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CAD, Cardiomyopathies, Valvular Disease, PE, CHD (Pericardial Disorders…

- - - - Pathophysiology
        
        Occurs with rapidly formed effusions --> increased pressure in pericardium throughout cardiac cycle --> RV unable to expand into maximally stretched pericardium --> left-ward bulging of interventricular septum --> decreased LVEDV --> decreased CO & SBP during inspiration
        
        S/S
        
        Chest pain, dyspnea, near-syncope
        
        Generally more comfortable sitting forward
        
        Recent Sx related to causes of tamponade
        
        Physical Exam
        
        Beck's Triad
        
        Elevated JVP
        
        Hypotension
        
        Diminished heart sounds (often w/ narrow pulse pressure)
        
        Tachycardia, other HF S/S
        
        Pulsus paradoxus
        
        Decreased/absent cardiac impulse (ECG)
        
        Often friction rub
- - - - Chronic Ischemic Heart Disease
        
        Chronic stable angina
        
        Variant & vasospastic angina
        
        Silent myocardial ischemia
  - - - Pathophysiology
        Arteriosclerosis = Hardening of arteries
        Atherosclerosis = Type of arteriosclerosis, is narrowing of arteries
        1. Damage to arterial endothelial cells (HTN, smoking, ++BG, hypercholesterolemia)
        
        2. Formation of Foam Cells
        
        LDL & monocytes move between endothelial cells into tunica intima (via diapedesis)
        
        Monocytes release free radicals, which oxidize LDL
        
        Monocytes engulf LDL --> Foam Cells
        
        Positive feedback system
        
        3. Formation of plaque
        
        Plaque grows larger
        
        T lymphocytes, platelets, & smooth muscles cells join foam cells --> plaque grows
        
        Platelets activate & form blood clot over plaque
        
        Overtime Ca2+ salts added --> hardened plaque with lipid core
        
        Collateral circulation forms to alleviate d/t hindered blood flow from partial blockage of artery
        
        4. Thrombus/Embolis
        
        Eventually may block vessel (thrombus)
        
        Can break off and occlude elsewhere (embolis)
        
        S/S
        
        Depends on location
        
        Heart: Chest pain/pressure, fatigue upon exertion, angina S/S
        
        Brain: Stroke-like symptoms (AKA Transient ischemic attack [TIA])
        
        Arms & legs: Leg/Arm pain when utilized
        
        Kidneys: HTN, renal failure
        
        Weak/absent pulse below narrowed area of artery
        
        Decreased BP in affected limb
        
        Bruits over arteries
        
        Tx
        
        Medications
        
        Cholesterol medications
        
        Antiplatelets
        
        Beta-blockers
        
        ACE Inhibitors
        
        Ca2+ channel blockers
        
        Diuretics
        
        Others
        
        Sx
        
        Angioplasty w/stent
        
        Endarterectomy
        
        Fibrinolytics
        
        Bypass
  - - - Dx Assessments
        
        Assessment
        
        ECG
        
        ST elevation
        
        T wave changes
        
        STEMI vs NSTEMI
        
        Serum tests (biomarkers for myocardial necrosis)
        
        Cardiac-specific troponin (TnI)
        
        0.7 ng/ml or higher = possible MI
        
        Troponin T (TnT)
        
        Primary biomarker (high specificity for myocardial tissue)
        
        0.07 ng/ml or higher = possible MI
        
        Creatinine kinase (CK-MB)
        
        TnI & TnT rise <3h after MI onset, and remain elevated for 7-10 days (useful for late MI Dx)
        
        Stress test w/ECG
        
        Echocardiography
        
        Angiogram
        
        S/S
        
        Sudden onset
        
        Severe & crushing pain, often substernal, radiating to left arm, neck, or jaw
        
        GI complaints (N&V)
        
        Complaints of fatigue & weakness
        
        Tachycardia, anxiety, restlessness, feelings of impending doom
        
        Pale, cool, moist skin
        
        Silent Atypical
        
        Asymptomatic, no evidence of CAD
        
        Persons who had a myocardial infarct and continue to have episodes of silent ischemia
        
        People with angina can have silent ischemia too
        
        Elderly, women, DM, HF
        
        Tx
        MONA TABS
        - Morphine - O2 - Nitrates (Nitroglycerin) - Aspirin - Thrombolytics - Anticoagulants - Beta-blocker - Sedatives
        
        Evidence of infarction --> immediate reperfusion Tx with fibrinolytic agent (<30min) or percutaneous coronary intervention (PCI, <90min)
        
        Insulin control important to maintain normal blood glucose (4.6-7.0 mmol)
        
        Post-Infarct Tx
        
        Thrombolytic therapy
        
        Revascularization interventions
        
        Coronary artery bypass grafting (CABG)
        
        Percutaneous coronary intervention (PCI)
        
        AKA angioplasty stent
        
        Atherectomy
        
        Cardiac rehabilitation programs
        
        Cardiac Remodelling post-STEMI
        
        Multiple progressive structural changes to maintain cardiac fx
        
        Both infarcted & non-infarcted areas of ventricle undergo progressive changes in size, shape, & thickness
        
        Early wall thinning at infarcted area --> healing --> hypertrophy & dilation of non-infarcted tissue
        
        Collectively termed ventricular remodelling
        
        Organic Nitrates: Nitroglycerin
        
        Is exogenous 'nitric oxide'
        
        1st line acute intervention
        
        SL tab/spray/IV
        
        1 SL tab q5min x 3 doses --> call EMS
        
        Longterm Tx
        
        Adrenergic Beta Blocker
        
        Metoprolol
        
        Atenolol
        
        CA2+ Channel Blockers
        
        Diltiazem
        
        Organic Nitrates
        
        Change route/drug to longer acting
        
        Antiplatelet Medications
        - ASA
        
        Blocks thromboxane A2 in degranulation
        
        Also COX-1 inhibition --> decreased platelet aggregation
        
        ASA (OTC, fast acting if chewed, effective MI 1st tx)
        
        - Clopidogrel (Plavix)
        
        Blocks ADP in degranulation
        
        Clopidogrel (PO)
        
        Glycoprotein 2B/3A receptor inhibitors
        - Abciximab (Reopro) - Integrilin - Aggrastat
        
        IV bolus --> continuous infusion
        
        Used in PTCA to prevent CVA/MI during procedure
        
        Thrombolytics
        
        Fibrinolysis = clot destruction
        
        The only drugs that destroy clots
        
        Stimulate TPa activation of plasmin --> clot destruction
        
        Tissue Plasminogen Activator (tPA) --> converts plasminogen to plasmin --> this enzyme digests fibrin strands --> circulation restored
        
        Endogenous cycle --> unwanted clots are removed
        
        Reteplase; tPA
        
        t1/2 = 13-16 min
        
        IV
        
        Pain management
        
        Combination of nitrates, analgesics (eg: morphine), O2, B-adrenergic blocking agents, reperfusion measures
        
        Nitroglycerin SL initially
        
        Possible IV nitroglycerin for Tx of ongoing ischemic pain, control of HTN, or management of pulmonary congestion
  - - - Causes
        
        Atherosclerotic plaque disruption
        
        Platelet aggregation
        
        Secondary hemostasis
        
        Pathophysiology
        
        Dynamic stenosis
        
        Ruptured/inflamed plaque
        
        S/S
        
        Symptoms at rest
        
        Supply-led ischemia
        
        Symptoms develop over short term
        
        Frequent/nocturnal symptoms
        
        Pain characteristics
        
        Occurs at rest/with minimal exertion for usually >20 min
        
        Severe and described as frank pain and of new onset
        
        Occurs with a pattern that is more severe, prolonged, or frequent than previously experienced
        
        Dx testing
        
        ECG changes at rest/with symptoms
        
        Troponin elevation
        
        Non-pharmacological Tx
        
        Smoking cessation
        
        Stress reduction
        
        Exercise
        
        Limiting cholesterol & saturated fats
        
        Weight reduction if obesity is present
        
        Avoidance of cold or other stresses that produce vasoconstriction
        
        Pharmacological Tx
        Antiplatelet
        - Aspirin
        
        Preferred antiplatelet for CAD
        
        Inhibits prostaglandins and thromboxane A2
        
        ADP Inhibitors
        - Ticlopidine - Clopidogrel
        
        May be used if aspirin contraindicated
        
        Irreversibly inhibits binding of ADP to its receptor on the platelets
        
        No effect on prostaglandin synthesis
        
        Platelet Receptor Antagonists
        - Abciximab
        
        Target single step in aggregation process
        
        Block receptor involved in the final common pathway for platelet adhesion, activation, & aggregation
        
        Treat acute coronary syndrome
- - - - Types
        
        Dilated
        
        Hypertrophic
        
        Restrictive
        
        Arrhythmogenic right ventricular
        
        Peripartum
        
        Primary Cardiomyopathy
        
        Genetic
        
        Hypertrophic
        
        Arrhythmogenic right ventricular
        
        Left ventricular noncompaction cardiomyopathy
        
        Inherited conduction system disorders
        
        Ion channel dysfunctions
        
        Secondary Cardiomyopathy
        
        Acquired cardiomyopathies
        
        Myocarditis
        
        Peripartum cardiomyopathy
        
        Stress cardiomyopathy
        
        Alcoholic cardiomyopathy
        
        Mixed Cardiomyopathy
        
        Dilated cardiomyopathy
        
        Restrictive cardiomyopathy
        
        Hypertrophic Cardiomyopathy
        
        Most common
        
        Most common cause of death
        
        Information
        
        Most common cardiomyopathy (heavily genetic)
        
        Most common cause of sudden cardiac death (SCD) in young athletes (mostly genetic)
        
        Pathophysiology
        
        L.ventricular hypertrophy (sometimes r.ventricle too) with...
        
        Thickening of ventricular septum
        
        Abnormal diastolic filling
        
        Cardiac arrhythmias
        
        May have intermittent left ventricular outflow obstruction
        
        S/S
        
        Can be asymptomatic
        
        Dyspnea
        
        Chest pain during exertion
        
        Exercise intolerance
        
        Syncopoe
        
        Palpitations
        
        1 more item...
        
        Tx of Cardiomyopathy
        
        Depends on type
        
        Medication
        
        Implanted pacemakers
        
        Implanted defibrillators
        
        Ventricular assist devices
        
        Ablation (alcohol septal ablation)
        
        Injection of absolute alcohol into septum to induce controlled necrosis of hypertrophied tissue
        
        Goal of tx is often symptom relief, some may eventually need heart transplant
- - - - S&S
        
        Signs of systemic infection (fever, positive blood culture)
        
        Change in existing heart murmur
        
        Evidence of embolic distribution of vegetative tissue
        
        Risk Factors
        
        Damaged endocardial surface
        
        Portal of entry to circulatory system
        
        Valvular disease, prosthetic heart valves, or congenital heart defects that create growth-prone environment
        
        Preexisting valvular or endocardial defects, gum/oral lesions may give bacteria access to bloodstream
  - - - Tx for RF & RHD
        
        Control acute inflammatory response + prevent cardiac complications and recurrence of disease
        
        Antibiotics
        - Penicillin - 1st gen. cephalosporins
        
        Anti-inflammatory drugs
        
        Selective restriction of activities
      - RF
        
        Acute Stage
        
        Hx of initiating streptococcal infection
        
        Involves mesenchymal connective tissue of the heart, blood vessels, joints, SC tissues
        
        Recurrent Phase
        
        Extension of the cardiac effects of the disease
        
        Chronic Phase
        
        Permanent deformity of heart valves
- - - - Diagnostic Imaging
        
        Pulmonary Angiography (gold standard)
        
        Chest X-ray
        
        Westmark Sign
      - Tx
        
        Fibrinolytic Tx
        - Streptokinase, Urokinase - Recombinant tissue plasminogen activator (serious cases)
        
        After... heparin Tx
- - - - Atrial Septal Defect
        
        Is an opening in atrial septum --> free passing blood between atria
        
        Seen in 10% of CHD
        
        Rarely have S&S of CHF or other CVD symptoms
        
        S&S
        
        Most asymptomatic but may be easily fatigable/mild growth stunting
        
        Cyanosis doesn't occur unless HTN is present
        
        Hyperactive precordium, RV heave, fixed widely split S2
        
        Systolic ejection murmur @ left sternal border
        
        Tx
        
        Sx closure generally recommended for secundum ASD w/ Qp:Qs Ratio >2:1
        
        Closure is elective for 2-5 year olds to avoid late complications
        
        Sx correction is done earlier in children w/CHF or significant pulmonary HTN
        
        Once pulmonary HTN w/shunt reversal occurs, this is considered too late
        
        Procedure mortality >1 %
    - - Pathophysiology
        
        PDA --> increased aortic pressure --> blood shunts L to R through the duct from aorta to PA --> increased pulmonary vascular disease d/t increased pressure
        
        S&S
        
        Small PDA usually asymptomatic
        
        Large PDA can result in symptoms of CHF, growth restriction, FTT
        
        Bounding aterial pulses
        
        Widening pulse pressure
        
        Enlarged heart, prominent apical impulse
        
        Classic continuous machinery systolic murmur
        
        Mid-diastolic murmur at the apex
        
        Tx
        
        Inhibitor of prostaglandin synthesis can be used in premature infants
        - Indomethacin
        
        Sx closure (required to prevent HF & pulmonary vascular disease)
        
        Mortality is <1%
    - - Tx
        - Arterial switch procedure (current standard)
        
        Procedure
        
        Aorta is reattached to pulmonary artery base, and pulmonary artery is reattached to aortic base. Then coronary arteries moved to left-sided great artery and any ventricular septal defects are closed during the same operation
        
        Corrects the relation of systemic and pulmonary blood flows
        
        Over 90% survival rates
        
        Preferably performed in 1st 2-3 weeks of life, before postnatal reduction in pulmonary vascular resistance occurs (where the left ventricle adjusts to the lower pulmonary pressure but becomes unable to sustain systemic blood flow)
        
        Possible complications
        
        Coronary insufficiency
        
        Supravalvular pulmonary stenosis and/or aortic regurgitation
        
        Dysrhythmias
    - - Pathophysiology
        
        Is a vascular disease
        
        Can start with infection
        
        Immune-mediated disease (inflammation in vasculature, valves, and eyes)
        
        Fever b/c of inflammation
        
        Inflammatory response to infection is disproportionately high
        
        Stages
        
        Acute phase
        
        Fever
        
        Conjunctivitis, rash, involvement of oral mucosa
        
        Redness and swelling of the hands and feet
        
        Enlarged cervical lymph nodes
        
        Subacute phase
        
        Defervescence
        
        Desquamation
        
        Convalescent phase:
        
        Complete resolution of symptoms until all signs of inflammation have disappeared after ~8 weeks
        
        Notes
        
        Cardiac involvement is the most important manifestation of Kawasaki disease.
        
        Coronary artery abnormalities develop in approximately 15% to 25% of children, manifested by coronary artery dilation and aneurysm formation as seen on 2D echocardiography
        
        Manifestations of coronary artery involvement include signs and symptoms of myocardial ischemia or, rarely, overt MI or rupture of the aneurysm.
        
        Pericarditis, myocarditis, endocarditis, heart failure, and arrhythmias also may develop.
        
        Death from Kawasaki disease is estimated to occur in less than 1% of patients and is almost always cardiac in nature, most often occurring during the convalescent phase of the illness, usually from thromboses or coronary arterial aneurysms
- - - - Pathophysiology
        
        Reduction in valve to 1/4 of its normal size --> severe obstruction to flow --> progressive pressure overload in left ventricle --> systolic & diastolic dysfunction + S&S of heart failure --> angina, syncope, and HF
        
        Tx
        
        Valve replacement most effective
        
        In children with congenital aortic stenosis: balloon valvotomy
        
        Statins & ACE Inhibitors to delay progression
    - - Pathophysiology
        
        IE, trauma, aortic dissection: Acute aortic regurgitation --> sudden large regurgitant volume to an unadapted left ventricle --> severe elevation in left ventricular diastolic pressure --> pulmonary edema
        
        Decrease in CO --> increase in HR & PVR --> regurgitation worsening
        
        S&S
        
        Palpitations (esp. lying down)
        
        Chest discomfort d/t pounding of heart against chest wall
        
        Tachycardia, head pounding, and premature ventricular contractions