Vascular Disorders: Varicose Veins and Thrombosis

• Varicose veins involve blood pooling, where veins become distended, tortuous (twisted), and palpable.
• Risk factors include age, being female, family history, DVT (deep vein thrombosis), pregnancy, and prior leg injury.
• Causes can be injury, disease, or gradual venous distention.

Chronic Venous Insufficiency (CVI)

• CVI is inadequate venous return over a long period.
• Symptoms include edema in the lower extremities and hyperpigmentation of the skin of the feet and ankles, often due to varicose veins or valvular incompetence.
• Venous stasis ulcers may occur due to poor circulation making tissues vulnerable to trauma and infection, leading to ulcer formation.

Thrombus Formation in Veins

• Obstruction of venous flow leads to increased venous pressure and capillary hydrostatic pressure.
• A thrombus is a blood clot attached to the vessel wall.
• Deep Vein Thrombosis (DVT) occurs primarily in lower extremities and is associated with venous stasis (immobility, age, heart failure), venous endothelial damage (trauma, surgery, IV medications), and hypercoagulable states (inherited disorders, pregnancy).
• A thromboembolus is a detached blood clot.
• Other causes include cancer, orthopedic surgery/trauma, heart failure, and immobility.
• Pulmonary embolism is a blockage in one of the pulmonary arteries in the lungs, usually caused by a blood clot that travels to the lungs, resulting in sudden sharp chest pain, shortness of breath (dyspnea), tachycardia, and coughing up blood.

Superior Vena Cava Syndrome (SVCS)

• SVCS involves gradual blocking or narrowing of the superior vena cava.
• SVCS Leads to venous distention of the upper extremities and head, it is considered an oncologic emergency.
• SVCS is caused by bronchogenic cancer, followed by other cancers, TB, or cystic fibrosis.
• Manifestations include edema and venous distension of the upper extremities.

Hypertension

• Hypertension is sustained systolic blood pressure of 130 mmHg or greater, or a diastolic pressure of 80 mmHg or greater.

Primary Hypertension

• Primary or essential/idiopathic hypertension is high blood pressure without an identifiable cause, potentially involving genetics or environmental factors.
• Risk factors include family history, age, being a smoker, obesity, alcohol consumption, gender at birth, race, and intake of sodium, potassium, and calcium.

Secondary Hypertension

• Secondary hypertension is caused by an underlying disorder, such as renal disease.
• It raises peripheral vascular resistance or cardiac output.

Complicated Hypertension

• Complicated hypertension involves chronic hypertensive damage to blood vessels and tissues, leading to target organ damage in the heart, brain, kidneys, and eyes.

Hypertensive Crisis

• A hypertensive crisis is rapid and progressive hypertension with a systolic BP of 180 mmHg or greater, or a diastolic BP of 120 mmHg or greater.
• It is life-threatening, and leads to stroke or cardiac failure, complications of pregnancy, drug use, or adrenal tumors.
• Hypertensive urgency is severe elevation in BP without organ damage.
• Hypertensive emergency involves target organ damage, affecting the heart, brain, or kidneys.

Pathologic Effects of Sustained, Complicated Primary Hypertension

• Heart: Increased workload combined with diminished blood flow leads to left ventricular hypertrophy, myocardial ischemia, and heart failure.
• Coronary Arteries: Accelerated atherosclerosis leads to myocardial ischemia, myocardial infarction, and sudden death.
• Kidneys: Reduced blood flow and increased pressure lead to glomerulosclerosis and decreased glomerular filtration, resulting in end-stage renal disease.
• Brain: Reduced blood flow and weakened vessel walls lead to transient ischemic attacks, cerebral thrombosis, aneurysm, hemorrhage, and acute brain infarction.
• Eyes (retinas): Retinal vascular sclerosis and increased pressure lead to hypertensive retinopathy, retinal exudates, and hemorrhages.
• Aorta: Weakened vessel wall leads to dissecting aneurysm.
• Arteries of Lower Extremities: Reduced blood flow and high pressures lead to intermittent claudication and gangrene.

ACE Inhibitors

• ACE inhibitors are a class of medications primarily used to treat high blood pressure, heart failure, and certain kidney conditions.
• They work by blocking angiotensin-converting enzyme which narrows blood vessels.

Orthostatic (Postural) Hypotension [OH]

• Orthostatic hypotension is a decrease in systolic (at least 20 mmHg) or diastolic (at least 10 mmHg) blood pressure within 3 minutes of standing.
• It is due to a lack of normal blood pressure response to gravitational changes.
• Acute orthostatic hypotension results from inadequate regulatory mechanisms (drug reaction).
• Chronic orthostatic hypotension is secondary to a specific disease (endocrine disorders).
• Manifestations include dizziness, blurring/loss of vision, and syncope (fainting).

Aneurysm

• An aneurysm is a local dilation or out pouching of a vessel wall, or cardiac chamber.
• True aneurysms involve weakening of all three layers of the vessel wall.
• False aneurysms are a pocket of blood outside the blood vessel that has a connection or opening to the inside of the blood vessels.
• The aorta is most susceptible, especially abdominal.
• Aneurysms are caused by atherosclerosis and hypertension.
• Effects include aortic dissection (acute aortic syndrome) or rupture.
• Risk factors include being male, smoking, increased age, and hypertension.

(Arterial) Thrombus Formation

• Arterial thrombus formation is where a blood clot remains attached to the vessel wall.
• Risk factors include initial injury/inflammation, obstruction of flow, and pooling (stasis).
• Artery occlusion can lead to gangrenous or eschar formation.

Embolism

• An embolism is a bolus of matter that is circulating in the bloodstream.
• Embolisms may include dislodged thrombi, air bubbles, amniotic fluid, bacteria, etc.

Peripheral Vascular Disease (PVD)

• PVD is a disease of the arteries that perfuse limbs due to atherosclerotic disease.

Thromboangiitis Obliterans (Buerger Disease)

• Thromboangiitis obliterans is a rare autoimmune disease of peripheral arteries strongly associated with smoking.
• Characterized by the formation of thrombi filled with inflammatory and immune cells.
• These thrombi become organized and fibrotic, resulting in permanent occlusion of arteries in the hands and feet.
• Causes pain and often leads to gangrenous lesions and amputation.

Raynaud Phenomenon

• Raynaud phenomenon is episodic vasospasm in arteries and arterioles of the fingers.
• Primary (Raynaud disease) is a vasospastic disorder of unknown origin.
• Secondary Raynaud phenomenon is related to other systemic diseases/conditions such as collagen vascular disease, pulmonary hypertension, hypothyroidism, or long-term exposure to a cold environment.

Atherosclerosis

• Atherosclerosis is plaque development.
• Atherosclerosis involves thickening and hardening of the vessel wall caused by the accumulation of lipid-laden macrophages in the arterial wall.
• Risk factors include diabetes, smoking, hyperlipidemia/dyslipidemia, hypertension, and autoimmunity.

Progression of Atherosclerosis

• It begins with endothelial injury, cellular proliferation, macrophage migration/adherence, LDL oxidation [foam cell formation], fatty streak, fibrous plaque, and complicated plaque.
• Results in inadequate perfusion, ischemia, and necrosis.
• Intermittent claudication with gradually increasing obstruction to arterial blood flow results in leg pain, and if a thrombus forms over the lesion, complete obstruction of flow can occur, causing severe pain, loss of pulse, and skin color changes.
• Results in inadequate perfusion, ischemia, necrosis.

Coronary Artery Disease (CAD)

• CAD is any vascular disorder that narrows or obstructs the coronary arteries, leading to myocardial ischemia.
• Atherosclerosis is the most common cause of CAD.
• It diminishes myocardial blood supply until ischemia is caused, where cells are alive but cannot function properly.

Conventional (Major) Risk Factors for Coronary Artery Disease

• Non-modifiable risk factors: advanced age, family history, gender at birth.
• Modifiable risk factors: dyslipidemia (abnormal levels of lipid proteins), hypertension, cigarette smoking, DM with insulin resistance, obesity/sedentary lifestyle, and atherogenic diet.

Criteria for Dyslipidemia

• Optimal Total Cholesterol: <200 mg/dL
• Near Optimal Total Cholesterol: <200 mg/dL
• Desirable Total Cholesterol: <200 mg/dL
• Low Total Cholesterol: <200 mg/dL
• Borderline Total Cholesterol: 200-239 mg/dL
• High Total Cholesterol: ≥240 mg/dL
• Optimal Low-Density Lipoprotein: <100 mg/dL
• Near Optimal Low-Density Lipoprotein: 100 - 129 mg/dL
• Desirable Low-Density Lipoprotein: none
• Low Low-Density Lipoprotein: none
• Borderline Low-Density Lipoprotein: 130-159 mg/dL
• High Low-Density Lipoprotein: ≥190 g/dL
• Optimal Triglycerides: <150 mg/dL
• Near Optimal Triglycerides: none
• Desirable Triglycerides: none
• Low Triglycerides: <150 mg/dL
• Borderline Triglycerides: 150-199 mg/dL
• High Triglycerides: ≥500 g/dL
• Optimal High-Density Lipoprotein: none
• Near Optimal High-Density Lipoprotein: none
• Desirable High-Density Lipoprotein: none
• Low High-Density Lipoprotein: none
• Borderline High-Density Lipoprotein: <40 mg/dL
• High High-Density Lipoprotein: ≥ 60g/dL

Nontraditional Risk Factors for Coronary Artery Disease

• Markers of inflammation and thrombosis, including high-density C-reactive protein, troponin I (TnI), adipokines, chronic kidney disease, air pollution/radiation, certain medications, and microbiome.

Coronary Atherosclerosis & Pathogenesis of CAD

• Chest pain may occur.
• Plaques can be stable or unstable.
• Thrombosis and vessel occlusion can occur.
• Lesions may be asymptomatic precursors.

Transient Myocardial Ischemia

• Transient myocardial ischemia develops if the flow of content or coronary blood is insufficient for metabolic demands.
• It involves local, temporary deprivation of coronary blood supply.
• Manifestations include stable angina pectoris (predictable chest pain without infarction), unstable angina (increased demand causes pain, then decreased demand = pain relief), Prinzmetal angina (unpredictable chest pain, often at rest), silent ischemia, and mental stress-induced ischemia (asymptomatic, indicator of future serious cardiovascular events).

Acute Coronary Syndrome

• Unstable angina results from reversible myocardial ischemia.
• Myocardial infarction is extended obstruction of myocardial blood supply causing monocyte necrosis.
• Prolonged ischemia (> 20 min) causes irreversible damage to the heart muscle.
• Non-ST elevation MI (non-STEMI) is subendocardial myocardial infarction.
• ST elevation MI (STEMI) is transmural myocardial infarction (wall-to-wall damage).

Serum Biomarkers

• Used for assessment.
• Myoglobin appears after acute MI.
• Myoglobin lacks specificity and rises in 1-4 hours, returning to normal within 24 hours.
• CK-MB rises in 4-12 hours and returns to normal within 36-48 hours.
• Troponin is the most sensitive and specific marker; it rises in 4-12 hours and may remain elevated for up to two weeks, making it most important.

MI Manifestations & Treatment

• Symptoms include sudden severe chest pain (may radiate/crush), nausea, vomiting, indigestion, diaphoresis (sweating), and dyspnea (SOB).
• Cardiomyocytes are lost at a rate of about 500 every second.
• Silent ischemia is when individuals feel no pain during MI (usually diabetics).
• Treatment involves; revascularization (PCI), administration of anti-thrombotics, ACE inhibitors, beta-blockers, pain relief, and fluid management
• Complications include dysrhythmia (abnormal heart rate), left ventricle failure, pericarditis (inflammation of the pericardium), Dressler post-infarction syndrome (delayed form of pericarditis), organic brain syndrome (irregular blood flow to the brain), aneurysms, and systemic and pulmonary thromboembolism.

CAD (coronary artery disease)

• Stable angina - Predictable
• Okay after rest
• Not MI
• Demand > supply
• Increase in activity = Angina Pectoris(chest pain)
• Acute Coronary Syndrome
• Unstable Angina: Plaque Rupture, Chest Pain even after rest (unpredictable)
• Heart Attack: formation of an embolus (NO 02 = 20 mins)
  • non STemi or STemi
• Cardiac Ischemia has varied results, see table on image provided for details