congestive heart failure
progressive
when heart cant match metabolic demands of tiss.
result from systolic or dyastolic dysfunction
Left HF causes
Ischemic heart disease
systemic hypertension
mitral/aortic vlave disease
primary myocardial disease
-> results mostly in rigth heart failure
deficient cardiac function
Pressure overload state
Hypertension
Aortic stenosis or coartaction
Volume overload states
Aortic insufficiency
Anemia (decreased oxygen carrying capacity)
Thyreotoxicosis (increased tissue demands)
Decreased myocardial contractility
MI
Cardiomyopathy
Disorders of cardiac conduction
LSHF symptoms
dyspnea
cough (bc of fluid transudation)
orthopnea (dyspnea in supine position)
paroxysmal nocturnal dypnea (dramatic breathlessness)
hypocic encephalopathy
hypoxic injury of bowl
decreased renal perfusion
RSHF causes
parenchimal lung disease
1.pul. hypertension
recurrent pul. thromboembolism
pul. vasoconstriciton (schlaf apnö)
=> pressure, volume overload
low myocardial contractiliy
RSHF symptoms
fatigue
dependent edema
cyanosis
anorexia
liver enlargement
etiopathogenensis of CHF
multifactorial, 90% the cause is unknown
arises from faulty embryogenesis during gestational weeks
3 through 8
Enviromental exposures
viruses (congenital rubella infection)
teratogens:talidomid,litium-> depression therapy
maternal diabetes, fetal alcohol sy
Genetic factors
familial forms of CHD
chromosomal abnormalities (Down, Turner)
3 groups based on hemodynamic and clinical consequenes
Malformation R-L shunt (early cyanosis)
MAlformation L-R shunt (late cyanosis)
malformation with obstructive lesion -> aortic coartation, aortic and pul. stenosis
Ventricular septal defects
MOST COMMON ANOMALY
opening between ventricles (90% membranous, 10% muscular)
50% spontaneous closure
atrial septal defects
most common anomalie in adults
asymptomatic
patent ductus arteriousus
blood flows between aorta and pulmonary aorta
didnt close in fetal development
Tetralogy of Fallot (TOF)
Cyanotic R-L shunt
severe symptoms
VSD
boot shaped heart
transposition of great arteries
functually seperated systemic and pul. circulation
=> emergency surgery after birth
Aortic coartation
constriction of aorta
r/L v hypertophy
infantile (hypertophy of aortic arch)
adult (folding of aorta)
50% + bicuspid aortic valve
ischemic heart disease results from
Reduced coronary blood flow
coronary atherosclerosis (>90%)
thrombosis
coronary vasospam emotional stages
arteritis
Diminished oxygenation or oxygen-carrying capacity
anemia,COPD, CO poisining
Diminished blood volume
hypotension, shock
Increased myocardialdemand
hypertrophy, tachycardia, hyperthyreosis , fever
clinical presentation of ischemic heart disease
Angina pectoris
Myocardial infarction
Chronic IHD with CHF
Sudden cardiac death
angina pectoris releaving drug
nirtoglycerin
necrosis of myocytes from abolute ischemia
major underlying cause = arterosclerosis
3 forms of MI
transmural
subendocardial
microscopic
transmural infarction
caused by epicardial vessel occlusion, due to acute plaque
change with thrombosis
within the distribution of a single coronary artery
involve full thickness of the ventriclular wall
ST-segment elevated MIs
MOST COMMON
intraplaque hemorrhage or plaque rupture
superimposed thrombosis and coronary occlusion
myocardial ischemia and dysfunstion
severe ischemia leads to ATP depletion and loss of contractile function within 60 sec
complete deprivation of blood flow for 20 to 30 min leads to irreversible injury
cinical symptoms of MI >80% pts ->
ECG abnormalities, cardiomyocyte-specific proteins without
subendocardial infarctions
MIs limited to the inner third of the myocardium
non-ST-segment elevated MIs
systemically diminished supply - hypoperfusion or hypoxia
lysis of a thrombotic occlusion before full- thickness infarction
chronic atherosclerotic disease in the setting of increased myocardial demand - tachycardia
Microscopic infarcts
Small vessels occlusion
Non-diagnostic ECG
vasculitis
embolization (valve vegetation or mural thrombi)
vessel spasm (catecholamines)
extreme emotional stress
tumors (pheochromocytoma)
cocaine
leading cause of sudden cardia death
coronary artery disease
conduction system scaring
acute ischemic injury
electrical irritability of myocardium distant from the conduction system
valvular heart disease
➢ congenital(bicuspidaorticvalve)
➢ acquired
➢ degeneration
➢ inflammatory processes (postinflammatory scaring)
➢ immune diseases
➢ changes secondary to myocardial disease
valvular heart disease rusult in
stenosis
insufficiency
degenerative valve disease
changes that affect the integrity of valvular extracellular matrix
➢ calcification (cuspal or annular)
➢ alterations in the ECM (myxomatous
degeneration)
➢ changes in the production of MMP or their inhibitors
➢ aging – repetitive mechanical stresses
most common cause of aortic stenosi s
calcification
calcific aortic stenosis
age-related lesions Asymptomatic / symptomatic / congenital bicuspid aortic valve
Cardiac output is maintained
Concentric left ventricular hypertrophy
High left ventricular pressure
Exhaustion of compensatory mechanisms:
Syncope, angina, CHF
Surgical intervention
myxomatous matrale valve
most common disease in women
Myxomatous degeneration of the mitral valve
One or both mitral leaflets prolapse into the left atrium during systole
0,5-2,4% adults, women 7-fold more
Primary
➢ defect of conective tissue synthesis, Marfan sy, systemic structural abnormalities in connective tissue..
Secondary
➢ injury of the valve myofibroblasts (chronic hemodynamic forces)
rheumatic valvular disease
rheumatic fever
Acute, immunologically mediated multisystem inflammatory disease
Atributed to host anti-streptococcal antibodies and/or T cells that cross-reacts with cardiac antigenes
Occuring in children 5-15 yrs after group A streptococcal infection (pharyngitis)
Rheumatic heart disease
progressive valve damage with fibrosis – most important clinical
feature (mitral valve 70% cases)
jones major criteria
➢ migratory polyarthritis of large joints
➢ carditis
➢ subcutaneous nodules
➢ erythema marginatum
➢ Sydenham chorea („St. Vitus dance”)
jones minor criteria
➢ fever
➢ arthralgias
➢ elevated CRP
➢ ECG changes
Infective endocarditis
microbial colonization or invasion of valves, leading to friable, infected vegetations, often with valve damage and destruction of the underlying cardiac tissue
Risc factors for IE
➢ Host factors
➢ neutropenia, immunodeficiency
➢ diabetes
➢ malignancy
➢ alcohol
➢ chronic infections (gut, oral cavity, urinary tract)
➢ trivial injuries
➢ cardiac abnormalities
➢ Congenital heart diseases
➢ Prosthetic heart valves
➢ IV drug abuse
➢ Dental or surgical procedure antibiotic prophylaxis
Acute IE
rapid onset
fever, rigor , malaise, wakness
staph aureus !!!
embolic complications
splenomegaly
high mortality
Subacute IE
no normal valve
Strep Viridans!!!!
small vegettaions lower mortality
complication s of IE
➢ Valvular and myocardial damage ➢ ring abscess
➢ calcification ➢ mycotic aneurisms ➢ arrhythmias
➢ Septicaemia, embolic complication
➢ Renal injury (septic infarcts, glomerulonephritis) ➢ Vasculitis
Nonbacterial thrombotic endocarditis
➢ Marantic endocarditis
➢ Underlying malignancy (mucinous adenocarcinoma)
➢ Prolonged debilitating illness ➢ Renal feilure
➢ Chronic sepsis
➢ Underlying hypercoagulable states ➢ DIC
➢ Hyperestrogenic states
Carcinoid heart disease
3 forms of cardiac myopathy
Dilated
hypertophic
restrictes
Dilated cardiomyopathy
90% of all myopathys
gradual 4 chambers hypertophy and dilatation
systolic dysfunction with hypocontraction
progessive CHF
etiology of dilated cardiomyopathy
Idiopathic
myocarditis
toxic (alcohol)
peripartum
iron overload
genetic
Arrhythmogenic rigth ventricular cardiomyopathy
➢ AD disorder characterized by predominantly right- sided failure and arrhythmia
➢ consider in young male with arrhythmia
➢ Mutation:
➢ genes encoding desmosomal junctional proteins
➢ Protein that interact with the desmosomes
➢ Death: secondary to progressive CHF or sudden death (fatal arrhythmia)
hypertrophic cardiomyopathy
myocardial hypertrophy
dyastolic dysfunction (defective diastolic felling)
ventricular outflow obstruction (1/3) due to systolic
anterior motion of the mitral valve
AD mutation of sarcomeric proteins, with variable expression
➢ Β-myosin heavy chain mutations
restrictive cardiomyopathy
➢ Primary disease in ventricular compliance
➢ Restriction of ventricular filling leading to reduced cardiac output (relaxation also problem)
➢ Idiopathic
➢ Associated with systemic diseases
➢ radiation fibrosis, amyloidosis, sarkoidosis, hemochromatosis...
endomyocardial fibrosis
disease of children and teens
africa, tropical
nutritional deficiency
helmintic infection
inflammatory
caused by infections/immune reactions
etiology of myocarditis
Infections
➢ Coxsackieviruses A and B, other enteroviruses, Influenza virus, HIV, CMV
➢ Protozoan Trypanosoma cruzi - Chagas disease (South America)
➢ Spirochete Borrelia burgdorferi – Lyma disease ➢ Trichinela spiralis (trichinosis) ➢ Toxoplasma gondii (cats) ➢ Corynebacterium diptheriae
➢ Noninfectiousvcauses
➢ Systemic disease of immune origin (SLE, poymyositis) ➢ drug hypersensitivity reaction
➢ Unknown cause: sarcoidosis, giant cell myocarditis
serous pericardial effusion
CHF hypoalbunminemia
serosanguineous effusion
trauma
malignancy
ruptures MI
aortic dissection
chylous effusion
mediastinal lymphatic obsruction
Pericarditis
➢ acute primary pericarditis
viral infection
bacterial viral fungal
➢ secondary
➢ disorders involving the heart or mediastinal structures
➢ systemic abnormalities
➢ chronic pericarditis
➢ delicate adhesions
➢ fibrotic scars that obliterate the pericardial space
➢ constrictive pericarditis
etiology of secondary pericarditis
➢ MI
➢ cardiac surgery
➢ Trauma
➢ Radiation
➢ Tumors
➢ Uremia
➢ autoimmune diseases
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