Cardiovascular Disorders - Detailed Notes

Cardiovascular Disorders: Diseases of Veins and Arteries

Venous Disorders

• Varicose Veins:

  • Occur across a spectrum from asymptomatic to chronic venous insufficiency.
  • Pooling of venous blood leads to vein dilatation, vessel elongation, and tortuous shaping.
  • Factors causing varicosity:
    • Vein obstruction
    • Incompetent vein valve
    • Dysfunction of the leg muscle pump impairs the venous muscle pump action
  • Leg varicose veins are a common manifestation.

• Chronic Venous Insufficiency:

  • Varicose veins can evolve into chronic venous insufficiency.
  • Chronic inadequate venous blood flow produces:
    • Venous hypertension
    • Circulatory (venous) stasis
    • Tissue hypoxia, leading to inflammation in veins and tissues.
  • Manifestations:
    • Leg edema
    • Hyperpigmentation and lipodermatosclerosis
    • Skin necrosis with ulceration and pain, resulting in venous leg ulcers

• Venous Thrombus Formation:

  • Thrombus: A clot attached to the vessel wall.
  • Thromboembolus: A detached and moving thrombus.
  • Deep vein thrombosis (DVT):
    • Occurs in iliac, femoral, popliteal, and tibial veins.
  • Superficial vein thrombosis:
    • Occurs in greater and lesser saphenous veins.

• Venous Thrombus Risk Factors:

  • Virchow’s Triad describes factors leading to venous thrombosis:
    • Venous stasis: Immobility, obesity, prolonged lower extremity dependency.
    • Endothelial damage: Tissue trauma.
    • Hypercoagulability: Immobility, smoking, malignancy, pregnancy, oral contraceptives, hormone replacement, elevated homocysteine level, antiphospholipid syndrome, inherited disorders (V Leiden factor or prothrombin gene abnormality).

• Venous Thrombosis Pathophysiology:

  • Clots are more common in venous circulation due to lower pressure.
  • Slower blood flow contributes to clotting.

• Venous Thrombosis Clinical Manifestations:

  • Often asymptomatic.
  • Diagnosis:
    • Positive serum D-dimer requires Doppler ultrasonography.
  • Venous inflammation can produce redness and pain in overlying skin/tissues.
  • Increased pressure in affected vein can cause extremity edema.
  • Pulmonary embolus is a life-threatening complication with potential fatality.

Hypertension

• Hypertension: Ongoing elevation of systemic arterial blood pressure.

• Types of Hypertension:

  • Isolated systolic hypertension: Systolic pressure above normal with normal diastolic pressure.
  • Primary (essential) hypertension: No known cause.
  • Secondary hypertension: Related to a primary diagnosis (e.g., kidney disease).

• Hypertension Risk Factors:

  • Genetics: Influencers related to renal excretion of sodium, insulin/insulin sensitivity, sympathetic nervous system activity, sodium/calcium transport at cell membrane, the renin-angiotensin-aldosterone system (RAAS).
  • Environment: Age, tobacco use, psychosocial stress, glucose intolerance, obesity, sleep apnea, family history, lower socioeconomic status, dietary factors (fats, sodium, potassium, alcohol).

• Pathophysiology of Hypertension:

  • Persistent increase in peripheral vascular resistance, circulating blood volume and cardiac output, or both.
  • Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV): CO = HR Imes SV
  • Changes in heart rate or stroke volume alter cardiac output.
  • Peripheral vascular resistance is increased by increased blood viscosity or decreased blood vessel diameter.

• Primary Hypertension:

  • 95% of cases, arising from interaction between physiological, genetic, and environmental factors.
  • Increase in peripheral vascular resistance and blood volume is influenced by inflammation, obesity hormones, endothelial dysfunction, and insulin resistance.
  • Pathophysiologic mechanisms include alterations in the:
    • Sympathetic nervous system activity
    • Renin-angiotensin-aldosterone system
    • Pressure-natriuresis relationship

• Secondary Hypertension:

  • Due to an underlying condition or medication that increases cardiac output, such as renal or adrenal disease.
  • If the cause is eliminated before permanent vascular damage, blood pressure is expected to return to normal.

• Sympathetic Nervous System Stimulation:

  • Causes: Inflammation, fluid loss, and pain.
  • Effects:
    • Increased heart rate.
    • Increased vasoconstriction, leading to increased peripheral resistance.
    • Increased insulin resistance.
    • Altered function of the blood vessel endothelial cell layer, including decreased production of nitric oxide (vasodilator).
    • Vascular remodeling.
    • Pro-coagulation (stimulation of clotting).
    • Increased release of renin and angiotensin, leading to involvement of the renin-angiotensin-aldosterone system.

• Renin-Angiotensin-Aldosterone System (RAAS):

  • Renin: An enzyme from kidneys.
  • Angiotensinogen: Circulating plasma protein.
  • Angiotensin I converts to Angiotensin II by Angiotensin-converting enzyme (ACE) which works in lung endothelium and destroys bradykinin (a vasodilator).
  • Angiotensin II: Potent vasoconstrictor that acts upon arterioles.

• Angiotensin II and Blood Pressure:

  • Promotes sodium reabsorption by kidneys.
  • Stimulates release of aldosterone by adrenals which leads to kidney and myocardial damage.
  • Makes blood vessels less elastic with a permanent increase in systemic vascular resistance.
  • Antidiuretic hormone (ADH) also influences blood pressure because it stimulates water reabsorption by kidneys and constricts arterial vessels, especially in splanchnic (gastrointestinal) circulation.

• Pressure-Natriuresis Relationship:

  • Excess sodium retention is a major mechanism of primary hypertension.
  • Individuals with hypertension have less renal excretion of sodium compared to individuals with the same blood pressure.
  • Increased blood volume caused by decreased renal excretion of sodium produces a shift in the normal pressure-natriuresis relationship.

• Natriuretic Hormones Action:

  • Natriuretic hormones (atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), C-type natriuretic peptide, and urodilatin) regulate renal sodium excretion and need adequate potassium, calcium, and magnesium.
  • Actions include:
    • Promotion of diuresis
    • Increase of renal blood flow and glomerular filtration rate
    • Inhibition of aldosterone (which normally stimulates renal absorption of sodium and water).
    • Promotion of systemic vasodilation
  • With hypertension, elevated ANP & BNP are related to increased ventricular hypertrophy, atherosclerosis, and heart failure.

• Inflammation and Hypertension:

  • Innate and adaptive immunity are activated by injury to the endothelial cell layer, leading to chronic inflammation.
  • Inflammation leads to decreased production of nitric oxide in the endothelium.
  • Nitric oxide contributes to vasodilation and protection against vessel damage from platelets.

• Hypertension and Target Organ Damage:

  • Cardiac: Left ventricular hypertrophy, coronary artery disease, heart failure.
  • Kidneys: Decreased perfusion.
  • Eyes: Retinal hemorrhages.

• Additional Cardiac Problems Due to Hypertension:

  • Heart workload increased; the heart must pump harder against increased systemic vascular resistance.
  • Myocardial oxygen consumption increased.

• Orthostatic (Postural) Hypotension:

  • Systolic blood pressure (SBP) decrease of at least 20 mmHg OR diastolic blood pressure (DBP) decrease of at least 10 mm Hg within 3 minutes of a change to standing position.
  • Common in elderly, especially in residential care or nursing homes.
  • Often affects those with dementia and Parkinson's disease.
  • Major risk for falls, injury, and death.
  • Involves autonomic nervous system dysfunction, including loss of usual sympathetic nervous system stimulation that increases vasoconstriction and increases heart rate with standing.
  • Blood pools in lower extremities related to gravity, and arterial blood pressure drops.

Vascular Aneurysms

• Localized dilation or outpouching of a vessel wall or cardiac chamber.

  • The most common site is the aorta due to its high pressure.
  • A false aneurysm is a hematoma on the outside vessel wall that connects with the inside of the vessel and is caused by a vascular graft or trauma.

• Vascular Aneurysm Pathophysiology:

  • Chronic hypertension creates mechanical stress in vessel wall resulting in inflammation.
  • Neutrophils, macrophages, and lymphocytes infiltrate the vessel wall.
  • Inflammatory proteases break down tissue, leading to vessel remodeling, calcification, and decreased elasticity.
  • Aneurysm becomes a blood reservoir and leads to decreased blood flow or decreased stroke volume if in the heart.
  • Aortic aneurysm is often asymptomatic until rupture causes pain, hypotension, and high mortality.
  • Cardiac aneurysm is possible in infarcted myocardium.

Arterial Thrombus Formation

• Form at sites of coagulation cascade activation:
  • Triggers: Inflammation, hyperlipidemia, hypercholesterolemia, autoimmune vasculitis, traumatic injury, infections, hypotension/shock, arterial pooling.
  • Clinical threats:
    • Artery occlusion with ischemia in tissue supplied by artery.
    • Thromboembolus that moves and occludes distal circulation.

Embolism

• Vessel occlusion by emboli other than from a blood clot.
  • Types: Air, amniotic fluid, bacterial, fat.
  • Outcomes:
    • Organ or extremity: Ischemia or infarction in tissue distal to occlusion.
    • Coronary, cerebral, or pulmonary artery embolism may be fatal.

Peripheral Artery Disease (PAD): Atherosclerosis

• Atherosclerosis within arteries that provide blood supply to limbs, especially the lower extremities.
  • Athere – fatty, Skleros – hard.
  • Gradual thickening of the intima and media arterial layers, leading to a narrowing of the vessel.
  • Consequences:
    • Partial or total vessel obstruction causing ischemia that can evolve into infarction.
    • Microthrombi formation and Thromboembolus.
    • Aneurysm.