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*Endocarditis Lecture*
Endocarditis – Definition, most common location
1. An infection of
the endothelial
surface of the
heart2. The most
location is the

Endocarditis Pathophysiology: Native Valve (6 Organisms?), Prosthetic Valve (Early, and late), IV drug users (1 organism)
Native Valve:
1. Staph aureus, CNS, Strep viridans, Strep bovis, enterococci, HACEK
Prosthetic Valve (10-30% of cases):
1. Early (w/in 2 months): CNS (Staph epi)
2. Late: Similar to native valve but with more fungal cases
IV drug users: Staph aureus.
Endocarditis – Presentation (3 Subacute, 3 Acute)
1. Mild toxicity
2. Present over weeks to months with rare metastatic infection
3. Most commonly S. viridans or enterococcusAcute:
1. Toxic presentation
2. Valve destruction and metastatic infection in days to weeks
*3. Usually caused by Staph aureus (Test Hint)*

6 Signs and Symptoms for endocarditis (2 Hallmarks, 4 other symptoms)

*1. Hallmark: NEW Murmur (90%)

2. Hallmark: Fever
Elderly pts may not have a fever (Test Hints)*

3. Fatigue, malaise, weight loss

4. Arthralgia, myalgia

5. Night sweats

6. Splenomegaly

PE Findings (3)
1. CHF
2. Systemic Embolization (Arterial or PE)
3. Cutaneous Manifestations
7 Cutaneous Manifestations (PJSORNR)
Cutaneous Manifestations:
1. Petechiae (conjunctiva or palatal)
2. Janeway Lesions (Small red spots in palms and soles)
3. Splinter Hemmorrhage (red lines on nail bed)
4. Osler’s Nodes (TENDER nodules on fingers and toes)
5. Renal manifestation (Failure, Hematuria, Infarction)
6. Neurologic Manifestations
7. Roth Spots (Pale retinal spots surrounded by hemorrhage)
FROM JANE Mnemonic
1. Fever
2. Roth’s spots
3. Osler’s nodes
4. Murmur
5. Janeway lesions
6. Anemia
7. Nail hemorrhages
8. Emboli
Diagnosis: Duke Criteria (Endocarditis is diagnosed if you meet 3 criteria)

Endocarditis is diagnosed if you meet:

1. 2 major criteria; or
2. 1 major and 3 minor; or
3. 5 minor criteria

4 Major Duke Criteria
1. 2 Positive Blood Cultures for organisms
2. Positive Echocardiogram for Oscillating mass on valve, root abcess, or vegetation.
3. New Regurgitant murmur
4. Single positive blood culture for C. Burnetii
6 Minor Duke Criteria
1. Predisposing heart condition/IV drug user
2. Fever (T>38 degrees C, 100.4 degrees F)
3. Vascular phenomenon
a) Arterial emboli, mycotic aneurysms, Janeway lesions
4. Immunologic phenomenon:
a) Osler’s nodes, Roth spots, GN, RF+
5. + cultures not meeting a major criteria
6. + echo not meeting a major criteria
Adjunctive Labs for Endocarditis (5 Labs)
1. CBC
2. ESR
3. CRP
4. RF often falsely positive
5. UA
Adjunctive Diagnostic Test (2)
1. EKG
2. CXR (CHF, Pleural Effusions)
Treatment: 2 modalities are used: (Antibiotics (3) & Surgical Debridement (2)
1. Subacute – wait to see what you are treating
2. Acute – Emperical therapy started promptly
3. Bactericidal agents in high doses x 6 weeksSurgical debridement:
1. Indicated in 25-40%

2. Indicated early unless they have had a cerebral infarction (then waiting 4 weeks is better)

Surgical Therapy NYHA FC III/IV Indications: 3 scenarios

1. CHF due to valve dysfunction

2. Unstable Prosthetic Valve

3. Failure to respond to antibiotics or difficult organisms (ie. Fungal, Brucella, VRE)

Endocarditis Prophylaxis: 3 important questions
1. Who?
2. When?
3. What?
Endocarditis Prophylaxis – Who (4 conditions)
1. Prosthetic Valve
2. Previous Endocarditis
3. Congenital Heart Disease
4. Cardiac Valvulopathy following transplantation
Endocarditis Prophylaxis – When (3 Procedures)

1. All dental procedures that involve manipulation of gums, or teeth.

2. Invasive procedures of the respiratory tract

3. Surgical procedures involving infected skin, or musculoskeletal tissues

Endocarditis Prophylaxis – What (3 antibiotic examples)
1. Amoxicillin
2. Cephalexin
3. Azithromycin
Cardiac Conditions no longer requiring Antibiotic Therapy (5)

1. Mitral valve Prolapse

2. Rheumatic Heart Disease

3. Bicuspid Valve Disease

4. Calcified

5. Congenital heart conditions:

*Pericarditis Lecture*
4 Pericardial Diseases

1. Acute Pericarditis

2. Pericardial effusion

3. Pericardial effusion with Tamponade

4. Constrictive Pericarditis

Pericarditis (Definiton, More common in what gender, and what age group?)

1. Definition – Inflammation of the Pericardium

2. More common in males

3. More common in young adults

Pericarditis – Etiology (6 causes)

1. Idiopathic: Most common cause – 26-86% of cases

2. Viral: 1-10% of cases
(Coxsackievirus B, Echovirus, Influenza)

3. Bacteria: Gram negative organisms are most common cause

4. RA and SLE and Scleroderma

5. Renal Failure

6. Hypothyroidism

Pericarditis Diagnosis (3)
1. EKG (ST elevation)
2. Chest X-Ray
3. Echo
Pericarditis - Chest X-ray (If uncomplicated? Description of the X-Ray, and what does it suggest?)
Pericarditis – Chest X-ray (If uncomplicated? Description of the X-Ray, and what does it suggest?)
1. Not helpful if
uncomplicated2. A water bottle heart
suggests a pericardial

Pericarditis – Treatment (2 Meds, Treat, 1 Procedure, How long should you treat it for?)

1. Anti-inflammatory Agents (Aspirin, NSAIDS)

2. Treat the underlying disorder

3. Pericardiocentesis (If there is an effusion, especially if purulent)

4. Treat until symptoms have been gone for one week

Pericarditis – 4 Complications

1. Chronic pericarditis

2. Pericardial effusions

3. Cardiac tamponade

4. Constrictive pericarditis

Chronic Pericarditis (Probable cause, Med treatment, What med is controversial)

1. Probably Autoimmune

2. Treatment: COLCHICINE

3. Steroids are controversial

Pericardial Effusion: (Definition, Cause? With enough pressure it will cause what?)
Pericardial Effusion: (Definition, Cause? With enough pressure it will cause what?)

1. An abnormal accumulation of fluid in the pericardial cavity

2. Malignancy causes 50% (often bloody effusions)

3. With enough pressure it will cause Cardiac Tamponade

Cardiac Tamponade (Description, Results in 4 things)
Compression on the
heart causes less
fillingThis results in:
1. Right sided CHF
2. Hypotension
3. Tachycardia
4. Shock

Cardiac Tamponade: Beck’s Triad (Test Hint) (3 clinical presentations, often associated with?)
1. Jugular venous distention
2. Hypotension
3. Muffled heart sounds (from fluid)
Often associated with clear lung fields
Pulsus Paradoxus (Definition, Normal, 3 Other causes)

1. The difference between the systolic blood pressure in expiration and the systolic pressure in inspiration (throughout the respiratory cycle)

2. Normal = <10 mm Hg

3. Other causes include: COPD, severe asthma, Pneumothorax

Cardiac Tamponade – Treatment
1. Pericardiocentesis –
Needle is advanced
under the xyphoid
toward the tip of
the left scapula2. Or: Echo-guided

Constrictive Pericarditis (Definition, inhibits what?, What is normal)

1. Rigid, scarred pericardium encircles the heart

2. Inhibits diastolic filling of both ventricles

3. Systolic contraction is normal

Constrictive Pericarditis: 7 Clinical Presentation (JHKPHDP)
1. Jugular Vein Distention
2. Hepatojugular reflux
*3. KUSSMAUL’S Sign – A paradoxical increase or lack of decrease in the jugular venous pressure with inspiration*
4. Pericardial knock – A prominent third heart sound
5. Hepatomegaly, Ascites
6. Diminished pulse volume
7. Pulsus Paradoxus is usually not present
Constrictive Pericarditis (Most common causes world wide, and in US, Chest X ray results?)

1. Most common cause worldwide is tuberculosis

2. Most common cause in the U.S. is idiopathic

3. Chest X-ray is usually unremarkable
With tuberculosis you may see pericardial calcifications

Constrictive Pericarditis: Imaging (2, The latter is helpful to distinguish from what condition?)

1. CT or MRI

2. MRI often helpful to
distinguish from
Restrictive CM

Constrictive Pericarditis: Treatments (Treatment for HF (2), Surgical treatment, DO NOT do what?)

1. Treatment for heart failure: Diuretics, salt restriction

2. SURGICAL: Radical pericardiectomy (entire removal of pericardium)

*3. DO NOT AFTERLOAD REDUCE constrictive pericarditis*

*Cardiomyopathies Lecture*
Systolic dysfunction (Decrease in 2 things, CO is maintained by? Compensatory mechanisms eventually… What happens to CO? What does it lead to?, characteristic of what condition?)
1. Decrease in myocardial contractility
2. Decrease in Left Ventricular Ejection Fraction (LVEF)
3. Cardiac output is maintained by: The Frank-Starling relationship (Higher stretch = Increased contractility
4. Compensatory mechanisms eventually fail, cardiac output decreases, leads to heart failure.
5. Characteristic of dilated cardiomyopathy
Diastolic Dysfunction (Description, Characteristic of what 2 conditions, EF status?)

1. LV relaxation and filling is abnormal and is accompanied by elevated filling pressures

2. Characteristic of both Hypertrophic Cardiomyopathy and Restrictive Cardiomyopathy

3. Ejection Fraction may be normal or reduced

Dilated Cardiomyopathy (Description, Invariably accompanied by, Can be caused by what? Most common cause for what?)
1. Dilation and impaired contraction of one or both ventricles
2. Invariably accompanied by an increase in total cardiac mass (hypertrophy)
3. Can be caused by genetics (Familial dilated cardiomyopathy)
*4. Most common cause for heart transplantation*
Dilated Cardiomyopathy: Genetics (Condition? Criteria?)

1. Familial dilated cardiomyopathy (FDC)

2. ≥ 2 family members meeting criteria for IDC

*(Recall the case she gave on the last day)*

Dilated Cardiomyopathy: Presentation (4, the first has 5 correlating symptoms)
A) Heart Failure:
1. Fatigue
2. Dyspnea on exertion/Shortness of breath
3. Orthopnea
4. Paroxysmal Nocturnal Dyspnea
5. EdemaB) Conduction abnormalities

C) Atrial and/or ventricular arrhythmias

D) Sudden death

Dilated Cardiomyopathy: Evaluation (5)
1. ECHO (Gold Standard)
2. Cardiac Enzymes (usually normal)
3. BNP (will be high)
4. ECG
5. Chest X-Ray (enlarged heart)
Dilated Cardiomyopathy: Management (Medical therapy of heart failure focuses on 3 main goals:) (Note: The first 2 goals provide what?, the last reduces what)
Medical therapy of heart failure focuses on 3 main goals:
1. Preload reduction
2. Afterload reduction
3. Inhibition of both the RAAS systems and vasoconstrictor neurohumoral factors produced by the sympathetic nervous system in patients with heart failure.
Note: The first 2 goals provide symptomatic relief, RAAS inhibition and Neurohumoral factors reduces morbidity and morality
Preload Reduction (Description, 3 possible meds)
1. Decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli.
1. Diuretics (including K+ Sparing but they inhibit RAAS)
2. ACE-I or ARB (Also inhibits RAAS)
After load Reduction (Increases what? Improves what? Which allows for what?, 1 Med, Improves 4 things, decreases, Use only after the patient has been)
1. Increases cardiac output and improves renal perfusion which allows for diuresis in the patient with fluid overload
1. Beta Blockers
a) Improve symptoms, exercise intolerance, cardiac hemodynamics, and LVEF.
b) Decrease mortality rates
c) Use only after patient has been diuresed
If Medical Therapy fails then what 4 treatments can be done.
1. Cardiac Resynchronization with a pacemaker
2. If that does not work you can put in an ICD
3. Next a Ventricular Assist Devices can be installed
4. Finally Heart transplant
Hypertrophic Cardiomyopathy (Description, Causes gross disorganization of, Completely caused by what? Most common cause of what? What intervention is effective at preventing that? Most common what?)
1. Heart muscle disease most often caused by mutations in one or several sarcomere genes
2. Causes Gross disorganization of the muscle bundles in the heart.
3. Completely caused by genetics
*4. Most common cause of sudden death in <35 yrs*
*5. Exercise restriction is effective at preventing sudden cardiac death*
*6. Most Common Cardiomyopathy*
Hypertrophic Cardiomyopathy: Presentation (Most patients, Affected individuals are often diagnosed as a result of what 3 things? 7 other symptoms, more common in which gender, presents at an earlier age in which gender? Which gender has more severe symptoms?)
1. Most patients with HCM have no symptoms
2. Affected individuals are often diagnosed as a result of:
a) Family screening
b) Detection of a murmur on a routine exam
c) Abnormal EKG
3. Dyspnea
4. Fatigue
5. Chest pain
6. Syncope (post exertional)
7. Palpitations
8. Heart Failure
9. Sudden Cardiac Death – typically caused by V-Fib
10. More common in males than females
11. Presents at an earlier age in females
12. Females tend to have more severe symptoms
HCM Murmurs: Caused by significant? Septal Hypertrophy murmur sound, and heard best at? Systolic anterior motion of the mitral valve murmur sound, and location?

Caused by significant LV outflow obstruction

Septal Hypertrophy:
1. Harsh crescendo-decrescendo systolic murmur that begins slightly after S1 and is heard best at the apex and lower left sternal border

Systolic anterior motion of the mitral valve:
1. Mid-late systolic murmur at the apex

Hypertrophic Cardiomyopathy (HCM): Diagnosis (3)

1. ECG: LVH (esp in absence of other CVD)

2. Echo

3. Chest X-Ray

Hypertrophic Cardiomyopathy: Management (Enhance impaired __ __ __ by 2 methods, Reduce obstruction caused by __ __ __ by 4 methods, Prevent __ __ with 2 methods)
Enhance impaired LV diastolic function:
1. Rate Control
2. Rhythm Control
Reduce obstruction caused by septal/mitral valve apposition:
1. Avoid dehydration
2. Negative inotropic drugs (Beta Blockers, CCBs)
3. Surgical septal myectomy
4. Dual chamber pacemaker
Prevent sudden death:
1. Implantable Cardiac Defibrillator
2. Refer children of patients with HCM to urgent echocardiography and genetic testing
Treatment for HCM (If they have Obstructive Physiology: (Avoid 2 drug types), If they do not have Obstructive Physiology or HF or Angina: (1), If they do not have Obstructive Physiology but have HF or Angina, and low EF: What 3 meds?)
If they have Obstructive Physiology:
1. Avoid vasodilator therapy and high dose diuretics
If they do not have Obstructive Physiology or HF or Angina:
1. Exam annual
If they do not have Obstructive Physiology but have HF or Angina, and low EF:
1. Diuretics and ACE or ARB
Prognosis for HCM (Mortality Rate, Most common reason)

1. Mortality rate is 4% per year

2. Sudden death is most common reason

Restrictive Cardiomyopathy (Stiff Heart Muscle) (Commonality?, State of the ventricle? Ventricular walls? Results in? Generally Normal what?, Which sided HF dominates over the other? Most cases are secondary to what? But some cases have… Which is most common cause?)
1. Less common than DCM and HCM
2. A nondilated ventricle with typically normal wall thicknesses
3. Ventricular walls that are rigid, resulting in *severe diastolic dysfunction* and restrictive filling with elevated filling pressures and dilated atria.
4. Generally normal left ventricular systolic function.
*5. Right heart failure tends to dominate over left heart failure*
6. Most cases are secondary to an identifiable disease but some cases have no clear cause (Amyloidosis is most common cause).
Restrictive Cardiomyopathy: Pathophysiology (Signs and symptoms of what condition are present, but what is the state of the ventricles? Ventricle function? What is preserved?

1. Signs and symptoms of heart failure are present, but the ventricles are not hypertrophic or dilated.

2. Left ventricular ejection fraction is normal or only slightly diminished, indicating that contractility is preserved.

Restrictive Cardiomyopathy: Presentation (Affected patients have symptoms and signs of both? The most common symptoms include (8 examples), 3 other symptoms)
1. Affected patients have symptoms and signs of both pulmonary and systemic congestion.
The most common symptoms include:
1. Dyspnea
2. Fatigue
3. Weakness
4. Exercise Intolerance
5. Peripheral edema
6. Palpitations
*7. Hepatosplenomegaly*, ascites, and anasarca.
8. S3 sound
3. Cough, orthopnea, paroxysmal nocturnal dyspnea
Restrictive Cardiomyopathy: PE (Signs are the same as what conditions (4 examples), 3 additional symptoms, Murmur Description.
1. Signs are the same as those of heart failure, including jugular venous distension, crackles in the lungs on auscultation, distant heart sounds, and lower extremity edema.
2. Increased JVP
3. Ascites
4. Increase JVP with inspiration (Kussmaul’s sign)
*5. Tricuspid/Mitral Regurgitation murmur/ Gallop (S3 and S4)*
Restrictive Cardiomyopathy: Diagnosis (4, Procedure looking for what 3 things?)
1. EKG (Afib, PAC, PVC)
2. Chest X-Ray
3. Elevated BNP
4. ECHOEndomyocardial biopsy:
1. amyloidosis,
2. sarcoidosis,
3. hemochromatosis

Restrictive Cardiomyopathy: Management (5)

1. No specific treatment

2. Treat heart failure

3. Treat underlying disease (amyloidosis, sarcoidosis, hemochromatosis)

4. Treat pulmonary hypertension

5. Heart transplant

*Heart Failure Lecture*
Causes of Systolic Dysfunction (Decreased Contractility) (Definition, 3 causes)

EF <50% = Systolic Dysfunction

1. Reduced muscle mass
2. Dilated cardiomyopathies
3. Vent. Hypertrophy (Pressure & Volume overload)

Causes of Diastolic Dysfunction (Restriction in ventricular filling) (5 Causes)
1. Vent. Stiffness
2. Vent. Hypertrophy
3. Myocardial Ischemia
4. Mitral or tricuspid valve stenosis
5. Pericardial disease
Prognosis of Systolic & Diastolic Heart Failure
5 year survival = 50%
How to Diagnose HF (Left sided HF, both)
Left Sided HF:
1. Kerley A & B Lines (on Chest X-ray)Both:
1. BNP

Left Sided Heart Failure: Common 2 Symptoms

1. Paroxysmal Nocturnal Dyspnea

2. Pulmonary Symptoms (Cough, crackles)

Right Sided Heart Failure: Most commonly caused by? Maybe secondary to what? 3 Symptoms
1. Most commonly caused by Left HF, but may be secondary to chronic pulmonary problems.
1. Distended Jugular Vein (Examined @ 30 degree angle)
2. Ascites
3. Increased Peripheral Venous Pressure
ACC/AHA: Stage A (Disease stage, and therapy)
1. No structural heart disease (asymptomatic)
1. ACEI or ARB
ACC/AHA: Stage B (Disease stage, and 3 meds for therapy)
1. Structural Heart disease (asymptomatic)
*1. ACE or ARB (First Line!!) Test Hint*
2. Beta Blockers
ACC/AHA: Stage C: Disease stage, 3 Symptoms, Therapy (5) Therapy in selected patients (4)
1. Structural heart disease (Symptomatic)
1. Shortness of breath
2. Fatigue
3. Decreased exercise capacity
2. ARB
3. Beta Blockers
4. Pacemaker
5. ICD
Therapy in selected patients:
1. Aldosterone Ant.
2. Diuretics *(Loops have no mortality benefit)*
3. Hydralazine/nitrates *(no mortality benefits)*
4. Digoxin
ACC/AHA: Stage D (Disease stage, 5 Therapies)
1. Refractory HF
1. Compassionate care or hospice
2. Transplant
3. Chronic inotropes
4. Mechanical Support
5. Experimental drugs
Objective 2: Demonstrate knowledge of pharmacological management of both diastolic and systolic heart failure.
Review HF Therapeutic Slides
*Nutrition Lecture*
Which dietary components or patterns are associated with hypertension (6)
1. High Salt Intake
2. Diet (high TG)
3. Inactivity
4. Smoking
5. Stress
6. Obesity
Which dietary components and foods does the DASH diet highlight? (2)

1. Rich in fruits, vegetables, low-fat dairy, whole grains, legumes*, nuts, fish, and poultry

2.High in fiber, low to moderate fat

Which foods are high in saturated (2), polyunsaturated (3), and monounsaturated fats (3)
Saturated Fat:
1. Mainly animal products: beef, lamb, pork, cream, butter, dairy
2. Some plants: palm and coconut oils
Polyunsaturated fat:
1. Omega-6: soybean, corn, safflower oils
2. Omega-3: fatty fish
3. Walnuts, sunflower
Monounsaturated fat:
1. Liquid oils
2. Avocado
3. Peanuts, almonds
What is the 2008 Physical Activity Guidelines for Americans (2)

1. Adults should exercise for at least 150 minutes per week

2. Include muscle-strengthening exercises at least twice per week

General calorie recommendations for weight loss (how much reduction is needed (2), what’s the lowest to go for women, and men).

1. To lose 1 pound a week, decrease calories by 500

2. Increase activity to lose up to 2 pounds a week

3. 1200 calories for women

4. 1500 Calories for men

What to recommend for a patient with high BP? (4, The second point has 2 components)
1. Reduce body weight
2. Begin DASH Diet
a) Reduce sodium intake to 2300 mg (1500 mg if possible)
b) Increase intake of fruits, veggies, and whole grains
3. Begin or increase physical activity
4. Refer to dietitian
What to recommend for a patient with high Cholesterol? (6) (reduce 3 things, Increase 2, 1 action)
1. Reduce body weight
2. Reduce intake of added sugars
3. Reduce intake of saturated fat and dietary cholesterol
4. Increase unsaturated fat intake
5. Increase fiber intake
6. Refer to dietitian
What to recommend when a patient is overweight? (5)
1. Suggest the DASH diet with a 300-500 calorie restriction
2. Begin or increase physical activity
3. Group programs
4. Self-monitoring with journals, apps
5. Refer to dietitian or behavior intervention group
*Congenital Heart Disease Lecture*
Congenital Heart Disease Risk Factors (5)
1. Prematurity
2. FH
3. Genetic syndromes
4. Maternal Factors (DM, HTN, Obesity, epilepsy)
5. Utero infections
Acyanotic Lesions: Left to Right Shunt (Increased Pulmonary Blood Flow (3), Normal Pulmonary Blood Flow (2)
Increased Pulmonary Blood Flow:
1. Atrial Septal Defect
2. Ventricular Septal Defect
3. Patent Ductus ArteriosusNormal Pulmonary Blood Flow:
1. Pulmonic Stenosis
2. Coarctation of the Aorta

Atrial Septal Defect (Most common? Type (2))
Atrial Septal Defect (Most common? Type (2))

1. Most common shunt lesion detected after 2 years of age

2. Acyanotic & Increased Pulmonary Blood flow

Atrial Septal Defect (Often ___ and discovered on? If there is evidence of ___ ___ ___ regardless of ___ what should be done? Diagnostic Method?)
1. Often asymptomatic and discovered on routine physical examination
2. If there is evidence of RV volume overload, regardless of symptoms, All atrial septal defects should be closed
3. Echocardiography is diagnostic
Atrial Septal Defect: Symptoms (In Children and adolescents , When do symtoms usually develop and due to what? 4 symptoms, May present with what?)

1. Children and adolescents usually asymptomatic

2. Symptoms develop in 4th and 5th decades due to right sided failure

3. Dyspnea, edema, atrial arrhythmias, pulmonary HTN

4. May present with paradoxical embolism (most commonly get caught in the lungs)

Atrial Septal Defect: Exam (Lift? Sound? CXR shows what 2 things?)

1. RV and PA lift

*2. Accentuated S1 with wide fixed split S2*

1. Enlarged heart,
2. prominent pulmonary artery

Atrial Septal Defect: Treatment (1)
Atrial Septal Defect: Treatment (1)
1. Surgical Repair
Patent Foramen Ovale (PFO) (Definition, No shunt unless what? What kind of finding is it?)

1. In 25% of patients the atrial septum forms completely but the foramen ovale fails to seal off completely

2. There is not a shunt unless the right atrial pressure is higher than the left atrial pressure (i.e. Valsalva)

3. Benign finding

Ventricular Septal Defect (Type, 2 possible sounds and why?, Larger defects may result in? Diagnostic measure?)
Ventricular Septal Defect (Type, 2 possible sounds and why?, Larger defects may result in? Diagnostic measure?)

1. Acyanotic & Increased Pulmonary Blood Flow

*2. A restrictive VSD is small and makes a louder murmur than an unrestrictive (large one)*

3. Larger defects may result in pulmonary hypertension if not repaired

4. Echocardiography is diagnostic

Physiology of large VSD (Pulmonary vascular resistance (PVR) at birth is __ and shunt is, 2-3 days after birth what happens? If not surgically corrected what happens? These changes later cause what?

1. Pulmonary vascular resistance (PVR) at birth is high, and shunt is R to L

2. 2-3 days after birth, PVR decreases to 10% of systemic resistance, and a large L to R shunt develops

3. If not surgically corrected, reactive pulmonary vascular changes occur that initially improve symptoms by decreasing blood flow.

4. These changes later cause pathologic irreversible changes and eventually a reversal in shunt termed Eisenmenger Syndrome

Ventricular Septal Defect: Symptoms (Small and intermediate size VSDs, Large VSDs (2), Intermediate size lesions progression?
Small and intermediate size VSDs:
1. Fairly asymptomatic in childhoodLarge VSDs:
1. Can present with CHF symptoms/shock in infancy

Intermediate size lesions:
1. Variable slow changes can occur with development of right sided failure symptoms, progression to Eisenmenger’s Syndrome

Ventricular Septal Defect: Physical Exam Murmur description and location, Wide physiologically __ __, Normal ECG with which condition?

*1. High pitched, harsh, grade IV-VI holosystolic murmur in tricuspid area radiating to right of sternum*

2. Wide physiologically split S2

3. Normal ECG with small VSD

Eisenmenger Syndrome: (Condition? Shunt development?, Can occur with what 3 conditions?

1. Pulmonary hypertension

2. Instead of a left to right shunt, a right to left shunt develops

3. Can occur with ASD, VSD, PDA

Management for a small VSD (If the patient is asymptomatic (1), If murmur does not resolve by 12 months of age do what?)
If the patient is asymptomatic:
1. Regular follow-up until murmur is gone2. If murmur does not resolve by 12 months of age, echo at age 3

Managing a moderate to large VSD (Typically become symptomatic when? Monitor for manifestations of 7 conditions, If asymptomatic what to do?)
1. Typically become symptomatic within the first month of life
2. Monitor for manifestations of (see below) and treat accordingly:
a) heart failure
b) tachypnea,
c) shortness of breath,
d) poor weight gain,
e) failure to thrive,
f) diaphoresis
g) pulmonary hypertension
3. If asymptomatic – annual echocardiograms
Managing Symptomatic Patients (Treat what 2 conditions? If something is elevated when should surgical repair take place?, If what type of shunt is present when should surgical closure happen?)

1. Treat heart failure and pulmonary hypertension with medical therapy

2. If Pulmonary Artery pressure is elevated surgical repair should occur within first 6 months.

3. If significant left to right shunt is present, surgical closure should occur within 1st year.

Endocarditis Prophylaxis (2)

1. If VSD repaired and A dental or respiratory tract procedure using a prosthetic material or device within 6 months of the repair – antibiotic therapy is necessary

2. If VSD repaired with a residual defect at the site, antibiotics should be used for all dental and respiratory tract procedures.

Patent Ductus Arteriosus (Type, Murmur sound and location, Diagnostic method?)
Patent Ductus Arteriosus (Type, Murmur sound and location, Diagnostic method?)

1. Acyanotic & Increased Pulmonary Blood Flow

2. A continuous murmur over the left pulmonary area (with or without a thrill is common)

3. Echocardiography is diagnostic in children.

Patent Ductus Arteriosus: Physiology

1. During fetal life, normal blood flow from the main pulmonary artery to aorta shunts blood away from the lungs

2. After birth, the ductus constricts, and flow usually ceases during the first 24 – 48 hours after birth; the closed ductus becomes the ligamentum arteriosum

3. Reversal of blood flow through the ductus from the aorta to the pulmonary artery occurs as pulmonary vascular resistance drops, creating a left to right shunt

Patent Ductus Arteriosus: Clinical Presentations (Small PDAs (1), Large PDAs (3), Pulses (2)
Small PDAs:
1. Usually asymptomaticLarge PDAs:
1. HF
2. Growth restriction
3. Failure to thrive

3. Bounding arterial pulses

4. Widened pulse pressure

Patent Ductus Arteriosus: Management: IN premature infants? PDA requires what? Why is treatment needed?
1. *Indomethacin*, Aspirin can be used in *premature infants*
2. PDA requires surgical or catheter closure
3. To treat heart failure and to prevent pulmonary vascular disease
Coarctation of the Aorta (Type, Usual presentation is (2), Some patients may have what condition? How do they affect systolic and diastolic pressures? Diagnostic method?

1. Acyanotic & Normal Pulmonary Blood Flow

2. Usual presentation is systemic hypertension
Associated with bicuspid aortic valve

3. Some patients may have Turner (XO) Syndrome

4. Systolic & Diastolic pressures are higher in the upper extremities than in the lower extremities

5. Echo is diagnostic

Coarctation of the Aorta: Presentation (Infancy/childhood (2), Older children/adolescents/adults (5)
1. Respiratory distress
2. Acute congestive heart failureOlder children/adolescents/adults
1. Exertional fatigue
2. Leg claudication
3. Left ventricular failure
4. Endocarditis
5. Aneurysmal rupture

Coarctation of the Aorta: Examination (BP and Pulse effects, 2 Visible pulsations? CXR shows what 2 things, 2 EKG findings, ECHO displays what?

1. Hypertension in upper extremities, slow-rising or absent pulse in lower extremities; radiofemoral delay

2. Visible suprasternal and supraclavicular pulsations

3. CXR- *rib notching*; increasing prominence of left ventricular size with age

4. EKG- normal or LVH

5. Echo- Displays coarctation

Coarctation of the Aorta: Management (1)
1. Placing a wire or mesh stent
Cyanotic Lesions: With increased pulmonary blood flow (1), With decreased pulmonary blood flow (3)
With increased pulmonary blood flow:
1. Transposition of the great arteriesWith decreased pulmonary blood flow
1. Tetralogy of Fallot
2. Tricuspid Atresia
3. Ebstein’s Anomaly

Transposition of the Great Arteries (Lesion Type, Which gender does it occur in more? Blood flow? Venous return? Creates 2 separate...?
Transposition of the Great Arteries (Lesion Type, Which gender does it occur in more? Blood flow? Venous return? Creates 2 separate…?

1. Cyanotic & Increased Pulmonary Blood Flow

2. Males > Females

3. Blood flows from RV to aorta (instead of PA)

4. Blood flows from LV to pulmonary arteries (instead of aorta)

5. Venous return is normal

6. Creates two separate parallel circulations

Transposition of the Great Arteries: Presentation (Typically presents before, 2 other presentations)
1. Typical presentation is before 30 days of age
2. *Cyanosis* (dependent on intercirculatory mixing)
3. Tachypnea
Transposition of the Great Arteries: Prognosis (If not treated what will happen? Data on mortality rates in first week, first month, first year without treatment
1. If patients do not receive treatment, most will die within the first year of life.
2. About 30 percent of untreated patients die in the first week,
3. 50 percent in the first month
4. 90 percent within the first year of life
Transposition of the Great Arteries: Examination (ECG will show what? CXR will show what? ECHO shows what?
Transposition of the Great Arteries: Examination (ECG will show what? CXR will show what? ECHO shows what?

1. ECG: Right ventricular hypertrophy

2. CXR: Small base of the heart, *”egg on a string”*

3. Echocardiogram: Great vessels are switched

Transposition of the Great Arteries: Management (2 types of surgery)
Transposition of the Great Arteries: Management (2 types of surgery)
1. Arterial Switch
2. Atrial Switch
Tetralogy of Fallot (Lesion type, Four Components, Most predominate…? Diagnostic method, Should be corrected when?)

1. Cyanotic/Decreased Pulmonary Blood Flow

*Four components
1. Ventricular septal defect
2. Overriding aorta
3. Pulmonary stenosis
4. Right ventricular hypertrophy* (Test Hint)

2. Most predominant cyanotic congenital heart lesion diagnosed after 1 year of age

3. Echo is diagnostic

4. Should be corrected early in life

Tetralogy of Fallot: Presentations: Depends on the degree of what? Children with severe obstruction and inadequate pulmonary flow typically present when? Children with moderate obstruction and balanced pulmonary and systemic flow may be noticed when? They can also present with what? Children with minimal obstruction may present with what 2 conditions?)
Depends on degree of pulmonary stenosis:
1. Children with severe obstruction and inadequate pulmonary flow typically present in the immediate newborn period with profound cyanosis.
2. Children with moderate obstruction and balanced pulmonary and systemic flow *may be noticed during elective evaluation for a murmur*. *These children may also present with hypercyanotic (“tet”) spells* when RVOT is obstructed during periods of agitation
3. Children with minimal obstruction may present with pulmonary overcirculation and heart failure.
Tetralogy of Fallot: Physical Exam (Patients demeanor, __ spells when?, Murmur caused by what, and sound description?, CXR description.
Tetralogy of Fallot: Physical Exam (Patients demeanor, __ spells when?, Murmur caused by what, and sound description?, CXR description.

1. Typically comfortable and in no distress

2. “Tet” spells when agitated

3. Murmur
a) Due primarily to the right ventricular outflow obstruction. b) typically crescendo-decrescendo with a harsh systolic ejection quality

4. CXR: Boot shaped heart

Tetralogy of Fallot: Early Management (Palliative Shunt: 3 components)
1. Palliative Shunt
a) Uncommon.
b) Produce a systemic to pulmonary shunt provide stable pulmonary blood flow required for survival, and allow a deferral of elective complete repair:
c) For patients who cannot undergo cardiac surgery immediately
Tetralogy of Fallot: Management (Intracardiac Repair (4 components) (Relief of…, Complete separation between…, Preservation of…, Minimizes post-procedure…)
1. Intracardiac Repair
a) Relief of RV Outflow Tract obstruction
b) Complete separation between the pulmonary and systemic circulations
c) Preservation of right ventricular function
d) Minimize post-procedure pulmonary valvular incompetence
*Pregnancy and Heart Disease Lecture*
6 Normal Cardiovascular changes associated with pregnancy (Test Hint) (2 things decrease, 4 things increase)
1. Decreased systemic and pulmonary vascular resistance
2. Decrease in BP
*3. Increased BV
4. Increased HR
5. Increased SV*
6. Increased CO
4 Normal cardiology findings on History during pregnancy
1. Palpitations
2. Fatigue
3. Dyspnea
4. Reduced exercise tolerance
4 Normal cardiology findings on PE during pregnancy
1. Tachycardia
2. Mid-systolic murmur at left base
3. Continuous murmur (Venous increased mammary flow)
4. Peripheral Edema
4 Cardiological Risk Factors for Maternal Complications During Pregnancy
*1. NYHA Functional Class >II)
2. LVEF <40%*
3. Left sided obstructive lesions
4. Previous History of arrhythmias with clinical impact or stroke or heart failure
Risk for Maternal Mortality caused by various heart disease: Group 1, Group 2, Group 3, Group 4)
Group 1 (Mortality (0-1%)
1. ASD, VSD, PDA, Corrected tetralogy of FallotGroup 2: (5-15%)
1. Aortic stenosis, coarctation without valve involvement, Tetralogy of Fallot (uncorrected)

Group 3: (25-50%)
1. Marfans, MI, Pulmonary HTN, Cardiomyopathy

Group 4: (>50%)
1. CHF, Advanced pulmonary edema

Preeclampsia (Definition)
Defined as a diastolic blood pressure increase of 15 mm of mercury over baseline
Severe Pre-eclampsia (Gestational Age, Maternal BP, Proteinuria, What else is present?)
1. Gestational Age (Weeks): >20
2. Maternal BP: >160/110
3. Proteinuria >5g/24hr
4. No Seizures present
Eclampsia (Test Hint) (Gestational Age, Maternal BP, Proteinuria, What else is present?)
Eclampsia (Test Hint) (Gestational Age, Maternal BP, Proteinuria, What else is present?)
1. Gestational Age (Weeks): >20
2. Maternal BP: >160/110
3. Proteinuria >5g/24hr
4. Seizures present
Eclampsia Treatment
1. Give Mg+
2. Usually have to deliver the baby
Peripartum Cardiomyopathy (5) (Description, Commonly associated with what 2 things? Common age group? Higher risk of what? Generally occurs when?)
1. Dilated Cardiomyopathy that becomes apparent by the last month of pregnancy or within 6 weeks of delivery
2. Commonly associated with gestational hypertension and drugs use to stopped uterine contractions
3. Occurs more commonly in women over the age of 30
4. Higher risk of re-occurrence with future pregnancies
5. Generally in the 1st or 2nd pregnancy
FDA Class of Medicines During Pregnancy (5 Classes)
A) Studies show no risk
B) No evidence of risk in humans, fetal harm is remote
C) Chance of fetal harm but benefits outweigh risk
D) Positive evidence of risk, potential benefit in pregnant women may outweigh risk
X) Contraindicated
Alexa’s Material
In general, coronary artery disease (CAD) leads to:
A) hypoxemia.
B) coronary artery dilation.
C) systolic hypertension.
D) myocardial ischemia.

Consequences of myocardial ischemia can include all of the following clinical consequences, EXCEPT:

A) chest pain.
B) hypertension.
C) conduction disturbances leading to arrythmias.
D) decreased ventricular contractility/pumping.


Unstable angina is a sign of:

A) electrical conduction problems in the heart.
B) impending myocardial infarction.
C) decreased myocardial oxygen demand.
D) mild to moderate atherosclerosis.


Which of the following is the most common cause of a myocardial infarction in an individual with coronary artery disease (CAD)?

A) Embolization of the plaque in the atherosclerotic coronary artery
B) Complete obstruction of the coronary artery by the developing plaque
C) Fat embolus
D) Formation of a blood clot in the atherosclerotic coronary artery


All of the following are known causes of or contributing factors to acute myocardial ischemia or infarction, EXCEPT:

A) anemia.
B) autoimmune disease.
C) cocaine use.
D) chest trauma.


Which of the following mechanisms causes cell injury after the myocardium is reperfused following a period of severe hypoxia during a myocardial infarction?

A) The mitochondria are overwhelmed by the high concentrations of oxygen.
B) Reactive oxygen species are formed, which cause free radical injury.
C) Excessive amounts of lactic acid disrupt the pH of the cytoplasm.
D) Excessive amounts of lactic acid disrupt the pH of the cytoplasm.

Primary pulmonary hypertension leads to:
A) right ventricular failure that is diastolic in nature.
B) left ventricular failure that is diastolic in nature.
C) right ventricular failure that is systolic in nature.
D) left ventricular failure that is systolic in nature.

Which of the following problems is most likely to cause an increase in ventricular preload and cause decompensation in a person with left ventricular failure?

A) A deep vein thrombosis (DVT) in the left femoral vein
B) An arterial blood pressure of 150/92 mm Hg
C) Fluid overload caused by renal failure
D) Pulmonary hypertension


Why does long term primary (systemic) hypertension eventually lead to left ventricular failure that is diastolic in nature?

A) Oxygen delivery to the left ventricle is reduced because of the high blood pressures
B) The left ventricle gradually dilates due to the high systemic blood pressures
C) Increased afterload leads to left ventricular hypertrophy
D) Hypertension is a common cause of valve disease.


How does activation of the renin-angiotensin-aldosterone system help the body maintain blood pressure in left ventricular failure?

A) The hormones released stimulate the heart to contract with more force.
B) The hormones released help resolve the edema.
C) The hormones released increase systemic vascular resistance and blood volume.
D) The hormones released help to reduce myocardial workload.


Which of the following hemodynamic changes occur in left ventricular failure (LVF) that is systolic in nature?

A) Decreased systemic vascular resistance
B) Increased left ventricular preload
C) Increased venous return to right ventricle
D) Decreased right ventricular afterload


Why is an elevation in the plasma levels of B-type natiuretic peptide (BNP) an indication that a patient may have heart failure?

A) Elevated BNP levels are a common cause of hypertension which often leads to heart failure.
B) Elevated BNP is a common cause of fluid overload which exacerbates heart failure.
C) BNP is released whenever stroke volumes decrease.
D) BNP is released when the kidneys retain fluid to compensate for the drop in CO and blood pressure.


Long term exposure to catecholamines and angiotensin II in chronic congestive heart failure results in all of the following problems except:

A) abnormal diastolic filling due to ventricular hypertrophy and fibrosis.
B) abnormal ventricular dilation due to destruction of collagen proteins.
C) apoptosis and death of myocardial cells.
D) altered contractility due to contractile protein (actin and myosin) abnormalities.


Which of the following statements correctly describes why inflammation plays an important role in the progression of chronic heart failure?

A) Neutrophils are attracted into the ventricles and phagocytose healthy cells.
B) Free radicals cause widespread myocardial cell injury.
C) Cytokines such TNF-α cause myocardial hypertrophy and apoptosis.
D) Histamine released by mast cells in the myocardium causes progressive cell injury.


Why does chronic left ventricular failure (LVF) eventually cause right ventricular failure (RVF)?

A) Decreased pulmonary vascular resistance increases RV preload.
B) Cardiac output from the LV to the RV is reduced.
C) Blood flow from the vena cavas into the right atrium and ventricle is reduced.
D) Pulmonary hypertension from LVF causes right ventricular hypertrophy.


A patient is diagnosed with chronic obstructive pulmonary disease. Which of the following cardiac conditions often develops from this condition?

A) Congestive heart failure
B) Diastolic left ventricular failure
C) Myocardial infarction
D) Right ventricular failure


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