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Comprehensive vocabulary flashcards covering cardiovascular/perfusion, hematology/VTE, digestion/bowel elimination, immunity/sepsis, infection control precautions, and dosage calculation concepts.
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Peripheral Arterial Disease (PAD) Etiology
Inadequate tissue perfusion caused by impaired arterial blood flow reaching the extremities.
Chronic Venous Insufficiency Etiology
Inadequate venous return causing blood to pool in the lower extremities.
Intermittent Claudication
Ischemic muscle pain characteristic of PAD that worsens with walking and exertion and is relieved by rest; can advance to rest pain in severe disease.
Chronic Venous Insufficiency Pain
Aching and heaviness in the legs that worsens after prolonged standing and typically improves with leg elevation.
PAD Skin and Temperature Findings
Cool, shiny, thin skin with decreased hair growth, exhibiting pallor on elevation and dependent rubor.
Chronic Venous Insufficiency Skin Findings
Warm or normal extremity temperature with brown hemosiderin staining, edema, and stasis dermatitis.
Hemosiderin Staining
Brownish skin discoloration occurring on the lower legs in chronic venous insufficiency due to red blood cell breakdown in pooled blood.
Dependent Rubor
A reddish-blue discoloration of the extremity when dangling in a dependent position, characteristic of severe peripheral arterial disease.
PAD Pulses and Capillary Refill
Weak, diminished, or absent peripheral pulses accompanied by delayed capillary refill.
Chronic Venous Insufficiency Pulses and Refill
Peripheral pulses are usually present and palpable, and capillary refill is often preserved.
Arterial Ulcer Characteristics
Punched-out, deep, pale, and dry wounds with minimal drainage located on the toes, feet, and bony pressure points.
Venous Stasis Ulcer Characteristics
Shallow, irregular, and moist wounds with substantial drainage located near the medial ankle and lower leg.
PAD Edema Presentation
Minimal to absent swelling unless a coexisting non-arterial cause is present.
Chronic Venous Insufficiency Edema Presentation
Common lower extremity swelling that typically worsens by the end of the day.
PAD Limb Positioning Guideline
Avoid prolonged leg elevation if it worsens ischemic pain; avoid compression therapy unless ordered after arterial status assessment.
Venous Insufficiency Limb Positioning Guideline
Elevate the legs above heart level and apply compression therapy if ordered and arterial perfusion is confirmed adequate.
Compression Therapy Precaution in Arterial Disease
Never apply compression to suspected significant arterial disease without first verifying arterial circulation and ankle-brachial index (ABI).
DVT Massage Contraindication
Never massage a limb with a suspected deep vein thrombosis due to the critical risk of dislodging the clot into a pulmonary embolism.
Peripheral Arterial Disease (PAD) Risk Factors
Smoking, diabetes mellitus, hypertension, dyslipidemia, older age, atherosclerosis, chronic kidney disease, physical inactivity, and family history.
Neurovascular Assessment Components
Bilateral comparison of pain, pallor/color, temperature, pulses (palpation or Doppler), capillary refill, sensation, movement, and swelling.
6 Ps: Pain
Sudden, severe discomfort or pain out of proportion to exam findings indicating acute arterial compromise.
6 Ps: Pallor
Unnatural paleness of the affected limb indicating compromised arterial blood flow.
6 Ps: Pulselessness
Absent or significantly diminished distal pulse indicative of acute arterial occlusion.
6 Ps: Paresthesia
Tingling, numbness, or altered sensation in an extremity indicating ischemic nerve compromise.
6 Ps: Paralysis
Weakness or inability to move an extremity; represents a late, ominous sign of severe arterial compromise.
6 Ps: Poikilothermia
The affected limb becomes cool or cold because it takes on ambient temperature due to absent arterial perfusion.
Acute Limb Ischemia
A vascular emergency characterized by sudden limb pain, cold/pale skin, new numbness/weakness, or absent pulse requiring immediate notification of the provider or rapid response.
PAD Thermal Protection Teaching
Avoid heating pads, hot water bottles, and direct heat sources due to impaired sensation and thermal burn risk; protect extremities from cold exposure.
Ankle-Brachial Index (ABI) Formula
The ankle systolic blood pressure divided by the brachial systolic blood pressure.
Normal Ankle-Brachial Index (ABI) Range
An ABI value generally between 1.00 and 1.40.
Ankle-Brachial Index (ABI) Value Supporting PAD
An ABI value less than or equal to 0.90.
Ankle-Brachial Index (ABI) Value Indicating Noncompressible Arteries
An ABI value greater than 1.40, suggesting rigid, calcified arteries.
Stable Angina
Predictable chest discomfort induced by exertion or emotional stress that is relieved by rest or prescribed sublingual nitroglycerin, without myocardial necrosis.
Unstable Angina
New, worsening, more frequent, or rest chest pain representing acute coronary syndrome that is not reliably relieved by rest and lacks troponin elevation.
Non-ST-Elevation Myocardial Infarction (NSTEMI)
Myocardial injury manifested by elevated cardiac troponins without persistent ST-segment elevation on a 12-lead ECG.
ST-Elevation Myocardial Infarction (STEMI)
Acute myocardial injury with qualifying persistent ST-segment elevation on ECG, indicating acute coronary occlusion requiring immediate emergency reperfusion.
Myocardial Infarction Red Flags
Substernal pressure or tightness, radiation to arm/jaw/back, dyspnea, diaphoresis, nausea, and unexplained fatigue.
Atypical MI Presentation
Subtle or non-classic symptoms such as unusual fatigue, shortness of breath, or nausea commonly seen in older adults, females, and patients with diabetes.
Suspected ACS Priority First Actions
Activate emergency response/911, assess ABCs and vital signs, obtain a rapid 12-lead ECG, draw troponin, administer aspirin if indicated, and administer targeted oxygen/nitroglycerin per safety parameters.
12-Lead ECG Timing Target in ED
Commonly obtained within 10minutes of arrival for patients presenting with chest pain or suspected acute coronary syndrome.
ACS Oxygen Administration Rule
Reserved only for documented hypoxemia, respiratory distress, or specific protocol orders rather than automatic routine administration.
Nitroglycerin Hemodynamic Precautions
Assess blood pressure before and after administration; avoid if severe hypotension is present or in suspected right-ventricular infarction.
Nitroglycerin and PDE-5 Inhibitor Interaction
Strictly contraindicated within recent use of phosphodiesterase-5 inhibitors (e.g., sildenafil, tadalafil) due to the risk of life-threatening, refractory hypotension.
Heart-Healthy Dietary Guidelines
Reduce saturated and trans fats, sodium, processed meats, and added sugars while emphasizing vegetables, fruits, whole grains, legumes, nuts, lean proteins, and unsaturated fats.
Low-Density Lipoprotein (LDL)
The primary atherogenic lipoprotein targeted in cardiovascular risk reduction therapy.
High-Density Lipoprotein (HDL)
Cardioprotective lipoprotein involved in reverse cholesterol transport from peripheral tissues back to the liver.
Statins (HMG-CoA Reductase Inhibitors) Mechanism
Medications that inhibit cholesterol synthesis in the liver to lower circulating LDL levels and decrease cardiovascular event risk.
Pre-Cardiac Catheterization Nursing Assessments
Verify informed consent, assess iodine/radiopaque contrast allergies, evaluate renal function, document baseline distal pulses and neurovascular status, check vitals, review bleeding history, and verify NPO status.
Metformin and Radiopaque Contrast Precaution
Discontinue metformin prior to or at the time of contrast procedures and withhold per protocol to avoid contrast-induced acute kidney injury and lactic acidosis.
Post-Cardiac Catheterization Assessments
Continuous ECG/vitals monitoring, inspecting access puncture site for bleeding/hematoma, checking distal pulses/color/temperature/sensation, and assessing urine output and chest pain.
Post-Femoral Access Positioning
Enforce strict bedrest with the affected leg kept straight for the prescribed duration to prevent femoral arterial bleeding.
Retroperitoneal Hemorrhage Clinical Signs
Unexplained hypotension, tachycardia, and back or flank pain following femoral cardiac catheterization.
Contrast-Associated Acute Kidney Injury Prevention
Encourage adequate oral or IV hydration before and following cardiac catheterization if not clinically contraindicated.
Left-Sided Heart Failure Clinical Manifestations
Pulmonary congestion symptoms including dyspnea, orthopnea, bilateral pulmonary crackles, cough, hypoxemia, paroxysmal nocturnal dyspnea, and pulmonary edema.
Right-Sided Heart Failure Clinical Manifestations
Systemic venous congestion symptoms including dependent peripheral edema, jugular venous distention (JVD), hepatomegaly, ascites, and rapid fluid weight gain.
Heart Failure with Reduced Ejection Fraction (HFrEF)
Systolic heart failure characterized by impaired ventricular contraction and reduced ejection fraction, commonly ≤40%.
Heart Failure with Preserved Ejection Fraction (HFpEF)
Diastolic heart failure characterized by impaired ventricular relaxation and filling, where ejection fraction is preserved (often ≥50%) despite clinical congestion.
Left Ventricular Ejection Fraction (LVEF)
The percentage of end-diastolic blood volume pumped out of the left ventricle with each contraction.
Worsening Heart Failure Indicators
Rapid weight gain, worsening peripheral edema, increasing dyspnea/orthopnea, decreasing oxygen saturation, new lung crackles, confusion, decreased urine output, tachycardia, or hypotension.
Acute Decompensated Heart Failure Positioning
Place the patient in an upright, high-Fowler's position to reduce venous return and optimize diaphragmatic expansion.
IV Loop Diuretic Response Evaluation in HF
Measure hourly urine output, daily weight trends, lung sounds, oxygen saturation, resolution of peripheral edema, renal panels, and electrolytes.
Heart Failure Daily Weight Protocol
Weigh every morning immediately upon waking after voiding, using the same scale and similar clothing.
Heart Failure Weight Gain Reporting Thresholds
Notify the provider for a weight gain of 2–3lb in 24hours or 5lb within one week.
NSAID Precaution in Heart Failure
Avoid nonsteroidal anti-inflammatory drugs because they cause sodium and water retention and attenuate renal function, worsening heart failure.
Diuretic Monitoring Priorities
Assess intake and output, daily weight, blood pressure/orthostasis, potassium, magnesium, sodium, BUN/creatinine, and signs of volume depletion.
Hypertension "Silent Killer" Concept
Chronic elevated arterial pressure causes progressive, asymptomatic vascular damage leading to MI, HF, stroke, nephropathy, and retinopathy.
Hypertensive Emergency
Severe blood pressure elevation accompanied by acute target-organ injury (e.g., encephalopathy, stroke, ACS, pulmonary edema, aortic dissection, or acute renal failure).
Hypertensive Urgency
Severe blood pressure elevation without evidence of acute target-organ damage, requiring prompt evaluation and gradual outpatient/inpatient medication titration.
Hypertensive Emergency Blood Pressure Reduction Goal
Requires monitored, controlled IV medication titration to prevent precipitous drops in perfusion pressure that could cause cerebral or myocardial ischemia.
Metoprolol Pharmacologic Class and Action
Beta-1 selective adrenergic blocker that decreases heart rate, blood pressure, myocardial contractility, and cardiac workload.
Metoprolol Pre-Administration Assessment
Check apical heart rate and blood pressure; hold medication based on specific provider parameters (commonly HR <60beats/min or systolic BP <90–100mmHg).
Metoprolol Hypoglycemia Precaution
Beta-blockers can mask classic adrenergic signs of hypoglycemia (e.g., tachycardia, tremors), leaving diaphoresis as the primary recognizable indicator.
Atorvastatin Patient Education and Adverse Effects
Report unexplained muscle pain, tenderness, weakness, or dark/tea-colored urine immediately due to the risk of myopathy or rhabdomyolysis; monitor liver enzymes.
Aspirin Antiplatelet Mechanism
Irreversibly inhibits platelet cyclooxygenase, reducing thromboxane A2 formation and preventing platelet aggregation.
Lisinopril Mechanism of Action
Angiotensin-converting enzyme (ACE) inhibitor that blocks conversion of angiotensin I to angiotensin II, decreasing systemic vascular resistance and afterload.
Lisinopril Adverse Effects and Contraindications
Causes dry persistent cough, hyperkalemia, renal impairment, and angioedema; contraindicated during pregnancy.
ACE Inhibitor Angioedema Presentation
Rapid swelling of the lips, tongue, pharynx, or face representing a life-threatening airway emergency requiring immediate medical intervention.
Losartan Pharmacologic Class and Advantage
Angiotensin II receptor blocker (ARB) that blocks angiotensin II receptors; provides hemodynamic benefits similar to ACE inhibitors with a significantly lower incidence of cough.
Digoxin Mechanism of Action
Cardiac glycoside that exerts positive inotropic effects (increases contractility) and negative chronotropic/dromotropic effects (slows AV node conduction).
Digoxin Pre-Administration Check
Auscultate the apical pulse for one full minute; withhold and contact the provider if the heart rate is below ordered parameters (typically <60beats/min in adults).
Digoxin Toxicity Clinical Manifestations
Anorexia, nausea, vomiting, fatigue, confusion, blurred vision, green-yellow halos around objects, and cardiac dysrhythmias.
Electrolytes Increasing Digoxin Toxicity Risk
Hypokalemia and hypomagnesemia enhance digoxin binding, significantly increasing the risk of life-threatening digitalis toxicity.
Furosemide Mechanism of Action
Loop diuretic that inhibits the Na+-K+-2Cl− cotransporter in the thick ascending limb of the loop of Henle, promoting potent diuresis.
Furosemide Adverse Effects
Hypokalemia, hypomagnesemia, hyponatremia, dehydration, orthostatic hypotension, elevated BUN/creatinine, and ototoxicity with rapid IV push.
Spironolactone Mechanism and Electrolyte Effect
Aldosterone receptor antagonist (potassium-sparing diuretic) that promotes sodium/water excretion while conserving potassium, risking hyperkalemia.
Spironolactone Dietary Precaution
Instruct patients to avoid potassium supplements and potassium-based salt substitutes to prevent dangerous hyperkalemia.
Nitroglycerin Mechanism of Action
Direct nitric-oxide mediated smooth muscle relaxation resulting in peripheral vasodilation, primarily reducing venous preload and myocardial oxygen demand.
Clopidogrel Pharmacologic Class and Clinical Indication
Oral P2Y12 platelet adenosine diphosphate (ADP) receptor antagonist used in acute coronary syndromes, coronary stents, PAD, and ischemic stroke.
Clopidogrel Post-Stent Adherence
Do not discontinue clopidogrel prematurely following stent placement without cardiology authorization due to the severe risk of acute stent thrombosis.
Pentoxifylline Mechanism and Indication
Rheologic agent that decreases blood viscosity and improves red blood cell flexibility to enhance microcirculatory flow in intermittent claudication.
Unfractionated Heparin Mechanism
Binds to antithrombin III to accelerate inactivation of factor Xa and thrombin (factor IIa).
Heparin Reversal Agent
Protamine sulfate binds and neutralizes unfractionated heparin and partially neutralizes low-molecular-weight heparin.
Enoxaparin (LMWH) Administration Technique
Inject subcutaneously into the anterolateral or posterolateral abdominal wall; do not massage the site; do not expel the prefilled air bubble prior to injection.
Warfarin Mechanism of Action
Vitamin K antagonist that inhibits hepatic synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and regulatory proteins C and S.
Warfarin Reversal Agents
Vitamin K (phytonadione) reverses routine elevated INR; severe or life-threatening hemorrhage requires prothrombin complex concentrate (PCC) or fresh frozen plasma.
Warfarin Dietary Education
Maintain a consistent day-to-day intake of vitamin K-rich foods (green leafy vegetables) rather than eliminating them completely, to prevent fluctuating INR levels.
Cardiac Troponin I and T
The preferred, highly sensitive biomarkers for diagnosing myocardial necrosis; levels rise within hours of injury and can remain elevated for days.
Serial Troponin Testing Rationale
A single early negative troponin does not exclude acute coronary syndrome; sequential trending paired with ECG and clinical symptoms is mandatory.
Creatine Kinase-MB (CK-MB)
Cardiac enzyme marker that rises after injury but returns toward baseline quicker than troponin, making it useful in identifying early reinfarction.
B-Type Natriuretic Peptide (BNP / NT-proBNP)
Neurohormone released from ventricular myocytes in response to increased intracardiac wall tension and volume stretch, supporting HF diagnosis.