Diseases of the Heart

A clinical syndrome resulting from deficient cardiac stroke volume with inability of the cardiac output to keep up with the venous return.

Resulting in:

Inadequate perfusion of the tissues from insufficient cardiac output.

• 1. Ischemic heart disease
• 2. Hypertension
• 3. Valvular disease (aortic stenosis or mitral regurgitation) - (NOT mitral valve stenosis)
• 4. Primary myocardial disease

Forward Failure is heart failure secondary to: decreased Cardiac Output.

Backward Failure is heart failure secondary to: increased workload and/or increased pressure load and/or increased blood volume.

• 1. Forward
• 2. Backward
• 3. Backward
• 4. Forward

Left ventricular hypertrophy and dilation (increased volume).

Primarily Lungs, Brain, and kidney.

• 1. Chronic passive congestion and pulmonary edema (predisposes for pneumonia)
• 2. "Heart failure cells" - hemosiderin laden macrophages - and brown induration of lungs

• Clinically:
• 1. Dyspnea (difficulty breathing) - most common
• 2. Orthopnea (difficulty breathing lying down)
• 3. Paroxysmal nocturnal dyspnea
• 4. Cough
• 5. Cyanosis

• Cerebral hypoxia resulting in:
• 1. Irritability
• 2. restlessness
• 3. stupor
• 4. coma (perhaps - extreme)

• Reduced renal perfusion results in:
• 1. fluid retention
• 2. peripheral edema

• 1. L-CHF
• 2. Valvular disease - pulmonic stenosis or tricuspid regurgitation
• 3. Congenital left-to-right shunts
• 4. Intrinsic lung diseases
• 5. Cardiomyopathy or myocarditis

• 1. Backward
• 2. Backward
• 3. Backward
• 4. Backward
• 5. Forward

• 1. Liver (nutmeg liver) (scarring around central vein)
• 2. Spleen (congestive splenomegaly)
• 3. Kidney (fluid retention)
• 4. Brain (congestion and hypoxia)
• 5. Subcutaneous tissues (peripheral edema and possible anasarca)
• 6. Portal system (hypertension; maybe ascites)

• 1. Medications
• 2. Hospitalizations
• 3. Changes in health status
• 4. Exercise tolerance and fatiguability
• 5. Dyspnea

• 1. Make sure pt has taken meds on day of appointment
• 2. Consider orthopnea and orthostatic hypotension
• 3. Stress reduction protocol
• 4. Baseline vitals at start of appointment
• 5. Monitor vitals during procedure (don't dismiss until vitals are with 10-20% of baseline)

Heart disease featuring an imbalance between supply and demand for oxygen to the myocardium.

• 1. Angina pectoris (AP)
• 2. Myocardial Infarction (MI)
• 3. Sudden Cardiac death (SCD)
• 4. Chronic Ischemic Heart Disease (CIHD) - Most common

One third to one fourth!

Yes

Severe coronary atherosclerosis with stenosing plaques.

A plaque that obstructs 70% o 80% of the coronary artery lumen, but usually asymptomatic unless there is an increased demand.

A stenosing plaque that occludes approximately 90% of the lumen causing symptoms at rest.

Intraluminal thrombosis overlying a ruptured or fissured plaque (often resulting in coronary crisis).

Paroxysmal attacks of substernal or precordial chest pain or discomfort caused by myocardial ischemia that falls precariously short of inducing infarction.

Left shoulder or arm, even jaws.

Pain is due to a transient reversible myocardial hypoxia.

• 1. Typical Angina (stable angina)
• 2. Prinzmetal Angina
• 3. Unstable Angina

Ischemia due to stenosing atherosclerosis compounded with increased myocardial demand.

Attacks are brought on by exertion/stress and are relieved by rest.

Attacks attributed to vasospasm (sudden constriction of b.v.) which may be superimposed on a fixed stenosis.

Attacks may appear even at rest and are relieved by vasodilators such as nitroglycerin.

A change in the usual pattern of attacks (freq, duration) brought about by multiple mechanisms.

Attacks forewarn imminent danger of a subsequent acute MI!

• 1. Know health history
• 2. Have pt's meds handy (Nitroglycerine)
• 3. Stress reduction protocol

Ischemic (hypoxic) necrosis of the myocardium.

• 1. Single most frequent cause of death in U.S.
• 2. 1.5 million suffer from MI per year and 1/3rd of them die.
• 3. Men are more likely to suffer an MI, especially at 50 year old range.

• 1. Transmural
• 2. Subendothelial

When ischemic necrosis involves the full thickness of the ventricular wall. (most common/serious, usually left ventricle)

Necrosis involves not more than the inner one third to half of the thickness of the wall.

Primarily its the severe coronary narrowing/stenosis from atherosclerotic plaques.

Thrombosis - initiated by plaque fissure, rupture, or intraplaque hemorrhage.

For transmural infarcts, 90-95% of cases have superimposed thrombosis.

Also: platelet activation, vasospasm, hypotensive episode, increased myocardial demand.

• 1-2 minutes - Loss of contractility
• 10 minutes - 50% depletion of ATP
• 20-40 minutes - Irreversible cell injury
• 8-12 hours - Gross pallor
• End of first week - Soft yellow lesion has red rim
• 7-10 days - Lesion maximally soft and weak (susceptible to rupture)
• 7th week - Lesion completely healed by scarring

• 1. infarction of papillary muscle
• 2. Rupture of infarcted papillary muscle - usually lethal
• 3. Fibrinous pericarditis - scar tissue adhesions between pericardium and pericardial sac results in loss of mobility
• 4. Mural thrombosis with risk of embolization - forms over area of infarction on wall of heart
• 5. Rupture of infarct may cause cardiac tomponade - occurs 7 to 10 days after infarct
• 6. Ventricular aneurysm - disrupts the "electrical conduction system" causing arythmias

• 1. Symptoms
• 2. ECG changes
• 3. Elevations of specific serum enzymes

• Symptoms may be
• 1. Prodromal
• 2. concurrent
• 3. asymptomatic

• Symptoms may occur days or weeks ahead and can include:
• 1. fatigue
• 2. dyspnea
• 3. change in angina pattern

• 1. Sweating (diaphoresis)
• 2. Nausea and vomiting
• 3. Breathlessness

10 to 20% are uncomplicated with a complete recovery

80 to 90% develop complications

• 1. Arrhythmias (majority) (early)
• 2. Cardiogenic shock (death) (early)
• 3. Rupture of wall, septum, or papillary muscle (early)
• 4. Embolism of a mural thrombus (early)
• 5. Development of Left ventricular CHF (late)

• * 50% die before reaching the hospital
• * of those reaching the hospital more than 10% die
• * 30% still die within first year

• 1. Coronary bypass surgery
• 2. Angioplasty (balloon)
• 3. Cardiac stents (metal stent)
• 4. Anticoagulant/ antiplatelet meds (Coumadin, Aspirin/Plavix)
• 5. Lifestyle - Important - Don't smoke, eat well, exercise

Unexpected death from cardiac causes within 1 hour of the onset of acute symptoms.

300,000

Ischemic Heart Disease

1. Marked stenosing atherosclerosis of at least one coronary artery...

2. The ultimate mechanism: development of a lethal arrhythmia (asystole, ventricular fibrillation)

AED, install pacemaker

Appears insidiously in older people developing ECG changes and congestive heart failure as a consequence of long-term, progressive ischemic myocardial damage.

Heart may be normal weight or smaller, and dark brown.

Microscopically one will see myocardial atrophy, lipofuscin deposits in the myocytes, and diffuse fibrosis around vessels.

• * May be asymptomatic until CHF develops
• * Years prior to CHF - angina or MI
• * Scarring of conduction system may cause arrhythmias
• * Most die of unrelated causes

Diagnosis is based on left ventricular hypertrophy and the absence of other cardiac changes.

Hypertension predisposes to atherosclerosis. While CO is maintained, the hypertrophied heart eventually fails!

Affected lung structure or function --> increased resistance to blood flow through lungs --> pulmonary hypertension --> right ventricular enlargement

Temporary right ventricular dilation without hypertrophy.

Characterized by right ventricular hypertrophy without ventricular dilation!

A category of disease characterized by cardiac malformations present at birth (not always recognized).

A heart murmur.

• 1. Left-to-right shunt: late cyanosis
• 2. Right-to-left shunt: early cyanosis
• 3. Obstruction without cyanosis

• 1. Normal color at first
• 2. Over time, right heart pressure overloads left pressure leading to a reversal of flow
• 3. Unoxygenated blood is then circulated causing cyanosis

• 1. Cyanosis from the outset
• 2. allow for paradoxical emboli to enter systemic circulation

• 1. Coarctation of the aorta
• 2. Aortic stenosis
• 3. Pulmonic stenosis

• 1. Ventricular Septal defect (VSD)
• 2. Atrial Septal defect (ASD)
• 3. Patent Ductus Arteriosus

Ventricular septal defect

There is a hole present in the ventricular septum, with 90% occuring in the thin membranous portion just below the aortic valve.

• * Very small (<.5 cm) may close spontaneously.
• * Small to medium may produce jet lesions that predispose to IE
• * Large holes produce sever shunting with consequent cyanosis and pulmonary complications.

A hole in the atrial septum above the level of the valves.

Symptoms may not develop for years, larger lesions can cause heart failure from severe pulmonary HTN.

Patent Ductus Arteriosus

A congenital heart defect that occurs when the ductus joining the pulmonary artery to the aorta fails to close at birth.

• * Machine-like murmur and systolic thrill.
• * L-2-R flow becomes R-2-L flow resulting in late onset cyanosis.

• 1. Tetralogy of Fallot
• 2. Transposition of the Great Vessels

• 1. Ventricular septal defect
• 2. Dextraposed aorta that overrides the ventricular septal defect
• 3. Obstruction of right ventricular outflow
• 4. Right ventricular hypertrophy

Degree of obstruction of right ventricular outflow.

Left-to-right shunting without cyanosis.

right-to-left with cyanosis and pulmonary HTN

Reversed position of the pulmonary artery and aorta.

There is a reversed position of the pulmonary artery and aorta, as well as venous input being transposed.

It is the most lethal heart shunt, prognosis is bad! With the corrected, a patient can live, but they have weaker cardiac function.

Coarctation of the Aorta - a constriction within the aorta.

Also known as floppy valve syndrome, the valve leaflets prolapse, ballooning backward toward the left atrium during systole.

It is the most common cardiac valve disease in the US

20-40 year old females.

• * Mild cases have no untoward consequences
• * Mitral valve regurgitation
• * With regurgitation - Infective Endocarditis

An acute febrile, immune-mediated inflammatory disease, affecting mostly children, that follows shortly after an infection with group A B-hemolytic strep!

No, is is a post-streptococcal response.

• 1. M protein of strep evokes antibodies that are reactive with human epitopes
• 2. The antibodies stimulate the immune system to produce acute systemic disease
• 3. After dz subsides, there may be permanent damage to tissues, specifically heart valves.

Aschoff body

Fibrinous (bread-and-butter) pericarditis.

Valves develop vegetations along leaflet edges, which become fibrotic and then calcified. Stenosis and regurgitation follows.

2-3 weeks after

• * Joint pain/swelling
• * Skin rash
• * Heart murmur

• 1st time = 66%
• 2nd time = 100%

Colonization or invasion of the heart valves by microbiologic agents, leading to local formation of thrombotic masses laden with organisms - infective vegetations.

All heart tissue if affected, but especially heart valve leaflets.

• 1. Microorganisms in
• 2. Circulating blood in a
• 3. Susceptible host

alpha strep, Strep viridans (dental related)

S. aureus

• 1. IV drug use
• 2. Dental procedures
• 3. Surgical procedures
• 4. Urinary tract catheterization
• 5. IV catheterization
• 6. Respiratory and skin infections

• 1. Cardiac abnormalities
• 2. Prosthetic heart valves
• 3. Intravenous drug use

• 1. Rheumatic heart disease
• 2. Congenital heart defects
• 3. Mitral valve prolapse with regurgitation
• 4. SLE
• 5. Previous use of phen-fen

low virulence organisms

Gradual onset with fever, malaise and weight loss. Clubbing of digits is common. Course is over weeks to months.

Virulent organisms.

Rapid onset and may be explosive. Symptoms may include high fever, shaking chills, and weakness.

• 1. changing heart murmur
• 2. enlarged spleen

• 1. Valve damage
• 2. Cardiogenic shock
• 3. Septic emboli - hemorrhages of skin and mucosa, splinter hemorrhages of nails
• 4. Fibrinous pericarditis

Start with I.V. broad spectrum antibiotics. Then do aggressive antimicrobial therapy aimed at the specific organism cultured from patient.

• 1. Review pt's health history to determine if a pt is at risk for IE
• 2. Determine if pt at risk falls in AHA guideline for IE prophylaxis
• 3. Pre-medicate only those with greatest risk of adverse outcomes if they were to get IE

• 1. Cardiac conditions associated with the highest risk of adverse outcome from endocarditis.
• 2. Dental procedures for which prophylaxis is recommended

• 1. prosthetic cardiac valve
• 2. Previous IE
• 3. Congenital heart disease
• 4. Cardiac transplant recipients who develop cardiac valvulopathy

• 1. Unrepaired cyanotic CHD
• 2. Completely repaired congenital heart defect with prosthetic material within the last 6 months
• 3. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic device

Those that involve manipulation of the gingival tissue or the periapical region of teeth or perforation of the oral mucosa.

Amoxicillin, 2 gm by mouth, 1 hour before dental appointment

There are five alternate regimens. Two include cephalosporins which wouldn't be given because of potential cross-reactivity. So No, there are really three.

• 1. Clindamycin - 600 mg by mouth - one hour prior
• 2. Azithromycin - 500 mg by mouth - one hour prior
• 3. Clarithromycin - 500 mg by mouth - one hour prior

Myocardial inflammation, primarily bc of infection, sufficient to cause clinical manifestations.

Non-inflammatory myocardial disease that is not attributable to pressure or volume overload, usually caused by myocardial abnormalities or dysfunction.

• 1. Effusions - non-inflammatory
• 2. Exudates - inflammatory
• 3. Blood - due to rupture or trauma - rapid accumulation results in cardiac tamponade

Inflammation involving the pericardial surface of the heart.

Almost always viral

Fibrinous