Cardiovascular Lecture Review

Flashcards covering key vocabulary terms and definitions from lectures on Arrhythmia, Heart Failure, Valvular Heart Disease (Aortic Stenosis, Aortic Regurgitation, Mitral Stenosis, Mitral Regurgitation), Coronary Artery Disease, Pericarditis, Pericardial Effusion with Tamponade, Atherosclerosis, Hypertension, and Shock.

Wolff-Parkinson-White syndrome

A condition characterized by a reentrant tachyarrhythmia, occurring in approximately 1 in 1000 persons, due to an accessory pathway.

Accessory Pathway

A bundle of normal atrial or ventricular tissue in Wolff-Parkinson-White syndrome that bypasses the AV node, leading to pre-excitation of the ventricle.

Pre-excitation

Conduction of cardiac impulse to the ventricles over an accessory pathway rather than through the AV node, causing a short PR interval and a wide QRS with a delta wave on ECG.

Delta Wave

A slurred upstroke of the QRS complex seen on an ECG, characteristic of ventricular pre-excitation in Wolff-Parkinson-White syndrome.

Reentrant Tachycardia

A type of rapid heartbeat initiated when a cardiac impulse travels in a circular fashion due to two parallel connections (like the AV node and an accessory pathway), allowing for continuous propagation.

Heart Failure (HF) Categories

Four general categories accounting for almost all causes of heart failure: inappropriate workload, restricted filling, myocyte loss, and decreased myocyte contractility.

Systolic Dysfunction (Heart Failure)

A condition where the heart's pumping ability is reduced, shifting the isovolumic systolic pressure curve downward, reducing stroke volume and cardiac output.

Diastolic Dysfunction (Heart Failure)

A condition where the heart's ability to relax and fill is impaired (normal contractility), shifting the diastolic pressure-volume curve to the left, increasing left ventricular end-diastolic pressure.

Compensatory Mechanisms (Systolic HF)

The heart's responses to systolic dysfunction: increased preload, increased catecholamine release, and cardiac myocyte hypertrophy/ventricular volume increase.

Aortic Stenosis Causes

The most common causes include congenital abnormalities (unicuspid, bicuspid, fused leaflets), rheumatic heart disease, and degenerative valve disease from calcium deposition.

Syncope (Aortic Stenosis)

Caused by decreased cerebral perfusion due to fixed obstruction, transient atrial arrhythmias with loss of effective atrial contribution, or ventricular arrhythmias.

Angina Pectoris (Aortic Stenosis)

Caused by comorbid coronary artery disease, compensatory ventricular hypertrophy increasing oxygen demand and compressing vessels, or rarely, calcium emboli from calcified valves.

Aortic Regurgitation Causes

Pathogenesis divided into valvular causes (congenital, rheumatic heart disease, ankylosing spondylitis, infective endocarditis) and aortic causes (aortic aneurysm, connective tissue disorders, aortic inflammation, dissection).

Pathophysiology of Aortic Regurgitation

Blood entering the ventricle from both the left atrium and aorta during diastole, causing abnormally high volume load, leading to eccentric hypertrophy, huge ventricular volumes, and a widened aortic pulse pressure.

Clinical Manifestations of Aortic Regurgitation

Shortness of breath (due to heart failure/pulmonary edema), hyperdynamic pulses, widened pulse pressure, three distinct murmurs, a third heart sound, and a laterally displaced apical impulse.

Mitral Stenosis Causes

Most commonly rheumatic heart disease, less commonly calcific mitral valve disease, congenital mitral stenosis, or collagen vascular disease.

Pathophysiology of Mitral Stenosis

Obstruction of flow through the mitral valve (area < 1 cm2 usually), elevating left atrial, pulmonary venous, and right-sided pressures, often leading to dilation and reduced systolic function of the right ventricle.

Clinical Manifestations of Mitral Stenosis

Shortness of breath and hemoptysis, atrial arrhythmias (e.g., atrial fibrillation), thrombus formation in the left atrium with embolic events, and a diastolic rumble with an opening snap on auscultation.

Mitral Regurgitation Causes

Ruptured chordae tendineae, ruptured or dysfunctional papillary muscles, perforated leaflet, inflammatory causes (e.g., rheumatic heart disease), destruction from myxomatous degeneration or calcification, and congenital abnormalities.

Pathophysiology of Mitral Regurgitation

Regurgitation of blood into the left atrium during systole, leading to dilation and hypertrophy of the left ventricle and atrium. Acute cases result in sudden volume overload and pulmonary edema due to prominent atrial v waves.

Clinical Symptoms of Mitral Regurgitation

Shortness of breath (chronic HF, acute pulmonary edema), fatigue (lack of forward blood flow), and palpitations/cardioembolic events due to left atrial enlargement and atrial fibrillation.

Stable Angina

Chest pain associated with coronary artery disease that occurs only with exertion and has been stable over a long period.

Unstable Angina

Chest pain associated with coronary artery disease that occurs at rest and comes and goes, often due to transient thrombotic occlusion from plaque fissuring.

Myocardial Infarction (MI)

Myocyte damage and death resulting from angina that continues uninterruptedly for a prolonged period, typically due to a fixed and persistent thrombus from deep arterial injury.

Pathophysiology of Stable Angina

Results from a fixed narrowing of coronary arteries, usually a 90% reduction at rest or 50% during exercise, causing ischemia as cardiac demand rises.

Pathophysiology of Unstable Angina

Caused by fissuring of atherosclerotic plaque leading to platelet accumulation, transient thrombotic occlusion (10-20 minutes), platelet-released vasoconstrictive factors, and endothelial dysfunction.

Pathophysiology of Myocardial Infarction

Deep arterial injury from plaque rupture causes formation of a relatively fixed and persistent thrombus, which leads to myocyte damage and death.

Clinical Manifestations of Coronary Artery Disease

Chest pain (angina), shortness of breath, a fourth heart sound (due to systolic/diastolic dysfunction), shock, bradycardia or tachycardia, and nausea and vomiting (ischemic episodes can be silent).

Pericarditis Clinical Presentation

Severe, sharp, retrosternal chest pain radiating to the back, worse with lying flat or deep breathing, better with leaning forward, and often accompanied by a pericardial rub.

Pericardial Rub

A high-pitched musical, squeaking sound, often with two or more components (systolic, early diastolic, late diastolic), originating from friction between visceral and parietal pericardial surfaces, pathognomonic for pericarditis.

Kussmaul Sign

An inappropriate increase in the jugular venous pulsation level with inspiration, seen in constrictive pericarditis due to prolonged inflammation and fibrosis.

Pericarditis Causes

Infection (e.g., coxsackievirus), inflammation from collagen vascular disease, neoplasm, metabolic conditions (chronic kidney disease), injury (MI, trauma, radiation), and idiopathic.

Beck Triad

Three classic signs of pericardial tamponade: hypotension, elevated jugular venous pressure, and muffled heart sounds.

Paradoxic Pulse (Pericardial Tamponade)

A marked inspiratory decline in systemic arterial pressure and left ventricular stroke volume due to decreased left ventricular end-diastolic volume, caused by increased right ventricular filling bowing the interventricular septum to the left during inspiration.

Causes of Pericardial Effusion and Tamponade

Similar to pericarditis: infection, inflammation from collagen vascular disease, neoplasm, metabolic (renal disease), injury (MI, trauma, aortic dissection), and idiopathic.

Atherosclerotic Plaque Formation

Begins with LDL infiltration into the subendothelial region, oxidation of LDL, activation of macrophages and immune proteins, formation of foam cells and fatty streaks, proliferation of vascular smooth muscle cells, macrophage apoptosis, plaque necrosis, inflammation, and eventual fibrous cap formation.

Atherosclerosis and Cardiovascular Disease

Can cause angina pectoris (coronary artery narrowing >75% for cellular ischemia during exertion) or myocardial infarction (clotting and occlusion leading to myocyte death).

Treatable Risk Factors for Atherosclerosis

Hyperlipidemia, cigarette smoking, hypertension, diabetes mellitus, and obesity (especially abdominal obesity).

Hypertensive Retinopathy

Narrowed arterioles, retinal hemorrhages, exudates, and papilledema observed on funduscopic examination, indicative of long-standing or severe hypertension.

Left Ventricular Hypertrophy (HTN)

Enlargement of the heart's pumping chamber, detectable by echocardiography, ECG, or physical examination, a physical finding in long-standing hypertension.

Renal Bruits (HTN)

Sounds heard over the renal arteries, indicating narrowing of these arteries, a physical finding in long-standing hypertension.

Causes of Hypertension

Essential hypertension (most common), renal diseases (renovascular, parenchymal), endocrine disorders, obesity/metabolic syndrome, drug-related factors, and other conditions (pre-eclampsia, coarctation, sleep apnea).

Nitric Oxide Synthase (NOS) Disruption and Blood Pressure

Inhibiting NO production or genetically ablating endothelial NOS in mice leads to an increase or sustained elevation in blood pressure, suggesting NO's role in chronic blood pressure lowering.

Hypovolemic Shock

A major pathophysiologic form of shock caused by loss of blood or fluid.

Distributive Shock

A major pathophysiologic form of shock caused by widespread dilation of blood vessels.

Cardiogenic Shock

A major pathophysiologic form of shock caused by decreased cardiac output.

Obstructive Shock

A major pathophysiologic form of shock caused by blockage, such as from a massive pulmonary embolism.

Specific Forms of Hypovolemic Shock

Hemorrhagic (blood loss), Traumatic (bleeding into damaged tissues), Surgical (blood loss, tissue bleeding, dehydration), Burns (plasma loss from burn surfaces), and Fluid losses (vomiting, diarrhea, sweating).

Anaphylactic Shock

A specific form of distributive shock where an accelerated allergic reaction releases histamine, causing marked vasodilation, a fall in blood pressure, and warm skin.

Neurogenic Shock

A specific form of distributive shock caused by sudden loss of sympathetic autonomic activity, resulting in vasodilation, pooling of blood in veins, reduced venous return, and decreased cardiac output, with warm skin.

Septic Shock

A specific form of distributive shock involving loss of plasma into tissues ('third spacing') leading to hypotension, and toxins that depress the myocardium, typically with warm skin.

Wolff-Parkinson-White syndrome

A condition characterized by a reentrant tachyarrhythmia, occurring in approximately 1 in 1000 persons, due to an accessory pathway.

Accessory Pathway

A bundle of normal atrial or ventricular tissue in Wolff-Parkinson-White syndrome that bypasses the AV node, leading to pre-excitation of the ventricle.

Pre-excitation

Conduction of cardiac impulse to the ventricles over an accessory pathway rather than through the AV node, causing a short PR interval and a wide QRS with a delta wave on ECG.

Delta Wave

A slurred upstroke of the QRS complex seen on an ECG, characteristic of ventricular pre-excitation in Wolff-Parkinson-White syndrome.

Reentrant Tachycardia

A type of rapid heartbeat initiated when a cardiac impulse travels in a circular fashion due to two parallel connections (like the AV node and an accessory pathway), allowing for continuous propagation.

Heart Failure (HF) Categories

Four general categories accounting for almost all causes of heart failure: inappropriate workload, restricted filling, myocyte loss, and decreased myocyte contractility.

Systolic Dysfunction (Heart Failure)

A condition where the heart's pumping ability is reduced, shifting the isovolumic systolic pressure curve downward, reducing stroke volume and cardiac output.

Diastolic Dysfunction (Heart Failure)

A condition where the heart's ability to relax and fill is impaired (normal contractility), shifting the diastolic pressure-volume curve to the left, increasing left ventricular end-diastolic pressure.

Compensatory Mechanisms (Systolic HF)

The heart's responses to systolic dysfunction: increased preload, increased catecholamine release, and cardiac myocyte hypertrophy/ventricular volume increase.

Aortic Stenosis Causes

The most common causes include congenital abnormalities (unicuspid, bicuspid, fused leaflets), rheumatic heart disease, and degenerative valve disease from calcium deposition.

Syncope (Aortic Stenosis)

Caused by decreased cerebral perfusion due to fixed obstruction, transient atrial arrhythmias with loss of effective atrial contribution, or ventricular arrhythmias.

Angina Pectoris (Aortic Stenosis)

Caused by comorbid coronary artery disease, compensatory ventricular hypertrophy increasing oxygen demand and compressing vessels, or rarely, calcium emboli from calcified valves.

Aortic Regurgitation Causes

Pathogenesis divided into valvular causes (congenital, rheumatic heart disease, ankylosing spondylitis, infective endocarditis) and aortic causes (aortic aneurysm, connective tissue disorders, aortic inflammation, dissection).

Pathophysiology of Aortic Regurgitation

Blood entering the ventricle from both the left atrium and aorta during diastole, causing abnormally high volume load, leading to eccentric hypertrophy, huge ventricular volumes, and a widened aortic pulse pressure.

Clinical Manifestations of Aortic Regurgitation

Shortness of breath (due to heart failure/pulmonary edema), hyperdynamic pulses, widened pulse pressure, three distinct murmurs, a third heart sound, and a laterally displaced apical impulse.

Mitral Stenosis Causes

Most commonly rheumatic heart disease, less commonly calcific mitral valve disease, congenital mitral stenosis, or collagen vascular disease.

Pathophysiology of Mitral Stenosis

Obstruction of flow through the mitral valve (area < 1 cm2 usually), elevating left atrial, pulmonary venous, and right-sided pressures, often leading to dilation and reduced systolic function of the right ventricle.

Clinical Manifestations of Mitral Stenosis

Shortness of breath and hemoptysis, atrial arrhythmias (e.g., atrial fibrillation), thrombus formation in the left atrium with embolic events, and a diastolic rumble with an opening snap on auscultation.

Mitral Regurgitation Causes

Ruptured chordae tendineae, ruptured or dysfunctional papillary muscles, perforated leaflet, inflammatory causes (e.g., rheumatic heart disease), destruction from myxomatous degeneration or calcification, and congenital abnormalities.

Pathophysiology of Mitral Regurgitation

Regurgitation of blood into the left atrium during systole, leading to dilation and hypertrophy of the left ventricle and atrium. Acute cases result in sudden volume overload and pulmonary edema due to prominent atrial v waves.

Clinical Symptoms of Mitral Regurgitation

Shortness of breath (chronic HF, acute pulmonary edema), fatigue (lack of forward blood flow), and palpitations/cardioembolic events due to left atrial enlargement and atrial fibrillation.

Stable Angina

Chest pain associated with coronary artery disease that occurs only with exertion and has been stable over a long period.

Unstable Angina

Chest pain associated with coronary artery disease that occurs at rest and comes and goes, often due to transient thrombotic occlusion from plaque fissuring.

Myocardial Infarction (MI)

Myocyte damage and death resulting from angina that continues uninterruptedly for a prolonged period, typically due to a fixed and persistent thrombus from deep arterial injury.

Pathophysiology of Stable Angina

Results from a fixed narrowing of coronary arteries, usually a 90% reduction at rest or 50% during exercise, causing ischemia as cardiac demand rises.

Pathophysiology of Unstable Angina

Caused by fissuring of atherosclerotic plaque leading to platelet accumulation, transient thrombotic occlusion (10-20 minutes), platelet-released vasoconstrictive factors, and endothelial dysfunction.

Pathophysiology of Myocardial Infarction

Deep arterial injury from plaque rupture causes formation of a relatively fixed and persistent thrombus, which leads to myocyte damage and death.

Clinical Manifestations of Coronary Artery Disease

Chest pain (angina), shortness of breath, a fourth heart sound (due to systolic/diastolic dysfunction), shock, bradycardia or tachycardia, and nausea and vomiting (ischemic episodes can be silent).

Pericarditis Clinical Presentation

Severe, sharp, retrosternal chest pain radiating to the back, worse with lying flat or deep breathing, better with leaning forward, and often accompanied by a pericardial rub.

Pericardial Rub

A high-pitched musical, squeaking sound, often with two or more components (systolic, early diastolic, late diastolic), originating from friction between visceral and parietal pericardial surfaces, pathognomonic for pericarditis.

Kussmaul Sign

An inappropriate increase in the jugular venous pulsation level with inspiration, seen in constrictive pericarditis due to prolonged inflammation and fibrosis.

Pericarditis Causes

Infection (e.g., coxsackievirus), inflammation from collagen vascular disease, neoplasm, metabolic conditions (chronic kidney disease), injury (MI, trauma, radiation), and idiopathic.

Beck Triad

Three classic signs of pericardial tamponade: hypotension, elevated jugular venous pressure, and muffled heart sounds.

Paradoxic Pulse (Pericardial Tamponade)

A marked inspiratory decline in systemic arterial pressure and left ventricular stroke volume due to decreased left ventricular end-diastolic volume, caused by increased right ventricular filling bowing the interventricular septum to the left during inspiration.

Causes of Pericardial Effusion and Tamponade

Similar to pericarditis: infection, inflammation from collagen vascular disease, neoplasm, metabolic (renal disease), injury (MI, trauma, aortic dissection), and idiopathic.

Atherosclerotic Plaque Formation

Begins with LDL infiltration into the subendothelial region, oxidation of LDL, activation of macrophages and immune proteins, formation of foam cells and fatty streaks, proliferation of vascular smooth muscle cells, macrophage apoptosis, plaque necrosis, inflammation, and eventual fibrous cap formation.

Atherosclerosis and Cardiovascular Disease

Can cause angina pectoris (coronary artery narrowing >75% for cellular ischemia during exertion) or myocardial infarction (clotting and occlusion leading to myocyte death).

Treatable Risk Factors for Atherosclerosis

Hyperlipidemia, cigarette smoking, hypertension, diabetes mellitus, and obesity (especially abdominal obesity).

Hypertensive Retinopathy

Narrowed arterioles, retinal hemorrhages, exudates, and papilledema observed on funduscopic examination, indicative of long-standing or severe hypertension.

Left Ventricular Hypertrophy (HTN)

Enlargement of the heart's pumping chamber, detectable by echocardiography, ECG, or physical examination, a physical finding in long-standing hypertension.

Renal Bruits (HTN)

Sounds heard over the renal arteries, indicating narrowing of these arteries, a physical finding in long-standing hypertension.

Causes of Hypertension

Essential hypertension (most common), renal diseases (renovascular, parenchymal), endocrine disorders, obesity/metabolic syndrome, drug-related factors, and other conditions (pre-eclampsia, coarctation, sleep apnea).

Nitric Oxide Synthase (NOS) Disruption and Blood Pressure

Inhibiting NO production or genetically ablating endothelial NOS in mice leads to an increase or sustained elevation in blood pressure, suggesting NO's role in chronic blood pressure lowering.

Hypovolemic Shock

A major pathophysiologic form of shock caused by loss of blood or fluid.

Distributive Shock

A major pathophysiologic form of shock caused by widespread dilation of blood vessels.

Cardiogenic Shock

A major pathophysiologic form of shock caused by decreased cardiac output.

Obstructive Shock

A major pathophysiologic form of shock caused by blockage, such as from a massive pulmonary embolism.

Specific Forms of Hypovolemic Shock

Hemorrhagic (blood loss), Traumatic (bleeding into damaged tissues), Surgical (blood loss, tissue bleeding, dehydration), Burns (plasma loss from burn surfaces), and Fluid losses (vomiting, diarrhea, sweating).

Anaphylactic Shock

A specific form of distributive shock where an accelerated allergic reaction releases histamine, causing marked vasodilation, a fall in blood pressure, and warm skin.