Master cardiac and vascular disorders in one comprehensive, exam-ready guide — from MI and PVD to heart failure and dysrhythmias.
This in-depth study guide (MED101) covers every major cardiac and vascular disorder you'll encounter in nursing school and on certification exams. Written in clear, organized sections with pathophysiology, symptoms, diagnostics, and management for each condition — it's the only cardiac-vascular guide you need.
What's Inside:
Myocardial Infarction (MI)
Pathophysiology: coronary thrombosis, ischemia, necrosis, inflammatory response
Cardiac markers: troponin I/T, myoglobin, CK-MB, LDH — timelines and sensitivity
ECG changes: ST elevation, T-wave inversion, Q waves — localization and extent
Symptoms: crushing chest pain, radiation, diaphoresis, nausea, left-sided HF signs
Complications: dysrhythmias, cardiogenic shock, ventricular rupture, aneurysm, embolism, pericarditis, mitral regurgitation, heart failure
Management: thrombolytics (2-hour window), PCI (1–2 hours), CABG, antiarrhythmics, oxygen, CCU monitoring
Post-MI rehab: activity progression, heart-healthy diet, medication adherence, psychosocial support
Peripheral Vascular Disease (PVD)
Causes: atherosclerosis, arteriosclerosis, vasoconstriction, thrombosis
Risk factors: smoking, obesity, hypertension, hyperlipidemia, diabetes, family history, sedentary lifestyle
Peripheral arterial disease symptoms: intermittent claudication, coldness, pallor, rubor on dependency, skin changes, weak pulses, cyanosis
Treatment: vasodilators, anticoagulants, exercise, lifestyle modification, bypass grafts, endarterectomy, amputation
Raynaud's Disease & Buerger's Disease
Raynaud's: episodic vasospasm, triggers, pallor/cyanosis/numbness, management with vasodilators, cold avoidance, sympathectomy
Buerger's: inflammatory occlusive disease in smokers, symptoms, critical tobacco cessation, vasodilators, amputation if necrotic
Aneurysm
Definition, risk factors (hypertension, arteriosclerosis, trauma, congenital weakness)
Signs: pulsatile mass, bruit, compression symptoms, rupture → hemorrhage/shock
Diagnosis: X-ray, aortography
Treatment: BP control, surgical repair, endovascular stenting, emergency surgery
Heart Failure
Pathophysiology: inability to pump sufficient blood, congestion + hypoperfusion
Types: left-sided (pulmonary congestion), right-sided (systemic congestion), systolic, diastolic
Causes: MI, hypertension, cardiomyopathies, valvular disease, cor pulmonale
Signs: fatigue, dyspnea, orthopnea, PND, crackles, tachycardia, edema, elevated BNP
Diagnosis: BNP, chest X-ray, echocardiogram, ABGs
Management: rest, low-sodium diet, fluid restriction, digoxin, diuretics, ACE inhibitors, beta-blockers, IABP, VAD, transplant
Pulmonary Edema
Mechanism: left ventricular failure → alveolar fluid accumulation
Symptoms: dyspnea, wheezing, orthopnea, frothy sputum, cyanosis, tachycardia
Treatment: inotropes, diuretics, vasodilators, oxygen, upright positioning
Hypertension
Definition: sustained BP 140/90 mmHg — "silent killer"
Types: essential (95%), secondary
Risk factors: age, race, family history, obesity, sodium, alcohol, smoking, stress
Diagnosis: multiple readings, home monitoring, ECG, labs (BUN, creatinine, cholesterol, triglycerides)
Management: lifestyle modification, diuretics, ACE inhibitors, calcium channel blockers, beta-blockers
Accelerated vs. malignant hypertension: retinal hemorrhages, papilledema, renal failure, stroke risk — IV antihypertensives
Varicose Veins
Etiology: valve incompetence, venous hypertension
Symptoms: heavy/tired legs, visible swellings, skin changes, ulcerations
Treatment: support stockings, sclerotherapy, vein ligation/stripping, wound care
Thrombophlebitis & Phlebothrombosis
Thrombophlebitis: inflammation + clot (superficial)
Phlebothrombosis: clot without inflammation (deep — DVT)
Signs: swelling, warmth, redness, tenderness, positive Homan's sign
Management: rest, elevation, warm compresses, anticoagulants, thrombectomy, vena cava filters
Lymphedema
Causes: lymphatic obstruction after surgery, radiation, infection
Symptoms: persistent swelling, skin tightness, thickening, ulcer risk
Management: elevation, compression, manual lymphatic drainage, exercise, surgery
Pulmonary Embolism (PE)
Pathophysiology: thrombus dislodges → pulmonary artery occlusion
Symptoms: sudden chest pain, dyspnea, tachypnea, hemoptysis, cyanosis
Treatment: anticoagulation (heparin, warfarin), thrombolytics, oxygen, embolectomy, vena cava filters
Cardiac Dysrhythmias
Bradycardia, tachycardia, atrial fibrillation, atrial flutter
Heart blocks: first-degree, second-degree (Wenckebach, Mobitz II), third-degree
Ventricular arrhythmias: PVCs, VT, VF, asystole
Treatments: medications, defibrillation, cardioversion, pacemakers, ICDs
Pacemaker Function & Patient Care
Temporary vs. permanent, demand vs. fixed-rate
Patient education: ID cards, daily pulse monitoring, symptom reporting, device evaluations
Cardiac Arrest & CPR
Step-by-step: responsiveness, airway, breathing, pulse, 30:2 compressions, AED, continue until help arrives
CABG & Cardiac Surgery Care
Graft vessels: saphenous vein, internal mammary artery
Preoperative: education, organ function, consent
Content preview
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Comprehensive Guide to Cardiac and Vascular Disorders
(MED101)
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Comprehensive Guide to Cardiac and Vascular
Disorders
Myocardial Infarction (MI) Definition and
Pathophysiology
MI is tissue necrosis in the heart muscle resulting from prolonged, total occlusion of
a coronary artery. This blockage is most commonly caused by coronary thrombosis,
where a blood clot forms within a coronary vessel, often secondary to
arteriosclerotic and atherosclerotic changes. The interruption of blood flow leads to
ischemia, triggering an inflammatory response. Damaged myocardial cells release
intracellular markers such as troponin, myoglobin, CK-MB, and LDH into the
bloodstream, which are essential for diagnosis. The extent of necrosis correlates with
the severity of the damage—the larger the infarcted area, the worse the prognosis.
Symptoms and Diagnostic Tests of MI
Patients typically present with sudden, severe chest pain that is often described as
crushing and may radiate to the shoulders, arms, jaw, teeth, or throat. This pain
persists despite rest and nitrates, indicating ischemia. Accompanying symptoms
include diaphoresis, nausea, vomiting, pallor, apprehension, and weakness. On
physical exam, signs of left-sided heart failure such as dyspnea, cyanosis, and cough
may be observed.
Diagnosis relies heavily on:
Serum cardiac enzymes: Troponin I and T are the most sensitive, elevating within 4-
6 hours and peaking at 12 hours.
Myoglobin: Elevates quickly (~2 hours) but has low specificity.
ECG changes: Elevation of the ST segment, T wave inversion, and the appearance
of Q waves within hours to days. These changes help localize and assess the
extent of infarction.
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Complications of Myocardial Infarction
MI can lead to life-threatening complications, including:
Dysrhythmias: Ranging from premature beats to ventricular fibrillation.
Cardiogenic shock: Due to extensive myocardial damage leading to inadequate
cardiac output.
Ventricular rupture: Soft necrotic tissue may rupture, causing hemopericardium
and cardiac tamponade.
Ventricular aneurysm: Outpouching that can lead to thrombus formation or
rupture.
Embolisms: Clots from aneurysms or infarcted tissue may dislodge.
Pericarditis: Inflammation of the pericardium.
Mitral regurgitation: Due to papillary muscle dysfunction.
Heart failure: From loss of functional myocardium, leading to pulmonary edema
and systemic congestion.
Medical and Surgical Management of MI
Immediate Interventions:
Thrombolytic therapy: Administered within 2 hours of symptom onset to dissolve
clots, using agents like streptokinase, urokinase, or r-TPA. Contraindicated in
cases of recent hemorrhage, uncontrolled hypertension, or bleeding disorders.
Percutaneous Coronary Intervention (PCI): Such as angioplasty or stenting, ideally
within 1-2 hours.
Coronary Artery Bypass Grafting (CABG): Used when PCI is not feasible or in
multivessel disease.
Supportive and Symptomatic Care:
Analgesics (e.g., nitrates, opioids) for pain relief.
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Antiarrhythmic drugs: Sodium channel blockers, beta-blockers, calcium channel
blockers.
Oxygen therapy: To relieve hypoxia.
Anticoagulants and antiplatelets: To prevent further clot formation.
Monitoring in CCU: Continuous ECG, vital signs, and assessment for early signs of
deterioration.
Surgical Options:
CABG: To bypass obstructed arteries.
Ventricular assist devices (VAD) or artificial hearts in severe cases.
Ventricular repair or transplantation: For end-stage failure.
Post-MI Rehabilitation and Nursing Care
Rest and activity: Gradual increase as tolerated.
Diet: Heart-healthy, low-fat, low-sodium.
Medication adherence: Including beta-blockers, ACE inhibitors, statins.
Psychosocial support: Address anxiety, depression.
Patient education: Recognizing symptoms of reinfarction, lifestyle modifications,
smoking cessation, stress management.
Peripheral Vascular Disease (PVD) Overview and Causes
PVD involves occlusive disorders affecting the peripheral arteries and veins, often
due to atherosclerosis, arteriosclerosis, vasoconstriction, or thrombosis. It
predominantly affects older adults and is characterized by slow healing, pain, and
progressive deterioration of blood flow to distal tissues.
Risk Factors: