NUR 411 - Adult Health III Exam 2 Study Guide

Adult Health III, NUR 411 – Exam 2 Study Guide

Care of the Patient in Shock
The Big Picture – Cardiac Output (CO)

  • Cardiac Output is a crucial measure of heart function.

    • Definition: Total blood amount the ventricle pumps out in 1 minute.

    • Calculation: Heart Rate x Stroke Volume = Cardiac Output

    • Normal Range: 4L to 6L per minute.

  • Key Drivers of CO: Changes can be achieved by altering one of three parameters:

    • Preload

    • Afterload

    • Contractility

The Three Factors of Stroke Volume

  • Stroke volume refers to the amount of blood ejected with each heartbeat and depends on three key factors:

    1. Preload (The Stretch)

    • Analogy: Like pulling back on a slingshot.

    • Definition: Amount of filling in heart chambers and stretching of cardiac muscle at end of diastole.

    • Frank-Starling Law: More stretch leads to a more forceful contraction (contracting heart muscle).

      • Result: More Stretch = Higher Stroke Volume

    • What Affects Preload:

      • Central Venous Pressure (CVP): Pressure of blood returning to the heart, increases with vasoconstriction.

      • Volume: Total blood volume influences preload.

      • Venous Return: Blood flow returning from the body.

    1. Afterload (The Resistance)

    • Analogy: Like pushing against a heavy door.

    • Definition: Tension the ventricle must generate to eject blood during systole.

    • What Affects Afterload:

      • Chamber pressure, volume, and wall thickness.

      • Left vs Right Heart Resistance:

        • Left Ventricle: Faces Systemic Vascular Resistance (SVR - hypertension increases it).

        • Right Ventricle: Faces Pulmonary Vascular Resistance (RV - hypertension increases resistance here).

    • Consequence: Higher afterload increases cardiac workload, leading to hypertrophy over time.

    1. Contractility (The Squeeze)

    • Definition: The strength of muscle contraction, independent of stretch/resistance.

    • Physiological Mechanism: Heart muscle cells generate force during contraction.

      • Increasing Force = Increasing Stroke Volume and Ejection Fraction.

    • Factors Increasing Contractility (Positive Inotropes):

      • Sympathetic Stimulation (fight or flight response).

      • Catecholamines (adrenaline).

      • Inotropic Drugs.

    • Factors Decreasing Contractility (Negative Inotropes):

      • Vagal Stimulation (rest and digest period).

      • Advanced Heart Failure.

      • Acute Myocardial Infarction (heart attack) or Chronic Ischemic Disease.

The Vital Number – Mean Arterial Pressure (MAP)

  • MAP is often a better indicator in shock than classic BP readings because it assesses organ perfusion.

  • Definition: Average arterial pressure during one cardiac cycle.

  • Importance: Serves as the perfusion pressure for vital organs.

  • Critical Thresholds:

    • MAP > 60: Minimum to sustain organ viability in an average adult.

    • MAP < 60: Not sufficient to perfuse organs leading to ischemia and failure.

  • How to Calculate MAP:

    • Given the heart rests twice as long in diastole as it works in systole, the formula gives more weight to diastolic pressure.
      MAP=DBP×2+SBP3\text{MAP} = \frac{{\text{DBP} \times 2 + \text{SBP}}}{3}

    • Example Calculation (BP of 120/80):

      • Double Diastolic: $80 \times 2 = 160$

      • Add Systolic: $120 + 160 = 280$

      • Divide by 3: 2803=93.3\frac{280}{3} = 93.3

      • MAP = 93.3 mmHg

Goals in Treating Shock

  • Priority: Maintain organ viability through effective blood circulation.

  • Primary Goal: Maintain adequate Cardiac Output (4L-6L) to ensure organ perfusion and adequate oxygen delivery.

  • Indicators of Success:

    • MAP: At least 60 mmHg (ideally between 60-70).

    • Systolic Blood Pressure (SBP): > 90 mmHg.

    • Oxygen Saturation: > 95%.

Hemodynamic Parameters and Normal Values

  • Cardiac Output (CO):

    • Normal Range: 4-6 L/min.

    • Definition: Total volume pumped by the ventricle per minute.

  • Cardiac Index (CI):

    • Normal Range: 2.4-4.0 L/min/m² .

    • Definition: Cardiac Output per body surface area for accurate assessment relative to body size.

  • Central Venous Pressure (CVP):

    • Normal Range: 2-4 mmHg.

    • Definition: Pressure in the right atrium from the blood volume.

  • Stroke Volume (SV):

    • Normal Range: 60-70 mL.

    • Definition: Volume of blood ejected with each heartbeat.

  • Systemic Vascular Resistance (SVR):

    • Normal Range: 900-1400 dynes/sec/cm⁻⁵.

    • Definition: Resistance against which the left ventricle pumps blood into systemic circulation.

    • Key Concept: An increase in SVR decreases cardiac output.

  • Pulmonary Vascular Resistance (PVR):

    • Normal Range: 30-100 dynes/sec/cm⁻⁵.

    • Definition: Resistance against which the right ventricle pumps blood into the pulmonary system.

What Is Shock?

  • Definition: It is a severe, whole-body continuum of inadequate fuel (oxygen) delivery to tissues and organs.

  • Core Problem: There is inadequate oxygen delivery to tissues leading to a systemic failure response.

  • Chain Reaction:

    • Oxygen and tissue perfusion requirements are unmet.

    • Leads to abnormal cellular metabolism.

    • Develops into a systemic life-threatening emergency.

Classifications of Shock

  • Shock is categorized according to the underlying cause of perfusion failure:

    • Hypovolemic: Low volume/fluid due to loss.

    • Cardiogenic: Heart’s failure to pump effectively.

    • Obstructive: Physical blockage hindering circulation (e.g., cardiac tamponade, pulmonary embolism).

    • Distributive: Circulatory blood volume is present but not adequately utilized (e.g., in sepsis, neurogenic, anaphylactic shock).

System-By-System Manifestations (Signs and Symptoms)

  • Compensatory Responses: When the body enters shock, it prioritizes blood flow to vital organs (brain, heart) while restricting it to other systems.

Cardiovascular (Heart and Vessels)

  • Compensatory Mechanisms:

    • Heart rate increases (tachycardia) in an effort to maintain cardiac output, yet may present as weak.

    • Reduced blood pressure with narrowed pulse pressure.

    • Central Venous Pressure (CVP) decreases reflecting reduced preload.

    • Peripheral Perfusion Impairments include:

    • Postural Hypotension (blood pressure drops on standing).

    • Collapsed veins (flat neck and hand veins).

    • Slow capillary refill times.

    • Diminished pulses in extremities.

Respiratory (Lungs)

  • Compensatory Mechanisms:

    • Increased respiratory rate (tachypnea).

    • Shallow breathing pattern (Kussmaul breathing).

    • Gas Exchange Changes:

    • PaCO₂ increases (carbon dioxide retention).

    • PaO₂ decreases (hypoxia).

    • Signs of cyanosis, especially around lips/nail beds.

Neuromuscular (Brain and Nerves)

  • Early Indicators: Anxiety, restlessness, and increased thirst (body requests more fluids).

  • Late Indicators:

    • Decreased CNS activity progressing to lethargy or coma.

    • Generalized muscle weakness.

    • Diminished or absent deep tendon reflexes.

    • Sluggish pupillary response to light.

Kidney (Renal System)

  • Highest risk for shutdown in shock situations:

    • Decreased urine output (urate retention).

    • Increased urine specific gravity (dark, concentrated urine).

    • Urine Contents:

    • Presence of sugar and acetone indicating stress response.

    • Possible proteinaceous fluid due to kidney permeability changes.

Gastrointestinal (Gut)

  • Perfusion shifts from gut to vital organs, slowing overall mobility.

    • Signs:

    • Decreased sounds or absent bowel sounds.

    • Symptoms of nausea/vomiting, constipation, abdominal pain.

Integumentary (Skin)

  • Skin Condition: Cool to cold, pallor progressing to mottled or cyanotic appearance.

  • Texture: Moist and clammy.

  • Mouth: Dry with a paste-like coating.

The Four Stages of Shock

  • Shock is progressive and may start unnoticed but escalates rapidly if not treated.

  1. Initial (Early) Stage

    • Phase Characteristics: Silent phase, difficult to detect signs externally.

    • MAP Change: Decrease by < 10 mmHg from baseline.

    • Clinical Signs: Slightly increased heart and respiratory rates; vital organs not yet disrupted.

  2. Nonprogressive/Compensatory Stage

    • Phase Characteristics: Body activates hormonal responses to restore pressure.

    • MAP Change: Decrease by 10-15 mmHg from baseline.

    • Hormonal Responses:

    • Renin secretion causing vasoconstriction.

    • Release of epinephrine/norepinephrine for strong vasoconstriction.

    • Antidiuretic hormone (ADH) leads to water retention.

    • Aldosterone causing sodium and water retention.

    • Clinical Signs: Decreased urine output and hypoxia in non-vital organs possible but not permanent damage yet.

  3. Progressive Stage

    • Phase Characteristics: Compensatory mechanisms fail; vital organs starving.

    • MAP Change: Sustained decrease of > 20 mmHg from baseline.

    • Clinical Signs:

    • Mental: A sense of impending doom, confusion, increased thirst.

    • Physical: Rapid/weak pulse, cool/moist skin, cyanosis in mucosa.

    • Renal: Anuria (no urine output).

    • Decreased oxygen saturation: drops by 5-20%.

  4. Refractory (Irreversible) Stage

    • Characteristics: Massive cell death due to insufficient oxygen. Body fails to respond to treatment.

    • Clinical Signs: Rapid loss of consciousness, non-palpable pulse, cold extremities, shallow respirations, unmeasurable oxygen saturation.

  • Multiple Organ Dysfunction Syndrome (MODS): A life-threatening complication arising from unresolved shock ultimately leading to failure and a cycle of toxicity and damage.

Hypovolemic Shock

  • Definition: Resulting from low circulating blood volume leading to decreased MAP.

  • Main Consequence: Oxygen needs unmet due to insufficient fluid.

  • Causes of Volume Loss:

    • External Loss:

    • Hemorrhage (trauma, GI bleeding, surgical).

    • Internal Loss:

    • Hemothorax, ruptured aortic aneurysm, hemorrhage into abdomen.

    • Fluid Loss:

    • Burns, severe diarrhea/vomiting, renal failure, or high-output states.

  • Clinical Manifestations:

    • Cardiovascular: BP (hypotension), pulse (tachycardia, weak).

    • Respiratory: increased rate, possible low saturation.

    • Renal: decreased output.

    • Skin: cool, clammy.

    • Neurological: decreased reflexes, confusion.

  • Management Goals:

    • Stop source of fluid loss and restore volume.

    • Non-Surgical: Fluid resuscitation through IV therapy.

      • Types of Fluids:

    • Crystalloids: Normal saline, ringers lactate.

    • Colloids: Proteins/starch-based solutions.

    • Blood products: PRBCs, FFP.

    • Drug Therapy:

    • Vasoconstrictors (e.g., Dopamine, Norepinephrine).

    • Inotropic agents (e.g., Dobutamine).

    • Myocardial perfusion enhancers.

  • Surgical Management: Depends on underlying cause (vascular repairs, wound repair, closure of bleeding ulcers).

Cardiogenic Shock

  • Definition: Impaired heart muscle function leading to poor pumping capability (typical following myocardial infarction).

  • Causes:

    • Structural: valve dysfunction, septal ruptures, papillary muscle rupture.

    • Rhythm Issues: bradycardia/tachycardia problems.

  • Clinical Manifestations: Similar to unresponsive conditions leading to inadequate perfusion.

  • Management Goals: Support heart function, relieve/blockage if present.

    • Drug Therapy: Nitrates, inotropes (to help heart squeeze).

    • Mechanical Interventions: IABP (intra-aortic balloon pump), PCI (coronary angioplasty).

Distributive Shock

  • Definition: Blood volume is intact but improperly distributed.

  • Causes:

    • Loss of sympathetic tone, vascular dilation.

  • Types are divided by what causes vessels to lose constriction:

    • Neural Induced: Lack of normal responsiveness to vasoconstrictive signals.

    • Chemical Induced: Severe allergic reactions or infections.

  • Sepsis Progression: Initial local infection leading to systemic inflammatory responses can destroy tissues and incapacitate organ function.

Anaphylactic Shock

  • Definition: Severe allergic reaction leading to life-threatening systemic effects.

  • Clinical Presentation: Symptoms: confusion, wheezing, tachycardia, hypotension, rash/urticaria.

  • Management Goals:

    • Priority to assess and manage the airway.

    • Administer epinephrine; change IV and administer fluids quickly.

Investigations and Treatment of Shock

  • Diagnostic Approach: Need to monitor vitals, signs of organ dysfunction, measure blood parameters (WBC, lactate).

    • Laboratory Assessments: Incorporate urine analysis, ABGs to measure the state of metabolic imbalances.

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