment
  • Complete examination
• Initial Step (2/2):
  • Gastric dilation decompression
  • Urinary catheterization

Management of Cardiogenic Shock

• Acute pulmonary edema:
  • Give furosemide, morphine, oxygen/intubation
• Check blood pressure: -Systolic BP ≥ 100 mm HG: no signs/symptoms of shock -Systolic BP 70-100 mmHg: signs/symptoms of shock -Systolic BP <70 mmHg: signs/symptoms of shock (consider vasodilators/inotropic agents/intraortic balloon pumps/extracorporeal life support)

Distributive Shock

• Caused by excessive vasodilation, impairing blood distribution to organs.
• Common causes include sepsis and anaphylaxis.

Septic Shock

• A subset of sepsis with more severe circulatory, cellular, and metabolic abnormalities.
• Characterized by hypotension requiring vasopressors to maintain MAP above 65 mmHg despite adequate volume resuscitation, along with serum lactate >2 mmol/L.

Anaphylactic Shock

• A life-threatening hypersensitivity reaction resulting from an IgE-mediated response or a non-IgE event.
• It often involves multiple organ systems (e.g., skin, respiratory, cardiovascular) and can be fatal if not treated promptly.

Neurogenic Shock

• A devastating consequence of spinal cord injury (SCI).
• It manifests as hypotension, bradyarrhythmia, dysregulation, and temperature disturbances.

Obstructive Shock

• A form of shock caused by mechanical obstruction of blood flow to the heart, specifically the left ventricle.
• Common causes are tension pneumothorax, cardiac tamponade, and pulmonary embolus.

Treatment of Obstructive Shock

• Tension pneumothorax: Needle decompression
• Cardiac tamponade: Pericardiocentesis

Treatment of Anaphylactic Shock

• Stop the trigger.
• Maintain airway.
• Give epinephrine (adrenaline).
• Administer IV fluids.
• Administer other drugs (corticosteroids, antihistamines, bronchodilators) as needed.

This quiz explores key concepts related to leadership qualities and emotional intelligence in the workplace. It evaluates the distinctions between experts and novices, effective problem-solving traits, and approaches to personal development. Test your knowledge on the factors that enhance team collaboration and emotional intelligence.