1. Acquired Heart Disease Tricia Santos MS3 Diagnostic Radiology December 2005

2. Diagnosing heart disease the “old fashioned” way History Physical Exam Chest Radiograph

3. Approach to evaluation of the Heart on Chest Radiograph Evaluate the heart for: Evaluate the heart for: –Pericardial disease –Myocardial disease –Valvular disease Evaluate the vessels for: Evaluate the vessels for: –Pressure and flow changes –Intravascular volume status –Edema

4. Size Matters When looking for heart disease, first ask yourself, “Is the heart big or small?”

5. Pericardial and Myocardial disease= Global enlargement Small Heart Constrictive Pericarditis Constrictive Pericarditis Restrictive Cardiomyopathy Restrictive Cardiomyopathy Big Heart Pericardial Effusion Pericardial Effusion Myocardial Failure Myocardial Failure

6. Small Heart Pericardial or Myocardial Disease? Use physical exam to differentiate Use physical exam to differentiate Kussmaul’s sign and pericardial knock are consistent with constrictive pericarditis Kussmaul’s sign and pericardial knock are consistent with constrictive pericarditis Pericardial Calcifications Small Heart

7. Globally Enlarged Heart Pericardial Disease Pericardial Effusion Pericardial Effusion –“Oreo” Sign Fluid collection between epicardial and retrosternal fat pads 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 RA pressures are high due to constriction and therefore do not allow blood to easily return to the RA

8. Oreo Sign

9. Globally Enlarged Heart Myocardial Disease Myocardial Failure Myocardial Failure –NARROW vascular pedicle Patients are usually on diuretics Patients are usually on diuretics –Leads and Lines Outline the walls of the chambers if no effusion is present Outline the walls of the chambers if no effusion is present

10. Myocardial Failure

11. Myocardial Failure or Pericardial Effusion?

12. Wide Vascular Pedicle Visible Borders of Mediastinum Pericardial Effusion

13. Myocardial Failure or Pericardial Effusion? Gehlbach, Brian K., et al. The Pulmonary Manifestations of Left Heart Failure. Chest. 2004; 125: 669-682.

14. Myocardial Failure or Pericardial Effusion? Gehlbach, Brian K., et al. The Pulmonary Manifestations of Left Heart Failure. Chest. 2004; 125: 669-682. Globally enlarged heart Narrow VPW Myocardial Failure

15. Valvular Disease = Unequal chamber enlargement Small/Normal Heart Valvular Stenosis Valvular Stenosis - Chambers are pressure overloaded - Mild dilation of chambers may be seen, but general hypertrophy is not seen on chest radiograph Big Heart Valvular Insufficiency Valvular Insufficiency - Chambers are volume overloaded - Marked dilation of chambers

16. Aortic Stenosis Chest radiograph 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: 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

17. Aortic Stenosis Why narrow vascular pedicle with decreased pulmonary blood flow? Low LV output → decreased circulating blood volume → decreased venous return and RV output 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 Increase in circulating atrionatriuretic factor → decreased total blood volume → decreased venous return and RV output

18. Aortic Stenosis

19. Mitral Stenosis Chest radiograph 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 Possibly secondary to displaced/compressed LUL veins from LA –Narrow vascular pedicle Physical Exam Physical Exam –Faint diastolic murmur (rumble) –Opening snap –Loud S1

20. Atrial Septal Defect Why?

21. Atrial Septal Defect…Why? Narrow VPW LV Dilation LUL Oligemia Pulmonary Venous HTN

22. Mitral Insufficiency Chest Radiograph Chest Radiograph –Marked dilation of LA –Pulmonary flow inversion Physical Exam Physical Exam –Holosystolic blowing murmur Radiates to axilla Radiates to axilla No change with inspiration No change with inspiration –S1 and S2 may be inaudible or difficult to hear –Systolic apical thrill

23. Tricuspid Insufficiency Chest radiograph Chest radiograph –Marked dilation of RA –Wide vascular pedicle Physical Exam Physical Exam –Holosystolic blowing murmur Increases with inspiration/increased venous return 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

24. Mitral and Tricuspid Insufficiency

25. Evaluate the vessels: Pulmonary Blood Flow Increased with shunt vascularity Increased with shunt vascularity Decreased with cephalization Decreased with cephalization Flow inversion occurs with chronic left heart failure and mitral stenosis Flow inversion occurs with chronic left heart failure and mitral stenosis

26. Normal Pulmonary Flow Pulmonary veins have no valves, therefore they are directly affected by pressures in the LA 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 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 Gravity makes it more difficult for blood to return to the LA from the lower lobe veins, therefore LL vessels are larger

27. Pulmonary Flow Inversion Occurs with long-standing elevated LAP Occurs with long-standing elevated LAP Actual cause of redirection of blood is unknown 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 ↑ 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 Flow inversion is not reversible with treatment

28. Pulmonary Flow Left to Right Shunts ASD, VSD, and PDA originally shunt blood to the right side of the heart and pulmonary circulation ASD, VSD, and PDA originally shunt blood to the right side of the heart and pulmonary circulation Pulmonary flow INCREASES Pulmonary flow INCREASES Narrow vascular pedicle secondary to decreased systemic flow Narrow vascular pedicle secondary to decreased systemic flow Small aorta due to decreased LV output Small aorta due to decreased LV output PE: Listen for the presence of murmurs PE: Listen for the presence of murmurs –ASD: systolic, fixed split S2 –VSD: loud, harsh, holosystolic –PDA: “machine-like” systolic and diastolic

29. Increased or decreased flow?

30. Decreased with Cephalization Larger vessels Small Vessels

31. Evaluate the Vessels: Pulmonary Pressures Pulmonary Venous Hypertension Pulmonary Venous Hypertension –Caused by subacute to chronic impairment of pulmonary venous drainage, i.e. ↑ LAP Myocardial dysfunctionMyocardial dysfunction Mitral valve diseaseMitral valve disease ObstructionObstruction –Secondary signs include septal thickening, indistinct LL vessels, bronchial wall thickening Blood flow redistributes to the upper lobes Blood flow redistributes to the upper lobes Diminished pulmonary blood flow Diminished pulmonary blood flow

32. Evaluate the Vessels: Pulmonary Pressures Pulmonary Arterial Hypertension Pulmonary Arterial Hypertension –Caused by increased resistance or chronic increase in pulmonary flow –Cardiac causes include ASD, VSD, PDA, AV septal defects Chest Radiograph Chest Radiograph –Early PAH: Increased convexity of main pulmonary artery –Hilar vessels enlarge with decrease in size of peripheral vessels Physical Exam Physical Exam –Widely split S2 –Chronic PAH: elevated JVP, enlarged liver, peripheral edema Secondary to right heart failure Secondary to right heart failure

33. Evaluate the vessels Main Pulmonary Artery Enlarged main pulmonary artery – 3 types 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

34. Renal failure

35. Evaluate the Vessels: Intravascular Volume Status Increased intravascular volume leads to increased vascular pedicle width (VPW) 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 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 Therefore, there is a continuous column of blood from base of skull to femoral veins

36. Evaluate the Vessels Cardiac Causes of Wide VPW Chronic Left Heart Failure (wide VPW without diuretics) 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 Acute Right Heart Failure Acute Right Heart Failure –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 Chronic Right Heart Failure Chronic Right Heart Failure –Most commonly secondary to left heart failure –Enlarged RV, wide VPW, possible pleural effusions –PE: Right ventricular heave, elevated JVP, enlarged liver, peripheral edema Tamponade Tamponade –Wide VPW, but decreased pulmonary blood volume –PE: Pulsus Paradoxus Tricuspid Regurgitation Tricuspid Regurgitation –Enlarged RA from volume overload –PE: See previous slides

37. Chronic Right and Left Heart Failure Wide VPW, Enlarged RV and LV

38. Evaluate the Vessels: Cardiogenic Edema Cardiogenic edema occurs secondary to hydrostatic forces and therefore predominately occurs in the lower lobes 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) Most commonly secondary to left heart failure (acute or chronic) Vascular indistinctness Vascular indistinctness

39. Which represents edema?

40. Vascular IndistinctnessWell-defined vessels

41. Cardiogenic Edema and LHF Acute LHF Acute LHF –Extensive Edema –No flow redistribution –No change in VPW –NL Heart Size –Causes Massive MI Massive MI Abrupt onset valvular disease Abrupt onset valvular disease Ruptured papillary muscle Ruptured papillary muscle Chronic LHF Chronic LHF –Basilar Edema –Cephalization –VPW usually narrow –Enlarged cardiac silhouette –Most commonly ischemic cardiomyopathy

42. Cardiogenic Edema

43. In Summary Acquired heart disease can be diagnosed with a thorough history and physical exam and careful evaluation of the chest radiograph 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. This method provides an an inexpensive, non-invasive, and reliable way to diagnose heart disease.

44. References *Primary Sources: Milne, Eric N.C and Pistolesi, Massimo. Reading the Chest Radiograph: A Physiologic Approach. Mosby. 1993. Milne, Eric N.C and Pistolesi, Massimo. Reading the Chest Radiograph: A Physiologic Approach. Mosby. 1993. Gosselin, Marc. Radiographic Approach to Acquired Cardiopulmonary Disease. 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 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. 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. 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. Wesley, Ely E., et al. Using the Chest Radiograph to Determine Intravascular Volume Status. Chest. 2002; 121: 942-950.