Flashcards in Cardiovascular: Pathoma, BRS, First Aid Deck (318):
Ischemic heart disease is caused by what?
Partial or complete interruption of arterial blood flow to the myocardium
What is the main cause for interruption of arterial blood flow to myocardium?
Atherosclerosis of coronary arteries
Incidence of IHD increases with what?
How will ischemia present? (6)
2. Angina pectoris
3. Coronary steal syndrome
4. Myocardial infarction
5. Sudden cardiac death
6. Chronic ischemic heart disease
Frequency of IHD increases in patients who manifest what?
What does metabolic syndrome include?
1. Central obesity
2. Artherogenic lipid patterns
4. Insulin resistance
5. Proinflammatory state
What predisposes someone to metabolic syndrome?
What is angina pectoris?
Episodic chest pain that is caused by inadequate oxygenation of myocardium
How much stenosis or obstruction of a vessel is needed to cause angina?
Is there myocyte necrosis in angina?
What is the most common type of angina?
What precipitates stable angina?
Exertion or stress
Can't get enough blood (oxygen) to heart
What causes stable angina?
CAD of coronary arteries greater than 70%
How does stable angina present? 3
1. Chest pain less than 20 minutes that radiates to left arm or jaw
3. Shortness of breath
Why is the 20 minute interval important?
After that you get irreversible injury and cell death
What does an EKG show in stable angina?
ST segment depression
What relieves stable angina? (2)
2. Vasodilators like nitroglycerin
Function of nitroglycerin?
Vasodilation of veins mainly that decreases preload and decreases stress on myocardia
Unstable angina is chest pain that occurs when?
What causes unstable angina?
Rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery
What type of damage is occurring in unstable angina?
Reversible injury to myocytes
What does an EKG show on unstable angina?
ST segment depression
What relieves unstable angina?
Nitroglycerin: Vasodilation to decrease preload which decreases stress
What are unstable angina patients at risk for?
Progressing to full occlusion: Myocardial infarction)
Prinzmetal angina is due to what?
Coronary artery vasospasm
What is the timing of pain in prinzmetal angina?
Episodic/intermittent chest pain at rest
What type of damage occurs in prinzmetal angina?
Reversible injury to myocytes
What does prinzmetal EKG show?
ST segment elevation
What relieves prinzmetal angina? 2
1. Nitroglycerin: Decrease preload
2. Calcium channel blockers: Decrease spasm
What is the most important cause of morbidity from IHD?
What is myocardial infarction?
Necrosis of cardiac myocytes (so after 20 minutes)
What mainly causes a myocardial infarction?
Rupture of a atherosclerotic plaque with thrombosis and complete occlusion of coronary artery
Other causes of myocardial infarction? (3)
1. Coronary artery vasospasm (Complete prinzmetal)
3. Vasculitis (kawasaki's disease)
Symptoms of myocardial infarction?
1. Severe chest pain greater than 20 minutes that radiates to left arm/jaw
3. Dyspnea: Heart can't pump --> Fluid in lungs
Will nitroglycerin relieve myocardial infarction pain?
What ventricle is usually involved in an MI?
What is most common artery involved in MI?
Which causes an infarction where?
Infarciton of anterior wall of LV and anterior part of IV septum
What is 2nd most common artery involved in MI?
Which causes an infarction where?
Infarction of right ventricle, posterior wall of LV and anterior portion of IV septum
What is 3rd most common artery involved in MI?
Which causes an infarction where?
Infarction of lateral wall of LV
What are the 2 types of infarction based on heart layers involved?
Which is more common
1. Transmural: Entire ventricular wall from endo to epi. More common
2. Subendocardial infarction: Just 1/3 of the wall
ECG shows what during myocardial infarction?
1. During the initial subendocardial infarction, ST depression
2. During later transmural infarction, ST elevation
Why are there biomarkers for MI?
Irreversible damage to myocytes causes membrane breakdown thus releasing markers
What is the most SENSITIVE and most SPECIFIC cardiac marker?
When does troponin I peak?
How long does troponin I remain high after MI?
7 to 10 days
CK-MB is most useful for what?
When does CK-MB rise?
4-6 hours after infarction
When does CK-MB peak?
When does CK-MB return to normal? 72 hours
What is the gold standard for diagnosing MI in first 6 hours?
When does LDH peak?
How long does it last?
When does myoglobin peak?
How long does it last?
First 6 hours
Treatment of MI includes what? 6
1. ASA/Heparin: limit more thrombosis
2. Supplemental O2: minimize ischemia
3. Nitrates: Vasodilate --> Decrease preload
4. Beta-blocker: Slow heart rate --> Decrease O2 need + decrease arrhythmia
5. ACE inhibitor: Decrease dilatation
6. Fibrinolysis/Angioplasty: Destroy blockage/open up vessel
How does an ACE inhiabitor decrease LV dilatation? 2
1. Blocks ANG II production --> prohibit constriction of peripheral arterioles --> Decrease afterload
2. Block ANG II --> No aldosterone secreted --> No blood volume increase
Two injuries due to fibrinolysis and angioplasty?
1. Contraction band necrosis
What is contraction band necrosis?
Calcium will enter cell after blood flow is restored and cause contraction --> visible contraction bands
What is reperfusion injury?
Returning O2 rapidly to cell causes ROS to form --> Further damage the cells
What is a lab test for reperfusion injury?
See cardiac enzymes continue to rise after reperfusion
Less than 4 hours from infarction, what risks does patient have?
1. Cardiogenic shock: Heart fails --> Hypofusion
2. CHF: Dead tissue --> Can't pump--> Backs up into heart --> Decreased ejection fracture
Between 4 and 24 hours after infarction, what changes do you see macroscopically?
1. Dark discoloration
2. Coagulative necrosis: Karyolysis, pyknosis, karyorrhexis
Between 1 and 3 days what change do you see? 2
What is patient at risk for?
Neutrophils on scene
How does fibrinous pericarditis present in days 1-3?
Why does it occur?
Chest pain with friction rub
Transmural infarction --> Neutrophils enlame entire wall --> Debris into pericardium --> Pericarditis
How does MI present in days 4-7? 2
1. Yellow pallor
2. Macrophages on scene
What is important about days 4-7 after MI?
Cardiac wall is weakest due to macrophages eating all the dead material.
What are the 3 things a patient is at risk for 4-7 days after MI?
1. Rupture of ventricular free wall --> Blood leaks into pericardium --> Compresses heart --> Cardiac tamponade
2. Rupture of IV septum --> Shunt from LV to RV
3. Rupture of papillary muscle --> Mitral insufficiency
What causes rupture of papillary muscle?
Occlusion of right coronary artery
In weeks 1-3, what are the macroscopic changes? (2)
1. Red border as granulation tissue enters from edge
2. Granulation tissue with fibroblasts, collagen, and BV's
Months after, what changes does MI patient have?
1. White scar of Type 1 collagen
What risks does a patient with an MI have after months? (3)
1. Weak scar: leads to balloon like dilatation --> Aneurysm
2. Scar along heart wall --> Stasis --> Mural thrombus
3. Dressler syndrome
What happens in Dressler's syndrome?
Transmural infarct --> Pericardium leaks --> Form imune response against pericardium antigens --> Pericarditis 6-8 weeks after infarction
What is most common cause of death in first several hours after infarction?
What is sudden cardiac death due to?
How does sudden cardiac death appear? 2
1. Asymptomatic before
2. Less than 1 hour after symptoms arise
What usually causes sudden cardiac death?
Fatal ventricular arrhythmia
Most common etiology of sudden cardiac death?
90% of SCD patients have what pre-existing condition?
Less common etiologies of SCD? 3
1. Mitral valve prolapse
3. Cocaine abuse
Chronic ischemic heart disease is defined how?
Poor myocardial function
What is Chronic IHD due to?
Chronic ischemic damage (with or without MI)
What do chronic IHD patients progress to?
What is coronary steal syndrome?
Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion.
Congestive heart failure may be failure of what ventricle?
Right, Left or both
Causes of Left sided heart failure?
1. Ischemia: Decrease blood flow --> Damage myocardium --> Can't pump well
2. Hypertension: Get concentric LV hypertrophy to deal with stress --> Extra O2 demands --> Ischemic damage --> Can't pump well
3. Dilated cardiomyopathy: Stretch all four chambers --> Can't contract well
4. Myocardial infarction: Nonfunctional tissue --> Can't pump well
5. Restrictive cardiomyopathy: Can't fill heart well --> Can't pump enough out
6. Aortic and mitral valvular disease
Two main Clinical manifestations of LCHF?
1. Pulmonary congestion
2. Decreased forward perfusion
Pulmonary congestion from LCHF is due to what?
Heart can't pump blood forward --> Backs up -->blood accumulates in lung --> Pulmonary congestion
Why does pulmonary congestion result in dyspnea?
Increase in hydrostatic pressure --> Pulmonary edema --> Dyspnea
What is PND?
Dyspnea upon laying flat for several hours
What is othopnea?
Dyspnea if late flat for a few minutes?
What are crackles?
Fluid in lungs upon auscultation
Ruptured pulmonary capillaries in LCHF results in what?
Blood in alveoli --> Macrophages arrive to clean up --> Iron fills maccrophages --> Forms hemosiderin laden cells called heart failure cells.
What are the 5 clinical manifestations of pulmonary congestion?
5. Heart failure cells
Decreased forward perfusion results in activation of what?
RAS activation has what two effects?
Decreased blood flow to kidneys activates juxtaglomerular apparatus --> Release renin --> Release Ang II -->
1. Constrict arterioles --> Increase total peripheral resistance
2. Go to adrenal gland --> Release aldosterone --> Cause resorption of sodium --> Water follows --> Increase blood volume
OVERALL = Increase resistance --> Exacerbates problem
Main treatment for LCHF?
Right sided failure has what causes? 6
1. Left sided heart failure
2. Left-sided lesions
3. Pulmonary hypertension: Chronic lung disease/cor pulmonale --> Vessel constriction
4. Cardiomyopathy/Diffuse myocarditis
5. Tricuspid or pulmonary valvular disease
6. Left to right shunts
Most common cause of RCHF?
Backup into pulmonary circuit --> Backups into right heart
Isolated RCHF is usually due to what?
Clinical manifestations of RCHF? 4
1. Jugular vein backup --> JVD
2. Hepato and spleno congestion --> Hepatosplenomegaly + cardiac cirrhosis + nutmeg liver
3. Pitting edema: Due to increased hydrostatic pressure in low extremities.
4. Renal hypoxia: Fluid retention
Congenital defects arise when?
During embryogenesis weeks 3-8
Congenital heart defects are seen in what percentage of live births?
Most congenital defects are caused by what?
Undetermined = Sporadic
Congenital defects overall usually result in what?
Shunting between left and right circulations
What is most common congenital heart defect?
Ventricular septal defect
VSD is a defect associated with what syndrome?
Fetal Alcohol Syndrome
What happens with blood flow in VSD?
Blood enters right atrium and can enters normal low pressure RV over high pressure LV. However upon returning to LA, blood chooses low pressure RV instead of high pressure LV resulting in LEFT TO RIGHT SHUNT
How does size of defect affect symptoms in VSD?
Small VSD = asymptomatic
Large VSD = large amounts of blood entering RV --> increase of blood in pulmonary circuit --> Pulmonary hypertension
What does pulmonary hypertension from VSD result in over time?
P-HTN --> Right side to become high pressure --> Blood now shunts from high pressure right to low pressure left ventricle --> Deoxygenated blood in systemic circulation --> Cyanosis
The reversal of a shunt due to a change in pressure from pulmonary hypertension is known as what?
3 consequences of Eisenmenger's syndrome?
1. RV hypertrophy: Due to pumping against higher pressure
2. Polycythemia: Deox blood --> Hypoxemia --> Release EPO --> Increase RBC's
3. Clubbing: Change in fingernails from cyanosis
Treatment of VSD? (2)
1. Small VSD close on their own
2. Surgical closure
Atrial septal defect includes what five types?
1. Patent foramen ovale
2. Septum primum
3. Septum secundum
4. Sinus venosus
5. Lutembacher syndrome
Patent foramen ovale is clinically significant how?
It's not. 20-30% of people have it.
Septum primum/Ostium primum is associated with what consequence?
What genetic disease is associated with this?
Affects lower part of septum so it can affect AV valves.
Most common type of ASD is what?
Ostium/Primum secundum is a defect in what?
Sinus venosus affects what area?
Upper part of septum near SVC
Lutembacher syndrome has what two components?
2. Mitral stenosis
Atrial septal defect results in what type of shunt?
Left to right shunt
ASD presents how on auscultation? 2
1. Split S2
2. Loud S1
Why does split S2 occur in ASD?
Blood from high pressure LA crosses to low pressure RA --> Extra volume on right side --> Delayed closure of pulmonic valve --> Split S2
What is the S2 sound?
Pulmonary and aortic valves closing
What is an important complication of ASD?
Paradoxical emboli: DVT emboli enters RA normally but crosses over to LA and lodges in brian or extremities.
When are ASD symptoms seen?
What is the main one?
Late in life
Cyanosis due to Eisenmenger's syndrome from P-HTN
What is Patent ductus arteriosus?
Failure of ductus arteriosus to close.
PDA is associated with what situations? 2
1. Congenital Rubella
2. People living in high altitudes
What is the mechanism of PDA?
Blood enters RA --> RV --> Enters pulmonary artery --> Chooses to enter low pressure lungs over high pressure aorta --> LA --> Enters LV --> Enters aorta --> Chooses low pressure lungs over high pressure systemic circulation --> LEFT TO RIGHT SHUNT
What happens over time in PDA patients?
P-HTN develops --> Blood now chooses low pressure aorta over high pressure lungs --> Deox blood goes to LOWER extremities --> Cyanosis in lower extremities in late life.
How does PDA appear at birth?
Asymptomatic left to right shunt
What causes PDA to appear in adulthood?
What keeps the PDA open? 2
Low O2 tension
What are treatments for PDA? (2)
Function of indomethacin
Decrease prostaglandin E --> Close PDA
What is the quality of murmur in PDA?
Tetralogy of Fallot is caused by what?
Anteriosuperior displacement of infundibular septum
Tetralogy of Fallot has what four components?
Pulmonary infundibular stenosis
Right Ventricular Hypertrophy
Overriding aorta (of VSD)
Ventricular Septal Defect
What is the flow of blood in tetralogy of Fallot?
RA --> RV --> Due to stenosis --> Shunt to aorta = Right to left shunt
In babies, ToF results in what?
Cyanosis due to deoxygenated right sided blood entering systemic circulation.
What is shape of heart in ToF?
In adults, what will cause cyanosis to occur in ToF?
How do patients deal with ToF?
Squat --> Increase left sided pressure --> Decrease shunt --> Oxygenate more blood --> less cyanotic
The main point behind squatting with ToF?
Increased arterial resistance --> Decreases shunting
Treatment of ToF?
In transposition of great vessels, what happens?
Aorta comes off RV and Pulmonary artery comes off LV resulting in two independent circuits that do not connect.
Can a person with transposition of great vessels live?
Only if they somehow form a shunt.
How do you treat Transposition of great vessels?
Cause open PDA so that blood can mix
1. Give patient prostaglandin E
2. Surgically repair problem
What maternal condition is associated with Transposition of Great vessels?
How do ToGV patients present?
Early cyanosis since deox blood from right side enters aorta --> Systemic circulation
What is truncus arteriosus?
Truncus fails to divide providing one single large vessel coming from both ventricles.
How does blood flow in truncus arteriosus?
One vessels drains both ventricles but divides later --> Deox and ox blood mix --> Deox blood enters systemic circulation --> Cyanosis
What is tricuspid atresia?
Tricuspid valve orifice fails to develop
What does atresia mean?
Fail to form lumen of tube
In tricuspid atresia, how is the RV described?
In tricuspid atresia, what is the situation associated with?
What is flow of blood?
How does it present?
ASD: Right to left shunt
Tricuspid fails to form --> No blood to RV --> ASD forms --> Deox blood enters left side
Coarctation means what?
Narrowing of aorta
Coarctation of aorta is divided into what two forms?
Infantile and Adult
Infantile CoA is associated with what?
In infantile CoA, where is the coarctation?
Distal to aortic arch
Proximal to PDA
Describe the pressures in infantile CoA?
High pressure above coarctation
Low pressure below coarctation
What is mechanism of blood flow in infantile CoA?
RA--> RV --> PA --> Cross PDA to low pressure aorta below coarctation --> Deox blood in lower extremities --> Lower extremity cyanosis
What disease is associated with infantile CoA?
Is adult form of CoA associated with PDA?
Where is coarctation in adult CoA?
Distal to aortic arch?
Mechanism of blood flow in adult CoA?
Since narrowing is below arch --> High pressure above and low pressure below --> High pressure in UE + low pressure in LE
How does adult CoA present?
HTN in upper extremity
Hyptension with weak pulses in lower extremity
When is adult form of CoA found?
What defect is adult CoA associated with?
Bicuspid aortic valve
What X-ray feature is seen in adult CoA?
Notching of ribs
Collateral circulation develops across intercostal arteries --> Engorged arteries --> Notching of ribs
What is Turner's syndrome associated with in congenital heart defects?
Coarctation of Aorta (Infantile)
What are congenital defects are Down syndrome patients known for?
Such as? 3
Endocardial cushion defects
ASD, VSD, AV septal defect
Congenital rubella is associated with what congenital CV defects? 5
Septal defects: VSD,
Pulmonary artery stenosis
22q11 syndromes are associated with what CV defects? (2)
1. Truncus arteriosus
2. Tetralogy of Fallot
Marfan's syndrome is associated with what CV defects?
Aortic insufficiency and dissection
Infant of diabetic mother has what associated CV defects?
Transposition of great vessels
Noncyanotic congenital CV defects include what two types?
What are the diseases of noncyanotic congenital CV defects?
No shunts = 1. Aortic stenosis 2. CoA
L-2-R shunts = 1. PDA, ASD, VSD
Rank frequency of left to right shunt defects?
VSD > ASD > PDA
Right to left shunts are known as what? 3
What are the 5 T's of right to left shunts?
Tetralogy of Fallot
Transposition of great arteries
Total anomalous pulmonary venous return
What do most patients with truncus arteriosus also have?
What is total anomalous pulmonary venous return?
Pulmonary veins return to RA
Two types of valvular disease?
Stenosis and regurgitation
Acute rheumatic fever is what?
Systemic complication of pharyngitis due to Group A beta-hemolytic strep
How old are children usually with ARF?
How many weeks after strep throat is ARF seen?
5-15 years old
What is the etiology of ARF?
The Bacterial M protein of Group A strep resembles human tissues and causes type II hypersensitivity against own heart tissues.
What evidence prior to ARF must be had?
How is this accomplished? 2
Evidence of group A strep infection
ASO or anti-DNase B titer
Minor criteria for ARF? 2
Major criteria for ARF?
J = Joint problems = Migratory polyarthritis
O = Heart problems (pan-carditis)
N = Nodules in Skin
E = Erythema marginatum
S = Sydenham's chorea
What is first layer of heart to be affected in ARF?
Which results in what?
Tiny vegetations on mitral valve (possibly aortic as well) --> Regurgitation
Myocardium is second layer to be affected in ARF, what forms here?
Aschoff bodies of: Giant cells + Fibrinoid material (degenerated collagen) + Anitschkow Cells
How do anitschkow cells appear?
Slender wavy nuclei (Caterpillar nuclei)
Pericarditis in ARF presents how?
Which of the 3 layers of carditis is most likely to kill ARF patient?
What is erythema marginatum?
Rash that is more red on edges
Sydenham's chorea is what?
Rapid involuntary muscle movement
What is the First Aid acronym for Rheumatic fever facts?
V=Valvular damage (vegetation and fibrosis)
R = Red-hot joints (migratory polyarthritis)
S=St. Vitus' dance (Sydenham's chorea)
Rheumatic endocarditis has what happen in early stage?
Valve leaflets are red and swollen with tiny vegetations resulting in mitral valve regurgitation
As a consequence of healing, what changes do valves have in ARF?
Valves become thickened, fibrotic and deformed.
Chronic rheumatic valvular disease is result of what?
Valve scarring that results from rheumatic fever?
Chronic rheumatic valvular disease results in what?
Mitral valve stenosis leads to what?
Thickening of chordae tendinae and cusps
Aortic valve in CRV results in what?
Fusion of comissures
Fusion of comisures in aortic valve CRV results in what? (2)
1. Small orifice --> FIshmouth appearance
2. Stenosis --> Can't completely open valve
Mitral stenosis causes what pressure difference to develop?
Diastolic pressure higher in left atrium than in left ventricle
What is aortic stenosis
Narrowing of aortic valve orifice
What is aortic stenosis due to mainly? (2)
When does aortic stenosis present?
Late adulthood (>60 years old)
Two others causes of aortic stenosis?
Bicuspid aortic valve
Chronic rheumatic valve disease
Aortic valve is usually what organization?
What's the problem with bicuspid aortic valves?
Two cusps do the work of 3 --> increases risk for aortic stenosis
How does CRVD cause aortic stenosis?
It has mitral valve stenosis and fusion of aortic valve comissures
What is difference between "wear-and-tear" aortic stenosis and CRVD caused aortic stenosis
Wear and tear aortic stenosis has only the aortic valve affected, CRVD = mitral + aortic valve
Compensation in aortic stenosis leads to what? 2
1. longer asymptomatic stage
2. Systolic ejection click followed by crescendo-decrescendo murmur
Complications resulting from aortic stenosis? (3)
1. LV Hypertrophy: Due to pumping against stenotic valve
2. Angina and syncope with exercise: Stenosis reduces systemic blood flow --> Don't get enough during exercise
3. Microangiopathic hemolytic anemia: Blood cells rupture moving across bad valve
Treatment of aortic stenosis?
Replace valve after symptoms appear
Aortic regurgitation is what?
backflow of blood from aorta into LV during diastole
AR arises due to what? 4
Which is most common
1. Isolated aortic root dilation (Most common)
2. Syphilitic aneurysm
3. Valve damage (such as CRVD)
4. Non-dissecting aortic aneurysm
Why does aortic root dilatation cause AR?
Dilation of root --> Pulls valves apart --> Regurg occurs
Clinical features of AR? 7
1. Bounding pulses
2. Early blowing diastolic murmur
3. Pulsating nail bed
4. Head bobbing
5. Increasing pulse pressure
6. LV dilation
7. Eccentric hypertrophy of one part of ventricle
Treatment of AR?
What is the most common valvular lesion?
Mitral valve prolapse
What is mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole
Mitral valve prolapse is due to what?
Myxoid degeneration of valve making it floppy
What diseases commonly have mitral valve prolapse? 2
Marfan and Ehlers Danlos
Clinical features of MVP? 3
1. Mid-systolic click with systolic regurgitation murmur
3. Can turn into infective endocarditis
Treatment of MVP?
Mitral regurg involves what?
Reflux of blood from LV into LA during systole
Mitral regurg is a complication of what prior problem usually?
Mitral valve prolapse
Other causes of mitral regurg? 4
1. LV dilation
2. Infective endocarditis (Bad leaflets)
3. ARF (Mitral valve)
4. Papillary muscle rupture after MI
Clinical features of mitral regurgitation? 3
1. Holosystolic blowing murmur
2. Louder with squatting and expiration
3. volume overload and left-sided heart failure
Why does squatting make mitral regurg louder?
Increase systemic resistance --> less blood forward --> more blood backwards --> Louder murmur
Why does expiration make mitral regurg louder?
Increase in amount of blood entering LA --> Increase blood in LV --> increase in regurgitated blood
What is mitral stenosis?
Narrowing of mitral valve orifice
Cause of mitral stenosis?
Clinical symptoms of mitral valve stenosis?
1. Opening snap with diastolic rumble
2. Volume overload leads to dilation of LA
Consequences of dilated LA in mitral valve stenosis?
1. Pulmonary congestion: Overloading LA --> Blood backs up into pulmonary circuit --> Pulmonary congestion --> Edema + Alveolar hemorrhage --> Heart failure cells
2. Pulmonary HTN: Excess blood in circuit --> Rt heart pumps against --> Right heart fails
3. Atrial fibrillation: Dilation --> Abnormal wall movement --> Stasis --> Mural thrombi
What syndrome is tricuspid valve involved in?
The pulmonary valve is normally affected by what
Endocarditis is what?
Inflammation of endocardium (inner surface)
Endocarditis is usually the result of what?
General features of bacterial endocarditis? 3
1. Large soft vegetations on valvular surfaces
2. Ulceration and perforation of valves cusps
3. Rupture of chordae tendineae
Two classifications of bacterial endocarditis?
What is acute endocarditis caused by?
Highly virulent pathogens like staph aureus
Staph aureus is most common cause of endocarditis in what demographic?
IV drug abusers
Acute endocarditis like staph aureus is secondary to what?
What is state of valves that highly virulent bacteria like staph aureus inhabit?
What does acute endocarditis result in?
Large vegetations with rapid onset of symptoms due to destruction of valve
Subacute endocarditis is caused by what?
Less virulent bacteria like strep viridans
What is the most common cause of bacterial endocarditis?
Subacute endocarditis occurs on what state of valves?
Previously damaged valves such as congenital heart disease or valvular heart disease
What is result of subacute endocarditis?
subendocardium is exposed allowing for formation of thrombotic vegetations that do not destroy the valve.
What allows for bacteria in subacute endocarditis to inhabit a valve?
Bacteremia such as during a dental procedure
Staph epidermidis is most common in what?
Endocarditis of prosthetic valves
Strep bovis is seen in what patients?
Endocarditis of patients with underlying colorectal carcinoma
Endocarditis with negative blood cultures is due to what?
Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Clinical features of bacterial endocarditis? 8
2. Roth's spots
3. Osler nodes: Painful lesions on fingers/toes
4. Murmur: Vegetations disrupt flow
5. Janeway Lesions: nonpainful on palms/soles
7. Nailbed hemorrhage
8. Emboli (septic): Vegetations come off and lodge
What valve is most frequently involved in bacterial endocarditis?
Tricuspid valve bacterial endocarditis is associated with what?
IV drug abuse (Don't Tri Drugs)
Lab features of bacterial endocarditis? 5
1. Positive blood cultures
2. Microcytic anemia: Low hemoglobin, low MCV
3. Hepcidin traps iron
4. Ferritin will be hidden (Low TIVC)
5. TEE = best for detecting lesions on valves
Nonbacterial thrombotic endocarditis is what?
Where do vegetations arise?
What do they cause?
Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma
Mitral valve along lines of closure
Libman-Sacks endocarditis is what?
Sterile vegetations associated with SLE (lupus)
What makes the vegetations in Libman-Sacks endocarditis special?
What does it result in?
Vegetations present on surface AND undersurface of mitral valve
Results in mitral regurgitation
The cause of endocarditis of carcinoid syndrome is what?
Secretory products of carcinoid tumors (vasoactive peptides and amines)
What does endocarditis of carcinoid syndrome result in?
Thickened endocardial plaques
What is cardiomyopathy?
Disease of heart muscle that results in cardiac dysfunction
What is most common form of cardiomyopathy?
Dilated cardiomyopathy (90%)
Dilated cardiomyopathy involves dilation/stretching of what?
All four chambers of heart
What are causes of dilated cardiomyopathy? (6)
1. Idiopathic (Most common)
2. mutation (AD)
4. Alcohol abuse
5. Drugs: Doxorubicin, Cocaine
6. Pregnancy: late or right after birth
7. wet Beriberi
8. Chagas disease
Treatment of dilated cardiomyopathy?
Hypertrophic cardiomyopathy is what?
Massive hypertrophy of left ventricle
What causes hypertrophic cardiomyopathy?
Genetic mutations in sarcomere proteins (autosomal dominant)
Clinical features of hypertrophic cardiomyopathy? 3
1. Decreased cardiac output: Too much muscle --> Lose compliance --> Diastolic dysfunction
2. Sudden death due to ventricular arrhythmias
3. Syncope with exercise: IV septum creates block in LV --> Blood can't get out well
What genetic disease is associated with hypertrophic cardiomyopathy?
Microscopic features of hypertrophic cardiomyopathy?
Disoriented, tangled, hypertrophied myocardial fibers
Treatment of hypertrophic cardiomyopathy?
1. Beta blocker
2. Calcium channel blocker
Restrictive cardiomyopathy is what?
Diastolic problem of not being able to fill due to decreased compliance of ventricular myocardium.
Causes of restrictive cardiomyopathy?
Sarcoidosis: Granulomas in wall of heart
Hemochromatosis: Iron in wall of heart
Endocardial fibroelastosis: FIbrosis in endocardium
Loeffler Syndrome: Eosinophil infiltrate of heart
Which cause of restrictive cardiomyopathy is seen in children?
How does restrictive cardiomyopathy present? (3)
1. CHF: Can't fill heart --> Backs up
2. Low-voltage EKG
3. Diminished QRS amplitudes
Two cardiac tumor types?
Myxoma is what?
Mesenchymal proliferation with gelatinous appearance to tumor
Myxoma has abundant what?
Myxoma is most primary cardiac tumor in what demogrpahic?
Can myocytes form tumors?
How does myxoma present?
Pedunculated mass in left atrium obstructing the mitral valve --> Syncope
What is rhabdomyoma?
Hamartoma of cardiac muscle
Rhabdomyoma is most common primary cardiac tumor in what demographic?
Rhabdomyoma is associated with what disease?
Where does rhabdomyoma grow?
Are myxoma and rhabdomyoma benign or malignant?
What is the most common heart tumor?
Common metastases primary locations?
1. Breast carcinoma
2. Lung carcinoma
Metastases usually invade what layer of heart?
Resulting in what?
Myocarditis most often presents as what?
Biventricular heart failure in young people with no other major heart diseases
Myocarditis morphological characteristics? 2
1. Diffuse myocardial degeneration
2. Necrosis with inflammatory infiltrate
Myocarditis has what etiology?
What causes myocarditis in south america?
What is hydropericardium?
Accumulation of serous transudate in pericardial space
What causes hydropericardium?
Anything that can cause systemic edema.
Hypoproteinemia like in nephrotic syndrome or chronic liver disease
What is hemopericardium?
Accumulation of blood in pericardial sac
What causes hemopericardium?
Traumatic perforation of heart or aorta by myocardial rupture associated with MI
Five types of acute pericarditis?
Serous pericarditis is associated with what causes? (3)
2. Rheumatic fever
3. Viral infections
What is the liquid in acute pericarditis?
Protein-rich exudate with inflammatory cells
What is fibrinous/serofibrinous pericarditis characterized by?
What causes fibrinous/serofibrinous pericarditis? 5
2. Myocardial infarction
4. Dressler's syndrome
What is clinical finding in fibrinous/serofibrinous pericarditis?
Loud friction rub
Purulent/suppurative pericarditis is characterized by what?
What causes purulent/suppurative pericarditis?
Hemorrhagic pericarditis is characterized by what?
Bloody inflammatory exudate
What causes hemorrhagic pericarditis? 2
1. Tumor invasion
2. TB or other bacterial infection
Overall, acute pericarditis presents how? 5
1. Sharp pain
2. Aggravated by inspiration
3. Relieved by sitting up and leaning forward
4. Friction rub
5. ST segment elevation or depression
Chronic pericarditis has what etiology? 2
2. Pyogenic staph
Characteristics of chronic pericarditis? 4
1. Thickening and scarring of pericardium
2. Loss of elasticity
3. Mimics Right sided heart failure
4. Proliferation of fibrous tissue
Hypertrophy of left ventricle is caused by what? 2
Aortic or mitral valvular disease
Hypertrophy of right ventricle causes? 4
1. LV failure
2. Chronic lung disease
3. Mitral valve disease
4. Congenital heart disease with L-2-R shunt
Define cor pulmonale
Right ventircular hypertrophy secondary to prmary disease of pulmonary vasculature (P-HTN)
What is cardiac tamponade?
Compression of heart by fluid in pericardium --> leading to decreased cardiac output.