Tricia Santos MS3
Diagnostic Radiology
December 2005

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

When looking for heart disease, first ask yourself,

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 Pericardial Calcifications
Small Heart
• Kussmaul’s sign and pericardial knock are consistent with constrictive pericarditis

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 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
• 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
- Chambers are volume overloaded
- Marked dilation of chambers

• 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

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

• 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?

LUL Oligemia
Narrow VPW
Pulmonary
Venous HTN
LV Dilation

• 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

• 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

• 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

• 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
• 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
– 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
– Wide VPW, but decreased pulmonary blood volume
– PE: Pulsus Paradoxus
• Tricuspid Regurgitation
– Enlarged RA from volume overload
– PE: See previous slides

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

Vascular Indistinctness Well-defined vessels

• 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

• 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.

*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.
Internal Medicine.
1998; 158: 501-506
Archives of
• 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.