Cardiovascular Disorders Outline

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 dilation, vessel elongation, and tortuous shaping.
  • Causes:
    • Vein obstruction
    • Incompetent vein valve
    • Dysfunction of the leg muscle pump
  • Venous muscle pump is implied, but the mechanism is not described.

• Chronic Venous Insufficiency:

  • Varicose veins can evolve into this condition.
  • Chronic inadequate venous blood flow produces:
    • Venous hypertension
    • Circulatory (venous) stasis
    • Tissue hypoxia
    • Inflammation in veins and tissues
  • Manifestations:
    • Leg edema
    • Hyperpigmentation and lipodermatosclerosis
    • Skin necrosis with ulceration
    • Pain

• Venous Leg Ulcer

• Venous Thrombus Formation:

  • Thrombus: clot attached to vessel wall
  • Thromboembolus: detached and moving
  • Deep vein thrombosis (DVT):
    • Iliac, femoral, popliteal, tibial veins
  • Superficial vein thrombosis:
    • Greater saphenous vein
    • Lesser saphenous vein
    • Others

• Venous Thrombus Risk Factors:

  • 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.
  • Virchow’s Triad describes factors leading to venous thrombosis.

• Venous Thrombosis Clinical Manifestations:

  • Often asymptomatic
  • Serum D-dimer: if positive, Doppler ultrasonography
  • Venous inflammation: redness and pain in overlying skin/tissues
  • Increased pressure: extremity edema
  • Pulmonary embolus: life-threatening complication, potentially fatal

Hypertension

• Hypertension is ongoing elevation of systemic arterial blood pressure.

• Evidence-based parameters are revised periodically by organizations like the American Heart Association and the International Society of Hypertension.

• Types of hypertension:

  • Isolated systolic hypertension: systolic pressure above normal with normal diastolic pressure.
  • Primary (essential) hypertension: without a known cause.
  • Secondary hypertension: related to a primary diagnosis like kidney disease.

• Hypertension Risk Factors:

  • Genetics:
    • Multiple gene influencers:
      • Renal excretion of sodium
      • Insulin and insulin sensitivity
      • Activity of sympathetic nervous system
      • Defect of sodium and/or calcium transport at cell membrane
      • Activity of the Renin-angiotensin-aldosterone system (RAAS) – lack of renin inhibition
  • Environment:
    • Age
    • Tobacco use
    • Psychosocial stress
    • Glucose intolerance
    • Obesity
    • Sleep apnea
    • Family history
    • Lower socioeconomic status
    • Dietary factors: fats, higher sodium intake, lower potassium intake, excessive alcohol

• Pathophysiology of Hypertension:

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

• Pathophysiology of Hypertension (Continued):

  • Primary hypertension (95% of cases): arises from interaction between physiological, genetic, and environmental factors.
  • Increase in peripheral vascular resistance (PVR) 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 and effects of increased sympathetic nervous system activity:
    • Common causes include inflammation, fluid loss, and pain
    • Increased sympathetic nervous system stimulation leads to:
      • Increased heart rate
      • Increased vasoconstriction – increased peripheral resistance
      • Increased insulin resistance - leads to dysfunction of blood vessel endothelial cell layer
      • Altered function of the blood vessel endothelial cell layer - decreased production of nitric oxide, a vasodilator.
      • Vascular remodeling – change in blood vessel structure
      • Pro-coagulation - stimulation of clotting
      • Increased release of renin and angiotensin – leads to involvement of renin-angiotensin-aldosterone system

• Renin-Angiotensin-Aldosterone System (RAAS):

  • Renin: enzyme from kidneys
  • Angiotensinogen: circulating plasma protein
  • Angiotensin I
  • Angiotensin-converting enzyme (ACE) works in lung endothelium and destroys bradykinin, an important vasodilator
  • Angiotensin II: very potent vasoconstrictor that acts upon arterioles

• Angiotensin II and Blood Pressure:

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

• Pressure-Natriuresis Relationship:

  • Excess sodium retention is the major mechanism of primary hypertension.
  • Individuals with hypertension have less renal excretion of sodium compared with an individual with the same blood pressure reading.
  • Increased blood volume caused by decreased renal excretion of sodium produces 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 relate to increased ventricular hypertrophy, atherosclerosis, and heart failure.

• Inflammation and Hypertension:

  • Innate and adaptive immunity are activated by injury to 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. Endothelium is the innermost vessel lining

• 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
  • Heart must pump harder against increased systemic vascular resistance
  • Myocardial oxygen consumption increased

Hypotension

• Orthostatic (Postural) Hypotension:
  • SBP decrease of at least 20 mmHg OR DBP decrease of at least 10 mm Hg within 3 minutes of change to standing position.
  • Occurs in about one-third of people in residential care or nursing home.
  • Often affects those with dementia and Parkinson disease.
  • Major risk for falls, injury, and death.
  • Involves autonomic nervous system dysfunction.
  • 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 vessel wall due to bulging of all vessel layers or in a cardiac chamber.

• The most common site is the aorta due to its high pressure.

• A false aneurysm is hematoma on 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, 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 often asymptomatic until rupture causes pain and hypotension with high mortality.
  • Cardiac aneurysm possible in infarcted myocardium.

Arterial Thrombosis

• Arterial Thrombus Formation:
  • Form at site of coagulation cascade:
    • 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 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.

• Peripheral Artery Disease: Atherosclerosis Consequences:

  • Partial or total vessel obstruction
  • Ischemia can evolve into infarction
  • Microthrombi formation
  • Thromboembolus
  • Aneurysm