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2460 EXAM 1
| Question | Answer |
|---|---|
| What is the underlying problem in shock? | Inadequate tissue perfusion and oxygen delivery |
| What happens when tissues do not receive enough oxygen? | Cellular hypoxia → organ dysfunction |
| What are the 3 major shock types for Exam 1? | Septic, neurogenic, cardiogenic |
| Cardiogenic shock = what basic problem? | Pump failure |
| Septic shock = what major trigger? | Infection with systemic inflammatory/perfusion abnormalities |
| Neurogenic shock is associated with what major risk factor? | Spinal cord injury or spinal anesthesia |
| What are the stages of shock? | Compensatory → progressive → refractory/irreversible |
| Why is lactate important in shock? | Helps identify impaired tissue perfusion/anaerobic metabolism |
| What does MAP reflect? | Perfusion pressure to organs |
| What does a rising creatinine suggest in shock? | Worsening renal function/perfusion |
| First-line vasopressor listed for septic shock? | Norepinephrine |
| What medication increases contractility in cardiogenic shock? | Dobutamine |
| What does an inotrope do? | Increases force of cardiac contraction |
| What does a vasopressor do? | Raises vascular tone/BP to support perfusion |
| What is MODS? | Multiple Organ Dysfunction Syndrome |
| What is SIRS? | Systemic Inflammatory Response Syndrome |
| What is AFib? | Disorganized atrial electrical activity |
| What happens to atrial kick in AFib? | It is lost |
| Loss of atrial kick causes what? | ↓ ventricular filling → ↓ stroke volume/CO |
| Classic AFib ECG? | Irregularly irregular with absent discernible P waves |
| Major complication of AFib? | Thromboembolism/stroke |
| Does stroke risk disappear when AFib rate is controlled? | No |
| Priority question with AFib/RVR? | Is the patient stable or unstable? |
| Treatment listed for unstable AFib/RVR? | Synchronized cardioversion |
| Diltiazem is used for what in AFib? | Rate control |
| Metoprolol is used for what in AFib? | Rate control |
| Why are anticoagulants used in AFib? | Reduce thromboembolic/stroke risk |
| Why check K⁺ and Mg²⁺ in AFib | ? Abnormalities can increase dysrhythmia risk |
| Why check TSH/free T4? | Thyroid dysfunction can trigger AFib |
| Troponin evaluates what? | Myocardial injury/ischemia |
| Echo evaluates what? | Cardiac structure and function |
| What is hypoxemia? | Low oxygen in arterial blood |
| What is hypoxia? | Inadequate tissue oxygen |
| What is hypercapnia? | Elevated CO₂ |
| What is ventilation? | Movement of air into and out of lungs |
| What is perfusion? | Blood flow |
| What is V/Q mismatch? I | mbalance between ventilation and perfusion |
| What does an ABG assess? | Oxygenation, ventilation and acid-base status |
| What does pulse oximetry measure? | Oxygen saturation |
| What is orthopnea? | Difficulty breathing while lying flat |
| What is hemoptysis? | Coughing up blood |
| What is atelectasis? | Collapse/incomplete expansion of alveoli/lung tissue |
| What is pneumothorax? | Air in pleural space |
| What is hemothorax? | Blood in pleural space |
| What is ARDS? | Acute severe respiratory disorder causing major impairment in oxygenation |
| What is refractory hypoxemia? | Low blood oxygen that remains difficult to correct |
| What does albuterol do? | Bronchodilation |
| What does ipratropium do? | Anticholinergic bronchodilation |
| Why use corticosteroids in respiratory disease? | Reduce inflammation |
| CPAP/BiPAP are what type of ventilation? | Noninvasive |
| Endotracheal intubation is what type? | Invasive ventilation |
| What is the priority of end-of-life care? | Comfort, dignity and patient goals |
| Is decreased appetite expected near end of life? | Yes |
| What is Cheyne-Stokes breathing? | Cyclic changes in breathing with periods of apnea |
| Morphine at end of life treats what? | Pain and dyspnea |
| Lorazepam at end of life treats what? | Anxiety/agitation |
| Glycopyrrolate/scopolamine treat what? | Respiratory secretions |
| What is hospice? | Comfort-focused end-of-life care |
| What is palliative care? | Care focused on symptom relief and quality of life |
| What is DNR? | Do not resuscitate |
| What is DNI? | Do not intubate |
| What is an advance directive? | Document communicating healthcare wishes |
| What is autonomy? | Patient's right to make informed healthcare decisions |
| SHOCK: 76F, pneumonia. T 102.4, HR 126, RR 30, BP 86/48, SpO₂ 91%, confused, UO 15 mL/hr, lactate 4.3. Warm/flushed. What is occurring? | Septic shock/impaired perfusion. Infection + hypotension + ↑ lactate + AMS + oliguria. Warm skin suggests vasodilation/↓ SVR. |
| SHOCK: BP 108/68 → 96/60, HR 118, RR 26, anxious, cool skin, UO 20 mL/hr. BP isn't severely low. Why worry? | Compensatory shock. Tachycardia, vasoconstriction and fluid retention may maintain BP temporarily despite falling tissue perfusion. |
| CARDIOGENIC: Post-MI patient: BP 78/46, HR 122, crackles, JVD, cool clammy skin, UO 15 mL/hr. What links these findings? | Pump failure → ↓ CO + pulmonary congestion. Hypotension/oliguria = poor forward flow; crackles/JVD = backup/congestion. |
| SHOCK: Spinal injury. BP 76/40, HR 48, skin warm/dry. Which shock pattern? | Neurogenic shock. Loss of sympathetic tone → ↓ SVR + hypotension; loss of sympathetic cardiac stimulation can cause bradycardia. |
| SHOCK: After treatment, which trends show improved perfusion? | Improved LOC, BP/MAP, urine output and peripheral perfusion; decreasing lactate supports improving tissue perfusion. |
| ARF: SpO₂ 95% on O₂, but patient becomes drowsy; RR 8, shallow. Why is this an emergency? | Ventilation may be failing. SpO₂ measures oxygen saturation, not CO₂ removal. Hypoventilation can cause ↑ PaCO₂ and respiratory acidosis. |
| ARF ABG: pH 7.28, PaCO₂ 58, HCO₃ 25, PaO₂ 66. Interpret. | Acute respiratory acidosis + hypoxemia. ↓ pH + ↑ CO₂ = inadequate ventilation; low PaO₂ = impaired oxygenation. |
| RESP: Severe asthma patient was wheezing loudly; now breath sounds are barely audible and patient is drowsy. Better or worse? | WORSE—emergency. Minimal air movement + fatigue/↓ LOC may indicate impending respiratory failure. |
| ARDS: Sepsis patient develops severe dyspnea, bilateral infiltrates and persistent hypoxemia despite O₂. What process is occurring? | ARDS: inflammatory alveolar-capillary injury → permeability ↑ → noncardiogen |
| ARDS: Why can increasing oxygen alone fail to correct severe hypoxemia? | Fluid/collapsed alveoli create severe V/Q mismatch and shunting; blood passes poorly ventilated alveoli without adequate oxygenation.ic pulmonary edema → severe impaired gas exchange. |
| HF: HF patient: RR 32, SpO₂ 84%, diffuse crackles, orthopnea, anxious. Priority problem? | Acute pulmonary congestion impairing oxygenation. Upright position, ABC assessment, respiratory support and prescribed acute HF treatment. |
| HF: Weight +6 lb, edema, JVD, crackles, BNP ↑. What connects these findings? | Volume overload/congestion. Increased filling pressures cause systemic/pulmonary congestion and ventricular stretch. |
| HF: Confusion, cool extremities, BP 82/48 and UO 15 mL/hr. What are these telling you? | Poor cardiac output/systemic perfusion. Brain, skin, kidneys and BP show inadequate forward flow. |
| HF: Why can RAAS compensation eventually worsen HF? | RAAS causes vasoconstriction + Na⁺/water retention → ↑ afterload + preload → greater cardiac workload/congestion. |
| AFIB: HR 154 irregular, no distinct P waves, BP 118/72, alert, no chest pain. Rhythm/problem? | AFib with RVR; currently stable. Chaotic atrial activity + rapid irregular ventricular response. Assess rate and perfusion. |
| AFIB: AFib/RVR patient now BP 72/40, confused, diaphoretic with chest discomfort. What changed? | Hemodynamic instability. Tachyarrhythmia is impairing perfusion; anticipate urgent synchronized cardioversion. |
| AFIB: Why can HR 160 LOWER cardiac output even though HR is higher? | Very rapid rate shortens diastolic filling time; loss of atrial kick further ↓ filling → ↓ SV → potentially ↓ CO. |
| AFIB: Why is anticoagulation considered even after the ventricular rate improves? | AFib causes atrial blood stasis → thrombus formation → embolic stroke risk. Rate control does not eliminate thromboembolic risk. |
| COMPARE: Warm/flushed + infection + hypotension vs cool/clammy + crackles after MI. shock. | Warm/infection = septic shock. Cool + pulmonary congestion after MI = cardiogenic |
| COMPARE: Crackles + edema + JVD + weight gain vs severe hypoxemia + bilateral infiltrates after sepsis. | First suggests HF/cardiogenic congestion; second raises concern for ARDS, especially severe refractory hypoxemia after systemic insult. |
Created by:
Anmag002