Cardiovascular Health Concepts Quiz

Cardiovascular Emergencies

• Cardiovascular emergencies are a significant topic for PARA 2024 Winter 2023.

Cardiovascular Assessments

• Complete cardiac assessments will be covered in detail in a later term.
• There is no single question that definitively rules out cardiac ischemia.
• A thorough patient history is crucial for determining the best working differential diagnosis.
• Many cardiac emergencies have "classic" signs and symptoms, but atypical presentations also require careful consideration.

Cardiovascular Assessment History

• A complete history includes a history of presenting illness/symptoms.
• It further includes a detailed description of signs and symptoms (OPQRST+).
• Past medical history (possibly including family history) should be documented.
• Any current investigations, diagnoses, and ongoing concerns should be documented.

Terminology

• Ischemia: Decreased blood (and oxygen) supply to a body organ or part, usually due to a functional constriction or obstruction of a blood vessel.
• Infarction: Necrosis (tissue death) due to local ischemia.
• Necrosis: Localized tissue death in cells or a body structure resulting from disease or injury.
• Gangrene: Death of body tissue due to a lack of blood flow or bacterial infection.
• Perfusion: Pouring over or through, especially the passage of fluid through an organ or body area.
• Thrombus: Stationary mass of clotted blood or other formed elements that remains attached to its origin along the wall of a blood vessel.
• Embolus: A mass of blood clot/formed elements (like air, calcium fragments, or fat) that travels in the bloodstream before lodging in a vessel, obstructing circulation.
• Preload: Volume of blood returning to the right atrium of the heart.
• Afterload: Pressure/force the left ventricle needs to generate to open the aortic semilunar valve and pump blood into systemic circulation.

Vascular Disorders/Disease

• Arteries carry oxygenated blood from the heart to tissues, and regulate blood pressure and capillary flow.
• Veins return blood to the heart and help maintain cardiac contraction.
• Various vascular disorders have the potential to disrupt homeostasis of the system.

Dyslipidemia

• Dyslipidemia is an imbalance in the lipid components of the blood (triglycerides, phospholipids, and cholesterol).
• Cholesterol and triglycerides combine with water-soluble transport proteins in the blood, which is known as lipoprotein.
• Lipoproteins are categorized by their densities (five types).
• LDL (low-density lipoprotein) is the primary transport molecule for cholesterol moving from the liver to target tissues. It's often called "bad cholesterol".
• HDL (high-density lipoprotein) is the primary transport molecule for cholesterol moving from the tissues back to the liver. It's known as "good cholesterol".
• Cholesterol serves various functions, including in membrane and hormone synthesis.
• Dyslipidemia is characterized by increased total blood cholesterol, increased LDL cholesterol, and decreased HDL cholesterol.
• Risk factors for elevated LDL include smoking, excessive alcohol, sedentary lifestyle, poor diet, type 2 diabetes, and genetic predisposition.
• These factors also typically reduce HDL levels, exacerbating the imbalance.

Atherosclerosis

• Arteriosclerosis: Abnormal hardening and thickening of the arteries.
• Atherosclerosis: A type of arteriosclerosis causing fibrofatty lesions in the inner lining of large and medium-sized arteries. Risk factors are primarily dyslipidemia and its associated factors; males are typically at higher risk than premenopausal females, although this tends to balance out post-menopause.
• Lifestyle factors including quitting smoking and adopting healthier diets/activities drastically reduce the risk.
• Atherosclerosis is fundamentally an inflammatory condition with various triggers causing lesion and plaque formation in the artery's internal layer.
• Atherosclerotic plaque consists of smooth muscle cells, macrophages, leukocytes, collagen, elastin fibers, platelets, and a significant lipid core.
• The development of atherosclerotic plaque occurs through stages:
  1. Initial endothelial injury by triggers (smoking, high LDL, etc.).
  2. Inflammatory cells migrate and adhere to the injury site.
  3. Accumulating foam cells cause progressive lesion deterioration.
  4. Foam cells die and deposit necrotic debris and lipids causing vascular wall thickening. The bulging wall becomes prone to rupture/thrombotic occlusion.
• Endothelial cell injury is a primary initiating factor. Risk factors for damage include hypertension, smoking, elevated LDL levels, and immune mechanisms.
• Inflammatory cell migration to injury sites occurs. Inflammation is paramount to the initiation and progression of atherosclerosis.
• Lipid accumulation increases lesion progression.

Arteriosclerosis Clinical Manifestations

• Typically, symptoms do not appear for over 20 years of plaque buildup.
• Vary considerably depending on the affected blood vessels and extent of blockage.
• Atherosclerosis can cause reduced blood flow, leading to ischemia, sudden vessel obstruction (thrombosis, embolism), or aneurysm formation.
• Larger vessels are more prone to aneurysms; smaller vessels are often more prone to vessel occlusion.

Peripheral Artery Disease (PAD)

• A circulation disorder in the extremities that can cause ischemia, pain, impaired function, and potentially infarction/tissue necrosis.
• PAD is caused by atherosclerosis/arteriosclerosis in the peripheral arteries.
• Risk factors are similar to atherosclerosis.
• Diabetics and smokers are at higher risk.
• Symptoms typically manifest when there is a 50% narrowing of the vessel.
• PAD symptoms include issues like pain with walking, vague muscle aches and numbness, muscle atrophy, skin/subcutaneous tissue thinning, weak/absent peripheral pulses, and poor perfusion.

Raynaud Disease/Phenomenon

• A functional disorder caused by vasoconstriction in the arteries/arterioles of the fingers and occasionally toes.
• Cause of vasospasm may be due to cold exposure, strong emotions, or a vessel injury (e.g., frostbite or prolonged heavy machinery use).
• Clinical manifestations include distal pallor/cyanosis, cold sensations, and following vasospasm, intense redness, throbbing, and paresthesia.

Aneurysms

• An abnormal localized dilation of a blood vessel, occurring in arteries and veins.
• True aneurysms are bounded by a complete vessel wall, containing blood within the vessel itself.
• False aneurysms are characterized by localized dissection/tear in the inner vessel wall, leading to an extravascular blood accumulation and vessel enlargement.
• Types of aneurysm include:
• Berry aneurysm: A small, spherical dilation at a vessel bifurcation.
• Fusiform aneurysm: A total circumference dilation.
• Saccular aneurysm: A partial circumference dilation (sac-like).
• Dissecting aneurysm: Involves a tear in the intimal layer, with blood entering the vessel wall and dissecting to creating a blood-filled cavity.
• Atherosclerosis (weakening of the arterial walls) and tunica media degeneration are common causes.
• Aneurysms are often asymptomatic until rupture, but pre-rupture symptoms can vary depending on the site; Rupture symptoms include severe unrelenting pain; pulsatile masses may be present.

Dissecting Aortic Aneurysm

• An acute, life-threatening condition with hemorrhage into the arterial wall, causing longitudinal tearing and a blood-filled channel.
• It can occur anyplace within the aorta, most commonly the ascending and descending (thoracic) sections, just distal to the subclavian artery.
• The etiology is rooted in conditions weakening the aortic walls, including atherosclerosis.
• Types:
• Type A: involving the ascending aorta, possibly both ascending and descending.
• Type B: involving only the descending aorta.
• Clinical manifestations include abrupt tearing, excruciating pain (differing in location by ascending/descending aorta), hypotension, and hypovolemic shock.
• Aneurysm rupture requires immediate, life-saving interventions.

Varicose Veins

• Dilated, superficial veins, mainly appearing in the lower extremities.
• Commonly lead to venous insufficiency issues.
• Prone to rupture with minimal trauma, easily managed with direct pressure.

Deep Vein Thrombosis (DVT)

• Formation of thrombus and inflammatory response within deep veins, typically in the lower extremities.
• Pulmonary embolism (PE) is a severe complication.
• Virchow's triad defines risk factors:
• Stasis: Prolonged flights, bed rest, spinal cord injury (SCI).
• Hypercoagulability: Clotting deficiencies, oral contraceptives, hormone therapy, smoking.
• Vessel wall injury: Trauma, post surgery, intravenous lines (IVs), infection.
• Manifestations are usually asymptomatic, but symptoms may include pain, swelling, deep muscle tenderness, fever, and general malaise in the affected leg. Localized findings often include calf pain, swelling, redness, and warmth to the touch.

Hypertension

• Persistent elevation of arterial blood pressure (typically ≥140mmHg).
• Broadly classified as either primary (essential) or secondary.
• Primary Hypertension: High blood pressure without evidence of a specific underlying cause.
• Associated with age, gender (incidence higher in males), family history, high sodium intake, dyslipidemia, smoking, alcohol consumption, sedentary lifestyle, obesity, and insulin resistance.
• Secondary Hypertension: High blood pressure resulting from another underlying cause.
• Clinical manifestations are typically asymptomatic until target organ damage starts.
• High blood pressure damages organs and blood vessels, particularly those in the kidneys, heart, and brain, triggering inflammation and atherosclerosis.

Hypertensive Emergency

• This is a potentially lethal complication of hypertension characterized by abruptly high blood pressure spikes (>180/120 mmHg).
• Prompt treatment is crucial due to worsening target organ damage.
• Complications include ischemia stroke, cardiac ischemia, and retinal hemorrhage.

Orthostatic Hypotension

• Abnormal drop of 20mmHg or more in blood pressure upon standing.
• Symptoms can range from asymptomatic to dizziness or syncope.
• Common causes include normal aging, hypovolemia, prolonged bed rest, pharmacologically induced effects, and autonomic nervous system disorders.

Disorders of Cardiac Function

• This is a broad category of issues impacting the heart.

Layers of the Heart

• The heart comprises the epicardium (outer layer of the serous pericardium), myocardium (muscular layer), and endocardium (inner layer).

Endocarditis

• Inflammation of the endocardium, usually caused by an infectious agent.
• Often caused by illicit intravenous drug use.
• Lesions initially affect heart valves, potentially spreading through the heart layers.
• Symptoms include fever, chills, malaise, and other signs of systemic infection.
• Emboli formation may occur and lodge in other parts of the body, leading to various symptoms, including a myocardial infarction (MI) or cardiac ischemia.
• Cardiac muscle inflammation (myocarditis) or pericardium inflammation (pericarditis) can develop with extensive infection spread.
• Valve destruction may cause congestive heart failure.

Myocarditis

• Inflammation of the myocardium, sometimes involving a viral or bacterial/fungal infection, occasionally autoimmune, or related to hypersensitivity to certain drugs.
• Symptoms vary depending on the cause and severity, ranging from asymptomatic to cardiogenic shock.
• Infection signs (fever, chills, malaise), embolus formation, heightened clotting (inflammation mediators), and myocardium irritation leading to reduced contractility can occur.
• Heart failure/cardiogenic shock may be present.

Pericarditis

• Pericardium inflammation (a double-layered membrane—visceral and parietal—surrounding the heart).

• Fluid (pericardial fluid) buildup between the layers lubricates the heart during motion.

• Pericarditis promotes increased permeability, allowing plasma proteins to enter the pericardial fluid.

• It may lead to adhesion/scarring between the serous layers.

• Clinical Manifestations:

  • Chest pain, often described as sharp and abrupt in the precordial region, potentially radiating to neck, back, abdomen, or sides.
  • Worst with deep breathing, swallowing, or positional changes.
  • Relieving factors include upright or slightly leaning forward positions which ease venous return.
  • ECG changes include widespread ST elevation and PR segment depression.

Pericardial Effusion/Tamponade

• Pericardial cavity fluid accumulation (usually from inflammatory/infectious causes).
• Pericardial Tamponade: Fluid accumulation severely compresses the heart, reducing cardiac output.
• May result from trauma, myocardial infarction (MI), dissecting aneurysms, or tumors.
• Pathogenesis: Fluid accumulation impact on the heart's mechanics, decreasing preload, stroke volume, and cardiac output.
• Blood backs up into the venous system, causing jugular venous distension (JVD).
• Clinical Manifestations:
  • Beck's triad: jugular venous distension (JVD), muffled heart sounds, hypotension.
  • Pulsus paradoxus: weakened or absent arterial pulse during inspiration.
  • ECG changes: nonspecific T-wave changes & low QRS voltage.

Cardiomyopathies

• Conditions of the myocardium (heart muscle) that often lead to mechanical and/or electrical dysfunction.
• Presents with inappropriate ventricular hypertrophy or dilation.
• It may affect the heart alone or be part of generalized systemic disorders leading to cardiovascular death or heart failure.
• Primary: Heart-confined disorder.
• Secondary: Myocardial changes due to other systemic conditions.

Coronary Artery Disease (CAD)

• Impaired coronary blood flow, commonly due to atherosclerosis.
• Potential complications include myocardial ischemia, angina, myocardial infarction (MI), cardiac arrhythmias, heart failure, and sudden cardiac death.
• Risk Factors: Cigarette smoking, hypertension, dyslipidemia, diabetes, advancing age, obesity, sedentary lifestyle.
• Pathogenesis: Divided into ACS and chronic ischemic heart disease.
• Subtypes of ACS include unstable angina and myocardial infarctions (MI).
• Types of chronic ischemic disease include:
• Stable angina
• Variant (vasospastic) angina
• Silent myocardial ischemia

Coronary Arteries

• Two major coronary arteries originate from the coronary sinus just above the aortic valve.
• They spread over the heart's surface (epicardium) as major branches that spread into the myocardium.
• The left coronary artery (LCA) divides into the left anterior descending (LAD) and circumflex arteries.
• The right coronary artery (RCA) supplies the posterior heart, septum, sinoatrial (SA) node, and atrioventricular (AV) node.
• Collateral circulation is important.
• Anastomoses (cross-connections) between adjacent channels will form if the primary supply is inadequate.

Myocardial Oxygen - Supply and Demand

• Imbalance of oxygen supply and demand within the heart can lead to myocardial ischemia, myocardial infarction(MI), or sudden cardiac death.
• Supply: Determined by capillary inflow and hemoglobin's ability to transfer oxygen.
• Demand: Determined by heart rate (HR), stroke volume (SV), and systolic blood pressure and myocardial wall stress. Ischemic issues may occur due to hypoxia, anemia, or carbon monoxide poisoning.

Chronic Ischemic Heart Disease

• Insufficient blood supply to the heart (ischemia) from coronary arteries.
• Common factors include atherosclerosis and vasospasm.
• Types include stable angina, variant angina (vasospastic), and silent myocardial ischemia. Note cardiac activity tolerance effects.
• Silent Myocardial Ischemia: Ischemia without chest pain. Can range from a mild condition to full-blown myocardial infarction.
• Stable Angina: Characteristic fixed partial obstruction causing ischemic chest pain. Increase in baseline MVO2 (metabolic rate for oxygen) is the trigger for pain. Common symptom resolution is rapid when rest is achieved or with nitroglycerin

Acute Coronary Syndrome (ACS)

• Acute and potentially dangerous situation where there is severe obstruction in coronary blood flow leading to MI or potentially death.
• Key symptoms and findings:
• Unstable angina: chest pain that doesn't resolve with rest and nitroglycerin.
• Non-ST-segment elevation myocardial infarction (NSTEMI).
• ST-segment elevation myocardial infarction (STEMI).
• Clinical Manifestations: Characterized by ischemic chest pain (constricting, squeezing), potentially radiating to the left shoulder, jaw, or arm. Shortness of breath, nausea, vomiting, epigastric discomfort, fatigue, anxiety, tachycardia, and pale, cool, diaphoretic skin are common accompanying symptoms.
• ECG changes: widespread ST segment elevation & PR segment depression.
• Serum biomarkers (cardiac enzymes): troponin and creatine kinase levels increase with damage to myocardial cells

Heart Failure

• A complex condition characterized by decreased cardiac output/pulmonary congestion due to functional/structural heart disorders.

• Causes: Coronary artery disease (CAD), hypertension (HTN), cardiomyopathy, and valvular heart disease.

• Heart failure is often a progressive condition that may be acute in origin (STEMI).

• Types include:

  • Right-sided: Results from right ventricle failure. Blood backs up into the systemic venous system, leading to peripheral edema (swelling), jugular venous distension (JVD), hepatomegaly (liver enlargement), portal hypertension, abdominal distention, and other conditions. Common causes of right-sided failure include pulmonary HTN, lung issues (e.g., COPD) and valve disorders.
  • Left-sided: Results from left ventricle failure. Blood backs up into the pulmonary circulation. Common causes of left ventricular failure include hypertension, MI, & valve disorders. Symptoms include dyspnea, orthopnea, crackles (in lungs), edema, and other symptoms.

• Clinical Manifestations:

  • Right-sided: Peripheral edema, JVD
  • Left-sided: Pulmonary congestion, orthopenea, crackles/rales, hypoxia
  • Other: Fatigue, SOB, weight gain, ascites, weakness, mental confusion

Shock

• A sudden and dramatic failure of the circulation resulting in cellular hypoxia.
  • Causes: Altered cardiac function (cardiogenic), decreased fluid/blood volume (hypovolemic), vasodilation (distributive), & obstructions (obstructive).
  • Cardiogenic: Decreased cardiac output due to heart failure.
  • Hypovolemic: Reduced circulating fluid volume.
  • Distributive: Vasodilation disrupting normal circulation.
  • Obstructive: Blockage hindering blood flow.

Electrophysiology

• A review of the heart's electrical conduction system and its components.
• Sinoatrial (SA) Node: Heart's pacemaker (60-100 bpm) producing P-waves.
• Atrioventricular (AV) Node: Delays impulse conduction (40-60 bpm) between atria & ventricles
• Internodal Pathways: Transmit impulse from SA Node to AV Node.
• Bachmann's Bundle: transmits signal from SA to left atrium.
• Bundle of His: transmits electrical signal to right and left ventricle bundles
• Purkinje Fibers: Deliver conducted impulses through the ventricular tissue, initiating the ventricular contraction (depolarization).
• Action Potential Phases: Each phase is a critical step representing electrical changes leading to heart contraction; the sequential change in electrical potential across a cell membrane.
• Phases occur in each part of heart's activity: rest, depolarization (contraction signals), early repolarization, plateau phase, & rapid repolarization (recovery).

Cardiovascular Trauma

• Myocardial Contusion: Bruising of the heart muscle.
  • Associated with deceleration forces, like collisions with the chest wall or spine.
  • Characterized by local contusion, hemorrhage, edema, and damage to myocardial tissue.
  • Coronary arteries damage causes myocardial disruptions - ischemia
  • Conductive cell damage can trigger cardiac arrhythmias and left-sided heart failure from backup of fluid into the lungs.
• Myocardial Rupture: Tear in the heart wall.
  • Almost always fatal due to the severity and potential for life-threatening complications.
  • Presents with pericardial tamponade, arrhythmias, hypovolemia, & heart failure.
• Commotio Cordis: A condition resulting from significant, blunt force trauma or other sudden impact in the relative refractory or supernormal excitatory periods during cardiac repolarization phase of the heartbeat. This can cause sudden cardiac arrest & ventricular fibrillation (VF). This is a sudden, dangerous event.

Test your knowledge on key concepts of cardiovascular health, including ischemia, dyslipidemia, and atherosclerosis. This quiz covers definitions, risk factors, and the role of HDL and veins in the cardiovascular system. Perfect for students studying health sciences or anyone interested in understanding heart health.