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Shock: A Comprehensive Guide to Understanding and Managing Shock, Exams of Nursing

Montana State UniversityNursing

A detailed overview of shock, a life-threatening condition characterized by decreased tissue perfusion and impaired cellular metabolism. It covers various aspects of shock, including its classifications, compensatory mechanisms, stages, and management strategies. The document also explores the impact of chronic diseases on shock and provides insights into the role of fluid resuscitation and other interventions. This resource is valuable for healthcare professionals and students seeking a comprehensive understanding of shock.

Typology: Exams

2024/2025

Available from 03/18/2025

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NRSG 327 FINAL EXAM QUESTIONS WITH THE LATEST SCORE
Shock -- Answer ✔✔ syndrome characterized by decreased tissue perfusion and
impaired cellular metabolism
Results in an imbalance between supply and demand for oxygen and nutrients
Classifications of shock -- Answer ✔✔ hypovolemic
Cardiogenic
Distributive (sepsis, anaphylaxis and neurogenic)
Cardiac Output (CO) and calculation -- Answer ✔✔ Amount of blood pumped in 1
minute (~5 L)
Stroke volume x heart rate
Preload and what is it determined by? -- Answer ✔✔ the volume of blood in the
ventricles at the end of diastole
Determined by:
- venous return
-ability of ventricle to stretch, relax and fill
Afterload and what is it determined by? -- Answer ✔✔ the force, or resistance, against
which the ventricles have to pump in order to eject the blood
3 Vs it is determined by:
-vessel tone
-valve
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pfd
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Download Shock: A Comprehensive Guide to Understanding and Managing Shock and more Exams Nursing in PDF only on Docsity!

NRSG 327 FINAL EXAM QUESTIONS WITH THE LATEST SCORE

Shock -- Answer ✔✔ syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Results in an imbalance between supply and demand for oxygen and nutrients Classifications of shock -- Answer ✔✔ hypovolemic Cardiogenic Distributive (sepsis, anaphylaxis and neurogenic) Cardiac Output (CO) and calculation -- Answer ✔✔ Amount of blood pumped in 1 minute (~5 L) Stroke volume x heart rate Preload and what is it determined by? -- Answer ✔✔ the volume of blood in the ventricles at the end of diastole Determined by:

  • venous return
  • ability of ventricle to stretch, relax and fill Afterload and what is it determined by? -- Answer ✔✔ the force, or resistance, against which the ventricles have to pump in order to eject the blood 3 Vs it is determined by:
  • vessel tone
  • valve
  • viscosity What is contractility determined by? -- Answer ✔✔ - preload
  • the stimulatory effect of the SNS
  • external factors that affect the amount of calcium in myocardial cell What is Starling's Law? -- Answer ✔✔ Stretching of heart muscle fibers causes increased force of contraction (e.g., more blood going to heart - > heart pumps harder> more CO) In HF - this mechanism doesn't work (more blood coming in, but heart doesn't pump harder) Mean arterial pressure equation -- Answer ✔✔ SBP+2(DBP)/ Compensated stage of shock -- Answer ✔✔ - refers to a state in which the body has activated hormonal and chemical compensatory mechanisms to help maintain homeostasis
  • the body is able to maintain CO and SV
  • CELLULAR DAMAGE IS STILL OCCURING
  • if it is corrected at this stage, pt will recover Neural compensatory mechanisms in shock -- Answer ✔✔ SNS activation
  • baroreceptors in the aortic arch and carotid bodies sense changes in blood flow
  • stimulates release of epinephrine and norepinephrine Epinephrine mechanism -- Answer ✔✔ - beta receptors increase HR (chronotropic),
  • increases BP (afterload),
    • vasoconstriction to legs,
  • increase myocardial contractility,
  • increased RR (chemoreceptors), normal WOB, normal SPO
  • thirst
  • slightly restless, possible mild confusion, decreased concentration, increased glucose
  • mild tachycardia, strong pulses centrally, possible slightly weaker peripherally, normal bp (decreased bp is one of the first changes)
  • decrease urine output, urine conc, hypoactive bowels Uncompensated (progressive ) stage of shock -- Answer ✔✔ - stage when compensatory mechanisms fail
  • O2 supply and demand becomes imbalanced
  • decreased cellular perfusion =decreased O2/glucose delivery And leads to inability to remove waste
  • accumulation of CO2= vasodilation What happens when there is decreased perfusion? -- Answer ✔✔ - less o2 delivery
  • cell functions fail the Na/K pump so more Na in cell therefore more water therefore more swelling
  • cells in cardiovascular system fail; fluid leaks into interstitial spaces and lungs leading to anasarca
  • body switches from aerobic to anaerobic metabolism because of lack of o2. This leads to buildup of lactic acid leading to acidosis
  • acidosis interferes with hgb, and makes arterioles less responsive to epi/norepi
  • acidosis also reduces contractility and interferes with clotting
  • CO2 will also start to accumulate, causing vasodilation, venous pooling and formation of blood clots in our microcirculation MODS (multiple organ dysfunction syndrome) -- Answer ✔✔ presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention Signs and symptoms of progressive stage of shock -- Answer ✔✔ neuro:
  • restless, confusion, decreasing GCS
  • MAP of <60 results in ischemic cell death Cardiac:
  • tachycardia, diminished/no peripheral pulses and increasing cap refill,
  • dysrhythmias (especially pvcs)
  • low BP MAP<60mmg
  • widening pulse pressure
  • skin pale, cold, clammy, mottled periphery
  • myocardial perfusion problems Respiratory
  • increased rate and WOB
  • abnormal lung sounds
  • dyspnea
  • decreased O2 sats (may need ear probe)
  • abgs show hypoxemia and metabolic acidosis or both metabolic and respiratory acidosis if CO2 is climbing GI:
  • n&V
  • decreased BS Renal:
  • less than 30cc/hr urine output
  • concentrated
  • increased BUN/Creat Irreversible (refractory) stage of shock -- Answer ✔✔ - refers to the stage where the amount of cellular damage and cell death is so great that significant and permanent organ damage occurs
  • microthrombi are formed from blood pooling in the small vessels that cause vessel occlusion and tissue ischemia
  • clot formation uses up clotting factors and platelets
  • then hemorrhages occur d/t no factors/platelets available and activation of the fibrinolytic system (in order to break down the clots) which can cause increased bleeding What chronic diseases might impact pts experience of shock? -- Answer ✔✔ - neuro/ETOH (confusion, unable to verbalize)
  • prev MI/HF (and consequent meds might lower HR)
  • HTN (meds that lower BP)
  • copd
  • ESLD
  • ESRD
  • chronic inflammation (corticosteroids mask S&S of infxn)
  • PEDS (less circulating volume and unable to vasoconstrict) and GERI Hypovolemic shock -- Answer ✔✔ decrease in intravascular volume; blood or fluid How much fluid loss= hypovolemic shock? -- Answer ✔✔ - patients can compensate for up to 15% total blood loss (in a female pt 6L)
  • greater than 30% is when compensatory mechanisms fail
  • depends on age, how much muscle, nutrition, hydration, disease What are some volume losses not associated with blood loss -- Answer ✔✔ - diarrhea
  • vomiting
  • burns greater than 40%
  • diuresis; diabetic ketoacidosis What are areas in which life threatening hemorrhage can occur? -- Answer ✔✔ - chest: 3 - 4 L
  • thighs: 1L
  • abdomen/pelvis: 3L
  • outside the body: total volume How much blood volume does a typical adult have -- Answer ✔✔ about 5-6L Isotonic, hypertonic and hypotonic crystalloids? -- Answer ✔✔ isotonic: osmolality matches plasma
  • 0.9% NS, RL Hypertonic: higher concentration of electrolytes
  • 3% nacl, D10W, D Hypotonic: lower concentration of electrolytes
  • 0.45% NS, D5W (once dextrose has been metabolized) Colloids -- Answer ✔✔ - contain large molecules so they remain in the intravascular compartment
  • expand plasma by drawing fluid form the extravascular space (oncotic pressure)
  • require less volume than crystalloids
  • i.e. FFP, albumin, hetastarch, pentastarch What is the RBC:FFP ratio? -- Answer ✔✔ 2: What is tranexamic acid? -- Answer ✔✔ Antifibrinolytic Used to treat or prevent excessive blood loss How do you know if your interventions for hypovolemic shock are working? -- Answer ✔✔ CCU:
  • central venous pressure
  • arterial pressure
  • plasma enzyme cascade What happens during the plasma enzyme cascade -- Answer ✔✔ - MAC: membrane attacking complex Causes holes in capillaries
  • fibrin: creates clots in microvascular circulation
  • bradykinin: causes massive vasodilation
  • prostaglandins (arachidonic acid): vasodilation SIRS (systemic inflammatory response syndrome) and symptoms -- Answer ✔✔ SIRS is widespread inflammation that can occur in infection, trauma, shock, ect. May result from or lead to MODS. Most frequently associated with sepsis. Fever >38 or < Tachycardia >90 bpm Tachypnea >20 breath/min Leukocytosis >12 or < Why is septic shock a hyperdynamic state? -- Answer ✔✔ increased CO and decreased SVR Signs and symptoms of septic shock -- Answer ✔✔ - tachycardia (narrow pulse pressure and tachycardia are the earliest signs of shock)
  • tachypnea
  • hypotension
  • temperature dysregulation
  • decreased urine output
  • altered neurological status
  • GI dysfunction
  • DIC
  • ARDS What is sepsis accompanied by -- Answer ✔✔ increased glycolysis and hyperlactatemia (due to hyperkinetic state) What is the diagnostic test for severity of sepsis -- Answer ✔✔ lactate levels Sepsis bundles: surviving sepsis campaign, what is the initial resuscitation for sepsis and septic shock? -- Answer ✔✔ 1. Measure lactate level (remeasure if it is >2mmol/L)
  1. Obtain blood cultures before administering antibiotics
  2. Administer broad-spectrum antibiotics
  3. Rapidly administer 30ml/kg crystalloid for hypotension or lactate >4mmol/L
  4. Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a MAP >65 mmhg How much fluid should you give following the first 3 hours of sepsis presentation? -- Answer ✔✔ 30ml/kg As much as 6-10L of isotonic crystalloids and 2-4 L of colloids are needed in the first 6 hours to achieve target CVP of 8- 12 mmhg

And circulatory failure due to massive vasodilation What are the life-threatening responses to anaphylaxis? -- Answer ✔✔ bronchoconstriction and laryngeal edema Signs and symptoms of anaphylactic shock -- Answer ✔✔ - Decreased BP

  • Increased HR
  • Increased RR
  • Wheezing, stridor
  • Swelling of lips and tongue, angioedema Flushing, pruritus, urticaria Resp distress Anxiety, confusion, dizziness Sense of impending doom What is the treatment for anaphylactic shock in order? -- Answer ✔✔ - epinephrine (x q10-15min)
  • antihistamines
  • steroids What is the action of epinephrine? -- Answer ✔✔ alpha: increases vascular constriction and reduces edema Beta: dilates airways, increases force of contraction and decreases histamine release (blocks histamine agonists and other vasodilating/broncho constricting substances released) Also stabilizes mast cells that reduces release of harmful mediators

What is the preferred route and location of epinephrine -- Answer ✔✔ vastus lateralus IM because of increased rate and concentration. Higher and rapid maximum plasma concentrations compared with deltoid What are the second and third line drugs for anaphylaxis -- Answer ✔✔ Benadryl (diphenhydramine) Ranitidine (third line treatment) What is the difference in action between Benadryl and ranitidine? -- Answer ✔✔ Benadryl works on H1 receptors Ranitidine works on H2 receptors and helps prevent delayed or late phase rxns by blocking the h2 pathway What do H1 receptors do? -- Answer ✔✔ - bronchoconstriction/resp distress

  • cough d/t vagus nerve stimulation
  • edema due to increased permeability of veins and capillaries
  • nasal congestion due to increased secretion from mucous glands
  • pain and pruritus due to stimulation of sensory peripheral nerve endings
  • dilation of capillaries causing skin flushing What do H2 receptors do? -- Answer ✔✔ - increase secretion of gastric acid and pepsin
  • increase rate and force of myocardial contraction
  • decreased immunologic and proinflammatory rxns Why would you not administer antihistamines alone in anaphylaxis? -- Answer ✔✔ - slow onset
  • minimal effect on bp
  • vasomotor center depression: drugs (barbiturates), severe pain, hypoglycemia (insulin shock d/t decreased glucose to brain, decreased SNS) Spinal shock -- Answer ✔✔ loss of reflexes below level of injury Similar to high levels of spinal anaesthesia How quickly can neurogenic shock occur? -- Answer ✔✔ it is a hemodynamic phenomenon that can occur within 30 mins of a spinal cord injury at the T5 vertebra or above and can last up to 6 weeks Can brain damage alone cause shock -- Answer ✔✔ no not usually What happens in neurogenic shock -- Answer ✔✔ - loss of sympathetic tone causes massive vasodilation. This allows for unopposed parasympathetic control of the heart
  • inhibition of baroreceptors
  • impaired thermoregulation What are the signs and symptoms of neurogenic shock -- Answer ✔✔ - poikilothermia (initially warm then takes on temp of environment; risk of hypothermia)
  • hypotension
  • bradycardia
  • temp dysregulation Treatment for neurogenic shock -- Answer ✔✔ - maintain normal hr (atropine)
  • maintain BP (sbp>90 MAP>60)
  • maintain normothermia

How should you administer IV fluids in neurogenic shock -- Answer ✔✔ 30ml/h to maintain u/o and SBP > What is atherosclerosis? -- Answer ✔✔ abnormal accumulation of lipid substances and fibrous tissue lining arterial wall Describe the process of atherosclerosis -- Answer ✔✔ 1. Injury to vessel wall by risk factors

  1. Inflammation occurs and macrophages infiltrate injured tissue, becoming foam cells because they ingest fat
  2. Smooth muscle cells proliferate and form a fibrous cap= atheromas (plaque)
  3. Because this plaque increases blood turbulance, it ruptures. Then platelets are activated and coagulation cascade occurs resulting in a fibrin clot and a thrombus Risk factor for men for atherosclerosis -- Answer ✔✔ - men have greater risk and especially if they are 55.
  • women postmenopausal are at great risk too because estrogen is cardioprotective Heredity risk factor for heart disease -- Answer ✔✔ - 1st deg relative with CV dx at 55 or younger for men
  • 1st deg relative with cv dx at 65 or younger for women Modifiable risk factors for heart disease -- Answer ✔✔ - elevated serum lipid levels/cholesterol
  • obesity
  • htn
  • tobacco
  • dm

How can DM increase platelet aggregation -- Answer ✔✔ hyperglycemia can cause dyslipidemia What is released during times of intense stress -- Answer ✔✔ catecholamines, increasing risk for a cardiovascular event Max drinks for women and men -- Answer ✔✔ women: 2drinks/day, 10/week Men: 3drinks/day, 15/week How do drugs like cocaine increase risk of CV event -- Answer ✔✔ increase homocysteine (also released with breakdown of protein) This damages blood vessels, promotes plaque buildup, alter clotting mechanisms What is metabolic syndrome aka syndrome x? -- Answer ✔✔ - group of risk factors that increase risk for heart disease, stroke and diabetes

  • 3 or more of these conditions:
  • high blood cholesterol
  • high blood pressure
  • obesity (abdominal fat)
  • high blood sugar
  • low HDL What is angina -- Answer ✔✔ chest pain that is the result of myocardial ischemia Types of angina -- Answer ✔✔ stable
  • follows a predictable pattern
  • relieved with rest/medication Unstable
  • unexpected
  • risk for heart attack, dysrhythmia or sudden death Variant (aka prinzmetals angina)
  • happens spontaneously at rest
  • very pain, between midnight and 8am
  • caused by coronary artery spasm (close to a blockage) Microvascular angina (aka cardiac syndrome x)
  • chest pain but without any apparent blockage in coronary arteries
  • caused by improper functioning of coronary arteries Atypical angina
  • vague chest discomfort, SOB, fatigue, nausea, back or neck pain or burning indigestion
  • women more likely Triggers for angina -- Answer ✔✔ - exertion
  • cold
  • eating (blood in gut so decreased supply)
  • stress (catecholamines) Difference between NSTEMI and STEMI -- Answer ✔✔ NSTEMI = Non-ST elevation MI (partial thickness infarction) - will see ST depression. STEMI = ST elevation MI (Full thickness infarction) Collateral circulation -- Answer ✔✔ arterial branching aka arterial anastomoses.