S3 Week 2 Pathology

Front 1

What is valvular stenosis?

Back 1

The failure of a valve to open completely, obstructing forward flow.

Front 2

What is valvular insufficiency?

Back 2

Insufficiency results from failure of a valve to close completely, thereby allowing reversed flow.

Front 3

Calcific Aortic Stenosis:

Back 3

- The most common degenerative valvular disease.
- Usually age related
- Can be related to congenital bicuspid valves (more prone to calcification)
- The hallmark of calcific aortic stenosis is heaped-up calcified masses on the outflow side of the cusps.
- Significant outflow obstruction leads to left ventricular pressure overload with concentric hypertrophy.
- The hypertrophied myocardium tends to be ischemic and angina can develop.
- Syncope may develop due to poor perfusion of the brain.
- Sytolic and diastolic dysfunction collude to cause CHF, and cardiac decompensation eventually ensues.

Front 4

Myxomatous Mitral Valve:

Back 4

- Also called mitral valve prolapse.
- One or more of the mitral valve leaflets are "floppy", and balloon back into the left atrium during systole.
- Affects women much more than men.
- Histologically, the essential change is thinning of the fibrosa layer of the valve, with expansion of the middle spongiosa layer with increased deposition of myxomatous (mucoid) material.
- Common in Marfan syndrome and other disorders of connective tissue.
- Most patients are asymptomatic; auscultation will reveal midsystolic clicks caused by abrupt tension on the redundant valve leaflets and chordae tendineae as the valve attempts to close.
- May lead to regurgitation and CHF.

Front 5

Rheumatic Valvular Disease Part 1:

Back 5

- Rheumatic fever is an acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks after an episode of group A beta-hemolytic strep pharyngitis.
- Acute rheumatic heart disease is the cardiac manifestation of RF and is associated with inflammation of the valves, myocardium or pericardium.
- Chronic valvular deformities are the consequence of RHD; characterized by diffuse and dense scarring of valves resulting in permanent dysfunction (mitral stenosis being most common).
- Chronic RHD is characterized by organization of the acute inflammation and subsequent scarring. Changes to the mitral valve include leaflet thickening, commisural fusion and shortening and thickening of the chordae tendineae.
- The functional consequence of RHD is valvular stenosis and regurgitation.
- With tight mitral valve stenosis, the left atrium dilates and may harbor mural thrombi.
- Congestive changes in the lungs may lead to right ventricular hypertrophy.
- With pure mitral stenosis, the left ventricle is generally normal.

Front 6

Rheumatic Valvular Disease Part 2:

Back 6

- Pathogenesis:
Acute RF is a hypersensitivity reaction induced by host antibodies elicited by group A streptococci. The M proteins of the bacteria induce host antibodies that cross-react with antigens in the heart, joints and other tissues.

- Clinical Features:
Acute RF typically appears in children between 5-15. Symptoms occur 2-3 weeks after an episode of pharyngitis. Streptolysin O or DNAase can be detected in most patients.
The predominant clinical manifestations are arthritis and carditis. Begins with a migratory polyarthritis accompanied by fever. Features of the carditis are pericardial friction rubs and arrythmias.
Chronic rheumatic carditis does not cause problems for years or decades after the initial episode of RF.
- Patients will have cardiac murmurs, hypertrophy and dilation, CHF and often arrythmias and thromboembolic complications.

Front 7

Jones Criteria for diagnosis of acute RHD:

Back 7

Diagnosis is made by serological evidence of a previous strep infection, in conjuction with two or more of the following Jones criteria:
1. Carditis
2. Migratory polyarthritis of the large joints
3. Subcutaneous nodules
4. Erythema marginatum of the skin
5. Sydenham chorea; a neurological disorder with involuntary, purposeless, rapid movements.

* One of the Jones criteria and two minor manifestations (fever, arthralgia or increased CRP) are also sufficient to make the diagnosis.

Front 8

Histopathology of rheumatic carditis:

Back 8

Rheumatic carditis may affect all three layers of the heart. Examination of often reveals Aschoff bodies, an area of focal fibrinoid necrosis surrounded by inflammatory cells, including lymphocytes, plasma cells and macrophages, that later resolve to form fibrous scar tisuse.

Front 9

Pathophysiology of mitral valve stenosis:

Back 9

In MS there is obstruction to blood flow from the LA to the LV generating an abnormally high pressure in the LA.
The high LA pressure is transmitted to the pulmonary circulation causing increased pulmonary venous and capillary pressures. This may cause transudation of plasma into the lung interstitium and alveoli; leading to dyspnea and other symptoms of CHF.
If highly elevated, collateral channels between pulmonary and bronchial veins may open and rupture, leading to hemoptysis.
Elevation of LA pressure can result in either "passive" or "reactive" changes; reactive changes lead to hypertrophy and fibrosis of the pulmonary arterioles which can decrease the blood flow through the lungs. This can cause back up into the RV; leading to hypertrophy and right sided heart failure.
LA dilation stretches the atrial conduction fibers and may lead to atrial fibrillation. This causes cardiac output to fall further due to shortened diastole.
LA dilation can lead to intra-atrial thrombus formation; possibly causing stroke. The bigger the LA gets, the higher the risk. The better the blood flow, the lower the risk.

Front 10

Clinical symptoms of mitral stenosis:

Back 10

Early manifestations are those of dyspnea and reduced exercise capacity.
With more severe MS dyspnea occurs even at rest. Orthopnea and PND occrs. May see jugular venous distention, hepatomegaly, ascites and peripheral edema. Compression of the recurrent laryngeal nerve by the enlarged pulmonary artery or LA may cause hoarseness

Front 11

Examination findings with mitral valve stenosis:

Back 11

Increased S1 sound resulting from the high pressure gradient between the LV and LA.
There will also be an opening "snap" that follows S2. This results from the sudden tensing of the chordae tendineae and stenotic leaflets on opening of the valve. The OS is followed by a low frequency decrescenod murmur caused by turbulent flow across the valve during diastole.

Front 12

Etiology of mitral valve regurgitation:

Back 12

MR may result from structural abnormalities of the mitral annulus, valve leaflets, chordae tendineae or the papillary muscles.

Front 13

Pathophysiology of mitral valve regurgitation:

Back 13

In MR, a portion of the LV stroke volume is ejected backward into the low pressure LA during sytole.
This causes; an elevation of the LA volume and pressure, a reduction of forward cardiac output and a volume related stress on the LV because the regurgitated volume returns to the LV in diastole along with normal pulmonary venous return.
In acute MR, symptoms include rapid pulmonary congestion and edema.
In chronic MR, the LA dilates and cardiac output decreases. This leads to weakness and fatigue along with atrial fibrillation.

Front 14

Summary of differences between acute and chronic MR:

Back 14

ACUTE: normal LA size and compliance --> High LA pressure --> High pulmonary venous pressure --> Pulmonary congestion and edema

CHRONIC: Increased LA size and compliance --> more normal LA and pulmonary venous pressures, but low forward cardiac output

Front 15

Examination findings with MR:

Back 15

Patients will have an apical holosystolic murmur that radiates to the axilla.
This murmur may resemble the murmur of AS. The way to tell the difference is to have the patient clench his fists:
Systemic vascular resistance increases and the severity of the MR murmur will intensify

In addition, an S3 may be heard reflecting increased volume returning to the LV in early diastole.

Front 16

Mitral valve prolapse:

Back 16

Mitral valve prolapse is a common and usually asymptomatic billowing of the mitral leaflets into the LA during ventricular systole sometimes accompanied by MR.
Usually the posterior leaflet is enlarged and the normal dense collagen and elastin matrix of the fibrosa is fragmented and replaced with loose connective tissue.
More common in women with thin, lean bodies.
Will hear a midsystolic click and late systolic murmur.

Ocassionally, rupture of the chordae can cause sudden severe regurgitation and pulmonary edema.

Front 17

Aortic stenosis:

Back 17

Most often caused by age related calcification, but may also be caused by congenitally deformed aortic valves, atherosclerotic valve disease and rheumatic disease.
In AS, blood flow across the aortic valve is impeded during sytole. Increased LV pressure is needed to drive blood into the aorta and hypertrophy results (reducing compliance of the LV). This in turn causes hypertrophy of the LA. Development of atrial fibrillation can cause marked clinical deterioration.

Front 18

Syptoms of advanced AS:

Back 18

1. Angina: develops due to increased myocardial oxygen demand because of increased muscle mass and decreased supply due to higher diastolic ventricular pressure.
2. Exertional syncope: Increased blood flow is impossible due to stenosis of the valve, plus exercise vasodilates peripheral vessels leading to decreased cerebral perfusion.
3. CHF: Increased LV diastolic volume and pressure can lead to increased pressure in the LA. This can lead to pulmonary venous congestion.

Angina: median survival of 5 years
Syncope: 3 years
CHF: 2 years
Afib: 6 months

Front 19

Examination of patient with aortic stenosis:

Back 19

Key features of advanced AS include:
A coarse late peaking systolic ejection murmur.
Weakened (parvus) and delayed (tardus) upstroke of the carotid artery owing to obstructed LV outflow.

Other findings may include an S4 because of atrial contraction into a still LV, and reduced or absent aortic component of the second heart sound.

Front 20

Aortic regurgitation:

Back 20

In AR, abnormal regurgitation of blood from the aorta into the LV occurs during diastole. So with each contraction, the LV must pump the extra volume plus the normal volume.
In acute AR: the LV is of normal size. The increased volume/pressure in the LV is transmitted to the LA and pulmonary circulation, often producing dyspnea and pulmonary edema.
In chronic AR: the LV compensates and hypertrophies. There is a significant difference between systolic and diastolic aortic pressure; a widened pulse pressure is a hallmark of AR.
Decreased aortic diastolic pressure results in decreased myocardial perfusion, when coupled with LV hypertrophy, can cause angina.

Front 21

Presentation and examination of AR:

Back 21

Common symptoms of AR include dyspnea on exertion, fatigue, decreased exercise intolerance and the uncomfortable sensation of a forceful heartbeat associated with high pulse pressure.

Physical exam may show bounding pulses and a blowing murmur of AR in early diastole along the left sternal border.

Front 22

Tricuspid stenosis:

Back 22

Is rare and usually a consequence of RHD. The opening snap and diastolic murmur of TS are similar to those of MS, but the murmur is heard closer to the sternum and it intensifies on inspiration.
The neck veins are distended as a result of right atrial contraction against the stenotic tricuspid valve.
Patients may develop abdominal distention and hepatomegaly owing to passive venous congestion.

Front 23

Tricuspid regurgitation:

Back 23

TR is usually functional rather than structural; it develops because of RV enlargement.

Physical signs of TR are waves in the jugular veins and a pulsatile liver because of regurgitation of RV blood into the systemic veins.

The systolic murmur of TR is heard at the lower left sternal border; louder on inspiration.

Front 24

Pulmonic stenosis:

Back 24

Is rare and its cause is almost always congenital deformity of the valve.

Front 25

Pulmonic regurgitation:

Back 25

Most commonly develops in the setting of severe pulmonary hypertension and results from dilation of the valve ring by the enlarged pulmonary artery.
Auscultation reveals a high-pitched decrescendo murmur along the left sternal border that is similar to AR.

Front 26

Anatomy of the heart valves:

Back 26

Front 27

Histology of a normal aortic valve:

Back 27

Front 28

Histology of a normal mitral valve:

Back 28

Front 29

How does the blood supply to the annulus and leaflets in a valve differ?

Back 29

The annulus is supplied by myocardial vessels.
The leaflets are supplied by diffusion from heart blood.

Front 30

Picture of a calcified stenotic aortic valve:

Back 30

Front 31

Possible mechanisms of mitral valve regurgitation:

Back 31

SAM: systolic anterior motion

Front 32

Picture of infective endocarditis:

Back 32

Front 33

Picture of calcification of an anulus:

Back 33

Front 34

Consequences of increased pressure vs. volume overload:

Back 34

Front 35

Consequences of acute vs. chronic stenosis/regurgitation:

Back 35

Front 36

Etiology of common valvular pathology:

Back 36

Front 37

Pathology of acute and chronic rheumatic heart disease:

Back 37

Front 38

Findings in chronic rheumatic heart disease:

Back 38

Front 39

Histology of mitral valve in chronic rheumatic heart disease:

Back 39

Front 40

Fibrosis of the aortic and mitral valve seen in chronic rheumatic heart disease:

Back 40

Front 41

Major types of aortic valve stenosis:

Back 41

 Major types of aortic valve stenosis. A, Normal aortic valve. B, Congenital bicuspid aortic stenosis. A false raphe is present at 6 o’clock. C, Rheumatic aortic stenosis. The commissures are fused with a fixed central orifice. D, Calcific degenerative aortic stenosis

Front 42

How would arythmyias occur with mitral annular calcification?

Back 42

The AV node may be affected as calcification approaches.

Front 43

Histology of mitral valve prolapse:

Back 43

Front 44

Histology comparison of normal vs. myxomatous mitral valve:

Back 44

Front 45

Concentric vs. Eccentric Hypertrophy:

Back 45

Front 46

Graphs of mitral valve stenosis:

Back 46

Front 47

What is responsible for hemoptysis in MS?

1. Pulmonary venous hypertension
2. Pulmonary arterial hypertension
3. Elevated right atrial pressure

Back 47

Pulmonary venous hypertension

Front 48

The most likely cause of atrial fibrillation in a patient with long-standing MS is?

1. Left ventricle enlargement
2. Right atrial enlargement
3. Right ventricular element
4. Left atrial enlargement

Back 48

Left atrial enlargement

Front 49

What is the best test to assess mitral valve stenosis?

Back 49

Transesophogial electrocardiography

Front 50

Recommended pharmacological treatment for mitral valve stenosis:

Back 50

Initial: Na restriction + diuretics

With progression: B-blockers or CCB

If A fib + M.S. – Coumadin (INR 2-3)

Front 51

Graph of mitral valve regurgitation:

Back 51

Front 52

Radiograph of chronic mitral valve regurgitation:

Back 52

Front 53

Radiograph of acute mitral valve regurgitation:

Back 53

Front 54

Graph of aortic stenosis:

Back 54

Front 55

Pathophysiology of angina in AS:

Back 55

Front 56

Recommended medical treatment for aortic stenosis:

Back 56

- Statins may help decrease progression of calcific AS

- Endocarditis prophylaxis only needed if previous history of I.E.

- ACE inhibitors /B-Blockers can be used for patients with CAD and preserved ejection fraction

Front 57

Graph of aortic regurgitation:

Back 57

Front 58

Normal vs Aortic regurgitation pressures:

Back 58

Front 59

Medical treatment of aortic regurgitation:

Back 59

- Acute AR: IV vasodilators/diuretics; B-blockers are contraindicated

Chronic AR: Diuretics first/ACE, CCB, hydralazine might be helpful
- Control of Systolic pressure to < 140 mm Hg
- Nitroglycerine can be tried for angina

Front 60

Disorders of impulse formation in arrythmias:

Back 60

No signal from the pacemaker site

Development of an ectopic pacemaker:
- May arise from conduction cells (most are capable of spontaneous activity)
- Usually under control of SA node, if it slows down too much conduction cells could become dominant.
- Often a result of other injury (ischemia, hypoxia)

Development of oscillatory afterdepolariztions:
- Can initiate spontaneous activity in nonpacemaker tissue
- May be result of drugs (digitalis, norepinephrine) used to treat other cardiopathologies

Front 61

A normal EKG broken down into pieces:

Back 61

The P wave represents the depolarization of the atria.
The PQ segment represents the time the atria are contracting.
The QRS complex represents the depolarization of the ventricles.
The ST segment represents the time the ventricles are contracting.
The T wave represents the ventricles are repolarizing.

Front 62

Calculation of heart rate from EKG:

Back 62

Front 63

Characteristics of sinus bradycardia:

Back 63

Front 64

Characteristics of sinus arrhythmia:

Back 64

Front 65

Characteristics of a 1st degree AV block:

Back 65

*This EKG shows a normal QRS complex

Front 66

Type I 2nd degree AV block (Mobitz I):

Back 66

Usually asymptomatic, but with accompanying bradycardia can cause angina and syncope especially in the elderly—will need pacing if symptomatic.
Also can be caused by drugs that slow conduction (BB, CCB, digoxin)
Correct if reversible cause, avoid meds that block conduction

Front 67

Type II 2nd degree AV block (Mobitz II):

Back 67

Front 68

3rd Degree AV block:

Back 68

Complete dissociation of P waves and QRS complexes; the SA node and AV-branch are firing at thier own rates.

Front 69

Limb lead translation to electrical impulses on an EKG:

Back 69

Front 70

Diagram of all limb leads together:

Back 70

Front 71

Placement of precordial leads:

Back 71

Front 72

Indications for a pacemaker:

Back 72

Front 73

EKG of a patient with a pacemaker:

Back 73

Red circled areas are some of the “pacing spikes” you can see on an EKG of a patient with a pacemaker.
Ventricular pacing results in slower conduction and a widened QRS complex.

Front 74

What does ICD stand for (in regards to a pacemaker)?

Back 74

Implantable cardioverter defibrillator.

Front 75

Overview of the cardiac conduction system:

Back 75

Front 76

How to determine ST segment elevation or depression:

Back 76

- Starts with the J point (where the QRS ends)
- Ends with the beginning of the T wave
- Elevation or depression of the ST segment is measured 0.08 seconds (2 small squares) to the right of the J point

Front 77

Regions of an EKG and the areas of the heart they represent:

Back 77

-ST segment elevation in leads I and aVL represent a lateral infarction
-Anteroseptal infarctions show ST segment elevation in leads V1 to V4.
-ST elevation in V4 to V6 is typical of an anterolateral infarction
-ST elevation in II, III and aVF is typical of inferior infarction.

Front 78

Measurement of ST deviation part 2:

Back 78

Front 79

Hyperacute T waves in acute MI:

Back 79

Front 80

Rule 1 for reading EKG:

Back 80

Rule 1:
The PR interval is the time from initiation of depolarisation of the atria to initiation of the depolarisation of the ventricles. The PR interval should be 120 to 200 milliseconds, or 3 to 5 little squares. A longer PR may imply a block in conduction and a shorter interval indicates a vulnerability to arrhythmias.

Front 81

Rule 2 for reading EKG:

Back 81

Rule 2:
The QRS complex is due to depolarisation of the ventricles. The width of the QRS complex should not exceed 110 ms (less than 3 little squares). A wider QRS is sometimes seen in healthy people, but may represent an abnormality of intraventricular conduction.

Front 82

Rule 3 for reading EKG:

Back 82

Rule 3:
The QRS complex should be dominantly upright in leads I and II. Slight disparities are likely to be acceptable.

Front 83

Rule 4 for reading EKG:

Back 83

Front 84

Rule 5 for reading an EKG:

Back 84

Front 85

Rule 6 for reading an EKG:

Back 85

Front 86

Rule 7 for reading an EKG:

Back 86

Front 87

Rule 8 for reading an EKG:

Back 87

Front 88

Rule 9 for reading an EKG:

Back 88

Front 89

Rule 10 for reading an EKG:

Back 89

Front 90

Deep Q wave seen in MI:

Back 90

Front 91

Causes of sinus tachycardia:

Back 91

Front 92

Three mechanisms of supraventricular tachycardia:

Back 92

Treatment:
- Carotid massage or adenosine commonly terminate the arrhythmia, esp, AV re-entry or AV nodal re-entry.
- Can also use CCB or beta blockers to terminate, if available
- Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stress

Front 93

AV nodal reentry tachycardia:

Back 93

- Is the most common form of paroxysmal supraventricular tachycardia in adults.
- In a normal heart there is a slow and fast pathway for conduction from the AV to the AV bundle. Normally the fast pathway wins out all the time.
- When the atria prematurely beat, the slow pathway is able to conduct both downwards and upwards into the atria, then back down the slow pathway, initiating a loop leading to tachycardia.
- An EKG will show normal QRS complexes with P waves buried in the complex. When P waves are visible they are at the end of the QRS complex and inverted, due to the reverse direction of electrical flow.
- Usually well tolerated, but in some will produce syncope, angina or pulmonary edema.

Front 94

AV re-entrant tachycardias:

Back 94

- Similar to AVNRT, except the re-entrant loop is composed of an accesory pathway of abnormal myoctyes that span the AV groove and connects atrial to ventricular tissue separately from the normal conduction system.

Depending on the characteristics of the pathway, one of two things can occur:
1) Ventricular preexcitation syndrome
2) PSVT

Front 95

Wolff-Parkinson-White syndrome:

Back 95

- WPW patients have an accessory pathway between the atrium and ventricle. This allows bypass of the AV node.
- Simulation of the ventricle begins earlier than normal, and the PR interval of the EKG is shortened.
- But the electrical spread through the myocardium is slower than that of the normal purkinje fiber system....
- As normal conduction through the AV node occurs, ventricular depolarization represents a combination of both electrical impulses.
- As a result, the QRS complex in patients with WPW is wider than normal and demonstrates an abnormally slurred initial upstroke, called a delta wave.

Front 96

Impulse conduction in WPW syndrome:

Back 96

Note the shortened PR interval and slurred upstroke of the delta wave.

Front 97

Characteristics of atrial flutter:

Back 97

Front 98

Characteristics of atrial fibrillation:

Back 98

Front 99

EKG findings with hypo and hyperkalemia:

Back 99

Front 100

Characteristics of premature atrial contraction:

Back 100

Front 101

Characteristics of premature ventricular contraction:

Back 101

Front 102

Non-sustained ventricular tachycardia:

Back 102

- Need to exclude heart disease with Echo and stress testing
- If normal, there is no increased risk of death
- May need anti-arrhythmia treatment if sxs
- In presence of heart disease, increased risk of sudden death
- Need referral for EPS and/or prolonged Holter monitoring

Front 103

Characteristics of ventricular fibrillation:

Back 103

Front 104

Factors affecting myocardial oxygen supply:

Back 104

- The supply of oxygen to the myocardium depends on the oxygen content of the blood and the rate of coronary blood flow.
- The predominance of coronary perfusion takes place during diastole. Perfusion pressure of the coronary arteries can be approximated by the aortic diastolic pressure.
- The heart normally extracts the maximal amount of oxygen from the blood; therefore any increase in demand must be met by an increase in flow.
- During states of hypoxia, ADP and AMP accumulate and are degraded to adenosine, a potent vasodilator.
- Adenosine decreases calcium entry into smooth muscle cells leading to relaxation and vasodilation.

Front 105

Endothelial factors affecting myocardial oxygen supply:

Back 105

- Vasodilators produced by the endothelium include NO, prostacyclin and EDHF.
- Vasoconstrictor is Endothelin 1.

- NO produced by endothelium diffuses into smooth muscle cells; stimulated by thrombic agents, Ach and shear stress of blood flow.

- Prostacyclin is released from endothelium in response to hypoxia, shear stress, Ach and platelet products.

- EDHF released by the endothelium hyperpolarizes and relaxes smooth muscle cells. It is stimulated by Ach. It is more important in relaxing small arterioles than larger arteries.

-Endothelin 1 is a potent vasoconstrictor stimulated by thrombin, angiotensin II, epinephrine and shear stress.

Front 106

Neural factors affecting myocardial blood supply:

Back 106

- Both sympathetic and parasympathetic components.
- Stimulation of a-adrenergic receptors results in vasoconstriction.
- Stimulation of b2-receptors promote vasodilation.

* Although stimulation of a-receptors may initially cause vasoconstriction, stimulation will also increase O2 consumption through increased HR and contractility leading to metabolite production and a net vasodilation.

Front 107

The three major determinants of myocardial oxygen demand:

Back 107

1) Ventricular wall stress: wall stress increases with systolic ventricular pressure. Increased wall stress increases myocardial O2 consumption.
Conversely, a hypertrophied ventrical has less stress and a decreased O2 consumption.

2) Heart rate: increased rate increases oxygen demand.

3) Contractility: Increased contractility increases O2 demand.

Front 108

Pathophysiology of ischemia; fixed vessel narrowing:

Back 108

- The length of a stenotic vessel, and more importantly the degree of narrowing the stenosis causes greatly effects the hemodynamic significance.
- The larger proximal vessels are more prone to atherosclerosis, while the smaller distal vessels can dilate to compensate for reduce flow, up to a point.
- When dilation of distal vessels can no longer compensate, during times of increased oxygen demand myocardial ischemia results.
- At 90% compromisation, dilation cannot compensate at all and ischemia develops even at rest.

Front 109

Pathophysiology of ischemia; endothelial cell dysfunction:

Back 109

- In normal persons, increased O2 demand results in vasodilation of coronary vessels.
- In patients with dysfunctional endothelium (atherosclerosis) an impaired release of endothelial vasodilators results in vasoconstriction.
* It makes sense if the endothelium is damaged, that all the endothelial vasodilatory factors would be decreased
- Impaired release of NO and prostacyclin allows platelets to aggregate and to secrete their potentially harmful procoagulants and vasoconstrictors.

Front 110

Other causes of myocardial ischemia:

Back 110

- Decreased perfusion pressure due to hypotension (hypovolemia or septic shock)
- Severely decreased blood oxygen content (marked anemia or impaired oxygenation of the blood by the lungs)

- A profound increase in myocardial oxygen demand can cause ischemia (from rapid tachycardia, profound acute hypertension or severe aortic stenosis)

Front 111

Consequences of ischemia:

Back 111

- During ischemia, myoctyes convert from aerobic to anaerobic metabolic pathways. Metabolic products such as lactate, serotonin and adenosine accumulate locally. One or more of these activate pain receptors in the C7 through T4 distribution.
- The accumulation of local metabolites and abnormalities of ion transport may precipitate dangerous arrhythmmias
- There are four possible outcomes of myocardial damage caused by ischemia; irreversible necrosis, rapid and full recovery, stunned myocardium and hibernating myocardium.

Front 112

Stunned myocardium:

Back 112

Refers to tissue that, after suffering a period of severe ischemia (but not necrosis), demonstrates prolonged systolic dysfunction even after the return of normal blood flow.
Contractile function gradually recovers. The magnitude of the stunning is proportional to the ischemia. This state likely just fell short of causing irreversible necrosis.

Front 113

Hibernating myocardium:

Back 113

Refers to tissue that manifests chronic vetricular contractile dysfunction in the face of a persistantly reduced blood supply.
In this situation, irreversible damage has not occured and function can promptly improve if blood flow is restored.

Front 114

Stable angina:

Back 114

Chronic stable angina is generally caused by fixed, obstructive plaques in one or more coronary arteries. The pattern of symptoms is usually related to the degree of stenosis.
A pattern of chronic, predictable, transient angina during exertion or emotional stress is termed stable angina.

Patients with variable-threshold angina may experience symptoms at random; due to inappropriate vasoconstriction even at rest.

Front 115

Unstable angina:

Back 115

A patient with chronic stable angina may experience a sudden increase in the tempo and duration of ischemic episodes, occuring with lesser degress of exertion and even at rest. This acceleration of symptoms is known as unstable angina, which can be a precursor to an MI.
Usually results from rupture of an unstable plaque with subsequent platelet aggregation and thrombosis.

Front 116

Variant Angina:

Back 116

Can occur due to coronary artery spasm, even in the absence of plaques.
Though to be an early manifestation of dysfunctional endothelium even before atherosclerosis can be seen.
Can often occur at rest.

Front 117

What kind of ischemia is common among diabetic patients?

Back 117

Silent ischemia; may be due to impaired pain sensation resulting from peripheral neuropathy

Front 118

Clinical features of chronic stable angina:

Back 118

- Angina is most often described as a pressure, discomfort, tightness, burning, or heaviness in the chest. It is not sharp or stabbing and does not vary with movement or breathing. It usually lasts at least a few minutes but no more than 10; but always more than a few seconds. The patient may perform the Levine sign when describing the symptom.

- Discomfort is usually diffuse rather than localized. Most often located in the retrosternal area and radiates to the shoulders and inner aspects of the arms especially on the left side.

- During an attack, generalized sympathetic and parasympathetic stimulation may result in tachycardia, diaphoresis, nausea, shortness of breath, fatigue and weakness.

Front 119

Precipitants and risk factors for chronic stable angina:

Back 119

- Angina is caused by conditions that increase myocardial oxygen demand. These include physical exertion, anger and emotional excitement. Also large meals or cold weather can cause problems.
- Angina is quickly relieved by nitroglycerin.

- Patients may compensate by reducing activities of daily living.

- Ask patients about other risk factors that predispose to atherosclerosis and CAD: smoking, hypercholesterolemia, hypertension, diabetes and family history of premature coronary disease.

Front 120

Diagnosis of chronic stable angina:

Back 120

- Distinguish from GERD, esophageal spasm, biliary pain, pericarditis and chest wall pain.

- Murmurs may be detected during an acute attack of angina.
- Check for carotid or femoral bruits.

Front 121

What stain is specific for endothelial cells?

Back 121

CD31

Front 122

Which coronary vessels are more susceptible to atherosclerosis, the sub-epicardial vessels or the
Intramyocardial (resistance) vessels?

Back 122

The sub-epicardial vessels

Front 123

Coronary artery anatomy:

Back 123

Three-dimensional reformatted images of CT coronary angiograms showing the right coronary artery (long black arrow), left main (large white arrow), left anterior descending coronary artery (white arrowheads) and a diagonal branch (short black arrow), and left circumflex coronary artery (small white arrows). A segment of the coronary venous circulation is also seen (black arrowheads).

Front 124

Diagram of metabolic effects of ischemia:

Back 124

Front 125

Mechanical effects of ischemia:

Back 125

Front 126

Electrical effects of ischemia:

Back 126

Front 127

Examples of different types of stenosis:

Back 127

Front 128

Injecting acetylcholine into coronary arteries would vasoconstrict or vasodilate or no change?

Back 128

Vasodilate; Ach causes vasocontriction when directly applied to smooth muscles cells, but when applied to the endothelial cells it will cause vasodilation (maybe because it induces other vasodilator factors to be released?)

Front 129

Pathogenesis of coronary thrombosis:

Back 129

Front 130

Back 130

Aortic insufficiency

Front 131

Back 131

Accelerated hypertension

Front 132

Back 132

2 cm long 90% lesion

Front 133

Laboratory tests to run in evaluating CAD:

Back 133

Front 134

Back 134

Patient 2

Front 135

Differences in an EKG of subendocardial or transmural MI:

Back 135

Front 136

Electrocardiographic stress tests:

Back 136

Front 137

Contraindications for a stress test:

Back 137

- Rest angina within 48 hrs
- Unstable rhythm
- Severe aortic stenosis
- Acute myocarditis
- Uncontrolled heart failure
- Severe pulmonary hypertension
- Active infective endocarditis

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Exercise treadmill test

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Left heart cath

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Back 140

Adenosine assisted nuclear stress test

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Treadmill nuclear stress test

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Outcomes of coronary thrombi:

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Histology of damaged myocardial tissue:

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Red wavy staining myocytes; or no change because it was very early.

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ST wave changes in MI:

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Front 146

Infarct location vs damaged areas:

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Front 147

What is the difference between STEMI and NSTEMI?

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NSTEMI (non-ST elevatation myocardial infarction): is a result of a partially occlusive thrombus; also called non-Q wave MI.

STEMI (ST-elevation myocardial infarction): is the reuslt of a complete occlusion of a coronary artery with more severe ischemia and a larger amount of necrosis; also called Q-wave MI.

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What does an S3 heart sound represent?

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Filling of an overloaded or non-compliant ventricle.

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What does an S4 heart sound represent?

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Atrial kick; contraction of the atria to push out the remaining blood into the ventricle.

Front 150

How to tell the difference between unstable angina, NSTEMI and STEMI:

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UA: patients symptoms (transient) + transient ST depression or T wave inversion

NSTEMI: Serum markers of necrosis + more persistent ST or T wave abnormalities

STEMI: More syptomatic with ST elevations on EKG + serum markers of necrosis

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The use of troponin and CK-MB in testing for MI:

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CK-MB rises 3-8 hours after an MI, peaks at 24 hours and returns to normal in 2-3 days.

Troponin: levels begin to rise 3-4 hours after MI, peak between 18-36 hours and decline slowly, allowing for detection for up to 10-14 days.

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What is hypertrophic cardiomyopathy?

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- Disease of the young
Incidence: 1 in 500 in the general population

- Asymmetric Left Ventricular Hypertrophy

- Genetic Transmission – Autosomal Dominant
Variable penetrance

-Individuals at risk for sudden death, syncope, life threatening arrhythmias

- Mutant cells cannot contract effectively and ultimately fibrose, so the other myocytes hypertrophy to take up the slack

- Hugely hypertrophied intraventricular septum and left ventricle

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What are the most common genetic mutations in HCM?

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Myosin binding protein C
B-myosin heavy chain

Front 154

Histology of hypertrophic cardiomyopathy:

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Short, wide, hypertrophied fibers in chaotic directions
Numerous cardiac fibroblasts and extracellular matrix

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Mechanism of disease in hypertrophic cardiomyopathy:

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With exercise and increased heart rate, the volume in the left ventricle decreases due to less diastolic filling time, bringing the thickened walls closer together. This blocks off the aortic outflow tract. You may also hear a mitral valve regurgitation.

Front 156

Pathology and symptoms of HCM:

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Front 157

Is EKG or echocardiogram better for diagnosis of HCM?

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Echocardiogram, because it will show you areas of hypertrophy.

Front 158

Treatments for HCM?

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- Implantable defibrillator
- Beta blockers or calcium channel blockers

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What is Arrythmogenic Right Ventricular Dysplasia?

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- # 1 cause of sudden death in athletes in Italy

-Individuals are at risk of sudden death, heart failure, ventricular arrhythmias

- Genetic Transmission
Autosomal dominant
1/1000 – 1/5000 adults
Variable penetrance

Front 160

Histology of Arrythmogenic Right Ventricular Dysplasia:

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Clinical presentation of Arrythmagenic right ventricular dysplasia:

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Early symptoms include palpitations and syncope. Over time the right heart fails and can progress to left heart failure as well.

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Treatment of arrhythmagenic right ventricular dysplasia:

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- Implanted defibrillator
- Antiarrythmic drugs

Front 163

What is dilated cardiomyopathy?

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Heart muscle disorder defined by dilatation and impaired systolic function of both ventricles in the abscence of CAD, valvular diseases, or pericardial disease.

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What are some causes of dilated cardiomyopathy?

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- 33% are genetic

- Other acquired causes are:
Prolonged hypertensive heart disease
Myocarditis
Chemotherapy
Radiotherapy
Alcohol
Cocaine
Hemochromatosis
Thiamine Deficiency(Beri-Beri Heart Disease)
Endocrinopathies
Autoimmune diseases

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Gross appearance of heart with dilated cardiomyopathy:

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Development of thrombi in left and right ventricles are common due to stasis of blood flow.

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Histology of dilated cardiomyopathy:

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Front 167

Pathophysiology of alcohol induced dilated cardiomyopathy:

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Front 168

Complications of dilated cardiomyopathy:

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Front 169

Peripartum cardiomyopathy:

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Tocolysis: medications used to induce delivery

Front 170

Presentation and diagnosis of peripartum cardiomyopathy:

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Clinical presentation:
Similar to other dilated CM

Diagnosis:
Diagnosis of exclusion
No previous history of heart disease.
Endomyocardial biopsy: Sens:50% Specif:99%
Cardiac MRI: might help but can’t reveal specific pattern

Prognosis:
> 50% - Improvement to normal or near-normal ejection fraction.
4% will require heart transplant
9% die of complications of heart transplant

Treatment:
Similar other DCM; HF treatment

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Increase

Front 172

Restrictive cardiomyopathy:

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Restrictive cardiomyopathy is characterized by abnormally rigid ventricles with impaired diastolic filling but usually normal or near normal systolic function.
This condition results from either fibrosis or scarring of the endocardium or infiltration of the myocardium by an abnormal substance.
The most common cause of restrictive cardiomyopathy is amyloidosis.

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Gross appearance of restrictive cardiomyopathy:

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Front 174

Histology of restrictive cardiomyopathy with amyloidosis:

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Front 175

Key Points from the cardiomyopathy lecture:

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Front 176

Hemangiomas (benign tumors):

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- Characterized by increased numbers of normal or abnormal vessels filled with blood.
- Common in infancy and childhood. Most regress spontaneously.
- The majority are superficial and localized to the head or neck
- Some can occur internally; mostly in the liver.

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Capillary hemangioma:

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- The most common hemangioma
- Occurs in the skin, subcutaneous tissue and mucous membranes of the oral cavities and lips.
- The "strawberry" type of the skin found in newborns is very common; it grows rapidly in the first few months then fades at age 1-3 and completely regresses by age 7 in most cases.

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Picture of capillary hemangioma and a regressed one:

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Front 179

Cavernous hemangioma:

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- Are characterized by large, dilated vascular channels; compared with capillary hemangiomas, cavernous hemangiomas are less well circumscribed and more frequently involve deep structures.
- Although benign in nature, they may be locally destructive and not spontaneously regress; therefore requiring surgery.

Front 180

Gross and micro of a cavernous hemangioma:

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Front 181

Pyogenic Granuloma (a benign hemangioma):

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- A rapidly growing peduncular red nodule on the skin, gingival or oral mucosa; it bleeds easily and is often ulcerated.
- 1/3 of lesions develop after trauma.
- The proliferating capillaries are often accompanied by extensive edema and an acute and chronic inflammatory infiltrate.
- "Pregnancy tumor" occurs in the gingiva of 1% of pregnant women. These lesions can spontaneously regress after pregnancy or undergo fibrosis.

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Simple (capillary) Lymphangioma (benign):

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These are composed of small lymphatic channels predominately occuring in the head, neck and axillary subcutaneous tissue.
- They are slightly elevated and sometimes pedunculated lesions 1-2 cm in diameter.
- Histology shows networks of endothelium lined spaces that are distinguished from capillary channels by the absence of blood cells.

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Cavernous Lymphangioma (cystic hygroma) (benign):

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- These lesions are typically found in the neck or axilla of children.
- Are common in the neck of patients with Turners syndrome
- These lesions can occassionally be enormous and may fill the axilla or produce gross deformaties about the neck.
- Tumors are composed of massively dilated lymphatic spaces.

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Glomus Tumors (benign):

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- Painful tumors originating from modified SMC's of the glomus body.
- Commonly found under the fingernails.

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Nevus Flammus (benign):

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- A birthmark; the most common form of ectasia.
- Include the "port wine stain" birthmark; these lesions tend to grow and not fade.

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Spider Telangiectasia (benign):

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- Grossly resembles a spider
- Blanches when pressure is applied.
- Frequently associated with hyperestrogenic states; pregnancy or cirrhosis

Front 187

Hereditary Hemorrhagic Telangiectasia (benign):

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- Also called Osler-Weber-Rendu disease
- An autosomal dominant disorder
- Malformations of dilated capillaries and veins present from birth; widely distributed over the skin and oral mucous membranes, as well as in the respiratory, GI and urinary tracts.
- Ocassionally these lesions rupture, causing serious nosebleeds, GI bleeding or hematuria

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Kaposi Sarcoma (intermediate-grade tumor):

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A malignant neoplasm with endothelial (lymaphatic or vascular) differentiation and often has spindle cell morphology in addition to presence of vascular channels. Has multiple clinical presentations including classic cutaneous form (less aggressive), Endemic African and AID-related (most aggressive) types. Human herpesvirus 8 (HHV8) also known as Kaposi sarcoma-associated herpesvirus (KSHV) is considered the causative agent of all forms of Kaposi sarcoma. Tumor cells stain for CD31 and HHV8 related protein.

Front 189

Histology of Kaposi Sarcoma:

Back 189

Front 190

Hemangioendothelioma (intermediate grade tumor):

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- Wide spectrum of vascular neoplasms with histology and clinical behaviors intermediate between benign, well differentiated hemangiomas and frankly anaplastic angiosarcomas.
- Involves medium sized and large veins.

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Angiosarcoma (malignant tumor):

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- Malignant endothelial neoplasms.
- Older adults are more commonly affected with no gender preference.
- Occur most often in the skin, soft tissue, breast and liver.
- Hepatic angiosarcomas are associated with carcinogenic exposures; arsenic, thorotrast, and PVC.
- Can also develop in the setting of lymphedema, usually after mastectomy for breast cancer.
- Can also be induced by radiation or by foreign material introduced into the body accidentally.
- Stain positive for CD31 and vonWillebrand Factor

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Histology of angiosarcoma:

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Front 193

Gross appearance of angiosarcoma:

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Front 194

Hemangiopericytoma (malignant tumor):

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- Rare tumors derived from pericytes; myofibroblast like cells that are normally arranged around capillaries and venules.
- Most common in the lower extremities.
- Spindle cell proliferation outside the basal lamina of blood vessels. Biological behavior ranges form local recurrence to high metastatic potential
- Tumor cells stain for CD 34

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What are the most common tumors of the heart?

Back 195

Metastatic tumors
Some tumors have more predilection for spread to the heart; lung, lymphoma, breast cancer, leukemia, melanoma, liver and colon.

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Cardiac Myxomas (benign):

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Cardiac myxoma are most common cardiac tumor in adults and arises specifically from endocardial surface. Tumors probably arise from primitive pluriopitential mesenchymal cells. Mean age of detection is 50. Slight female preponderance.
Clinical presentation: Classical triad;
Constitutional – fever, arthralgia, weight loss, fatigue, malaise. Tumor cell elaborate interleukin 6 (IL-6) a mediator of acute phase reactants
Valvular obstruction, mostly mitral , Classic- ball valve obstruction, may mimic rheumatic mitral stenosis, heart failure, arrhythmia
Embolization of tumor fragments in systemic circulation , mostly to brain and extremities
Diagnostic and Imaging studies:
Chest Xray – may show cardiomegaly and sometime calcification in the mass
Echocardiography is the main diagnostic modality
CT and MR performed prior to surgery to delineate surgical margins
Blood work – acute phase reactants
Pathlogy:
70% arise from left atrium from fossa ovalis. Soft glistening mass with areas of hemorrhage attached with a pedicle (stalk) to endocardium
Neoplasm consists of myxoma cells ( cells with stellate appearance, abundant cytoplasm which may show focal endothelial differentiation . Cells are embedded in abundant acid mucopolysaccharide ground substance
Differential diagnosis: Mural thrombus . Occur in background of underlying cardiac disease. Most commonly in patients with atrial fibrillation with or without mitral valve disease (stenosis causing stasis). Most common location in atrial appendage and NOT atrium. Ventricular thrombi are usually superimposed on underlying acute or healed myocardial infarct. The thrombi generally consists of layered clots and microscopically may show focal myxoid areas (early fibrosis) in addition to signs of old hemorrhage (hemosiderin pigmented macrophages)
Treatment: surgical excision

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Gross appearance of cardiac myxoma:

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Histology of cardiac myxoma:

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Front 199

Cardiac Rhabdomyomas (benign):

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Cardiac rhabdomyomas are the most common neoplasms of neonates, infant and children < 16 yrs.
Rhabdomyomas most likely are hamartomas (malformation) rather than true neoplasms.
50% of cases are associated with Tuberous sclerosis complex (hamartomas of brain, kidney, retina, skin and heart).
Autosomal dominant inheritance, Disruption of Tumor suppressor genes (TSC1 – hamartin) and TSC2- tuberin) .
Most commonly arise in free wall of ventricles. May present with outflow tract obstruction, arrhythmias or heart failure.
Some tumors spontaneously regress. Appear as solid fleshy mass. Microscopically m marked vacuolization of cytoplasm (glycogen).
May mimic glycogen storage disease

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Cardiac Angiosarcomas (malignant):

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Angiosarcoma are the most common sarcomas with differentiation to specific cell type. Undifferentiated sarcoma is the most common primary malignancy overall.
Age 40-50. Right atrium most commonly involved. Generally present with advanced disease (metastases) and may extend into pericardium,
Clinical presentation _ right atrial mass with valve dysfunction, hemopericardium or from metastases.
Pathology – polypoid masses with infiltration, and microscopically evidence of vascular differentiation (capillary or venous type vessels). Tumors cells express endothelial markers (CD31, CD34m,fFcator VIII)
Poor prognosis
Undifferentiated sarcoma – most common sarcoma of heart. Age distribution similar to angiosarcoma. Most commonly arise from left atrium My present with mitral valve stenosis, pulmonary hypertension. 1/3 of the patients present initially with metastases.
Polypoid tumors with infiltration. No significant endothelial differentiation.

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Histology of angiosarcoma 2:

Back 201

Front 202

"Most Commons" for cardiac masses:

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Front 203

Rheumatic Fever:

Back 203

- Initial episode is a disease of children and young adults ( 5-15 years of age)
- Recurrent RF can be common in young adults
- 3-6% of the population is susceptible
- Susceptibility appears to be inherited

- Incubation is usually 3 weeks (1-5)
- Sore throat can be subclinical
- Most common symptoms:
Polyarthritis (60-75%)
Carditis (50-60%)
Chorea (jerky movements) ( 2- 30%)
Erythema marginatum (<5%)
Subcutaneous nodules (<5%)

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Pancarditis in Rheumatic Fever:

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- 60% of patients with ARF progress to RHD.
- Valvular damage is the hallmark of rheumatic carditis
- ARF causes inflammation on the mitral valve with mitral regurgitation as a result
- Myocarditis can be present affecting conduction pathways; leads to P-R interval prolongation.

Front 205

Erythema Marginatum from Rheumatic Fever:

Back 205

Front 206

Antigen mimics in acute rheumatic fever:

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- Recently, found T cells specific for streptococcal M protein peptides cross react with self proteins in the heart.

Disease presents pathologically as inflammation of the heart valve

Antibodies against the group A carbohydrate on the valve surface endothelium upregulate cell adhesion molecules such as VCAM-1 on activated surface endothelium of the valve.
M protein-reactive T cells extravasate into the valve through the surface endothelium by binding to cell adhesion molecules such as VCAM-1.

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Pathology of acute rheumatic fever:

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Front 208

Gross and histology of acute rheumatic fever:

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Front 209

Clinical diagnosis of acute rheumatic fever:

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- Fever- usually significant > 39 centigrade
- Elevated inflammatory markers: c-reactive protein and sedimentation rate
- Elevated leukocyte count
- Evidence of preceding strep infection: Anti - streptolysin O and anti-Dnase titers

- Rheumatic fever is mainly a clinical diagnosis:
No single diagnostic sign
No specific laboratory test
Diagnosis based on Modified Jones Criteria and evidence of recent strep infection.

Front 210

Jones Criteria for diagnosis of acute rheumatic fever:

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Front 211

Pathogenic pathway in the development of RF:

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Front 212

Treatment of acute rheumatic fever:

Back 212

- PNC p.o. 500mg bid for 7 days OR benzathine PCN IM 1.2 million units once

- Salicylate or NSAI’s- for fever and arthitis

- Primary prevention- treat streptococcal pharyngitis within 9 days of onset

- Secondary prevention- important due to the fact that patients who have had RF have a higher incidence of recurrence

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Pathophysiology of myocarditis:

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Front 214

Clinical presentation of myocarditis:

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Front 215

Evaluation of myocarditis:

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Treatment- similar to other types of heart failure with systolic dysfunction ( ACE, BB, diuretics)

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Histology of myocarditis:

Back 216

Front 217

Causes of myocarditis:

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Front 218

More causes of myocarditis:

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Front 219

Presentation and prognosis of myocarditis:

Back 219

- Acute presentation:
Children, adolescents
Viral prodrome (viremia)
Immune activation (injury)
Remodelling/repair

Chronic presentation:
Adults
Insidious onset
Ventricular dysfunction → cardiomyopathy

Prognosis:
Acute presentation:
Mild carditis→ recovery
Severe
1/3 residual dysfunction
1/3 recover
1/3 → trasnplantation / death, chronic course

Giant cell /chronic active myocarditis
Poor prognosis

Front 220

Diagnosis of myocarditis:

Back 220

Echocardiography and cardiac MRI are most useful diagnostic tools

Front 221

Causes of endocarditis:

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Front 222

Histology of infective endocarditis:

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Front 223

Active infective endocarditis

Back 223

Healed infective endocarditis lesion

Front 224

Common problems associated with infective endocarditis:

Back 224

Infarcts in the spleen, coronary septic embolus, renal embolization leading to acute glomerulonephritis.

Front 225

Gross and histo appearance of non bacterial thrombotic endocarditis:

Back 225

Note that the lesions are evenly spaced around the valve as opposed to the single or bunched lesions in infective endocarditis.

Front 226

Causes of pericarditis:

Back 226

Infectious:
Viral
Tuberculosis
Bacterial

Noninfectious (More common):
Post myocardial infarction
Uremia
Neoplastic
Radiation induced
Rheumatic diseases
Drug induced

Front 227

Possible outcomes of pericarditis:

Back 227

- Effusion
Hemodynamic consequences
- Complete resolution
Viral infection
- Chronic fibrosing inflammation
Constructive pericarditis

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Back 228

Front 229

Clinical presentation of pericarditis:

Back 229

- History of previous viral syndrome is common
- Pain usually abrupt and severe and pleuretic
- Precordial with radiation to left shoulder, left upper extremity, and left trapezius ridge ( most specific historical symptom for pericarditis )
- Pain relieved by leaning forward and worse by laying flat

- Sinus tachycardia
- Low grade fever
- Pericardial friction rub ( present in 85% of patients )
- Rub can be evanescent and best heard at LSB with patient leaning forward
- 3 Phase rub corresponds to: ventricular systole, early diastolic filling, and atrial contraction

Front 230

Diagnosis of pericarditis:

Back 230

- Elevated white blood cell count with mild lymphocytosis in viral/idiopathic disease. If bacterial, severe elevations with left shift noted
- Elevation of sed rate and C-reactive protein can be seen
- Modest elevation of cardiac enzymes ( troponin I and CK MB) can be seen

CXR- usually normal. Enlarged cardiac shadow can occur with pericardial effusions / tamponade

Echo- Usually normal but is done to exclude silent effusion

Front 231

Complications of pericarditis:

Back 231

Pericardial effusion- Small effusions common

Pericardial tamponade- In one series ( Imazio M, Circulation 2007 ) present in 3.1% of patients

Pericardial constriction- ( Imazio M, Circulation 2007) 1.5%

Relapse of pericarditis- 15-30%
NSAIDS and aspirin and colchicine (used for gout) can prevent recurrences

Front 232

Pericardial Effusion:

Back 232

Front 233

Pericardial Tamponade:

Back 233

Severe elevation of pericardial pressures will overcome the diastolic pressures in all 4 chambers of the heart. This is called “equalization of pressures” ( diastolic pressure on all 4 chambers will = pericardial pressures )


The above will result in impaired diastolic filling → Decrease LV filling → decrease stroke volume → decrease cardiac output → hypotension

Front 234

Pericardial Tamponade consequences:

Back 234

Beck’s triad: Distant or absent heart tones, JVD, hypotension
Pulsus paradoxus: Exaggerated systolic B/P drop during inspiration

Septum has to move over to the left to accept increased venous return; makes less space for blood in the left ventricle

Front 235

Treatment of pericardial tamponade:

Back 235

Pericardiocentesis- Patient at 45 degrees, needle inserted in below the xiphoid process angled toward the left shoulder. A catheter is then passed and pressure recordings are compared to right side of the heart
( concomitant right heart cath). There should be
equalization of pressures across all 4 chambers and
pericardial space

Catheter is maintained in place for 48 hours for continual drainage

Front 236

Constrictive pericarditis:

Back 236

Complication of pericarditis whereby the fluid in the pericardium over time becomes organized with fusion of the pericardial layers followed by fibrous scar formation


Over time calcium can form in the pericardial sac and can be useful in diagnosis with chest radiography or CT scanning

Systolic contraction remains uninhibited

Diastolic relaxation is abruptly interrupted when the relaxing myocardium comes in contact with the stiff pericardium

When the right ventricle, while filling, comes into contact with the non-compliant pericardium ventricular filling is abruptly halted

Front 237

Pathophysiology of constrictive pericarditis:

Back 237

Clinical features:
- Fatigue, hypotension and reflex tachycardia
- Right sided failure- JVD, peripheral edema, ascites,
hepatomegaly
- Positive Kussmal sign- Increase of jugular venous
distention during inspiration
- Early diastolic “knock” in patients with calcium
surrounding the heart

Front 238

Diagnosis of constrictive pericarditis:

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