Transcript Acquired-Heart

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
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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
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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
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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
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Correlates with increased flow
Ex: ASD
2. PA larger than draining veins
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Correlates with increased pressure
Ex: Hypertension
3. Equally enlarged PA and veins + wide vascular pedicle
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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)
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Enlarged cardiac silhouette, cardiogenic pulmonary edema, cephalization
Most common cause is ischemic
PE: S3, S4 gallop, basilar crackles
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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
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Most commonly secondary to left heart failure
Enlarged RV, wide VPW, possible pleural effusions
PE: Right ventricular heave, elevated JVP, enlarged liver, peripheral edema
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Wide VPW, but decreased pulmonary blood volume
PE: Pulsus Paradoxus
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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
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Extensive Edema
No flow redistribution
No change in VPW
NL Heart Size
Causes
• Massive MI
• Abrupt onset valvular
disease
• Ruptured papillary muscle
• Chronic LHF
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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.