Exam Study Guide 2 PDF

EXAM 2 Shock Overview Definition: Shock is a life-threatening condition where blood flow is insufficient to meet the body’s needs, leading to organ dysfunction. MAP: 2x Diastolic + Systolic DIVIDED by 3 Stages of Shock 1. Compensatory Stage: a. Symptoms: Normal BP, elevate...

EXAM 2 Shock Overview Definition: Shock is a life-threatening condition where blood flow is insufficient to meet the body’s needs, leading to organ dysfunction. MAP: 2x Diastolic + Systolic DIVIDED by 3 Stages of Shock 1. Compensatory Stage: a. Symptoms: Normal BP, elevated HR, normal CO, elevated RR. b. Treatment: Identify underlying cause, monitor VS for subtle changes, provide early interventions. 2. Progressive Stage: a. Symptoms: BP drops, MAP decreases, shallow RR, increasing HR, worsening LOC. b. Treatment: Support respiratory system, monitor BGL ( 90 bpm o Respiratory rate > 20 breaths per minute o WBC count > 12,000/mm³ or < 4,000/mm³ Pathophysiology Mechanisms: o Massive vasodilation  o Increased capillary permeability o Clot formation in microcirculation Effects: Imbalance between cellular oxygen supply and demand, leading to cell hypoxia and death. Sources of Infection Common sources include: o Catheters o Wounds o Lungs o Genitourinary (GU) tract o Gastrointestinal (GI) tract o Heart o Skin o Blood o Head High-Risk Groups Pediatrics and elderly Immunocompromised individuals Those with comorbidities Recent hospitalizations Sepsis survivors Prolonged antibiotic use Clinical Manifestations Tachycardia Tachypnea Warm, flushed skin; increased temperature Altered level of consciousness (ALOC) Decreased urine output (UO) Normal to low blood pressure (BP) Multiple Organ Dysfunction Lungs: Endothelial damage leads to edema and poor gas exchange. Heart: Leaky capillaries lead to low BP and blood volume. Kidneys: Low perfusion and hypoxia lead to renal failure. GI Tract: Hypoxia and stress can cause ulcers. Liver: Hypoperfusion and hepatocyte damage lead to liver failure.  Nervous System: Inflammatory molecules disrupt the blood-brain barrier (BBB), leading to edema and slowed cerebral function. Diagnostic Procedures Serum lactate levels Blood cultures (x2 from different sites before antibiotics) Cultures from suspected infection sources (wound, urine, sputum) Urinalysis (UA) Complete blood count (CBC) and comprehensive metabolic panel (CMP) Chest X-ray Sepsis Bundles 3-Hour Bundle: o Measure lactate level o Obtain blood cultures before antibiotics o Administer broad-spectrum antibiotics o Administer 30mL/kg IV fluid 6-Hour Bundle: o Administer vasopressors if hypotension persists (MAP > 65 mm Hg) o Re-evaluate lactate levels Nursing Interventions Provide oxygen to meet increased demands Establish IV access (preferably two or a central line) Initiate central venous pressure (CVP) monitoring (normal: 2-6 mmHg) Administer fluids and antibiotics (within 1 hour of arrival) Administer vasopressors (MAP > 65 mmHg) Measure urine output (>0.5 mL/kg/hr) Repeat lactate draw Monitor and control blood glucose levels (90-180 mg/dL) Septic Shock Defined as acute circulatory failure with refractory hypotension. Indicators of progression to septic shock include: o BP 70/38 after fluid bolus o Serum lactate > 2 mmol/L o Need for norepinephrine to maintain MAP > 65 mmHg o CVP > 12 mmHg ENDO Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Definition: Excessive release of ADH (vasopressin) from the pituitary gland, leading to water reabsorption by the kidneys and excretion of sodium, causing hyponatremia and hypervolemia. Risk Factors More common in children, elderly, and hospitalized patients. CNS disturbances: Stroke, hemorrhage, trauma, infection, mental illness. Malignancies: Primarily small cell lung cancer. Certain medications: Tegretol, Trileptal, SSRIs. Surgery: Hypersecretion of ADH in response to pain. Hormone deficiencies: Hypopituitarism, hypothyroidism. Secondary to diseases: HIV, hypothyroidism, pulmonary diseases. Hereditary: Mutation in vasopressin 2 receptors in kidneys. Assessment Findings Early symptoms: Nausea, vomiting, malaise. Altered level of consciousness (ALOC). Weight gain without edema. Signs of fluid volume excess: Hypertension, tachycardia, bounding pulses. Headache, lethargy, seizures. Severity of symptoms increases as sodium levels drop, potentially leading to permanent neurological damage and death. Laboratory Tests and Diagnostics Urinalysis: Increased sodium and urine osmolality. Blood work: Decreased blood osmolality, electrolyte panel, blood glucose, renal function (BUN, creatinine), lipid profile, liver function tests, serum cortisol, thyroid panel. Imaging: X-ray and CT if pulmonary disease is suspected. Schwartz and Bartter Clinical Criterion: o Serum sodium < 135 mEq/L. o Serum osmolality < 275 mOsm/kg. o Urine sodium > 40 mEq/L. o Urine osmolality > 100 mOsm/kg. o Normal skin turgor and BP.  o No other causes of hyponatremia. o Hyponatremia correctable by fluid restriction. Nursing Care Monitor ABCs and VS. Monitor neurological status and implement seizure precautions. Restrict fluids to prevent further hemodilution. Monitor weight and I/O. Monitor electrolytes and for signs of fluid overload (EKG, lung sounds, VS). Administer salt tablets or 0.9% sodium chloride if sodium is low. Administer loop diuretics if giving salt to decrease urine concentration. Provide a safe and calm environment. Identify underlying cause while monitoring fluid status and electrolytes. Pharmacology Demeclocycline: Corrects fluid and electrolyte imbalance by stimulating urine flow. Monitor renal function. Vasopressin antagonists (Tolvaptan, Conivaptan): Promote water excretion without sodium loss, rapidly increase sodium levels. Monitor liver function. Loop diuretics: Increase water excretion. IV fluid (hypertonic solution 3% sodium chloride): Increase sodium levels. Patient and Family Education Follow strict fluid intake guidelines. High salt and protein diet. Educate on signs and symptoms of hypo- and hypernatremia. Educate on seizure precautions and management. Compliance with treatment and medications. Diabetes Insipidus (DI) Definition: Deficiency of ADH (antidiuretic hormone), leading to reduced ability of kidneys to collect and concentrate urine, resulting in excessive urine production. Types 1. Primary DI: Damage or defect in hypothalamus or pituitary gland. 2. Secondary DI: Infection, tumors, head trauma, brain surgery affecting ADH production. 3. Nephrogenic DI: Kidneys unresponsive to ADH due to medications or kidney damage. Risk Factors Head injury, family history of DI, brain surgery, infections, metabolic disorders, tumors, radiation, certain medications (e.g., lithium, demeclocycline). Assessment Findings Increased thirst, excessive urination (4-30 liters/day), tachycardia, hypotension, poor skin turgor, poor peripheral pulses, ALOC, ataxia, dry mucous membranes. Laboratory Tests and Diagnostics Urinalysis: Decreased urine specific gravity, pH, osmolality, sodium, potassium. Blood work: Increased sodium, potassium, blood osmolality. Blood glucose test to rule out diabetes mellitus. MRI. Water deprivation test: Induces dehydration to assess body’s response. ADH stimulation test: Differentiates between neurogenic and nephrogenic DI. Nursing Care Monitor ABCs and VS. Weigh patient daily. Educate on diet (avoid diuretic-like foods such as caffeine). Assess skin and treat dehydration. Ensure fluid intake matches urine output. Address electrolyte imbalances. Treatment Neurogenic DI: Administer desmopressin (replaces vasopressin). Nephrogenic DI: Correct underlying cause, address electrolyte issues, administer thiazide diuretics. Pharmacology Desmopressin: Synthetic ADH, caution in cardiac patients. Thiazide Diuretics: For nephrogenic DI. NSAIDs: Reduce urine volume when combined with thiazides. Prostaglandin Inhibitors: Increase water absorption by kidneys. Patient and Family Education Low salt and protein diet. Prevent dehydration by matching fluid intake with urine output. Monitor for signs of dehydration. Diabetic Ketoacidosis (DKA) Definition: Uncontrolled hyperglycemia leading to high serum and urine ketones, resulting in metabolic acidosis. Rapid onset, typically over 24 hours. Risk Factors Illness/infection, missing insulin doses, non-adherence to diabetic regimen, alcohol, drug use, untreated or undiagnosed diabetes, stress, certain medications. Assessment Findings Polyuria, polydipsia, polyphagia, unintentional weight loss, nausea, vomiting, abdominal pain, weakness, ALOC, fruity odor breath, Kussmaul respirations, dehydration. Laboratory Tests and Diagnostics Blood work: Glucose > 300 mg/dL, present ketones, normal to low sodium, normal to high potassium, high osmolality, elevated BUN/creatinine. Arterial Blood Gas: Metabolic acidosis. Urinalysis: Ketones, large amounts of glucose. Nursing Care Assess ABCs, VS, and neurological status. Correct hyperglycemia: Administer IV fluids, insulin IV, sodium bicarbonate. Replace electrolytes: Monitor potassium levels. Reverse acidosis. Treat underlying condition. Patient and Family Education Check urine for ketones when BGL is elevated. Prevent dehydration. Be aware of triggers. Monitor BGL. Take insulin as prescribed, even on sick days. Importance of exercise and healthy diet. Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) Definition: Profound hyperglycemia associated with dehydration, absence of ketones, gradual onset. Risk Factors Common in adults 50-70 years old, inadequate fluid intake, decline in kidney function, lack of sufficient insulin, illness, infection, certain medications, stress, more common in Type 2 diabetics. Assessment Findings Polyuria, polydipsia, polyphagia, unintentional weight loss, orthostatic hypotension, ALOC, seizures, blurred vision, headaches. Laboratory Tests and Diagnostics Blood work: Glucose > 600 mg/dL, absent ketones, normal to low sodium, normal to high potassium, high osmolality, elevated BUN/creatinine. Arterial Blood Gas: Absence of acidosis. Urinalysis: Absence of ketones. Nursing Care Assess ABCs, VS, and neurological status. Correct hyperglycemia: Administer IV fluids, insulin IV, sodium bicarbonate. Replace electrolytes: Monitor potassium levels. Aim to reduce BGL by 75-100 mg/dL/hr to prevent rapid decrease and cerebral edema. Do not drop BGL lower than 300 mg/dL. Patient and Family Education Check urine for ketones when BGL is elevated. Prevent dehydration. Be aware of triggers. Monitor BGL. Take insulin as prescribed, even on sick days. Importance of exercise and healthy diet. Key Differences ADH Levels: o DI: Low ADH or kidneys unresponsive to ADH. o SIADH: Excessive ADH. Urine Output: o DI: High urine output (dilute urine).  o SIADH: Low urine output (concentrated urine). Serum Sodium: o DI: High serum sodium (hypernatremia). o SIADH: Low serum sodium (hyponatremia). Fluid Balance: o DI: Dehydration, fluid loss. o SIADH: Fluid retention, hypervolemia. NEURO Guillain-Barré Syndrome (GBS) Definition: An autoimmune disorder where the body’s immune system attacks the peripheral nerves, leading to muscle weakness and paralysis. Risk Factors: Often follows an infection (respiratory or gastrointestinal), vaccination, or surgery. Assessment Findings: o Symmetrical and ascending muscle weakness starting in the lower extremities. o Paresthesia (tingling or prickling sensation). o Decreased or absent deep tendon reflexes. o Respiratory muscle weakness in severe cases. o Autonomic dysfunction (e.g., fluctuating blood pressure, heart rate abnormalities). Labs and Diagnostic Findings: o Elevated protein levels in cerebrospinal fluid (CSF) from lumbar puncture. o Electromyography (EMG) and nerve conduction studies show slowed nerve conduction. Nursing Management: o Monitor respiratory function and prepare for possible mechanical ventilation. o Manage pain and prevent complications such as pressure ulcers and deep vein thrombosis (DVT). o Provide physical therapy to maintain muscle strength and flexibility. Patient Education:  o Inform about the potential for recovery, although it may take weeks to months. o Encourage participation in rehabilitation programs. GB-The patient reports a weak cough Amyotrophic Lateral Sclerosis (ALS) Definition: A progressive neurodegenerative disease affecting motor neurons, leading to muscle weakness and atrophy. Risk Factors: Genetic predisposition, age (most common between 40-70 years), and possibly environmental factors. Assessment Findings: o Muscle weakness and atrophy, starting in the limbs. o Fasciculations (muscle twitches). o Dysphagia (difficulty swallowing) and dysarthria (difficulty speaking). o Respiratory muscle weakness. o Cognitive function usually remains intact. Nursing Management: o Support respiratory function and manage symptoms. o Assist with activities of daily living (ADLs) and mobility. o Provide nutritional support and manage dysphagia. o Offer emotional support and end-of-life care planning. Patient Education: o Discuss the progressive nature of the disease and the importance of advance directives. o Encourage the use of assistive devices to maintain independence. Which of the following is considered a risk factor for amyotrophic lateral sclerosis? o HEAD TRAUMA Myasthenia Gravis (MG) Definition: An autoimmune disorder characterized by weakness and rapid fatigue of voluntary muscles due to impaired communication between nerves and muscles.  Risk Factors: Thymus gland abnormalities, family history, and other autoimmune diseases. Assessment Findings: o Muscle weakness that worsens with activity and improves with rest. o Ptosis (drooping eyelids) and diplopia (double vision). o Difficulty swallowing, chewing, and speaking. o Respiratory muscle weakness in severe cases. Labs and Diagnostic Findings: o Positive acetylcholine receptor antibody test. o Electromyography (EMG) shows decreased muscle response. o Tensilon test (edrophonium test) shows temporary improvement in muscle strength. Nursing Management: o Administer anticholinesterase medications (e.g., pyridostigmine). o Monitor respiratory function and prepare for possible mechanical ventilation. o Provide a balanced diet and manage dysphagia. o Educate on energy conservation techniques. Patient Education: o Teach about medication management and the importance of adhering to the treatment regimen. o Encourage regular follow-up with healthcare providers. o Myasthenia gravis is characterized by: ▪ Ptosis A patient is suspected of being in a myasthenic crisis after having a Tensilon (Edrophonium) test. Which test result best supports this diagnosis? ▪ Muscle weakness improves with the Tensilon injectuion Multiple Sclerosis (MS) Definition: A chronic autoimmune disease that affects the central nervous system (CNS), leading to demyelination and nerve damage.  Risk Factors: Genetic predisposition, environmental factors, infections, and vitamin D deficiency. Assessment Findings: o Fatigue, muscle weakness, and spasticity. o Visual disturbances (e.g., optic neuritis, diplopia). o Sensory changes (e.g., numbness, tingling). o Coordination and balance problems. o Bladder and bowel dysfunction. o Cognitive impairment. Labs and Diagnostic Findings: o MRI shows lesions or plaques in the CNS. o Lumbar puncture reveals oligoclonal bands in CSF. Nursing Management: o Administer disease-modifying therapies (e.g., interferon beta). o Manage symptoms with medications (e.g., muscle relaxants, corticosteroids). o Provide physical and occupational therapy. o Educate on lifestyle modifications and coping strategies. Patient Education: o Discuss the importance of medication adherence and regular monitoring. o Encourage a healthy lifestyle, including exercise and a balanced diet. Intracranial Pressure (ICP) Definition: The pressure exerted by the contents of the skull (brain tissue, blood, and cerebrospinal fluid). Normal ICP: 5-15 mm Hg. Causes of Increased ICP: Head injury, brain tumor, hemorrhage, infection, hydrocephalus. Assessment Findings: o Headache, vomiting, and altered level of consciousness (early signs). o Cushing’s triad (late signs): Hypertension with widening pulse pressure, bradycardia, and irregular respirations. o Pupillary changes and posturing (decorticate or decerebrate). Nursing Management: o Monitor neurological status and vital signs. o Elevate the head of the bed to 30 degrees to promote venous drainage. o Administer medications to reduce ICP (e.g., mannitol, hypertonic saline). o Avoid activities that increase ICP (e.g., coughing, straining).  Patient Education: o Explain the importance of following medical advice to manage ICP. o Educate on recognizing signs of increased ICP and when to seek medical help. Glasgow Coma Scale (GCS) Definition: A scale used to assess the level of consciousness in patients with acute brain injury. Components: o Eye Opening (E): ▪ 4: Spontaneous ▪ 3: To speech ▪ 2: To pain ▪ 1: None o Verbal Response (V): ▪ 5: Oriented ▪ 4: Confused ▪ 3: Inappropriate words ▪ 2: Incomprehensible sounds ▪ 1: None o Best Motor Response (M): ▪ 6: Obeys commands ▪ 5: Localizes to pain ▪ 4: Withdraws from pain ▪ 3: Abnormal flexion (decorticate posturing) ▪ 2: Extension (decerebrate posturing) ▪ 1: None Scoring: o Total score ranges from 3 to 15. o Severe brain injury: GCS ≤ 8. o Moderate brain injury: GCS 9-12. o Mild brain injury: GCS 13-15. ABGS Arterial Blood Gases (ABGs) Overview ABGs are a crucial diagnostic tool used to assess a patient’s oxygenation, ventilation, and acid-base status. The key components measured in an ABG are: pH: Indicates the acidity or alkalinity of the blood. PaCO₂: Partial pressure of carbon dioxide, reflecting respiratory function. HCO₃⁻: Bicarbonate, reflecting metabolic function. PaO₂: Partial pressure of oxygen, indicating oxygenation status. SaO₂: Oxygen saturation, indicating the percentage of hemoglobin saturated with oxygen. Normal ABG Values pH: 7.35 - 7.45 PaCO₂: 35 - 45 mm Hg HCO₃⁻: 22 - 26 mEq/L PaO₂: 80 - 100 mm Hg SaO₂: 95% - 100% ROME Method for ABG Interpretation The ROME method helps determine the primary cause of an acid-base imbalance: Respiratory Opposite: In respiratory disorders, pH and PaCO₂ move in opposite directions. Metabolic Equal: In metabolic disorders, pH and HCO₃⁻ move in the same direction. Steps for ABG Interpretation 1. Assess the pH: a. Normal: 7.35 - 7.45 b. Acidosis: < 7.35 c. Alkalosis: > 7.45 2. Determine the Primary Cause: a. Respiratory: Look at PaCO₂. i. Acidosis: PaCO₂ > 45 mm Hg ii. Alkalosis: PaCO₂ < 35 mm Hg b. Metabolic: Look at HCO₃⁻. i. Acidosis: HCO₃⁻ < 22 mEq/L ii. Alkalosis: HCO₃⁻ > 26 mEq/L 3. Check for Compensation: a. Uncompensated: pH is abnormal, and either PaCO₂ or HCO₃⁻ is abnormal.  b. Partially Compensated: pH is abnormal, and both PaCO₂ and HCO₃⁻ are abnormal. c. Fully Compensated: pH is normal, but both PaCO₂ and HCO₃⁻ are abnormal. Examples of ABG Interpretation Respiratory Acidosis pH: < 7.35 PaCO₂: > 45 mm Hg HCO₃⁻: Normal (uncompensated) or > 26 mEq/L (compensated) Causes: Hypoventilation, COPD, respiratory depression, airway obstruction. Respiratory Alkalosis pH: > 7.45 PaCO₂: < 35 mm Hg HCO₃⁻: Normal (uncompensated) or < 22 mEq/L (compensated) Causes: Hyperventilation, anxiety, pain, fever, hypoxemia. Metabolic Acidosis pH: < 7.35 HCO₃⁻: < 22 mEq/L PaCO₂: Normal (uncompensated) or < 35 mm Hg (compensated) Causes: Diabetic ketoacidosis (DKA), renal failure, lactic acidosis, diarrhea. Metabolic Alkalosis pH: > 7.45 HCO₃⁻: > 26 mEq/L PaCO₂: Normal (uncompensated) or > 45 mm Hg (compensated) Causes: Vomiting, gastric suctioning, diuretic use, excessive bicarbonate intake. Compensation Mechanisms Respiratory Compensation: The lungs adjust PaCO₂ to help normalize pH. o For Metabolic Acidosis: Increase ventilation to blow off CO₂. o For Metabolic Alkalosis: Decrease ventilation to retain CO₂. Metabolic Compensation: The kidneys adjust HCO₃⁻ to help normalize pH. o For Respiratory Acidosis: Retain HCO₃⁻. o For Respiratory Alkalosis: Excrete HCO₃⁻. Practice Problems 1. ABG Results: pH 7.30, PaCO₂ 50 mm Hg, HCO₃⁻ 24 mEq/L  a. Interpretation: Respiratory acidosis, uncompensated. b. Cause: Likely due to hypoventilation or respiratory depression. 2. ABG Results: pH 7.48, PaCO₂ 30 mm Hg, HCO₃⁻ 22 mEq/L a. Interpretation: Respiratory alkalosis, uncompensated. b. Cause: Likely due to hyperventilation (e.g., anxiety, pain). 3. ABG Results: pH 7.32, PaCO₂ 35 mm Hg, HCO₃⁻ 18 mEq/L a. Interpretation: Metabolic acidosis, uncompensated. b. Cause: Likely due to DKA or renal failure. 4. ABG Results: pH 7.50, PaCO₂ 48 mm Hg, HCO₃⁻ 30 mEq/L a. Interpretation: Metabolic alkalosis, partially compensated. b. Cause: Likely due to vomiting or excessive bicarbonate intake. Key Points to Remember ROME: Respiratory Opposite, Metabolic Equal. Compensation: The body attempts to normalize pH through respiratory or metabolic adjustments. Clinical Correlation: Always correlate ABG results with the patient’s clinical condition and history. CUSHINGS TRIAD Cushing’s Triad Overview Cushing’s Triad is a clinical syndrome that indicates increased intracranial pressure (ICP). It consists of three primary signs: 1. Hypertension (with widening pulse pressure) 2. Bradycardia 3. Irregular respirations Components of Cushing’s Triad 1. Hypertension with Widening Pulse Pressure Definition: Elevated systolic blood pressure with a significant difference between systolic and diastolic pressures. Mechanism: Increased ICP leads to reduced cerebral perfusion. The body responds by increasing systemic blood pressure to maintain cerebral blood flow. Clinical Significance: Indicates the body’s attempt to overcome increased ICP and maintain adequate cerebral perfusion. 2. Bradycardia Definition: Slower than normal heart rate. Mechanism: Increased ICP stimulates the vagus nerve, leading to a decrease in heart rate. Clinical Significance: Reflects the body’s response to increased pressure within the skull, affecting the autonomic nervous system. 3. Irregular Respirations Definition: Abnormal breathing patterns, such as Cheyne-Stokes respiration, Biot’s respiration, or ataxic breathing. Mechanism: Increased ICP affects the brainstem, which controls respiratory patterns. Clinical Significance: Indicates severe brainstem dysfunction due to increased ICP. Pathophysiology of Cushing’s Triad Increased ICP: Can result from head injury, brain tumor, hemorrhage, infection, or hydrocephalus. Cerebral Perfusion Pressure (CPP): CPP = MAP - ICP. As ICP increases, CPP decreases, leading to reduced cerebral blood flow. Autoregulatory Mechanisms: The body attempts to maintain cerebral perfusion by increasing systemic blood pressure. Brainstem Compression: Increased ICP can compress the brainstem, affecting vital functions such as heart rate and respiration. Causes of Increased ICP Head Injury: Trauma leading to bleeding, swelling, or hematoma. Brain Tumor: Mass effect causing compression of brain structures. Hemorrhage: Intracerebral, subarachnoid, or epidural bleeding. Infection: Meningitis or encephalitis causing inflammation and swelling. Hydrocephalus: Accumulation of cerebrospinal fluid (CSF) leading to increased pressure. Assessment and Diagnosis Neurological Examination: Assess for signs of increased ICP, including changes in level of consciousness, pupil size and reactivity, motor responses, and vital signs. Imaging: CT scan or MRI to identify the cause of increased ICP.  ICP Monitoring: Invasive monitoring using devices such as intraventricular catheters or subdural bolts to measure ICP directly. Management of Increased ICP Positioning: Elevate the head of the bed to 30 degrees to promote venous drainage. Medications: o Osmotic Diuretics: Mannitol to reduce cerebral edema. o Hypertonic Saline: To draw fluid out of brain tissue. o Sedatives: To reduce metabolic demand and control agitation. o Antihypertensives: To manage systemic blood pressure. Surgical Interventions: o Decompressive Craniectomy: Removal of part of the skull to relieve pressure. o Ventriculostomy: Insertion of a catheter to drain excess CSF. Monitoring: Continuous monitoring of neurological status and vital signs. Nursing Interventions Monitor Neurological Status: Frequent assessments of level of consciousness, pupil response, motor function, and vital signs. Maintain Airway and Breathing: Ensure adequate oxygenation and ventilation. Fluid Management: Monitor fluid balance and administer IV fluids as prescribed. Prevent Complications: Implement measures to prevent complications such as pressure ulcers, infections, and deep vein thrombosis (DVT). Educate Patient and Family: Provide information about the condition, treatment plan, and signs of increased ICP to watch for. Key Points to Remember Cushing’s Triad is a late sign of increased ICP and indicates a medical emergency. Early Recognition: Prompt identification and treatment of increased ICP are crucial to prevent permanent brain damage or death. Multidisciplinary Approach: Management involves a team of healthcare professionals, including neurologists, neurosurgeons, critical care nurses, and respiratory therapists. MINI TEST Shock Q: What is shock? A: Shock is a life-threatening condition where blood flow is insufficient to meet the body’s needs, leading to organ dysfunction. Q: What are the stages of shock? A: 1. Compensatory Stage 2. Progressive Stage 3. Irreversible Stage Q: What are the symptoms of the compensatory stage of shock? A: Normal BP, elevated HR, normal CO, elevated RR. Q: What are the symptoms of the progressive stage of shock? A: BP drops, MAP decreases, shallow RR, increasing HR, worsening LOC. Q: What are the symptoms of the irreversible stage of shock? A: Persistently low BP, multiple organ failure, unresponsive to treatment. Q: What is the pathophysiology of cardiogenic shock? A: Heart pump failure, decreased cardiac output. Q: What are the risk factors for hypovolemic shock? A: Hemorrhage, burns, dehydration, trauma, surgery, vomiting/diarrhea. Q: What is the treatment for neurogenic shock? A: Spinal stabilization, HOB 30 degrees, fluid resuscitation, DVT prevention, VS monitoring. Q: What are the common risk factors for septic shock? A: Indwelling catheters, antibiotic resistance, age, comorbidities, infections, surgeries, wounds. Q: What are the symptoms of anaphylactic shock? A: Low BP, high HR, elevated RR, nausea/vomiting, lightheadedness, rash, SOB, throat swelling, bronchoconstriction. Sepsis Q: What is sepsis? A: Sepsis is a systemic, dysregulated host response to infection leading to life-threatening organ dysfunction. Q: What are the SIRS criteria for sepsis? A: 1. Temperature > 38°C (100.4°F) or < 36°C (96.8°F) 2. Heart rate > 90 bpm 3. Respiratory rate > 20 breaths per minute 4. WBC count > 12,000/mm³ or < 4,000/mm³ Q: What are the mechanisms of sepsis pathophysiology? A: Massive vasodilation, increased capillary permeability, clot formation in microcirculation. Q: What are the common sources of infection leading to sepsis? A: Catheters, wounds, lungs, GU tract, GI tract, heart, skin, blood, head. Q: What are the high-risk groups for sepsis? A: Pediatrics and elderly, immunocompromised individuals, those with comorbidities, recent hospitalizations, sepsis survivors, prolonged antibiotic use. Q: What are the clinical manifestations of sepsis? A: Tachycardia, tachypnea, warm/flushed skin, increased temperature, altered level of consciousness (ALOC), decreased urine output (UO), normal to low blood pressure (BP). Q: What are the components of the 3-hour sepsis bundle? A: Measure lactate level, obtain blood cultures before antibiotics, administer broad-spectrum antibiotics, administer 30mL/kg IV fluid. Q: What are the indicators of progression to septic shock? A: BP 70/38 after fluid bolus, serum lactate > 2 mmol/L, need for norepinephrine to maintain MAP > 65 mmHg, CVP > 12 mmHg. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Q: What is SIADH? A: Excessive release of ADH (vasopressin) from the pituitary gland, leading to water reabsorption by the kidneys and excretion of sodium, causing hyponatremia and hypervolemia. Q: What are the risk factors for SIADH? A: CNS disturbances, malignancies, certain medications, surgery, hormone deficiencies, secondary diseases, hereditary factors. Q: What are the early symptoms of SIADH? A: Nausea, vomiting, malaise. Q: What are the laboratory findings consistent with SIADH? A: Increased sodium and urine osmolality, decreased blood osmolality, electrolyte panel, blood glucose, renal function, lipid profile, liver function tests, serum cortisol, thyroid panel. Q: What is the role of vasopressin antagonists in the treatment of SIADH? A: Promote water excretion without sodium loss, rapidly increase sodium levels. Q: What is a key management strategy for SIADH? A: Fluid restriction. Diabetes Insipidus (DI) Q: What is DI? A: Deficiency of ADH (antidiuretic hormone), leading to reduced ability of kidneys to collect and concentrate urine, resulting in excessive urine production. Q: What are the types of DI? A: 1. Primary DI 2. Secondary DI 3. Nephrogenic DI Q: What are the risk factors for DI? A: Head injury, family history of DI, brain surgery, infections, metabolic disorders, tumors, radiation, certain medications. Q: What are the common symptoms of DI? A: Increased thirst, excessive urination (4-30 liters/day), tachycardia, hypotension, poor skin turgor, poor peripheral pulses, ALOC, ataxia, dry mucous membranes. Q: What is the purpose of the water deprivation test in diagnosing DI? A: Assesses the body’s ability to concentrate urine in response to dehydration. Q: What is the treatment for neurogenic DI? A: Administer desmopressin (replaces vasopressin). Diabetic Ketoacidosis (DKA) Q: What is DKA? A: Uncontrolled hyperglycemia leading to high serum and urine ketones, resulting in metabolic acidosis. Rapid onset, typically over 24 hours. Q: What are the risk factors for DKA? A: Illness/infection, missing insulin doses, non- adherence to diabetic regimen, alcohol, drug use, untreated or undiagnosed diabetes, stress, certain medications. Q: What are the common symptoms of DKA? A: Polyuria, polydipsia, polyphagia, unintentional weight loss, nausea, vomiting, abdominal pain, weakness, ALOC, fruity odor breath, Kussmaul respirations, dehydration. Q: What is the role of insulin in the management of DKA? A: Helps lower blood glucose levels, reduce ketone production, and correct metabolic acidosis. Q: Why is checking urine for ketones important when blood glucose levels are elevated? A: It helps detect the presence of ketones, indicating the severity of DKA. Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) Q: What is HHNS? A: Profound hyperglycemia associated with dehydration, absence of ketones, gradual onset. Q: What are the risk factors for HHNS? A: Inadequate fluid intake, decline in kidney function, lack of sufficient insulin, illness, infection, certain medications, stress, more common in Type 2 diabetics. Q: What are the common symptoms of HHNS? A: Polyuria, polydipsia, polyphagia, unintentional weight loss, orthostatic hypotension, ALOC, seizures, blurred vision, headaches. Q: Why is gradual reduction of blood glucose levels important in HHNS management? A: To prevent rapid shifts in osmolarity, which can lead to cerebral edema. Q: Can HHNS lead to cerebral edema if blood glucose levels are reduced too rapidly? A: Yes. Guillain-Barré Syndrome (GBS) Q: What is GBS? A: An autoimmune disorder where the body’s immune system attacks the peripheral nerves, leading to muscle weakness and paralysis. Q: What are the common triggers for GBS? A: Respiratory or gastrointestinal infection, vaccination, surgery. Q: What are the common symptoms of GBS? A: Symmetrical and ascending muscle weakness starting in the lower extremities, paresthesia, decreased or absent deep tendon reflexes, respiratory muscle weakness, autonomic dysfunction. Q: What is the role of plasmapheresis in the treatment of GBS? A: Removes antibodies from the blood that are attacking the peripheral nerves. Q: How long can recovery from GBS take? A: Weeks to months. Amyotrophic Lateral Sclerosis (ALS) Q: What is ALS? A: A progressive neurodegenerative disease affecting motor neurons, leading to muscle weakness and atrophy. Q: What are the risk factors for ALS? A: Genetic predisposition, age (most common between 40-70 years), possibly environmental factors. Q: What are the common symptoms of ALS? A: Muscle weakness and atrophy, fasciculations, dysphagia, dysarthria, respiratory muscle weakness, cognitive function usually remains intact. Q: Why are advance directives important in ALS management? A: They allow patients to communicate their wishes for end-of-life care and medical interventions. Q: Is ALS a progressive neurodegenerative disease with no cure? A: Yes. Myasthenia Gravis (MG) Q: What is MG? A: An autoimmune disorder Cushing’s Triad Q: What is Cushing’s Triad? A: Cushing’s Triad is a clinical syndrome indicating increased intracranial pressure (ICP), consisting of hypertension (with widening pulse pressure), bradycardia, and irregular respirations. Q: What are the components of Cushing’s Triad? A: 1. Hypertension with widening pulse pressure 2. Bradycardia 3. Irregular respirations Q: What causes hypertension with widening pulse pressure in Cushing’s Triad? A: Increased ICP leads to reduced cerebral perfusion, causing the body to increase systemic blood pressure to maintain cerebral blood flow. Q: What causes bradycardia in Cushing’s Triad? A: Increased ICP stimulates the vagus nerve, leading to a decrease in heart rate. Q: What causes irregular respirations in Cushing’s Triad? A: Increased ICP affects the brainstem, which controls respiratory patterns, leading to abnormal breathing patterns. Q: What are the clinical significances of Cushing’s Triad? A: Indicates severe brainstem dysfunction due to increased ICP and the body’s attempt to overcome increased ICP and maintain adequate cerebral perfusion. Intracranial Pressure (ICP) Q: What is Intracranial Pressure (ICP)? A: The pressure exerted by the contents of the skull (brain tissue, blood, and cerebrospinal fluid). Q: What is the normal range for ICP? A: 5-15 mm Hg. Q: What are common causes of increased ICP? A: Head injury, brain tumor, hemorrhage, infection, hydrocephalus. Q: What are early signs of increased ICP? A: Headache, vomiting, altered level of consciousness. Q: What are late signs of increased ICP (Cushing’s Triad)? A: Hypertension with widening pulse pressure, bradycardia, irregular respirations. Q: What are the components of Cushing’s Triad? A: 1. Hypertension with widening pulse pressure  2. Bradycardia 3. Irregular respirations Q: How is ICP monitored? A: Using invasive devices such as intraventricular catheters or subdural bolts. Q: What are the management strategies for increased ICP? A: Elevate the head of the bed to 30 degrees, administer medications (mannitol, hypertonic saline, sedatives, antihypertensives), and surgical interventions (decompressive craniectomy, ventriculostomy). Q: What are the nursing interventions for increased ICP? A: Monitor neurological status, maintain airway and breathing, manage fluid balance, prevent complications, educate patient and family. Arterial Blood Gases (ABGs) Q: What are the key components measured in an ABG? A: pH, PaCO₂, HCO₃⁻, PaO₂, SaO₂. Q: What is the normal range for pH in ABGs? A: 7.35 - 7.45. Q: What is the normal range for PaCO₂ in ABGs? A: 35 - 45 mm Hg. Q: What is the normal range for HCO₃⁻ in ABGs? A: 22 - 26 mEq/L. Q: What is the normal range for PaO₂ in ABGs? A: 80 - 100 mm Hg. Q: What is the normal range for SaO₂ in ABGs? A: 95% - 100%. Q: What does the ROME method stand for in ABG interpretation? A: Respiratory Opposite, Metabolic Equal. Q: What does respiratory acidosis look like in ABGs? A: pH < 7.35, PaCO₂ > 45 mm Hg, HCO₃⁻ normal (uncompensated) or > 26 mEq/L (compensated). Q: What does respiratory alkalosis look like in ABGs? A: pH > 7.45, PaCO₂ < 35 mm Hg, HCO₃⁻ normal (uncompensated) or < 22 mEq/L (compensated). Q: What does metabolic acidosis look like in ABGs? A: pH < 7.35, HCO₃⁻ < 22 mEq/L, PaCO₂ normal (uncompensated) or < 35 mm Hg (compensated). Q: What does metabolic alkalosis look like in ABGs? A: pH > 7.45, HCO₃⁻ > 26 mEq/L, PaCO₂ normal (uncompensated) or > 45 mm Hg (compensated). Q: What are the compensation mechanisms for acid-base imbalances? A: Respiratory compensation: Lungs adjust PaCO₂ to help normalize pH. Metabolic compensation: Kidneys adjust HCO₃⁻ to help normalize pH.