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CARDIAC PATHOLOGY, ISCHEMIC HEART DISEASE (IHD), ENDOCARDITIS, CARDIAC…

- - - - Chest pain that arises with exertion or emotional stress <20 minutes Relieved by rest or nitroglycerin
      - Atherosclerosis of coronary arteries with > 70% stenosis Reversible injury to myocytes (no necrosis)
      - EKG shows ST-segment depression
    - - Chest pain that occurs at rest Relieved by nitroglycerin
        & High risk of progression to myocardial infarction
      - Rupture of an atherosclerotic plaque with thrombosis and
        incomplete occlusion of a coronary artery, reversible injury to myocytes (no necrosis)
      - EKG shows ST-segment depression-subendocardial ischemia
    - - Coronary artery vasospasm
      - EKG shows ST-segment elevation- transmural ischemia
      - Relieved by nitroglycerin or calcium channel blockers
  - - - Territory
        
        Occlusion of right coronary artery (RCA)
        
        Occlusion of left circumflex artery leads to infarction of lateral wall of the LV.
        
        Occlusion of left anterior descending artery (LAD)
      - Symptoms
        
        Severe, crushing chest pain > 20 minutes, radiates to the left arm or jaw, diaphoresis, and dyspnea; not relieved by nitroglycerin
      - Studies
        
        EKG
        
        1) ST-segment depression (subendocardial infarction)
        
        2) ST-segment elevation (transmural necrosis)
        
        Laboratory
        
        Troponin I gold standard, Levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days.
        
        CK-MB useful for detecting reinfarction days after an initial MI; levels rise 4-6 hours after infarction, peak at 24 hours, and return to normal by 72 hours.
      - Tx
        
        Supplemental O2 - minimizes ischemia (DONT OFER IF SO2>92% DUE TO RISK OF FREE RADICALS INJURY)
        
        Nitrates - Vasodilate veins and coronary arteries
        
        Aspirin and/or heparin - limits thrombosis
        
        β- blocker - slows heart rate, decreasing O2 demand and risk for arrhythmia
        
        ACE inhibitor - decreases LV dilation
        
        Fibrinolysis or angioplasty - opens blocked vessel
      - Cronology
        
        <4 horas no change, can lead to Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
        
        4-24 hrs Coagulative necrosis, can lead to Arrhythmia
        
        1-3 días, neutrophils infiltration, can leadto fibrinous pericarditis (chest pain with rub)
        
        4-7 días macrophages infiltration, can lead to rupture of ventricular free wall (tamponade), interventricular septum (shunt) or papillary muscle (mitral insufficiency)
        
        1-3 weeks, granulation, plump fibroblast, collagen and blood vesels.
        
        Months fibrosis, can lead to aneurysm, mural thrombus or Dressler syndrome
      - Mechanical Complications
        
        3-5 days
        
        Papillary muscle rupture→severe pulmonary edema, respiratory distress /// New early systolic murmur (acute MR) /// Hypotension/cardiogenic shock
        
        Interventricular septum rupture → chest pain // new holosystolic murmur // Hypotension- cardiogenic shock // Step up in O2 level from Right Atrium to Right Ventricle
        
        5 days-2 weeks
        
        Free wall rupture → Chest pain // Distant heart sounds // Shock, rapid progression to cardiac arrest
        
        Up to several months
        
        Left ventricular aneurysm → Heart failure // Angina, ventricular arrhytmias
  - - - Causes
        
        Common
        
        Acute ischemia;
        90% of patients have
        preexisting severe
        atherosclerosis.
        
        Less common
        
        Mitral valve prolapse
        Cardiomyopathy
        Cocaine abuse
  - - - Progresses to congestive heart failure (CHF)
- - - - Strep bovis
        
        Cause endocarditis in patients with colorrectal carcinoma
      - HACEK
        organism
        
        Haemophilus, Actinobacillus,
        Cardiobacterium, Eikenella, Kingella
        
        Associated with endocarditis with negative blood cultures
      - S. epidermidis
        
        Key organism to cause endocarditis of prosthetic valves
      - Libman-Sacks
        Endocarditis
        
        Sterile vegetations on both sides of mitral valve
        →Mitral regurgitation
        
        Associated with Lupus
      - S. Aureus
        
        Most common cause of endocarditis in IV drug users
        
        Acute endocarditis →Large vegetations destroy valve
        
        High Virulence can infect normal valves (tricuspid)
      - Nonbacterial
        Thrombotic
        Endocarditis
        
        Patients with Hypercoagulable state or with Adenocarcinoma
        
        Sterile vegetation on bicuspid valves →mitral regurgitation
      - S. viridans
        
        Most common cause of endocarditis →Dental procedure
        
        Subacute endocarditis→Small vegetations
        
        Low virulence don't destroy valve
      - Coxiella
        Burnetti
        
        Most common cause of culture negative endocarditis →Q fever
        
        Sterile vegetations on both sides of mitral valve
        →mitral regurgitation
- - - - Most common cardiac tumor in children
      - Usually seen in ventricle
      - Associated with tuberous sclerosis
  - - - Affects pericardium → pericardial effusion
        
        From:
        
        Breast
        
        Lung carcinoma
        
        Melanoma
        
        Lymphoma
  - - - Most common primary cardiac tumor in adults
      - Pedunculated mass in the left atrium →obstruction of the mitral valve → syncope
- - - - Decreased forward perfusion
        and pulmonary congestion
        
        Leads to pulmonary edema
        
        Dyspnea
        Paroxysmal nocturnal dyspnea
        Orthopnea
        Crackles
        
        Small, congested capillaries burst>>> leading to intraalveolar hemorrhage marked by hemosiderin-laden macrophages
        
        Decreased flow to kidneys leads to
        activation of renin-angiotensin system
        Fluid retention exacerbates CHF
      - Etiology
        
        -Ischemia
        -Hypertension
        -Dilated cardiomyopathy
        -Myocardial infarction
        -Restrictive cardiomyopathy.
      - Tx ACE inhibitor
    - - Cause Congestion
        
        -Jugular venous distension
        -Painful hepatosplenomegaly nutmeg liver →cardiac cirrhosis
        -Pitting edema (↑↑hydrostatic pressure)
      - Etiology
        
        -Left-sided heart failure
        -Left-right shunt
        -Chronic lung disease (cor pulmonale)
- - - - Complications
        
        Increased flow through the pulmonary circulation results in hypertrophy of pulmonary vessels and pulmonary hypertension
        
        Increased pulmonary resistance → reversal of shunt →late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy + polycythemia+ clubbing
      - Relatively asymptomatic at birth / can eventually reverse
      - Types
        
        VSD: Ventricular Septal Defect
        
        MOST COMMON CONGENITAL HEART DEFECT
        Associated with alcohol fetal syndrome
        
        Size determines
        age at presentation
        
        Small asymptomatic and close spontaneously
        
        Large need surgery // can lead to Eisenmenger syndrome.
        
        ASD: Atrial Septal Defect
        
        Most common type is ostium secundum
        -90% of cases Associated with Down Syndrome
        
        Split S2
        on auscultation
        
        Increased blood in right heart delays
        closure of pulmonary valve
        
        Paradoxical emboli are an important complication.
        
        PDA: Patent Ductus Arteriosus
        
        Associated with Congenital Rubella Shunting
        between the aorta and the pulmonary artery
        
        Asymptomatic at birth
        Continuous 'machine-like' murmur
        
        Tx: indomethacin to ↓↓PGE → PDA closure
        
        Can develope Eisenmenger syndrome, resulting in lower extremity cyanosis
        
        Normally shunts blood from the
        pulmonary artery to the aorta, bypassing the lungs
    - - Defects with right-to-left shunting usually
        present as cyanosis shortly after birth
      - Types
        
        TRANSPOSITION OF
        THE GREAT VESSELS
        
        Characterized by:
        
        Pulmonary artery arising from the left ventricle
        & Aorta arising from the right ventricle
        
        Associated with maternal diabetes
        
        Early cyanosis: Pulmonary & systemic do not mix
        
        Creation of shunt (allowing blood to mix) after
        birth is required for survival.
        
        PGE can be administered to maintain a PDA
        until definitive surgical repair is performed
        
        Results in hypertrophy of the right ventricle
        and atrophy of the left ventricle
        
        TRUNCUS
        ARTERIOSUS
        
        Characterized by:
        
        Single large vessel arising from both
        ventricles →Truncus fails to divide
        
        Associated with ASD
        
        Early Cyanosis
        
        TETRALOGY OF FALLOT
        
        Boot-shaped heart on x-ray
        
        Characterized by:
        
        1) Stenosis of the right ventricular outflow tract
        2) Right ventricular hypertrophy
        3) VSD
        4) Aorta that overrides the VSD
        
        Early cyanosis
        
        Patients squat (increased arterial resistance decreases shunting and allows more blood to reach the lungs)
        
        Degree of stenosis determines
        the extent of shunting and cyanosis
        
        TRICUSPID
        ATRESIA
        
        Characterized by:
        
        Valve orifice fails to develop; right ventricle is hypoplastic
        
        Associated with ASD
        
        Early Cyanosis
    - - Adult form
        (discovered in adulthood)
        
        Associations:
        
        NOT associated with PDA
        
        Coarctation lies after
        (distal to) the aortic arch
        
        Associated with Bicuspid Aortic Valve
        
        Hypertension in the upper extremities and hypotension with weak
        pulses in the lower extremities
        
        Collateral circulation across the intercostal arteries; engorged arteries - 'notching' of ribs on x-ray
      - Infantile form
        
        Associated with PDA
        
        PDA
        
        Coarctation lies after (distal to) the aortic
        arch, but before (proximal to) the PDA
        
        Turner syndrome
        
        Lower extremity cyanosis in infants-often at birth
- - - - Systemic complication of group A strep which presents 2-3 weeks after streptococcal pharyngitis //Resolves but can progress to chronic
      - Dx evidence of group A strep infection (elevated ASO or anti-DNAse B titer) + major (JONES) or minor criteria
        
        Mayor
        
        Joint migratory large polyarthritis
        O (pancarditis)
        -Endocarditis - Mitral valve -Small vegetations-regurgitation
        -Myocarditis - Aschoff bodies (focal area of chronic inflammation) + Anitschkow cells (reactive histiocytes with slender, wavy nucleus) + fibrinoid material and giant cells -most common cause of death
        Pericarditis - friction rub + chest pain
        Subcutaneous Nodules
        Erythema marginatum - nonpruritic rash with erythematous border on trunk and limbs
        Sydenham chorea
        
        Minor
        
        Fever and elevated ESR (non-specific)
      - Bacterial M protein mimics human protein
        and autoantibodies are generated
    - - Valve scarring - chronic rheumatic fever
        → Stenosis "Fish-mouth appearance"
      - Presentation:
        
        Mitral valve is most commonly affected - Fish Mouth
        
        Aortic valve is no. 2 - fusion of commissures
        
        Other valves rarely affected
      - Complication: Infective endocarditis
    - - Narrowing of the aortic valve orifice
        
        Etiology
        
        Normal wear and tear of valve
        
        Bicuspid aortic valve (speeds up wear and tear)
        
        Chronic rheumatic fever →Aortic valve fusion of commissures + mitral stenosis (that differentiate from other etiologies)
      - Presentation
        
        ↑ 60 years
        
        Crescendo-decrescendo murmur with systolic ejection click (click is when the valve opens)
      - Complications
        
        Concentric left ventricular hypertrophy →cardiac failure
        
        Angina with & syncope when exercise (decreased perfusion of heart and brain)
        
        Microangiopathic hemolytic anemia →schistocytes
      - Tx: Valve replacement
    - - Backflow of blood from the aorta into
        the left ventricle during diastole
        
        Etiology
        
        No. 1 Aortic root dilation due to
        syphilitic aneurysm/aortic dissection
        
        No. 2 Valve damage due to infectious endocarditis
      - Presentation:
        
        Increased pulse pressure (water-hammer pulse) due to stroke volume
        
        Diastolic pressure is low due to regurgitation
        
        LV dilation and eccentric hypertrophy due to volume overload
        **Pulse Pressure = Systolic Blood Pressure minus Diastolic Blood Pressure
      - Tx: Valve replacement once LV dysfunction develops
    - - Ballooning of mitral valve into
        left atrium during systole
        
        Etiology
        
        Accumulation of ground substance → Myxoid degeneration of the valve (floppy valve)
      - Presentation:
        
        Mostly asymptomatic
        
        Mid-systolic click followed by regurgitation murmur
        
        Murmur is softer with squatting (increased systemic resistance decreases left ventricular emptying)
      - Complications:
        
        Rare but infective endocarditis
        
        Arrhythmia
        
        Severe mitral regurgitation
      - Tx: Valve replacement
    - - Reflux of blood from the left ventricle into
        the left atrium during systole
        
        Etiology
        
        Complication of mitral prolapse
        
        LV dilation
        
        Infective endocarditis
        
        Acute rheumatic fever vegetation prevent smooth closing
        
        Papillary muscle rupture after MI
      - Presentation:
        
        Holosystolic "blowing" murmur; lower when squatting (increased systemic resistance decreases LV emptying) and expiration (increases blood return to LV)
        
        Volume overload and left sided failure
    - - Narrowing of the
        mitral valve orifice
        
        Etiology
        
        Chronic rheumatic disease
      - Presentation:
        
        Opening snap followed by diastolic rumble
        
        Volume Overload with dilation of left atrium:
        *Pulmonary congestion with edema and alveolar hemorrhage
        *Pulmonary HTN and eventual right sided heart failure
        *A-fib with mural thrombus
- - - - Massive hypertrophy of the left ventricle
        
        Etiology
        
        Autosomal dominant mutations in sarcomere proteins
      - FINDINGS
        
        Diastolic dysfunction (heart doesn't fill well)
        
        Sudden death in young athletes due to ventricular arrhythmias
        
        Syncope with exercise
        
        BIOPSY Myofiber hypertrophy with disarray
    - - Decreased compliance of the ventricular
        endo-myocardium that restricts filling during diastole
        
        Etiology
        
        Amyloidosis
        
        Sarcoidosis
        
        Hemochromatosis
        
        Endocardial fibroelastosis (in kids) → there's fibrosis and elastosis in endocardium
        
        Loeffler syndrome → eosinophilic inflammation of endocardium and myocardium
      - Findings:
        
        Presents as congestive heart failure
        
        EKG with low voltage and Diminished QRS amplitudes
    - - Dilation of all four chambers of the heart
        
        Most common form of cardiomyopathy
        
        ETIOLOGY:
        
        Idiopathic in most cases
        
        Mutation autosomal dominant
        
        Myocarditis - coxcakie virus most common pathogen
        Acute Infection → Death
        Chronic → Dilated cardiomyopathy
        
        EtOH abuse (HY)
        
        Drugs - doxorubicin, cocaine
        
        Pregnancy (HY) - in 3rd trimester or soon after birth
      - PHYSIOPATOLOGY
        Systolic dysfunction-ventricles cannot pump→ biventricular CHF
      - Complications: mitral & tricuspid regurgitation + Arrhythmia
      - Tx: Transplant
- - - - Occlusion of right coronary artery (RCA)
      - Occlusion of left circumflex artery leads to infarction of lateral wall of the LV.
      - Occlusion of left anterior descending artery (LAD)
    - - Severe, crushing chest pain > 20 minutes, radiates to the left arm or jaw, diaphoresis, and dyspnea; not relieved by nitroglycerin
    - - EKG
        
        1) ST-segment depression (subendocardial infarction)
        
        2) ST-segment elevation (transmural necrosis)
      - Laboratory
        
        Troponin I gold standard, Levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days.
        
        CK-MB useful for detecting reinfarction days after an initial MI; levels rise 4-6 hours after infarction, peak at 24 hours, and return to normal by 72 hours.
    - - Supplemental O2 - minimizes ischemia (DONT OFER IF SO2>92% DUE TO RISK OF FREE RADICALS INJURY)
      - Nitrates - Vasodilate veins and coronary arteries
      - Aspirin and/or heparin - limits thrombosis
      - β- blocker - slows heart rate, decreasing O2 demand and risk for arrhythmia
      - ACE inhibitor - decreases LV dilation
      - Fibrinolysis or angioplasty - opens blocked vessel
    - - <4 horas no change, can lead to Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
      - 4-24 hrs Coagulative necrosis, can lead to Arrhythmia
      - 1-3 días, neutrophils infiltration, can leadto fibrinous pericarditis (chest pain with rub)
      - 4-7 días macrophages infiltration, can lead to rupture of ventricular free wall (tamponade), interventricular septum (shunt) or papillary muscle (mitral insufficiency)
      - 1-3 weeks, granulation, plump fibroblast, collagen and blood vesels.
      - Months fibrosis, can lead to aneurysm, mural thrombus or Dressler syndrome
    - - 3-5 days
        
        Papillary muscle rupture→severe pulmonary edema, respiratory distress /// New early systolic murmur (acute MR) /// Hypotension/cardiogenic shock
        
        Interventricular septum rupture → chest pain // new holosystolic murmur // Hypotension- cardiogenic shock // Step up in O2 level from Right Atrium to Right Ventricle
      - 5 days-2 weeks
        
        Free wall rupture → Chest pain // Distant heart sounds // Shock, rapid progression to cardiac arrest
      - Up to several months
        
        Left ventricular aneurysm → Heart failure // Angina, ventricular arrhytmias
- - - - Common
        
        Acute ischemia;
        90% of patients have
        preexisting severe
        atherosclerosis.
      - Less common
        
        Mitral valve prolapse
        Cardiomyopathy
        Cocaine abuse
- - - - Cause endocarditis in patients with colorrectal carcinoma
    - - Haemophilus, Actinobacillus,
        Cardiobacterium, Eikenella, Kingella
        
        Associated with endocarditis with negative blood cultures
    - - Key organism to cause endocarditis of prosthetic valves
    - - Sterile vegetations on both sides of mitral valve
        →Mitral regurgitation
        
        Associated with Lupus
    - - Most common cause of
        endocarditis in IV drug users
        
        Acute endocarditis →Large vegetations destroy valve
        
        High Virulence can infect normal valves (tricuspid)
    - - Patients with Hypercoagulable
        state or with Adenocarcinoma
        
        Sterile vegetation on bicuspid valves →mitral regurgitation
    - - Most common cause
        of endocarditis →Dental procedure
        
        Subacute endocarditis→Small vegetations
        
        Low virulence don't destroy valve
    - - Most common cause of culture
        negative endocarditis →Q fever
        
        Sterile vegetations on both sides of mitral valve
        →mitral regurgitation
- - - - From:
        
        Breast
        
        Lung carcinoma
        
        Melanoma
        
        Lymphoma
- - - - -Left-sided heart failure
        -Left-right shunt
        -Chronic lung disease (cor pulmonale)
    - - -Jugular venous distension
        -Painful hepatosplenomegaly nutmeg liver →cardiac cirrhosis
        -Pitting edema (↑↑hydrostatic pressure)
  - - - -Ischemia
        -Hypertension
        -Dilated cardiomyopathy
        -Myocardial infarction
        -Restrictive cardiomyopathy.
    - - Decreased flow to kidneys leads to
        activation of renin-angiotensin system
        Fluid retention exacerbates CHF
      - Leads to pulmonary edema
        
        Small, congested capillaries burst>>> leading to intraalveolar hemorrhage marked by hemosiderin-laden macrophages
        
        Dyspnea
        Paroxysmal nocturnal dyspnea
        Orthopnea
        Crackles
- - - - Etiology
        
        Autosomal dominant mutations in sarcomere proteins
    - - Diastolic dysfunction (heart doesn't fill well)
        
        Sudden death in young athletes due to ventricular arrhythmias
        
        Syncope with exercise
      - BIOPSY Myofiber hypertrophy with disarray
  - - - Etiology
        
        Amyloidosis
        
        Sarcoidosis
        
        Hemochromatosis
        
        Endocardial fibroelastosis (in kids) → there's fibrosis and elastosis in endocardium
        
        Loeffler syndrome → eosinophilic inflammation of endocardium and myocardium
  - - - ETIOLOGY:
        
        Idiopathic in most cases
        
        Mutation autosomal dominant
        
        Myocarditis - coxcakie virus most common pathogen
        Acute Infection → Death
        Chronic → Dilated cardiomyopathy
        
        EtOH abuse (HY)
        
        Drugs - doxorubicin, cocaine
        
        Pregnancy (HY) - in 3rd trimester or soon after birth