heart

Question 1

cardiac pump problems

Answer 1

-Failure of the pump –MC problem
-contracts weakly and chambers cant empty properly— (systolic dysfunction)
-cant relax enough to allow ventricular filling – (diastolic dysfunction)

-Obstruction to flow- calcific aortic valve stenosis or cause increased ventricular chamber pressures (systemic hypertension) can overwork myocardium (has to pump against obstruction)
-Regurgitant flow
-Shunted flow - Defects (congenital or acquired) that divert blood, leading to pressure and volume overloads
-Disorders of cardiac conduction
-Rupture of the heart or major vessel - Loss of circulatory continuity

Question 2

CHF

Answer 2

-Heart cant pump blood adequately to meet demands of tissues
-Causes: Fluid overload, abrupt valvular dysfunction, MI
-Initially, compensatory to maintain organ perfusion:
-!!!!Frank-Starling mechanism: Increased filling volumes dilate the heart, enhancing contractility and stroke volume
-Activation of neurohumoral systems: aid heart function and/or regulate filling volumes and pressures
-Release of norepinephrine: elevates HR, augments myocardial contractility and increases vascular resistance
-Activation of RAAS: water and salt retention, increases vascular tone
-Release of ANP: counterbalances the RAAS by diuresis and vascular smooth muscle relaxation
-Myocardial adaptations
-Ventricular remodeling

Question 3

CHF causes

Answer 3

-decrease in EF - blood ejected from ventricle during systole- WNL- 45% to 65%

-Reduction in EF:
-ischemic injury
-inadequate adaptation to pressure or volume overload due to HTN or valvular disease
-ventricular dilation

-left ventricular hypertrophy, myocardial fibrosis, constrictive pericarditis, or amyloid deposition

Question 4

cardiac hypertrophy: patho and progression to HF

Answer 4

-increase in mechanical work of ventricle due to pressure overload, volume overload, or trophic signals (activation of β-adrenergic receptors) causes increase in !myocyte size (hypertrophy)!
-Pressure-overload hypertrophy (HTN or aortic stenosis): results in concentric wall thickness increase
-Volume-overload hypertrophy (valvular regurgitation): ventricular dilation

-Hypertrophied heart vulnerable to ischemia:
-Larger myocytes need more blood
-Larger heart has increased metabolism needs because of increased mass, heart rate, contractility – increase oxygen consumption

Question 5

flow chart

Answer 5

Question 6

LEFT sided HF: Causes

Answer 6

-Most often caused by:
-ischemic heart disease
-HTN
-Aortic and mitral valvular diseases
-Primary myocardial diseases

-Clinical and morphologic effects of left-sided CHF: consequence of passive congestion (blood backing up in the pulmonary circulation), stasis of blood in left-sided chambers, and inadequate perfusion of downstream tissues leading to organ dysfunction

-Systolic failure - insufficient EF (pump failure)

-Diastolic failure - LV abnormally stiff; HTN MCC

Question 7

left sided HF

Answer 7

-Enlarged heart, tachycardia
-volume overload (S3)
-increased myocardial stiffness (S4)

-lung micro will show “heart failure cells”
-dyspnea- blood tinged sputum
-tachy- heart has to work harder
-Moderate CHF: reduced EF leads to decreased renal perfusion -> activating RAAS -> leading to salt and water retention -> prerenal azotemia (excess nitrogen compounds in blood) -> may lead to renal failure
-Very severe- cerebral hypoperfusion can lead to hypoxic encephalopathy: irritability, loss of attention span, and restlessness; can progress to stupor and coma

Question 8

right sided heart failure causes

Answer 8

-MCC by left-sided HF
-isolated right-sided heart failure- lung diseases (cor pulmonale)
-Pulmonary congestion minimal; engorgement of systemic and portal venous systems pronounced

Question 9

right sided HF

Answer 9

-changes in liver, spleen, and gi:
-hepatomegaly- caused by passive congestion; Grossly: congested red-brown pericentral zones, with relatively normal-colored tan periportal regions, produce characteristic “nutmeg liver”
-congestive splenomegaly
-effusions in pleural, pericardial, or peritoneal spaces (ascites)

-Hallmark - foot/ankle (pedal) and pretibial edema
-Renal congestion more marked with right-sided heart failure = more fluid retention and peripheral edema, azotemia
-Hypoxia of CNS can also produce deficits of mental function

-FATIGUE
-“Dependent” edema
-JVD‏
-ASCITES, PLEURAL EFFUSION
-Cyanosis
-Increased peripheral venous pressure (CVP)

Question 10

CHF labs

Answer 10

-Usually both right and left sided HF
-Serum BNP
-Echocardiography- measure EF, wall motion, valvular function, and possible mural thrombosis
-Tx - underlying cause (valvular defect or inadequate cardiac perfusion)
-salt restriction, diuretics, inotropes (increase myocardial contractility), adrenergic blockers or ACE inhibitors (reduce afterload)

Question 11

CHD, L to R

Answer 11

-Left-to-right shunts (all have “D”s in their names) increase pulmonary blood flow but NOT initially associated with cyanosis; may develop pulmonary HTN

-Atrial Septal Defect - Usually asymptomatic until adulthood; increase only right ventricular and pulmonary outflow volumes

-Ventricular septal defect - MC; only 30% are isolated; often with TETRALOGY of FALLOT
-50% close spontaneously
-large - early right ventricular hypertrophy and pulmonary hypertension

-Patent Ductus Arteriosus -
-harsh “machinery-like” murmur

Question 12

congenital HD R to L shunts

Answer 12

-hypoxemia and cyanosis- pulmonary circulation is bypassed and poorly oxygenated venous blood shunts directly into systemic arterial supply

-Right-to-left shunts: (all have “T”s in their names)
-tetralogy of Fallot (TOF)!!!

Question 13

Answer 13

boot shaped heart
-tetralogy of fallot

Question 14

ischemic heart disease

Answer 14

-90% of IHD patients have ATHEROSCLEROSIS

-Angina Pectoris: Stable, Unstable
-MI‏
-Chronic IHD- > CHF
-Sudden Cardiac Death (SCD)‏

-“Acute” Coronary Syndromes:
-UNSTABLE ANGINA
-Acute myocardial infarction
-SCD (Sudden Cardiac Death)

Question 15

coronary artery patho in ischemic heart disease

Answer 15

dont need severe stenosis for an MI

Question 16

angina pectoris

Answer 16

-Chest pain
-Paroxysmal (sudden)‏
-Recurrent
-15 sec - 15 min.
-Reduced perfusion, but NO infarction!

-THREE TYPES
-STABLE: relieved by rest or nitro
-PRINZMETAL: SPASM is main feature, responds to nitro
-UNSTABLE (crescendo, PRE-infarction, Q-wave angina): pattern of increasingly frequent, prolonged (>20 min), or severe angina, usually occurring at rest -> associated with plaque disruption and superimposed partial thrombosis

Question 17

MI

Answer 17

-Transmural (full thickness) vs. Subendocardial (inner 1/3)
-Most are TRANSMURAL, and MOST are caused by coronary artery occlusion

-In the 10% of transmural MIs NOT associated with atherosclerosis:
-Vasospasm
-Emboli
-UNexplained

Question 18

lab enzymes

Answer 18

-EKG
-CK-MB
-Troponin
-C-reactive protein predicts risk of AMI in angina patients

-coagulation necrosis
CHARACTERIZED BY THE LOSS OF THE NUCLEUS
-TEST QUESTION

-A WEEK LATER AFTER MI -> AND YOU LOOK AT TISSUE -> GRANULATION TISSUE- A BUNCH OF MACROPHAGES, COLLAGEN, & NEW VESSELS
-TEST QUESTION

-if CK-MB is low it doesnt rule out MI -> must do troponins

Question 19

complications of MI

Answer 19

-Wall motion abnormalities
-Arrhythmias (usually within first 24 hours)!!!!- MC
-Rupture (4-5 days) – cardiac tamponade
-Pericarditis
-Dressler syndrome (autoimmune pericarditis 2 weeks – 2 months post MI)
-RV infarction
-Infarct extension
-Mural thrombus
-Ventricular aneurysm
-Papillary muscle dysfunction (regurgitation)
-CHF

Question 20

hypertensive heart disease

Answer 20

usually causes ventricular hypertrophy, CHF may develop, myocardial dysfunction, or sudden death

Question 21

mitral annular calcification

Answer 21

-Degenerative calcific deposits in the mitral valve usually develop in the fibrous annulus
-Irregular, stony hard, occasionally ulcerated nodules at base of the leaflets
-Usually does not affect valvular function; however, rarely can lead to:
-* Regurgitation by interfering with physiologic contraction of the valve ring
-* Stenosis by impairing opening of the mitral leaflets
-* Arrhythmias and occasionally sudden death by penetration of calcium deposits deep enough to impinge on AV conduction system
-Increases with age, more common in women and individuals with mitral valve prolapse

Question 22

mitral valve prolapse (MVP) aka myxomatoid degeneration of the mitral valve

Answer 22

-One or both mitral valve leaflets are “floppy” and protrude into left atrium during systole
-2% to 3% of adults in US, more common in women; mostly incidental finding, but may lead to serious complications in small minority
-parachute valve
-Cause not really known
-Uncommonly, associated with heritable disorders of connective tissue including Marfan syndrome
-!!Ballooning (hooding) of mitral leaflets; affected leaflets often enlarged, redundant, thick, and rubbery; associated tendinous cords may be elongated, thinned, or even ruptured, and the annulus may be dilated

Question 23

MVP: clinical features

Answer 23

-Usually asymptomatic
-Mid-systolic “click” (caused by abrupt tension on redundant valve leaflets and chordae tendineae as valve tries to close)
-May or may not be associated regurgitant murmur
-Diagnosis confirmed by echocardiography
-Minority of patients - occasional chest pain, dyspnea
-3% may develop Infective endocarditis, mitral insufficiency, arrythmias, stroke or other systemic infarct (from embolism of leaflet thrombi), sudden death

Question 24

rheumatic heart disease- just know ab pain carditis and joint pain

Answer 24

-Acute rheumatic carditis in active RF may progress to chronic rheumatic heart disease (RHD)

-RHD (chronic)- deforming fibrotic valvular disease, esp. of the mitral valve

-Migratory polyarthritis (large joints)
-Pancarditis (myocarditis, pericarditis, or endocarditis) -> all three layers
-Subcutaneous nodules (typically on extensor surfaces of extremities)
-Erythema marginatum, irregular circinate skin rash
-Sydenham chorea, a neurologic disorder with involuntary rapid movements
-Aschoff bodies (with plump activated macrophages called Anitschkow cells (aka “caterpillar cells”)

Question 25

chronic rheumatic heart disease

Answer 25

-Clinical manifestations appear years/decades after initial episode of RF: cardiac murmurs, cardiac hypertrophy and dilation, and heart failure
-Mitral valve: leaflet thickening, commissural fusion and shortening, and thickening and fusion of tendinous cords; calcification and fibrous bridging across valvular commissures create “fish mouth” stenosis!!!!!!!!

-MC CAUSE OF MITRAL STENOSIS IS CHRONIC RHEUMATIC HEART DISEASE !!!

Question 26

infectious endocarditis

Answer 26

-Microbial infection of heart valves; leads to formation of vegetations (thrombotic debris and organisms) often with destruction of underlying cardiac tissues; Most infections bacterial
-Acute IE usually caused by infection of previously normal heart valve by a highly virulent organism (e.g., Staphylococcus aureus ) that rapidly produces destructive lesions; Staph. aureus usually in IE among IV drug users
-S. aureus commonly found on skin can infect either healthy or deformed valves; responsible for 20% to 30% of cases
Subacute IE usually caused by organisms with lower virulence (e.g., viridans streptococci, usu oral cavity) that cause insidious infections of deformed valves with less destruction

-Other bacterial causes: enterococci and the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella , and Kingella ), commensals in oral cavity
-Disposing factor for endocarditis: bacteremia (or fungemia) from other infection, dental or surgical procedure, contaminated needle in IV drug abusers

Question 27

infectious endocarditis

Answer 27

-Vegetations on heart valves: friable, bulky, potentially destructive lesions containing fibrin, inflammatory cells, and bacteria; may be single or multiple, may involve more than one valve; can sometimes erode into underlying myocardium and produce an abscess (ring abscess)
-Vegetations of subacute endocarditis associated with less valvular destruction (v. acute IE)

-Acute endocarditis: rapid onset of fever, chills, weakness, and lassitude; in older adults only manifestations may be nonspecific fatigue, weight loss, and flulike syndrome
-Sepsis, arrhythmias (suggesting invasion into underlying myocardium and conduction system), and systemic embolization associated with poor prognosis
-If not treated, acute IE generally fatal
-Treatment: long-term (6 weeks or more) antibiotic therapy and/or valve replacement; reduces mortality
-For infections involving low-virulence organisms (e.g., S. viridans ), cure rate is 98%

Question 28

nonbacterial thrombotic endocarditis (NBTE)

Answer 28

-AKA marantic endocarditis
-Deposition of small (1 to 5 mm) sterile thrombi on leaflets of cardiac valves; micro shows bland thrombi, loosely attached to underlying valve; vegetations are nondestructive, do not elicit any inflammatory reaction
-Often in debilitated patients with cancer or sepsis
-Usually occurs on previously normal valves

-Hypercoagulable states predisposition:
-chronic DIC
-increased estrogen
-underlying malignancy (esp. mucinous adenocarcinomas secondary to procoagulant effects of tumor-derived mucin factor- can cause migratory thrombophlebitis aka Trousseau syndrome)
-indwelling catheters

Question 29

vegetations

Answer 29

-INFECTIVE >5mm
-NON-Infective <5mm
-dont need to memorize^

-Vegetations:
-1) rheumatoid = small, at chordae tendinae junction
-2) infectious = big (>5 mm)
-3) NBTE = non-bacterial thrombotic endocarditis (<5 mm)
-4) lupus (Libman-Saks) = BOTH sides

Question 30

cardiomyopathies

Answer 30

-DILATED (DCM)
-Systolic dysfunction

-HYPERTROPHIC (HCM)
-Diastolic dysfunction

-RESTRICTIVE (RCM)
-Diastolic dysfunction

Question 31

dilated cardiomyopathy

Answer 31

-Adults
-Progressively declining LVEF
-LVEF ~ prognosis

-3 Main causes
-Myocarditis
-Alcohol
-Adriamycin- chemo agent
-cocksackies - viral ;.

-Heart changes:
-4 chamber dilatation
-irregular hypertrophy
-Interstitial Fibrosis

Question 32

hypertrophic cardiomyopathy

Answer 32

-Also called IHSS, (Idiopathic Hypertrophic Subaortic Stenosis)
-GENETIC defects involving:
-Beta-myosin heavy chain!!!!!
-Troponin T
-Alpha-tropomyosin
-Myosin binding protein C

-PATHOLOGY: Massive hypertrophy, Asymmetric septum, DISARRAY of myocytes, INTERSTITIAL fibrosis
-CLINICAL: ↓chamber volume, ↓SV, ↓ diastolic filling
-Sudden death in young athletes can occur

-Disproportionate ventricular septal hypertrophy involving basal and midventricular regions

Question 33

dilated vs hypertrophic cardiomyopathy

Answer 33

Question 34

restrictive cardiomyopathy

Answer 34

-↓ ventricular compliance
-May be caused by amyloid, radiation fibrosis, sarcoidosis, etc.
-Chiefly affects DIASTOLE
-NORMAL chamber size and wall thickness
-THREE similar diseases affecting predominantly the SUBENDOCARDIAL area:
-Endomyocardial Fibrosis (African children)
-Loeffler Endomyocarditis (eosinophilic leukemia)
-Endocardial Fibroelastosis (infants)

Question 35

dilated vs hypertrophic vs restrictive cardiomyopathies

Answer 35

Question 36

myocarditis

Answer 36

-INFLAMMATION of MYOCARDIUM

-Mainly microbial
-COXACKIE A & B, CMV, HIV
-Trypanosoma cruzi (Chagas dis.), 80%
-Trichinosis
-Toxoplasmosis
-Lyme disease (5%)
-Diphtheria

-IMMUNE: Post-viral, rheumatic, SLE, drug hypersensitivity->alpha-methyl dopa, sulfas

Question 37

myocarditis: viral

Answer 37

-MC cause in US: viral infections ; Coxsackie viruses A and B and other enteroviruses account for most cases
-Less common causes: cytomegalovirus, HIV, and influenza
-Depending on pathogen and host, viruses potentially cause myocardial injury either as a direct cytopathic effect, or by eliciting a destructive immune response
-Myocardial injury produces inflammatory cytokines which can also cause myocardial dysfunction out of proportion to degree of actual myocyte damage

Question 38

other causes of myocarditis

Answer 38

-Protozoan Trypanosoma cruzi (Chagas disease - endemic in some regions of South America
-Trichinosis (Trichinella spiralis): most common helminthic disease associated with myocarditis
-Parasitic diseases, including toxoplasmosis
-Lyme disease caused by spirochete Borrelia burgdorferi (5% of patients affected): self-limited conduction system disorder
-In diphtheritic myocarditis, myocardial injury results from diphtheria toxin release by Corynebacterium
-AIDS-associated myocarditis may reflect inflammation and myocyte damage without clear etiologic agent, or myocarditis attributable directly to HIV or an opportunistic pathogen
-Noninfectious causes of myocarditis: immunologically mediated (hypersensitivity myocarditis) or idiopathic conditions with distinctive morphology (giant cell myocarditis) probably of immunologic origin
-Some chemotherapy may occasionally lead to fatal lymphocytic myocarditis

Question 39

pericardium

Answer 39

-Normally 30-50 ml clear serous fluid
-Visceral (epicardium)
-Parietal (Fibrous pericardium)

-PERICARDIAL EFFUSIONS TAMPONADE
-Ruptured MI
-Traumatic perforation
-Infective endocarditis
-Ruptured aortic dissection

Question 40

pericarditis

Answer 40

-SEROUS: Rheum. Fever (RF), SLE, scleroderma, tumors, uremia
-FIBRINOUS: MI (Dressler), uremia, radiation, RF, SLE, s/p open heart surgery
-PURULENT: infective, bacterial
-HEMORRHAGIC: Malignancy, TB
-CASEOUS: TB
-CHRONIC: (ADHESIVE, CONSTRICTIVE)

-The “bread and butter” pericarditis is classically and most often described in uremia or pericardial infections. What is the exudate? Ans: Fibrin
“Bread and butter” pericarditis = fibrinous pericarditis.

Question 41

cardiac tumors

Answer 41

-Primary cardiac tumors uncommon, most benign
-Five most common: no malignant potential, account for almost 90% of all primary heart tumors: myxomas, fibromas, lipomas, papillary fibroelastomas, and rhabdomyomas.

-Myxomas: most common primary tumor of the adult heart (benign)
-About 90% in the atria, left/right ratio 4:1
-Major clinical manifestations due to valvular “ball-valve” obstruction, embolization, or syndrome of constitutional symptoms, such as fever and malaise (tumor may produce cytokine IL-6)
-Surgical removal usually curative

-Rhabdomyomas: most frequent primary tumor of the pediatric heart (benign)
-50% of cases associated with tuberous sclerosis, with mutations in the tuberous sclerosis complex TSC1 or TSC2 tumor suppressor genes

-Primary malignant cardiac tumors: very rare, usually an angiosarcoma

Question 42

metastatic tumor to heart

Answer 42

-Occur in approximately 5% of patients dying of cancer
-Most frequent are lung and breast carcinomas, melanomas, leukemias, and lymphomas
-Clinical symptoms: symptomatic pericardial effusions or a mass-effect restricting cardiac filling
-Lung carcinoma or malignant lymphoma can infiltrate mediastinum, causing encasement, compression, or invasion of the superior vena cava with resultant obstruction to blood coming from head and upper extremities (superior vena cava syndrome)
-Renal cell carcinoma often invades the renal vein; can grow as a continuous column of tumor up the inferior vena cava lumen and into the right atrium, blocking venous return to the heart