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Transcript
Acquired Heart Disease Tricia Santos MS3 Diagnostic Radiology December 2005 Diagnosing heart disease the “old fashioned” way History Physical Exam Chest Radiograph Approach to evaluation of the Heart on Chest Radiograph • Evaluate the heart for: – Pericardial disease – Myocardial disease – Valvular disease • Evaluate the vessels for: – Pressure and flow changes – Intravascular volume status – Edema Size Matters When looking for heart disease, first ask yourself, “Is the heart big or small?” Pericardial and Myocardial disease= Global enlargement Small Heart • Constrictive Pericarditis • Restrictive Cardiomyopathy Big Heart • Pericardial Effusion • Myocardial Failure Small Heart Pericardial or Myocardial Disease? • Use physical exam to differentiate • Kussmaul’s sign and pericardial knock are consistent with constrictive pericarditis Pericardial Calcifications Small Heart Globally Enlarged Heart Pericardial Disease • Pericardial Effusion – “Oreo” Sign • Fluid collection between epicardial and retrosternal fat pads – WIDE vascular pedicle • RA pressures are high due to constriction and therefore do not allow blood to easily return to the RA Oreo Sign Globally Enlarged Heart Myocardial Disease • Myocardial Failure – NARROW vascular pedicle • Patients are usually on diuretics – Leads and Lines • Outline the walls of the chambers if no effusion is present Myocardial Failure Myocardial Failure or Pericardial Effusion? Myocardial Failure or Pericardial Effusion? Wide Vascular Pedicle Visible Borders of Mediastinum Pericardial Effusion Myocardial Failure or Pericardial Effusion? Gehlbach, Brian K., et al. The Pulmonary Manifestations of Left Heart Failure. Chest. 2004; 125: 669-682. Myocardial Failure or Pericardial Effusion? Globally enlarged heart Narrow VPW Myocardial Failure Gehlbach, Brian K., et al. The Pulmonary Manifestations of Left Heart Failure. Chest. 2004; 125: 669-682. Valvular Disease = Unequal chamber enlargement Small/Normal Heart Big Heart • Valvular Stenosis • Valvular Insufficiency - Chambers are pressure overloaded - Mild dilation of chambers may be seen, but general hypertrophy is not seen on chest radiograph - Chambers are volume overloaded - Marked dilation of chambers Aortic Stenosis • Chest radiograph – Decreased pulmonary blood flow with normal flow distribution – Narrow vascular pedicle – Increased LVP (may have mild LV enlargement) – Post stenotic dilation of aorta • Physical Exam: – Crescendo/decrescendo systolic murmur (may radiate to clavicles, carotid, or “beauty-sash” distribution) – Pulsus parvus et tardus – Diastolic rumble from associated aortic insufficiency Aortic Stenosis Why narrow vascular pedicle with decreased pulmonary blood flow? • Low LV output → decreased circulating blood volume → decreased venous return and RV output • Increase in circulating atrionatriuretic factor → decreased total blood volume → decreased venous return and RV output Aortic Stenosis Mitral Stenosis • Chest radiograph – – – – Mild LA dilation Increased LAP Pulmonary flow inversion LUL oligemia occurs in 16% of patients • Possibly secondary to displaced/compressed LUL veins from LA – Narrow vascular pedicle • Physical Exam – Faint diastolic murmur (rumble) – Opening snap – Loud S1 Atrial Septal Defect Why? Atrial Septal Defect…Why? LUL Oligemia Narrow VPW Pulmonary Venous HTN LV Dilation Mitral Insufficiency • Chest Radiograph – Marked dilation of LA – Pulmonary flow inversion • Physical Exam – Holosystolic blowing murmur • Radiates to axilla • No change with inspiration – S1 and S2 may be inaudible or difficult to hear – Systolic apical thrill Tricuspid Insufficiency • Chest radiograph – Marked dilation of RA – Wide vascular pedicle • Physical Exam – Holosystolic blowing murmur • Increases with inspiration/increased venous return – Elevated JVP with fused CV wave – Side-to-side head bob – Hepatojugular reflux – Hepatomegaly – Puslatile Liver – Ascites – Peripheral Edema Mitral and Tricuspid Insufficiency Evaluate the vessels: Pulmonary Blood Flow • Increased with shunt vascularity • Decreased with cephalization • Flow inversion occurs with chronic left heart failure and mitral stenosis Normal Pulmonary Flow • Pulmonary veins have no valves, therefore they • • are directly affected by pressures in the LA In the upright person, flow is greater in the lower lobes according to the West zones Gravity makes it more difficult for blood to return to the LA from the lower lobe veins, therefore LL vessels are larger Pulmonary Flow Inversion • Occurs with long-standing elevated LAP • Actual cause of redirection of blood is unknown – One theory suggests: ↑ LAP → basal edema → ↓ basilar compliance → ↓ negative interstitial pressure → vessels unable to stay open → ↓ diameter of vessels → ↑↑ resistance to flow → blood redirected to upper lobes – Others theorize that the cause is organic – Cardiac output is likely decreased in the presence of cephalization and edema • Flow inversion is not reversible with treatment Pulmonary Flow Left to Right Shunts • ASD, VSD, and PDA originally shunt blood to the • • • • right side of the heart and pulmonary circulation Pulmonary flow INCREASES Narrow vascular pedicle secondary to decreased systemic flow Small aorta due to decreased LV output PE: Listen for the presence of murmurs – ASD: systolic, fixed split S2 – VSD: loud, harsh, holosystolic – PDA: “machine-like” systolic and diastolic Increased or decreased flow? Decreased with Cephalization Larger vessels Small Vessels Evaluate the Vessels: Pulmonary Pressures • Pulmonary Venous Hypertension – Caused by subacute to chronic impairment of pulmonary venous drainage, i.e. ↑ LAP • Myocardial dysfunction • Mitral valve disease • Obstruction – Secondary signs include septal thickening, indistinct LL vessels, bronchial wall thickening • Blood flow redistributes to the upper lobes • Diminished pulmonary blood flow Evaluate the Vessels: Pulmonary Pressures • Pulmonary Arterial Hypertension – Caused by increased resistance or chronic increase in pulmonary flow – Cardiac causes include ASD, VSD, PDA, AV septal defects • Chest Radiograph – Early PAH: Increased convexity of main pulmonary artery – Hilar vessels enlarge with decrease in size of peripheral vessels • Physical Exam – Widely split S2 – Chronic PAH: elevated JVP, enlarged liver, peripheral edema • Secondary to right heart failure Evaluate the vessels Main Pulmonary Artery • Enlarged main pulmonary artery – 3 types 1. Large PA and large pulmonary veins – – Correlates with increased flow Ex: ASD 2. PA larger than draining veins – – Correlates with increased pressure Ex: Hypertension 3. Equally enlarged PA and veins + wide vascular pedicle – – Correlates with increased circulating blood volume Ex: Renal Failure Renal failure Evaluate the Vessels: Intravascular Volume Status • Increased intravascular volume leads to increased vascular pedicle width (VPW) • There are no valves in the veins from the base of the skull to the RA or from the RA down to the femoral veins • Therefore, there is a continuous column of blood from base of skull to femoral veins Evaluate the Vessels Cardiac Causes of Wide VPW • Chronic Left Heart Failure (wide VPW without diuretics) – – – Enlarged cardiac silhouette, cardiogenic pulmonary edema, cephalization Most common cause is ischemic PE: S3, S4 gallop, basilar crackles – – – Abrupt increase in VPW without pulmonary edema, possible pleural effusions Caused by sudden elevation of pulmonary vascular resistance (massive PE, bacterial emboli from IVDU, tumor emboli) PE: Elevated JVP – – – Most commonly secondary to left heart failure Enlarged RV, wide VPW, possible pleural effusions PE: Right ventricular heave, elevated JVP, enlarged liver, peripheral edema – – Wide VPW, but decreased pulmonary blood volume PE: Pulsus Paradoxus – – Enlarged RA from volume overload PE: See previous slides • Acute Right Heart Failure • Chronic Right Heart Failure • Tamponade • Tricuspid Regurgitation Chronic Right and Left Heart Failure Wide VPW, Enlarged RV and LV Evaluate the Vessels: Cardiogenic Edema • Cardiogenic edema occurs secondary to hydrostatic forces and therefore predominately occurs in the lower lobes • Most commonly secondary to left heart failure (acute or chronic) • Vascular indistinctness Which represents edema? Which represents edema? Vascular Indistinctness Well-defined vessels Cardiogenic Edema and LHF • Acute LHF – – – – – Extensive Edema No flow redistribution No change in VPW NL Heart Size Causes • Massive MI • Abrupt onset valvular disease • Ruptured papillary muscle • Chronic LHF – – – – – Basilar Edema Cephalization VPW usually narrow Enlarged cardiac silhouette Most commonly ischemic cardiomyopathy Cardiogenic Edema In Summary • Acquired heart disease can be diagnosed with a thorough history and physical exam and careful evaluation of the chest radiograph • This method provides an an inexpensive, non-invasive, and reliable way to diagnose heart disease. References *Primary Sources: • Milne, Eric N.C and Pistolesi, Massimo. Reading the Chest Radiograph: A Physiologic Approach. Mosby. 1993. • Gosselin, Marc. Radiographic Approach to Acquired Cardiopulmonary Disease. Secondary Sources: • Philbin, Edward F., et al. Relationship between Cardiothoracic Ratio and Left Ventricular Ejection Fraction in Congestive Heart Failure. Archives of Internal Medicine. 1998; 158: 501-506 • Baron, Murray G. Pericardial Effusion. Circulation. 1971; 44: 294. • Gehlbach, Brian K., et al. The Pulmonary Manifestations of Left Heart Failure. Chest. 2004; 125: 669-682. • Wesley, Ely E., et al. Using the Chest Radiograph to Determine Intravascular Volume Status. Chest. 2002; 121: 942-950.