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Circulation is the movement of blood throughout the body through one continuous circuit of blood vessels. Different organs have unique functions and, therefore, have different requirements, circulatory patterns, and regulatory mechanisms. Several of the most vital organs (including the brain, heart, and kidneys) have autoregulatory properties, meaning that they are able to maintain a relatively constant blood flow despite fluctuations in mean arterial pressure (MAP). In other cases, locally produced factors (such as adenosine, CO2, or NO) can produce local vasoconstriction or vasodilation, regulating blood flow under specific physiologic conditions.

Vascular Resistance, Flow, and Mean Arterial Pressure

Blood flows through the heart, arteries, capillaries, and veins in a closed, continuous circuit. Flow is the movement of volume per unit of time. Flow is affected by the pressure gradient and the resistance fluid encounters between 2 points. Vascular resistance is the opposition to flow, which is caused primarily by blood friction against vessel walls. Vascular resistance is directly related to the diameter of the vessel (smaller vessels have higher resistance). Mean arterial pressure (MAP) is the average systemic arterial pressure and is directly related to cardiac output (CO) and systemic vascular resistance (SVR). The SVR and MAP are affected by the vascular anatomy as well as a number of local and neurohumoral factors.

Tachyarrhythmias

A tachyarrhythmia is a rapid heart rhythm, regular or irregular, with a rate > 100 beats/min. Tachyarrhythmia may or may not be accompanied by symptoms of hemodynamic change. Pathologic tachyarrhythmias resulting in hemodynamic instability can be caused by intrinsic cardiac abnormalities, systemic diseases, or medication toxicity. Supraventricular arrhythmias are called narrow-complex tachycardias and originate in the sinoatrial (SA) node, atrial myocardium, or atrioventricular (AV) node. Ventricular arrhythmias originate below the AV node and are characterized by a wide QRS complex. Diagnosis is made by physical exam and ECG. Management is directed toward the type of tachyarrhythmia present and its underlying cause.

Portal hypertension

Portal hypertension is increased pressure in the portal venous system. This increased pressure can lead to splanchnic vasodilation, collateral blood flow through portosystemic anastomoses, and increased hydrostatic pressure. There are a number of etiologies, including cirrhosis, right-sided congestive heart failure, schistosomiasis, portal vein thrombosis, hepatitis, and Budd-Chiari syndrome. Most individuals are asymptomatic until complications arise, including esophageal varices, portal hypertensive gastropathy, ascites, and hypersplenism. The diagnosis is clinical, but it can be supported by ultrasound findings (and hepatic venous pressure gradient measurement in unclear cases). Management requires treating the underlying etiology and managing the complications. This can include nonselective beta blockers to prevent bleeding from varices, diuretics and sodium restriction for ascites, and transjugular intrahepatic portosystemic shunt for refractory complications.

Heart sounds

Heart sounds are brief, transient sounds produced by valve opening and closure and by movement of blood in the heart. They are divided into systolic and diastolic sounds. In most cases, only the first (S1) and second (S2) heart sounds are heard. These are high-frequency sounds and arise from aortic and pulmonary valve closure (S1), as well as mitral and tricuspid valve closure (S2). The third heart sound (S3) may be physiologic (e.g., athletes) or pathologic (e.g., congestive heart failure), and is related to abnormally rapid deceleration of early diastolic left ventricular inflow. The fourth heart sound (S4) is associated with contraction of the atria into partially-filled and non-compliant (stiff) ventricles. S4 is a pathologic sign in the young, but may be found in older individuals due to an age-related decrease in ventricular compliance. Additional sounds include murmurs (physiologic and pathologic), clicks, and snaps. These sounds are heard in individuals with structural abnormalities of the heart such as septal defects, valvular stenosis, and mitral regurgitation.

Long QT Syndrome

Long QT syndrome (LQTS) is a disorder of ventricular myocardial repolarization that produces QT prolongation on electrocardiogram (ECG). Long QT syndrome is associated with an increased risk of developing life-threatening cardiac arrhythmias, specifically torsades de pointes. The condition may be congenital or acquired. Congenital LQTS is attributed to genetic mutations affecting cardiac ion channels. Acquired LQTS usually results from drug therapy and/or electrolyte abnormalities. Patients can be asymptomatic or present with palpitations, syncope, seizures, and even sudden cardiac death. Diagnosis is established with ECG along with medical and family history, laboratory workup, and other cardiac tests. Treatment is determined by etiology. Acquired LQTS requires removal of the offending drug and correction of electrolyte abnormalities. Congenital LQTS management involves avoidance of triggers of arrhythmia, intake of beta-blockers, and placement of an implantable cardioverter-defibrillator (ICD).

Thoracic Aortic Aneurysms

Thoracic aortic aneurysm (TAA) is the abnormal dilation of a segment of the thoracic aorta, usually the ascending aorta. Most TAAs are due to degenerative aortic disorders, commonly in patients > 65 years of age. Genetic TAAs account for 20% of cases and are frequently found in younger patients. Most TAAs are asymptomatic (incidentally found in imaging) but could present with symptoms from its effects on surrounding structures. Aortic rupture is a life-threatening emergency. Among diagnostic imaging studies, computed tomography (CT) angiography is the most widely utilized. In asymptomatic cases, aortic expansion is monitored. Operative repair is recommended for symptomatic TAAs and increasing aortic diameter (criteria varies with location and underlying condition).

Atrioventricular Block

Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. The 1st-degree block is due to delayed conduction through the AV node. The 2nd-degree block is characterized by progressive conduction delay or intermittently blocked conduction. The 3rd-degree block involves total interruption in conduction between the atria and ventricles, causing complete AV dissociation. Patients may be asymptomatic or may present with syncope, chest pain, dyspnea, and bradycardia depending on the severity of the block. Electrocardiography (ECG) establishes the diagnosis, and treatment is based on the type of block and hemodynamic stability of the patient.

Veins

Veins are tubular collections of cells, which transport deoxygenated blood and waste from the capillary beds back to the heart. Veins are classified into 3 types: small veins/venules, medium veins, and large veins. Each type contains 3 primary layers: tunica intima, tunica media, and tunica adventitia. The venous circulation is a low-pressure system with much lower amounts of smooth muscle and elastic tissue, thinner walls, and larger lumens than arteries. Veins are capacitance vessels with significant compliance and the ability to distend and hold up to 70%–80% of blood volume at rest.

Capillaries

Capillaries are the primary structures in the circulatory system that allow the exchange of gas, nutrients, and other materials between the blood and the extracellular fluid (ECF). Capillaries are the smallest of the blood vessels. Because a capillary diameter is so small, only 1 RBC may pass through at a time. Capillaries are organized into capillary beds, which are extensive networks of branches and anastomoses. Blood flows from the metarterioles, into the capillaries, out the thoroughfare channel, and into venules. Continuous, fenestrated, and sinusoid (discontinuous) capillaries are the 3 primary types, and each has a slightly different structure. Capillary dysfunction can occur either as a result of or a contribution to the clinical manifestation of many clinical conditions.

Lymphadenopathy

Lymphadenopathy is lymph node enlargement (> 1 cm) and is benign and self-limited in most patients. Etiologies include malignancy, infection, and autoimmune disorders, as well as iatrogenic causes such as the use of certain medications. Generalized lymphadenopathy often indicates underlying systemic disease. Diagnosis relies on a thorough medical history and physical examination, which usually identify the underlying cause. When the cause is unknown, a biopsy may be necessary. Management is directed at the underlying infection, malignancy, or other cause.

Myocardial Infarction

MI is ischemia and death of an area of myocardial tissue due to insufficient blood flow and oxygenation, usually from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is most commonly with chest pain, but women and patients with diabetes may have atypical symptoms. Diagnosis is by clinical history, ECG changes, an increase in cardiac enzymes, and evidence of wall motion abnormalities on imaging. Management depends on the timing of the presentation and local resources with regard to thrombolytic therapy versus percutaneous intervention. All patients receive nitrates, pain control, aspirin, anticoagulation, and beta-blockers (unless contraindicated).

Hypertension

Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. The disorder can usually be managed with lifestyle modification and medications, but occasionally, vascular intervention or surgery are required. Age, sex, smoking, obesity, and diet are contributing factors to hypertension, which can lead to heart attack, stroke, congestive heart failure, and CKD if not managed properly. Many individuals with hypertension are undiagnosed or undertreated.

Uncontrolled Hypertension

Although hypertension is defined as a blood pressure of > 130/80 mm Hg, individuals can present with comorbidities of severe asymptomatic or “uncontrolled” hypertension (≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic) that carries with it a significant risk of morbidity and mortality. Despite the prolonged presence of hypertension, there may be no signs or symptoms of end-organ damage (e.g., brain, eyes, heart, kidneys) until function becomes decompensated or severely impaired. Individuals may present with clinical symptoms such as chest pain due to MI or focal neurologic changes associated with a cerebral infarction or intracranial hemorrhage. Diagnosis is made using serial blood pressure measurements and testing for end-organ damage. Management includes lowering the blood pressure and treating specific organ damage.

Myocarditis

Myocarditis is an inflammatory disease of the myocardium, which may occur alone or in association with a systemic process. There are numerous etiologies of myocarditis, but all lead to inflammation and myocyte injury, most often leading to signs and symptoms of heart failure. The course of myocarditis may vary based on the etiology and timeline of symptom progression. The diagnosis is supported by clinical findings, laboratory evaluation, and cardiac imaging. A definitive diagnosis by endomyocardial biopsy is rarely required. Management is supportive and aimed at addressing complications.

Chronic Venous Insufficiency

Chronic venous disease is a spectrum of disorders characterized by venous dilation and/or abnormal vein function in the lower extremities resulting from venous hypertension. "Chronic venous insufficiency" refers to the more severe forms of chronic venous disease. Skin changes typically distinguish chronic venous insufficiency from milder forms of venous disease (like varicose veins) and include skin pigmentation, stasis dermatitis, lipodermatosclerosis, and eventually, the development of ulcers. Diagnosis is usually based on physical exam findings alone, although venous duplex ultrasonography can provide additional information about the etiology, location, and extent of disease. The mainstay of management is compression therapy. A variety of surgical options also exist, including ablation, sclerotherapy, and valve repair. Venous ulcers are common as the disease progresses and are often very difficult to treat.

Aortic Dissection

Aortic dissection occurs due to shearing stress from pulsatile pressure causing a tear in the tunica intima of the aortic wall. This tear allows blood to flow into the media, creating a “false lumen.” Aortic dissection is most commonly caused by uncontrolled hypertension. Complications arise due to partial occlusion of vital branches off the aorta and reduced blood flow to the brain, visceral organs, and extremities. Patients often present with acute, tearing chest or back pain. Computed tomography is the diagnostic modality of choice. All type A dissections (ascending aorta) are a surgical emergency due to the risk of imminent rupture. Type B dissections (descending aorta) can be managed medically with impulse control using beta-blockers and calcium channel blockers. If there is evidence of malperfusion to visceral organs or extremities, aneurysm dilation to > 5 cm, retrograde extension into the ascending aorta, or intractable pain, the patient will need evaluation for endovascular or open repair.

Tetralogy of Fallot

Tetralogy of Fallot is the most common cyanotic congenital heart disease. The disease is the confluence of 4 pathologic cardiac features: overriding aorta, ventricular septal defect, right ventricular outflow obstruction, and right ventricular hypertrophy. The timing and severity of presentation usually depend on the degree of right ventricular outflow obstruction. Definitive diagnosis is usually established by echocardiogram. Chest X-ray may show the classic boot-shaped heart. Definitive treatment involves surgical repair. Long-term prognosis is good for surgically corrected disease, but cardiovascular morbidity is common.

Supraventricular Tachycardias

Supraventricular tachycardias are related disorders in which the elevation in heart rate is driven by pathophysiology in the atria. This group falls under the larger umbrella of tachyarrhythmias and includes paroxysmal supraventricular tachycardias (PSVTs), ventricular pre-excitation syndromes (i.e. Wolff-Parkinson-White syndrome), atrial flutter, multifocal atrial tachycardia, and atrial fibrillation. Sinus tachycardia (> 100/min) is not a pathologic arrhythmia. The diagnosis of these conditions can be made using electrocardiogram (ECG), and treatment differs depending on the condition.

Deep Vein Thrombosis

Deep vein thrombosis (DVT) usually occurs in the deep veins of the lower extremities. The affected veins include the femoral, popliteal, iliofemoral, and pelvic veins. Proximal DVT is more likely to cause a pulmonary embolism (PE) and is generally considered more serious. Ultrasound can visualize the thrombus and anticoagulation is the primary mode of treatment; the main objective is the prevention of development of a PE.

Abdominal Aortic Aneurysms

An aortic aneurysm is the abnormal dilation of a segment of the aorta. Abdominal aortic aneurysm is the most common aortic aneurysm, occurring frequently in the infrarenal area. Degenerative aortic disorders are the prevalent etiology, affecting patients > 60 years of age. Most aneurysms are asymptomatic, but can cause compression of surrounding structures or rupture, which is a life-threatening emergency. Diagnosis is often made by ultrasound. As aneurysmal rupture carries a high mortality rate, surveillance is recommended for asymptomatic cases to monitor aortic diameter. Elective surgery (the majority via endovascular aortic repair) is an effective way to reduce complications and aneurysm-related death. This surgery is performed based on aortic size, underlying condition, and associated symptoms.

Atrial Fibrillation

Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. There are many conditions that can cause AF, usually damage to the heart (e.g., coronary artery disease, previous myocardial infarction). Diagnosis is confirmed by an electrocardiogram that will show an “irregularly irregular” heartbeat with no distinct P waves and narrow QRS complexes. AF increases the risk of thromboembolic events. Treatment is primarily based on ventricular rate and rhythm control, which can be achieved through drugs and/or cardioversion. Anticoagulation is administered if the patient is at significant risk for thromboembolic events.

Arteries

Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Each of these types of arteries contain 3 primary layers: the tunica intima, tunica media, and tunica adventitia. In particular, the tunica media contains smooth muscle cells (allowing for vasoconstriction), and in the larger vessels, a significant amount of elastin (allowing these vessels to stretch and recoil in response to changes in pressure during systole and diastole).

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Cardiovascular Pathology

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