surface of the
heart2. The most
location is the
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.
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)*
*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
2. Systemic Embolization (Arterial or PE)
3. 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)
2. Roth’s spots
3. Osler’s nodes
5. Janeway lesions
7. Nail hemorrhages
Endocarditis is diagnosed if you meet:
1. 2 major criteria; or
2. 1 major and 3 minor; or
3. 5 minor criteria
2. Positive Echocardiogram for Oscillating mass on valve, root abcess, or vegetation.
3. New Regurgitant murmur
4. Single positive blood culture for C. Burnetii
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
4. RF often falsely positive
2. CXR (CHF, Pleural Effusions)
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)
1. CHF due to valve dysfunction
2. Unstable Prosthetic Valve
3. Failure to respond to antibiotics or difficult organisms (ie. Fungal, Brucella, VRE)
2. Previous Endocarditis
3. Congenital Heart Disease
4. Cardiac Valvulopathy following transplantation
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
1. Mitral valve Prolapse
2. Rheumatic Heart Disease
3. Bicuspid Valve Disease
5. Congenital heart conditions:
1. Acute Pericarditis
2. Pericardial effusion
3. Pericardial effusion with Tamponade
4. Constrictive Pericarditis
1. Definition – Inflammation of the Pericardium
2. More common in males
3. More common in young adults
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
2. Chest X-Ray
uncomplicated2. A water bottle heart
suggests a pericardial
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
1. Chronic pericarditis
2. Pericardial effusions
3. Cardiac tamponade
4. Constrictive pericarditis
1. Probably Autoimmune
2. Treatment: COLCHICINE
3. Steroids are controversial
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
heart causes less
fillingThis results in:
1. Right sided CHF
3. Muffled heart sounds (from fluid)
Often associated with clear lung fields
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
Needle is advanced
under the xyphoid
toward the tip of
the left scapula2. Or: Echo-guided
1. Rigid, scarred pericardium encircles the heart
2. Inhibits diastolic filling of both ventricles
3. Systolic contraction is normal
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
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
1. CT or MRI
2. MRI often helpful to
1. Treatment for heart failure: Diuretics, salt restriction
2. SURGICAL: Radical pericardiectomy (entire removal of pericardium)
*3. DO NOT AFTERLOAD REDUCE constrictive pericarditis*
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
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
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*
1. Familial dilated cardiomyopathy (FDC)
2. ≥ 2 family members meeting criteria for IDC
*(Recall the case she gave on the last day)*
2. Dyspnea on exertion/Shortness of breath
4. Paroxysmal Nocturnal Dyspnea
5. EdemaB) Conduction abnormalities
C) Atrial and/or ventricular arrhythmias
D) Sudden death
2. Cardiac Enzymes (usually normal)
3. BNP (will be high)
5. Chest X-Ray (enlarged heart)
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
1. Diuretics (including K+ Sparing but they inhibit RAAS)
2. ACE-I or ARB (Also inhibits RAAS)
1. Beta Blockers
a) Improve symptoms, exercise intolerance, cardiac hemodynamics, and LVEF.
b) Decrease mortality rates
c) Use only after patient has been diuresed
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
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*
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
5. Chest pain
6. Syncope (post exertional)
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
Caused by significant LV outflow obstruction
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
1. ECG: LVH (esp in absence of other CVD)
3. Chest X-Ray
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
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
1. Mortality rate is 4% per year
2. Sudden death is most common reason
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).
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.
The most common symptoms include:
4. Exercise Intolerance
5. Peripheral edema
*7. Hepatosplenomegaly*, ascites, and anasarca.
8. S3 sound
3. Cough, orthopnea, paroxysmal nocturnal dyspnea
2. Increased JVP
4. Increase JVP with inspiration (Kussmaul’s sign)
*5. Tricuspid/Mitral Regurgitation murmur/ Gallop (S3 and S4)*
2. Chest X-Ray
3. Elevated BNP
4. ECHOEndomyocardial biopsy:
1. No specific treatment
2. Treat heart failure
3. Treat underlying disease (amyloidosis, sarcoidosis, hemochromatosis)
4. Treat pulmonary hypertension
5. Heart transplant
EF <50% = Systolic Dysfunction
1. Reduced muscle mass
2. Dilated cardiomyopathies
3. Vent. Hypertrophy (Pressure & Volume overload)
2. Vent. Hypertrophy
3. Myocardial Ischemia
4. Mitral or tricuspid valve stenosis
5. Pericardial disease
1. Kerley A & B Lines (on Chest X-ray)Both:
1. Paroxysmal Nocturnal Dyspnea
2. Pulmonary Symptoms (Cough, crackles)
1. Distended Jugular Vein (Examined @ 30 degree angle)
3. Increased Peripheral Venous Pressure
1. ACEI or ARB
*1. ACE or ARB (First Line!!) Test Hint*
2. Beta Blockers
1. Shortness of breath
3. Decreased exercise capacity
3. Beta Blockers
Therapy in selected patients:
1. Aldosterone Ant.
2. Diuretics *(Loops have no mortality benefit)*
3. Hydralazine/nitrates *(no mortality benefits)*
1. Compassionate care or hospice
3. Chronic inotropes
4. Mechanical Support
5. Experimental drugs
2. Diet (high TG)
1. Rich in fruits, vegetables, low-fat dairy, whole grains, legumes*, nuts, fish, and poultry
2.High in fiber, low to moderate fat
1. Mainly animal products: beef, lamb, pork, cream, butter, dairy
2. Some plants: palm and coconut oils
1. Omega-6: soybean, corn, safflower oils
2. Omega-3: fatty fish
3. Walnuts, sunflower
1. Liquid oils
3. Peanuts, almonds
1. Adults should exercise for at least 150 minutes per week
2. Include muscle-strengthening exercises at least twice per week
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
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
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
2. Begin or increase physical activity
3. Group programs
4. Self-monitoring with journals, apps
5. Refer to dietitian or behavior intervention group
3. Genetic syndromes
4. Maternal Factors (DM, HTN, Obesity, epilepsy)
5. Utero infections
1. Atrial Septal Defect
2. Ventricular Septal Defect
3. Patent Ductus ArteriosusNormal Pulmonary Blood Flow:
1. Pulmonic Stenosis
2. Coarctation of the Aorta
1. Most common shunt lesion detected after 2 years of age
2. Acyanotic & Increased Pulmonary Blood flow
2. If there is evidence of RV volume overload, regardless of symptoms, All atrial septal defects should be closed
3. Echocardiography is diagnostic
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)
1. RV and PA lift
*2. Accentuated S1 with wide fixed split S2*
1. Enlarged heart,
2. prominent pulmonary artery
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
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
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
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
*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
1. Pulmonary hypertension
2. Instead of a left to right shunt, a right to left shunt develops
3. Can occur with ASD, VSD, PDA
1. Regular follow-up until murmur is gone2. If murmur does not resolve by 12 months of age, echo at age 3
2. Monitor for manifestations of (see below) and treat accordingly:
a) heart failure
c) shortness of breath,
d) poor weight gain,
e) failure to thrive,
g) pulmonary hypertension
3. If asymptomatic – annual echocardiograms
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.
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.
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.
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
1. Usually asymptomaticLarge PDAs:
2. Growth restriction
3. Failure to thrive
3. Bounding arterial pulses
4. Widened pulse pressure
2. PDA requires surgical or catheter closure
3. To treat heart failure and to prevent pulmonary vascular disease
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
1. Respiratory distress
2. Acute congestive heart failureOlder children/adolescents/adults
1. Exertional fatigue
2. Leg claudication
3. Left ventricular failure
5. Aneurysmal rupture
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
1. Transposition of the great arteriesWith decreased pulmonary blood flow
1. Tetralogy of Fallot
2. Tricuspid Atresia
3. Ebstein’s Anomaly
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
2. *Cyanosis* (dependent on intercirculatory mixing)
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
1. ECG: Right ventricular hypertrophy
2. CXR: Small base of the heart, *”egg on a string”*
3. Echocardiogram: Great vessels are switched
1. Arterial Switch
2. Atrial Switch
1. Cyanotic/Decreased Pulmonary Blood Flow
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
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.
1. Typically comfortable and in no distress
2. “Tet” spells when agitated
a) Due primarily to the right ventricular outflow obstruction. b) typically crescendo-decrescendo with a harsh systolic ejection quality
4. CXR: Boot shaped heart
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
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
2. Decrease in BP
*3. Increased BV
4. Increased HR
5. Increased SV*
6. Increased CO
4. Reduced exercise tolerance
2. Mid-systolic murmur at left base
3. Continuous murmur (Venous increased mammary flow)
4. Peripheral Edema
2. LVEF <40%*
3. Left sided obstructive lesions
4. Previous History of arrhythmias with clinical impact or stroke or heart failure
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
2. Maternal BP: >160/110
3. Proteinuria >5g/24hr
4. No Seizures present
2. Maternal BP: >160/110
3. Proteinuria >5g/24hr
4. Seizures present
2. Usually have to deliver the baby
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
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
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.
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:
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.
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