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Atherosclerosis (plaque buildup in coronary arteries)

Hypertension (HTN)

Hyperlipidemia (high LDL, low HDL)

Diabetes Mellitus

Smoking

Obesity

Sedentary lifestyle

Family history of CAD

Stress

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Atherosclerosis → Narrowing of coronary arteries

Reduced blood flow → Ischemia (angina)

Plaque rupture + Thrombus formation → Complete blockage

Myocardial Infarction (MI) → Myocardial cell death (necrosis)

Complications → Heart failure, arrhythmias, cardiogenic shock

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Stable Angina: Chest pain relieved by rest or nitroglycerin

Unstable Angina: Chest pain at rest, unpredictable

Myocardial Infarction (MI):

Severe, crushing chest pain (radiates to arm, jaw, back)

Diaphoresis (sweating)

Dyspnea

Nausea/vomiting

Pallor, cool clammy skin

Anxiety, feeling of impending doom

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ECG: ST-elevation (STEMI) or ST-depression (NSTEMI)

Cardiac Biomarkers:

Troponin I & T (most specific)

CK-MB (creatine kinase-muscle/brain)

Myoglobin

Echocardiogram: Assess heart function

Coronary Angiography: Identify blockages

Stress Test: Evaluate ischemia

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Acute MI Treatment (MONA-B):

Morphine – Pain relief

Oxygen – If hypoxic

Nitroglycerin – Vasodilation

Aspirin – Prevent clot formation

Beta-blockers – Reduce myocardial workload

Reperfusion Therapy:

Thrombolytics (tPA, streptokinase) – If PCI is unavailable

Percutaneous Coronary Intervention (PCI): Stent placement

Coronary Artery Bypass Graft (CABG): Severe blockages

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Monitor vital signs, ECG changes, and pain level

Administer oxygen, medications as prescribed

Educate on risk factor modification (diet, exercise, smoking cessation)

Encourage cardiac rehabilitation

Monitor for complications (heart failure, arrhythmias)

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Heart failure

Cardiogenic shock

Arrhythmias (ventricular fibrillation, atrial fibrillation)

Pericarditis

Recurrent MI

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1. Decreased Cardiac output related to reduced myocardial contractility due to ischemia as evidenced by decreased cardiac output.

2. Acute paint related to decreased myocardial oxygen supply leading to ischemia as evidenced by chest pain and anxiety and restlessness

3. Ineffective Cardiac tissue perfusion related to coronary artery occlusion and decreased blood flow to the heart as evidenced by weak pulses ad cool, clammy skin

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PAD:

Atherosclerosis (plaque buildup in arteries)

Smoking

Diabetes Mellitus

Hypertension

Hyperlipidemia

Obesity

Sedentary lifestyle

HTN:

High sodium intake

Chronic stress

Genetics

Renal disease

Endocrine disorders (Cushing’s, Hyperaldosteronism)

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PAD:

Atherosclerosis → Narrowing of arteries → ↓ Blood flow to extremities → Ischemia

HTN:

Increased systemic vascular resistance → ↑ Cardiac workload → Vascular damage

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PAD:

Intermittent claudication (pain in legs when walking)

Cold, pale extremities

Weak or absent pulses

Delayed wound healing

Dependent rubor (redness when dangling)

HTN:

Often asymptomatic

Headaches, dizziness

Blurred vision

Chest pain, palpitations

Epistaxis (nosebleeds)

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PAD:

Ankle-Brachial Index (ABI)

Doppler ultrasound

Angiography

HTN:

Blood pressure measurements (≥140/90 mmHg)

Electrocardiogram (ECG)

Lipid profile

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PAD Treatment:

Medications: Antiplatelets (Aspirin, Clopidogrel), Statins, Vasodilators

Surgical Interventions: Angioplasty, Bypass Surgery

Lifestyle Changes: Smoking cessation, exercise, low-fat diet

HTN Treatment:

Medications:

Diuretics (Hydrochlorothiazide)

ACE Inhibitors (Lisinopril)

Beta-blockers (Metoprolol)

Calcium Channel Blockers (Amlodipine)

Lifestyle Changes:

Low-sodium diet

Exercise

Stress reduction

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Monitor blood pressure, pulses, and circulation

Assess for complications (stroke, MI, gangrene, aneurysms)

Encourage smoking cessation and weight management

Teach foot care for PAD patients (avoid injury, wear proper footwear)

Educate on medication adherence and lifestyle modifications

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PAD: Critical limb ischemia, ulcers, amputation

HTN: Stroke, MI, kidney disease, heart failure

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1. Ineffective Peripheral Tissue Perfusion related to decreased arterial blood flow secondary to atherosclerosis as evidenced by intermittent claudication.

2. Risk for Decreased Cardiac Output related to increased afterload and myocardial workload due to hypertension as evidenced by Elevated blood pressure readings (≥140/90 mmHg).

3. Acute pain related to decreased oxygenation to tissues from PAD as evidenced by relief by dangling legs.

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How Are PAD, CAD, MI, and HTN Connected?

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How Are PAD, CAD, MI, and HTN Connected?

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All four conditions are linked by atherosclerosis—the buildup of fatty plaques in the arteries—which leads to poor circulation, increased cardiac workload, and oxygen deprivation in tissues.

1. Hypertension starts the damage:

Chronic high blood pressure puts constant stress on artery walls, making them stiff and prone to injury.

This damage allows cholesterol and other substances to build up, leading to narrowed arteries.

2. Coronary Artery Disease develops:

When atherosclerosis affects the coronary arteries, blood flow is restricted.

Patients may develop angina, shortness of breath, or fatigue due to decreased oxygen supply to the heart muscle.

3. A Myocardial Infarction occurs if CAD worsens:

If a plaque ruptures, a blood clot forms and completely blocks a coronary artery.

Without oxygen, the heart muscle begins to die → leading to an MI.

4. Peripheral Artery Disease shows that the whole vascular system is affected:

Atherosclerosis doesn’t just affect the heart—it can also block arteries in the legs and arms, PAD.

Patients with PAD often have pain when walking (claudication), cold extremities, slow-healing wounds, and weak pulses.

PAD and CAD often coexist—meaning if a patient has PAD, they likely have undiagnosed heart disease too.