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136 Cards in this Set

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  • Back
Explain the difference between concentric versus eccentric hypertrophy of the heart.
Concentric is due to an increased afterload. Eccentric is due to volume-overload (preload problem).
Holosystolic high pitched blowing murmur, loudest at the apex during systole. What heart murmur is this?
Mitral regurgitation.
Diamond shaped systolic ejection murmur following an ejection click. What heart murmur is this?
Where does it radiate?
Aortic stenosis. Radiates to carotids.
When does S3 and S4 heart sounds occur?
S3 occurs in early diastole. S4 (decreased compliance) occurs in late diastole (atrial systole).
Will there be left ventricular hypertrophy in mitral stenosis?
No. No volume overload.
What does mitral stenosis murmur sound like?
Opening snap in early diastole followed by a rumbling murmur.
What does an aortic regurgitation murmur sound like?
High pitched blowing diastolic murmur. S3 and S4 would be present because LV overload. Increased intensity on expiration.
What valve leaflet is hit by the dripping of blood from aortic regurgitation? Whats the murmur that is heard?
Anterior leaflet of the mitral valve. Austin-Flint murmur.
What is the most common cause of tricuspid stenosis? How do you differ tricuspid stenosis from mitral stenosis?
Infective endocarditis. Tricuspid stenosis is louder with inspiration.
What is the average weight of the heart? What is the average wall thickness of the left ventricle? Right ventricle?
Average weight = 250-300g in females, 300-350g in males
Thickness: RV = 0.3-0.5, LV = 1.3-1.5
What does azotemia indicate?
If perfusion deficit of the kidney becomes sufficiently severe, impaired excretion of nitrogenous products may cause azotemia. LHF can cause this.
What is anasarca?
Generalized massive edema.
What type of heart failure causes pulmonary edema?
Left sided heart failure.
What can be seen histiologically in the lungs of a person with chronic left heart failure?
Heart failure cells: alveolar macrophages engulfing RBC's and breaking them down into hemosiderin.
What is the main symptom of left heart failure?
Dyspnea.
Hydrostatic pressures increase where in right heart failure? Consequences?
Backward failure: venous system. Neck vein distension, hepatomegaly (nutmeg liver), pitting edema. Possibly ascites.
Paroxysmal nocturnal dyspnea. Right or left heart failure?
Left heart failure. aka Pillow orthopnea, sleeping upright decreases VR and decreases pulmonary congestion.
What type of heart failure does endotoxic shock cause?
High-output failure by mass vasodilation. Increase stroke volume (hyperthyroidism), decrease blood viscosity (severe anemia), and arteriovenous fistulas (Paget's disease) can also cause high-output heart failure.
How does estrogen protect against coronary artery disease?
Increases HDL.
How does cholestyramine protect against coronary artery disease?
Decreases LDL by decreasing bile acid reuptake. Body must make new bile from cholesterol.
What are the four types of ischemic heart disease?
Angina pectoris, sudden cardiac death syndrome, myocardial infarction, chronic ischemic heart disease?
What is sudden cardiac death syndrome? Cause of death?
Patient dead within one hour of onset of symptoms. Autopsy reveals no thrombus, but severe coronary artery disease (atherosclerosis). Cause of death is VT.
What is chronic ischemic heart disease?
Progressive onset of CHF due to small infarcts. Ejection fraction falls too low.
How do you determine if a patient with stable angina is a candidate for an angiogram?
If they have ST depression of > 1.5 on exertion.
What is the common cause/onset of Prinzmetal's variant angina? Male or female more common?
Prinzmetal angina is secondary to coronary artery spasm. W > M.
What does ST depression indicate?
Subendocardial ischemia.
What does the ST segment look like in Prinzmetal angina?
ST elevation.Vasospams effects the full thickness of endocardium causing transmural (full thickness) ischemia.
A patient who use to get pain on exertion now gets chest pain at rest. What do they have?
Unstable angina.
What is the most common manifestation of coronary artery disease?
Angina pectoris
What vessels can be used in coronary artery bypass graft?
Internal mammary artery graft (10 years) or saphenous veins (10 years). Saphenous veins undergo arterialization of the vessels, fibrosis, and occlusion common after 10 years.
What are the treatments for coronary artery diseases?
Angina pectoris stable and Prinzmetal: nitroglycerin, Ca-channel blockers.
Angina pectoris unstable: percutaneous transluminal coronary agnioplasty (PTCA), stenting, coronary bypass graft
MI: same as unstable angina plus thrombolysis
What is the difference between a myocardial infarction and angina pectoris?
Angina is myocardial ischemia without cellular necrosis (no infarction).
What is reperfusion injury?
Restored blood flow reintroduces oxygen and superoxide free radicals that damages cells.
What are the most common coronary artery occlusions in MI?
LAD > RCA > circumflex
What does the left anterior descending artery supply?
The anterior portion of the heart and the anterior 2/3rds of the IV septum.
What does the right coronary artery supply?
The posterior side of the heart. The posterior 1/3rd of the IV septum. The entire right ventricle. Also supplies posterior-medial papillary muscle of the mitral valve. AV node.
Obstruction of which can cause bradycardia: RCA or LAD?
RCA. It supplies the AV node.
How many hours/days after an MI is the heart the softest and at risk of rupture?

What type of necrosis do you see? After how many hours/days?
Between 3-7 days.

Coagulation necrosis (low oxygen) after ~12-24 hrs.
At point does tachycardia compromise filling of the coronary arteries?
180 bpm
What is this showing?
Day 7 of acute MI in the posterior wall of LV. Yellow area is surrounded by dark, red granulation tissue.
What is the appearance of an MI 1-3 days after event? 4-7?
1-3: myocyte nuclei disappear, neutrophils lyse dead myocardial cells.
4-7: red granulation tissue, macrophages removing necrotic debris.
Patient presents with severe retrosternal pain radiating down the left arm. The patient presents with sweating, anxiety, and hypotension. His symptoms are not relieved by nitroglycerin. What does he have?
MI
What does this show?
Fibrinous pericarditis
What does this show? Look at thin wall on the inferior portion of the ventricle.
Left ventricle aneurysm. Thin wall of scar tissue. Rupture is uncommon.
What is a mural thrombosis? How do you treat?
Thrombosis on the wall of the ventricle (most often LAD). Mixed characteristics of venous (stasis) clot and platelet-like clot. Asprin (platelet-like) and heparin/warfarin (venous-like).
MI complications:
Arrhythmia
Congestive heart failure
Rupture (anterior wall, posterior papillary muscle, IV septum)
Aneurysm (mural thrombus)
Fibrinous pericarditis (early, late autoimmune)
What is the most common arrhythmia caused by MI? Most common cause of death?
Ventricular premature beat. V-fib.
What is the consequence of an anterior wall rupture due to an MI? Where does the occlusion commonly occur?
Causes cardiac tamponade (fluid in pericardial cavity). This rupture is associated with thrombosis of the LAD coronary artery.
What is the consequence of an IV septal rupture as a result of an MI?
This rupture is associated with LAD coronary artery thrombosis. It produces a L to R shunt causing RHF.
What is the most common cause of death after a ventricular aneurysm?
A ventricular aneurysm as a result of an MI is clinically recognized within 4-8 weeks. CHF due to lack of contractile tissue is the cause of death.
What is Dressler's syndrome?
Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI.
Three weeks out of MI patient notices his chest bulging. What does he have? Whats the most common complication?
Ventricular aneurysm. Heart failure (<<EF)! (Not rupture).
CK-MB appears within ___to___ hours; peaks at ___ hours; disappears within ___to___ days.
4 to 8
24 hours
1.5 to 3
cTnI and cTnT appear within __to__ hours; peak at ___ hours; disappear within __to__ days.
3 to 6
24
7 to 10
How do you diagnose reinfarction?
CK-MB, because it shows up again 3 days later.
What is the LDH (1-2) flip?
Normally, LDH2 is higher than LDH1. In acute MI, LDH1 in cardiac muscle is released causing the "flip."

Appears within 10 hours; peaks at 2 to 3 days; disappears within 7 days
What murmur would you here with this pathology?
Click (midsystolic) followed by late systolic murmur (not snap, murmur). Most common valvular lesion.
Whats the pathophysiology of mitral valve prolapse?
Redundancy of valve tissue:
Myxomatous degeneration of the mitral valve leaflets due to excess production of dermatan sulfate
What valvular diseases most commonly causes hemolytic anemia with schistocytes?
Aortic stenosis
You hear an early diastolic murmur and notice a bunding pulses (water hammer pulse), head nodding, and a pulsating uvula. What is the diagnosis?
Aortic regurgitation.
What is shown?
Acute rheumatic fever. Uniform, verrucoid-appearing sterile vegetations appear along the line of closure of the mitral valve.
What is the pathogenesis of Rheumatic fever?
Pathology: Immune-mediated disease that follows group A streptococcal infection. Antibodies develop against group A streptococcal M proteins. Antibodies cross-react with similar proteins in human tissue. Type II hypersensitivity reaction
What causes Rheumatic fever?
Group A streptococcal pharyngitis.
How is acute rheumatic fever diagnosed?
Increased antistreptolysin (ASO) titers, positive throat culture, leukocytosis, increased PR interval, increased C-reactive protein.
What valvular disease are commonest in rheumatic fever?
Mitral regurgitation > aortic regurgitation. In chronic infection: mitral stenosis.
What are Aschoff bodies?
They are present in myocarditis caused by rheumatic fever. They are a central area of fibrinoid necrosis surrounded by reactive histiocytes.
What is Sydenham's chorea?
Reversible rapid, involuntary movements affecting all muscles. It results from childhood infection with Group A beta-hemolytic Streptococci (rheumatic fever).
Mitral senosis is most often caused by chronic rheumatic fever. Give four clinical findings in mitral stenosis.
Dyspnea (pulmonary capillary congestion).
Atrial fibrillation (atrial dilation/hypertrophy).
Pulmonary venous hypertension (leads to RVH).
Dysphagia for solids (compression of the esophagus).
Give the most common causes of mitral regurgitation.
Mitral valve prolapse, LHF, infective endocarditis, and dysfunction of the papillary muscle.
What causes aortic stenosis?
Dystrophic calcification of a normal or bicuspid aortic valve. Chronic rheumatic fever.
What causes aortic regurgitation?
Isolated aortic valve root dilation.
Infective endocarditis.
HTN.
Rheumatic fever.
Aortic dissection.
Coarctation
Name the microbial pathogens responsible for infective endocarditis.
Streptococcus viridians – most common cause of IE.
Staphylococcus aureus – most common cause of IE in IV drug abuse.
Staphylococcus epidermidis – most common cause of IE due to prosthetic device.
Streptococcus bovis – most common cause of IE in ulcerative colitis or colorectal cancer.
Patient presents with fever, splenomegaly, splinter hemorrhages, and a pansystolic murmur which is heard louder on expiration. What does this patient have?
Infective endocarditis causing mitral valve regurgitation.
What produces sterile vegetations on the mitral valve surface?
SLE associated Libman-Sacks endocarditis.
Patient presents with fever, chest pain, CHF. Labs show increased CK-MB, troponins. What virus could cause these symptoms? What protozoa?
Coxsackievirus. Trypanosoma cruzi. A lymphocytic infiltrate is highly predictive of coxsackievirus.
What are the clinical features of pericardial effusion?
Muffled heart sounds, hypotension associated with pulsus paradoxus, Kussmaul's sign (jugular vein distention).
Water bottle configuration on CXR.
Patient presents with hypotension and the heart on ausculation has a distinctive knock. What does this patient have?
Constrictive pericarditis. TB is the most common cause worldwide. the pericardial knock is due to the ventricles hitting the thickened parietal pericardium.
Define cardiomyopathy. What three types are there?
Group of diseases that primarily involve the myocardium and produce myocardial dysfunction.
Dilated, hypertrophic, restictive.
Name the causes of cardiomyopathy.
Idiopathic > genetic causes > drugs (doxorubicin, cocaine), postpartum > thiamine deficiency (EtOH).
Patient presents with an EF < 40%, CXR shows a global enlargement of the heart, and echo shows poor contractility. What type of cardiomyopathy is this?
Dilated.
What is the most common cause of sudden death in young individuals?
Hypertrophic cardiomyopathy. Familial form in young individuals: mutation in heavy chain of beta-myosin and in the troponins.
What is the pathophysiology of hypertrophic cardiomyopathy?
Hypertrophy IV septum + anterior MV leaflet drawn against septum = decreased CO.
Conduction system in the IV septum is damaged = sudden death.
How is the ejection murmur created by hypertrophic cardiomyopathy affected by preload?
Increased preload decreases the murmur (reclining, negative inotropic drugs).
What is Pompe's disease? Why type of cardiomyopathy can it cause?
Autosomal recessive glycogen storage disease. Lysosomal storage disease with a deficiency in alpha-glycosidase. The muscular weakness can lead to restrictive cardiomyopathy.
Name the infiltrative causes of restrictive cardiomyopathy.
Pompe's glycogenosis, amyloidosis, hemochromatosis. Sarcoidosis.
Loeffler endocarditis?
Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis
The afferent pain fibers from the heart run centrally in the thoracic cardiac branches of the sympathetic trunk and enter spinal cord segments at the same dermatome level as __to__.
T1 - T5
The innervation of the pericardium is supplied by the phrenic nerve. Pain sensation is referred to __to__ dermatomes.
C3 -C5
The epicardium is also known as what layer of the heart?
The visceral layer of serous pericardium.
What percent of cases is the cause of myocardial ischemia due to atherosclerotic coronary arterial obstruction?
90%. This IHD is often termed coronary artery disease.
During which weeks of embryogenesis do congenital heart defects occur?
Gestational weeks 3-8 when major cardiovascular structures develop.
What is the primary site for gas exchange in the fetus?
Chorionic villus.
What fetal vessel has the highest amount of oxygen? Lowest?
Highest: umbilical vein
Lowest: umbilical arteries (2)
Why do newborns have polycythemia?
HbF has a higher affinity for oxygen. To supply sufficient oxygen to tissue the baby increases the number RBC.
What vasodilator keeps the ductus arteriosus open?
Prostaglandin E2 made by the placenta.
What shunts lead to a step up in oxygen content? What shunt leads to a step down?
Step up = left-to-right (75 to 80)
Step down = right-to-left (95 to 80)
What are the clinical findings in left-to-right shunts?
Pulmonary hypertension which will cause right ventricular hypertrophy. Reversal of the shunt occurs when pressure in RV overrides LV pressure, which leads to cyanosis (Eisenmenger syndrome).
Name the left-to-right cardiovascular defect shunts.
ASD, VSD, AVSD, patent ductus arteriosus.
Name the types of atrial septal defects.
Secundum ASD (90%), primum ASD and sinus venosus (5% each). Patent foramen ovale is present in up to 1/3rd of individuals and may/may not be considered an ASD.
Atrial septal defects are associated with ______ and ______.
Fetal alcohol syndrome and Down syndrome. Down syndrome is actually an AVSD.
Which left-to-right cardiovascular shunt commonly spontaneously closes?
VSD. Types: membranous and infundibular VSDs.
Ventricular septal defects are associated with _____,_____, and _____.
Cri du chat syndrome, trisomy 13, and trisomy 18.
A continuous machine-like murmur is heard during systole and diastole. Additionally the patient has a pink upper body and a cyanotic lower body. Diagnosis?
Patent ductus arteriosus which as reversed to a right-to-left shunt.
Patent ductus arteriosus is associated with _____.

PDA can be closed with _____.
Congential rubella.

Indomethacin. Inhibits PGE2.
What are the clinical features of right-to-left shunt
Cyanosis. With chronic cyanosis patients can develop hypertrophic osteoarthropathy (clubbing), polycythemia, and infective endocarditis
Name the right-to-left cardiovascular shunts.
Tetralogy of Fallot, complete transposition of the great vessels, truncus arteriosus, tricuspid atresia, total anomalous pulmonary venous connection.
What are the four features of tetralogy of Fallot? Which feature determines the severity?
VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy. The degree of pulmonary stenosis determines the severity of the disease.
Name two cardioprotective shunts that would aid the survival of someone with tetraology of Fallot.
PDA and ASD.
What is the congenital defect in total anomalous pulmonary venous return?
Pulmonary vein empties oxygenated blood into the right atrium.
Name the obstructive congenital anomalies.
Coarctation of the aorta, pulmonary stenosis/atresia, and aortic stenosis/atresia.
Hows does adult and infantile aortic coarctation differ?
Infantile is preductal while adult is distal to the ligamentum arteriosum.
Patient presents with a systolic murmur, decreased blood pressure in the lower extremities (>10 mmHg less than upper), leg claudication and hypertension. What is your diagnosis?
Adult coarctation.
Infantile coarctation is associated with _____.
Turner's syndrome.
What is paradoxical embolization?
In right to left shunts, emboli from peripheral veins can bypass the normal filtration action of the lungs and enter the systemic circulation.
A 9 year old girl is diagnosed with acute rheumatic fever. Instead of recovering she dies. What is the cause of death?
The most common cause of death that occurs during acute rheumatic fever is cardiac failure secondary to myocarditis.
What is Sydenham chorea?
A central nervous system manifestation of acute rheumatic fever. It is characterized by involuntary, purposeless muscular movements, and bizarre grimaces, as well as emotional lability.
In what disease is the bundle of Kent present? What does the characteristic ECG look like?
Wolf-Parkinson White syndrome. ECG has prolonged QRS with a delta wave.
Describe the ECG tracing of atrial fibrillation. How do you treat?
Irregularly irregular and no discrete P waves. Coumadin to prevent clot formation.
Describe the ECG tracing of atrial flutter. How do you treat?
Sawtooth appearance. Class IA, IC or III antiarrhythmics.
Describe the ECG's of AV heart blocks.
First degree: prolonged PR (>.2)
Second degree: Mobitz I: progressively longer PR intervals till P wave is dropped. Mobits II: consistent PR's from beat to beat until one drops.
Third degree: independent atria and ventricular beats.
How would a LBBB appear on an ECG tracing?
Wide QRS which are mostly negative in V1-2. M morphology in V5-6.
How would a RBBB appear on an ECG tracing?
QRS is mostly positive with M morphology in V1-2. Large S wave in V5-6.
Tosades de pointes can be caused by:
a. prolonged PR
b. absent T
c. prolonged QT
d. tachycardia
c. Prolonged QT interval can predispose to torsades de pointes. It shows up on ECG as a sinusoidal waveform around the isoelectrical point.
Does hyperkalemia or hypokalemia increase the risk of ventricular fibrillation?
Hyperkalemia. Nerst equation includes -(K in/K out). Increasing K out makes the membrane potential less negative and closer to the threshold potential, therefore it is easier to elicit an AP.
What are the pacemaker rates at the SA, AV, and His-Purkinje system?
SA = 60-80, AV = 40-60, Purkinje = 20-40
What antiarrhythmic drug class is used to treat acute ventricular arrhythmias?
Class IB - lidocaine. Lidocaine is best used in post-MI conditions, because it acts on damaged tissue, not normal myocytes.
What is the best antiarrhythmic drug to use for paroxysmal supraventricular tachycardia?
Adenosine.
Hyperthyroidism can cause _____ in the heart.
Arrhythmia. Most often tachycardia.
What are the three types of atria fibrillation?
Paroxysmal - recurrent episodes that are self-limiting within 7 days
Persistent - recurrent episodes that are not self-limiting
Permanent - last than more than a year
What is the atrial rate (of impulses) in atrial fibrillation? In this condition what is the rate in the ventricles?
400-600 bpm, but most are blocked in the AV node and the ventricles are normally 80-180 bpm.
What antiarrhythmias would you use in atrial fibrillation to control the rate in the ventricles?
Beta blockers which suppress abnormal pacemakers by decreasing the slope of phase 4. Ca channels also work at the AV nodal cells (verapamil).
How many premature ventricular contractions qualifies as ventricular tachycardia?
3 or more.
What is sick sinus syndrome? What are some causes?
Both fast and slow arrhythmia due to a malfunctional SA node.
Can be caused by sarcoidosis, amyloidosis, Chagas, cardiomyopathies
In what situation is the antiarrhythmic Mg (2+) used?
Torsades de pointes and digoxin toxicity.
What antiarrythmic drug class can cause bradycardia?
Beta blockers.
What is the Jones criteria used for?
Diagnoses of Rheumatic Fever. Major criteria: erythema marginatum, migratory polyarthritis, subcutaneous nodules, chorea, carditis. Minor: fever, arthralgia, leukocytosis, increased ESR, ECG heart block, ASO, etc. Diagnosis: 2 major and + culture or 1 major, 2 minor, + culture.