Cardio Heavy Hitters

This striated muscle forms the walls of the heart.

Myocardium

This structure separates the right and left sides of the heart; it has an atrial portion and a ventricular portion.

Septum

This two-cusped left atrioventricular valve lies between the left atrium and left ventricle.

Mitral valve, also called the bicuspid valve

This three-cusped right atrioventricular valve lies between the right atrium and right ventricle.

Tricuspid valve

This valve lies between the right ventricle and pulmonary artery.

Pulmonary valve

This valve separates the left ventricle from the aorta.

Aortic valve

This is the normal blood-flow sequence through the heart and lungs.

Superior and inferior venae cavae, right atrium, tricuspid valve, right ventricle, pulmonary valve, pulmonary artery, lungs, pulmonary veins, left atrium, mitral valve, left ventricle, aortic valve, and aorta

This circulation carries blood through the body outside the lungs.

Systemic circulation

This circulation carries blood through the lungs.

Pulmonary circulation

This double-walled, well-lubricated membranous sac surrounds the heart, reduces friction, and allows movement during contraction.

Pericardium

This phase is the mechanical contraction phase of the heart.

Systole

This phase is the relaxation and filling phase of the heart.

Diastole

This natural pacemaker lies in the right atrial wall near the opening of the superior vena cava.

Sinoatrial node

This conduction-system structure lies in the lower right atrium along the interatrial septum.

Atrioventricular node

This is the usual impulse path from the natural pacemaker to ventricular contraction.

Sinoatrial node, atrioventricular node, bundle of His, then Purkinje fibers

These congenital lesions allow mixing of systemic and pulmonary blood because blood preferentially moves from high-pressure systemic circulation to low-pressure pulmonary circulation.

Left-to-right shunts

These are the three major left-to-right shunts in the slide deck.

Atrial septal defect, ventricular septal defect, and patent ductus arteriosus

This most common left-to-right shunt is a free communication between the atria.

Atrial septal defect

This left-to-right shunt is a free communication between the ventricles.

Ventricular septal defect

This persistent fetal vascular connection joins the pulmonary artery and aorta; it normally closes soon after birth.

Patent ductus arteriosus

This left-to-right shunt enlarges the right atrium, right ventricle, and pulmonary outflow tract.

Atrial septal defect

Cardiomegaly, increased pulmonary vascularity, a small aortic knob, and a small descending aorta with an enlarged pulmonary outflow tract point to this defect.

Atrial septal defect

This defect increases pulmonary blood flow and pulmonary venous return, producing diastolic overload of the left atrium and left ventricle.

Ventricular septal defect

This congenital defect produces an enlarged pulmonary trunk but usually does not enlarge the right ventricle on a chest radiograph.

Ventricular septal defect

An enlarged, somewhat triangular heart with increased pulmonary vascular volume and a very large pulmonary trunk suggests this congenital defect.

Ventricular septal defect

In this persistent fetal connection, blood moves from the high-pressure aorta into the lower-pressure pulmonary artery.

Patent ductus arteriosus

This left-to-right shunt enlarges the left atrium, left ventricle, and central pulmonary arteries and diffusely increases pulmonary vascularity.

Patent ductus arteriosus

This left-to-right shunt produces a prominent aortic knob because flow increases through the aorta proximal to the shunt.

Patent ductus arteriosus

This complication of any left-to-right shunt occurs when chronic high pulmonary flow raises pulmonary arterial resistance and pulmonary hypertension develops.

Eisenmenger syndrome

This pulmonary-hypertension pattern shows enlarged central pulmonary arteries with abrupt narrowing and pruning of peripheral pulmonary vessels.

Eisenmenger syndrome

This direction change can occur in a long-standing left-to-right shunt when pulmonary arterial pressure rises enough to balance or reverse the original shunt.

Right-to-left shunting

This is the most common cause of cyanotic congenital heart disease and combines four abnormalities.

Tetralogy of Fallot

This four-part congenital defect includes a high ventricular septal defect, pulmonary stenosis, an overriding aorta, and right ventricular hypertrophy.

Tetralogy of Fallot

In tetralogy of Fallot, this shunt allows unoxygenated venous blood to enter the left ventricle and systemic circulation, causing cyanosis.

Right-to-left shunting

An upturned and laterally displaced cardiac apex, decreased pulmonary vascularity, and a flat pulmonary outflow tract point to this cyanotic defect.

Tetralogy of Fallot

This French term describes the boot-shaped cardiac silhouette associated with tetralogy of Fallot.

Coeur en sabot

This congenital condition is a narrowing or constriction of the aorta, most commonly just beyond the branches to the head and arms at the distal aortic arch.

Coarctation of the aorta

Normal arm pressure with very low leg pressure is the classic clinical clue for this congenital aortic narrowing.

Coarctation of the aorta

Pressure erosion from dilated intercostal collateral vessels causes notching of these posterior ribs in coarctation of the aorta.

Fourth through eighth posterior ribs

Prestenotic dilation above a narrowed aortic segment plus poststenotic dilation below it produces this chest-radiograph sign.

Figure 3 sign

This esophagram sign is the reverse figure 3 impression caused by coarctation of the aorta.

Figure E sign

This disease is narrowing of the lumen of one or more coronary arteries.

Coronary artery disease

This deposition of fatty material on the inner arterial wall is the most common cause of coronary artery disease.

Atherosclerosis

Temporary oxygen insufficiency in the myocardium causes this severe chest pain, often radiating to the neck, jaw, or left arm and associated with tightness or suffocation.

Angina pectoris

These five factors in the slide deck predispose to coronary artery disease.

Hypertension, obesity, smoking, a high-cholesterol diet, and lack of exercise

This event occurs when a coronary artery is occluded, depriving part of the myocardium of blood and causing muscle-cell death.

Myocardial infarction

This invasive but definitive test shows coronary artery disease.

Coronary arteriography

This noninvasive test has high sensitivity and specificity for coronary narrowing greater than 50 percent.

Computed tomography coronary angiography

This revascularization procedure is commonly used for ischemic heart disease and its graft patency can be assessed with computed tomography coronary angiography.

Coronary artery bypass grafting

This term means that the heart cannot propel blood at a rate and volume sufficient to supply the tissues.

Congestive heart failure

Cardiac enlargement, redistribution of pulmonary venous blood flow, interstitial edema, alveolar edema, and pleural effusions describe this condition.

Left-sided heart failure

Enlarged superior pulmonary veins with decreased caliber of veins in the lower lungs describe this pulmonary venous pattern.

Redistribution of pulmonary venous blood flow

Pulmonary congestion and edema with little heart enlargement can occur in this acute event caused by coronary thrombosis.

Acute left ventricular failure

Dilation of the right atrium and right ventricle, often with lower-extremity edema, describes this form of heart failure.

Right-sided heart failure

Dilation of the superior vena cava and widening of the right superior mediastinum can be caused by this form of heart failure.

Right-sided heart failure

A cardiothoracic ratio greater than this percentage on a posteroanterior chest radiograph indicates cardiomegaly.

50 percent

This condition is abnormal accumulation of fluid in extravascular pulmonary tissues.

Pulmonary edema

This pressure change is the most common cause of pulmonary edema.

Elevation of pulmonary venous pressure

Loss of sharp pulmonary vascular markings and perihilar haze caused by fluid in the interstitial space indicate this type of pulmonary edema.

Interstitial pulmonary edema

These thin horizontal basal lines represent fluid in the interlobular septa during interstitial pulmonary edema.

Kerley B lines

Irregular, poorly defined patchy densities scattered through the lungs describe this type of pulmonary edema.

Alveolar pulmonary edema

A diffuse, bilateral, symmetric, fan-shaped central lung infiltration with peripheral sparing is this classic pattern of alveolar pulmonary edema.

Butterfly pattern, also called bat-wing pattern

Blunting or a meniscus at the lateral and posterior costophrenic angles indicates this fluid collection associated with pulmonary edema.

Pleural effusion

This chest position with a horizontal beam best shows a pleural effusion and whether the fluid layers freely.

Lateral decubitus position

This term means high blood pressure and is a leading cause of stroke and congestive heart failure.

Hypertension

This equation describes blood pressure in the slide deck.

Cardiac output multiplied by total peripheral resistance

This is the highest peripheral arterial pressure and occurs when the left ventricle contracts.

Systolic pressure

This is the peripheral arterial pressure when the left ventricle relaxes and fills from the left atrium.

Diastolic pressure

According to this slide deck, blood pressure above these values is defined as high blood pressure.

Systolic pressure above 140 millimeters of mercury or diastolic pressure above 90 millimeters of mercury

This is the most common screening examination for renovascular lesions causing hypertension.

Computed tomography angiography

This vascular disease often affects young adult women, is commonly bilateral, and is a major cause of renovascular hypertension.

Fibromuscular dysplasia

Alternating areas of narrowing and dilation in a renal artery create this characteristic appearance.

String-of-beads pattern

This condition results when long-standing high blood pressure narrows systemic vessels and raises resistance to blood flow.

Hypertensive heart disease

In hypertensive heart disease, the early response of the left ventricle to increased workload is this.

Left ventricular hypertrophy

Downward displacement of the cardiac apex, sometimes below the left hemidiaphragm, is a later sign of this condition.

Hypertensive heart disease

This localized arterial dilation most commonly affects the aorta, especially its abdominal portion.

Aneurysm

This aneurysm type involves only one side of the arterial wall.

Saccular aneurysm

This aneurysm type bulges around the entire circumference of the vessel wall.

Fusiform aneurysm

Most abdominal aortic aneurysms occur below these arterial origins, allowing a graft to be placed without injuring the kidneys.

Renal arterial origins

This catastrophic event may occur when an aneurysm enlarges and is not treated quickly.

Rupture with massive hemorrhage

Rapid deceleration, blast injury, and chest compression are mechanisms that can cause this potentially fatal injury.

Traumatic aortic rupture

In closed-chest trauma, this is the usual location of an aortic tear, distal to the left subclavian artery at the ductus arteriosus.

Aortic isthmus near the ductus arteriosus

Mediastinal widening and loss of the sharp aortic-knob margin after chest trauma suggest this injury.

Traumatic aortic rupture

This potentially life-threatening condition begins when an intimal disruption lets blood enter the aortic wall and separate its layers.

Aortic dissection

These two channels result when blood separates the layers of the aortic wall in a dissection.

True lumen and false lumen

This is the most common risk factor for aortic dissection in the slide deck.

Arterial hypertension

Sudden, sharp, severe chest, abdominal, or back pain that may fade even while rupture risk remains suggests this condition.

Aortic dissection

This proximal aortic-dissection category is fatal without immediate surgical treatment by graft placement.

Type A aortic dissection

This aortic-dissection category may be treated medically or with an endovascular stent placed in the true lumen.

Type B aortic dissection

A radiolucent flap within a dilated aorta on computed tomography is the key sign of this condition.

Aortic dissection

This arterial disorder causes wall thickening, hardening, loss of elasticity, fatty plaques, progressive narrowing, and possible occlusion.

Atherosclerosis

These fatty deposits develop in the intima during atherosclerosis.

Atherosclerotic plaques

Irregular densities along an arterial course on a radiograph are the common appearance of this vascular process.

Calcified atherosclerotic plaques

This balloon-catheter procedure relieves peripheral ischemia from atherosclerotic narrowing.

Percutaneous transluminal angioplasty

This term means an intravascular clot.

Thrombus

Slow blood flow, especially in veins, is this major cause of thrombus formation.

Stasis

Platelets can adhere and form a thrombus after this vessel-wall problem.

Endothelial injury or inflammation

This is all or part of a thrombus that detaches, enters the bloodstream, and lodges elsewhere to cause ischemia or occlusion.

Embolus

A clot that forms in the deep veins of the legs commonly sends fragments to these arteries.

Pulmonary arteries

An embolus from a damaged mitral valve can travel through the left ventricle and aorta to these organs.

Brain, kidney, or another systemic organ