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CARDILOGY - WEEK 2 - Coggle Diagram

- - - - PATHOPHYSIOLOGY:
        
        Mitral valve stenosis → obstruction of blood flow into the left ventricle (LV) → limited diastolic filling of the LV (↓ end-diastolic LV volume) → decreased stroke volume → decreased cardiac output (forward heart failure)
        Mitral valve stenosis → increase in left atrial pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema → pulmonary hypertension → backward heart failure and right ventricular hypertrophy
      - SYMPTOMS:
        
        Breathlessness (pulmonary congestion)
        
        Fatigue (low CO)
        
        Oedema, ascites (RHF)
        
        Palpitations (AF)
        
        Cough (pulmonary congestion)
        
        Hemoptysis (pulmonary congestion, PE)
        
        Chest pain (pulmonary HTN)
        
        Thromboembolic complications (stroke, ischemic limb)
        
        Hoarseness and dysphagia due to compressive forces of enlarged left atria
        
        Orthopnea and PND (RHF)
      - SIGNS
        
        Irregular pulse (AF)
        
        Mitral facies (rosy cheeks with bluish tinge aka malar flush)
        
        Apex tapping on S1
        
        RV heave if pulmonary HTN present
        
        Loud S1
        
        Opening snap
        
        Mid- diastolic murmur
      - AETIOLOGY
        
        Rheumatic
    - - PATHOPHYSIOLOGY:
        
        Acute MR: ↑ LV end-diastolic volume → rapid ↑ LA and pulmonary pressure → pulmonary venous congestion → pulmonary edema
        
        Chronic (compensated) MR: progressive dilation of the LV (via eccentric hypertrophy) → ↑ volume capacity of the LV (preload and afterload return to normal values) → ↑ end-diastolic volume → maintains ↑ stroke volume (normal EF)
        
        Chronic (decompensated) MR: progressive LV enlargement and myocardial dysfunction → ↓ stroke volume → ↑ end-systolic and end-diastolic volume → ↑ LV and LA pressure → pulmonary congestion, possible acute pulmonary edema, pulmonary hypertension, and right heart strain
      - SYMPTOMS
        
        Unwell and breathless, orthopnea, PND due to acute pulmonary oedema
        
        Fatigue
        
        Dry Cough
      - SIGNS
        
        Systolic Thrill
        
        Displaced apex beat
        
        Bibasilar crackles(inspiratory)
        
        Holosystolic murmur radiating to left axilla
        
        Cardiogenic shock: poor peripheral perfusion, tachycardia, tachypnea, hypotension
      - AETIOLOGY
        
        Mitral valve prolapse
        
        Dilate mitral valve
        
        post MI papillary dysfunction
        
        Rupture tendae chordinae
      - TREATMENT
        
        Treat heart failure including use of beta blocker and ACE, along with diuretics
        
        Valve replacement
        
        Mitraclip
        
        Tendyne
    - - PATHOPHYSIOLOGY:
        
        Narrowed opening area of the aortic valve during systole → obstruction of blood flow from left ventricle (LV) → increased LV pressure → left ventricular concentric hypertrophy, which leads to: Increased LV oxygen demand; Impaired ventricular filling during diastole → left heart failure; Reduced coronary flow reserve
        
        Initially, cardiac output (CO) can be maintained. Later, the decreased distensibility of the left ventricle reduces cardiac output and may then cause backflow into the pulmonary veins and capillaries → higher afterload (pulmonic pressure) on the right heart → right heart failure
      - SYMPTOMS:
        
        Asymptomatic in early disease
        
        Sudden death
        
        Three major symptoms of aortic valve stenosis, think: SAD (syncope, angina, dyspnea).
      - SIGNS:
        
        Low volume/amplitude plateau pulse and decreased pulse pressure (anacrotic pulse)
        
        Signs of pulmonary venous congestion
        
        Thrusting apex beat with lateral displacement
        
        Systolic thrill at base of heart, bifurcation of carotids and aorta
        
        Narrow split or reversed S2
        
        Harsh mid-systolic ejection murmur to carotids - (crescendo decrescendo)
        
        Early systolic ejection click
      - TREATMENT
        
        Treat CCF, surgery, TAVI (valve replacement)
      - AETIOLOGY:
        
        Degenerative calcification or congenital, less commonly rheumatic
    - - PATHOPHYSIOLOGY:
        
        General: Regurgitation of blood from the aorta into the left ventricle (LV) leads to: Increased systolic blood pressure and decreased diastolic pressure. Widened pulse pressure → water hammer pulse
        
        Acute AR: Because LV cannot sufficiently dilate in response to regurgitant blood, LV end-diastolic pressure increases rapidly → pressure transmits backwards into pulmonary circulation → pulmonary edema and dyspnea. Decreased cardiac output if severe → cardiogenic shock and myocardial ischemia
        
        Chronic AR: Initially, a compensatory increase in stroke volume can maintain adequate cardiac output despite regurgitation (compensated heart failure). Over time, increased left ventricular end-diastolic volume → LV enlargement and eccentric hypertrophy of myocardium → left ventricular systolic dysfunction → decompensated heart failure
      - SYMPTOMS:
        
        Exertional dyspnoea
        
        Fatigue
        
        Palpitations
        
        Exertional angina
      - SIGNS
        
        Collapsing (Water hammer) pulse
        
        Prominent carotid pulsations
        
        Diastolic thrill
        
        High-pitched, blowing, decrescendo early diastolic murmur
        
        LV enlargement
        
        Congestive HF
      - TREATMENT
        
        Treat complications. No specific treatment. Valve replacement if symptomatic..
      - AETIOLOGY:
        
        Congenital bicuspid valve
        
        Infective endocarditis
        
        Calcific AS
        
        Rheumtic
        
        Marfan's Syndrome
        
        Hypertention
        
        Aortic dissection
  - - - Congenital aortic stenosis
      - Congenital subvalvular aortic stenosis
      - Congenital supravalvular aortic stenosis
    - - Calcification & fibrosis of congenitally
        bicuspid aortic valve
      - Rheumatoid aortic stenosis (results from chronic systemic inflammation)
    - - Senile degenerative aortic stenosis
      - • Calcification of bicuspid valve
      - • Rheumatic aortic stenosis
  - - - Asymptomatic: good prognosis. Conservative management. Frequent review for development of angina, syncope and symptoms of low CO or heart failure.
      - Moderate = severe stenosis Doppler echo every 1-2yrs to detect progression
      - Symptomatic: prompt aortic valve replacement
    - - Valve replacement if symptomatic
- - - - High-yield secondary causes of dilated cardiomyopathy: ABCCCDD: Alcohol use, Beriberi, Cocaine, Coxsackie B virus, Chagas, Doxorubicin/Daunorubicin
    - - Causative factors decrease the contractility of myocardium → compensatory mechanisms (Frank-Starling law) are activated to maintain cardiac output → ↑ end-diastolic volume (preload) → myocardial remodeling → eccentric hypertrophy (sarcomeres added in series) and dilation of the ventricle → reduced myocardial contractility → systolic dysfunction and ↓ ejection fraction → heart failure
      - ↓ LV contractility due to dilation leads to left heart failure and eventually right heart failure
      - Left heart failure: decreased LV output leads to clinical features of left-sided heart failure via the following mechanisms: Diminished systemic perfusion → decreased perfusion of end organs → forward failure (e.g., renal/cerebral dysfunction, cold extremities). ↑ Pressure within the pulmonary circulation → pulmonary circulation congestion → impaired gas exchange and fluid extravasation into the interstitium and alveoli → backward failure with predominant pulmonary congestion (e.g., dyspnea, orthopnea, cardiac asthma)
      - Right heart failure : decreased right ventricular output → systemic circulation congestion → backward failure with predominant systemic congestion (see clinical features of right-sided heart failure)
    - - Dilated: Most common, idiopathic, alcohol also a common cause along with myocarditis, post partum persistent tachycardia. Results in HFrEF (systolic HF)
      - Hypertrophic
        
        Non obstructive: No outflow obstruction, no SAM. Results in diastolic HFpEF, arrythmias
        
        Obstructive (HOCM): obstruction at left ventricular outflow. Caused mitral regurgitation et al and results in arrythmias and HFpEF.
        
        Dizziness, syncope, angina, (SAD), SOB
        
        ECHO features: asymmetrical septal hypertrophy, LV outflow obstruction, systolic anterior motion of MV
      - Restrictive: RHF signs (JVP, dep edema, hepatomegaly, ascites) Diuretics are the only effective treatment
  - - - Family history: cardiovascular events in first-degree relatives below the age of 55 (♂)/65 (♀)
      - Age: males ≥ 45 years, females ≥ 55 years (postmenopause)
      - Ethnicity
    - - Smoking
      - Diabetes mellitus [3]
      - Arterial hypertension
      - Dyslipidemia [4]
      - High homocysteine levels (homocystinuria)
      - Obesity
      - High fibrinogen levels
      - Hyperphosphatemia
      - Stress
      - Increased alcohol consumption
  - - - SNAP
      - Cardiac rehab: Advice on SNAP and mental health
    - - ACUTE = MOAN/MONABASH
      - LONGTERM: ACE/ARB, STATIN, ASPIRIN, Beta Blocker
    - - Single Balloon Angioplasty
        
        Restenosis: 40% chance
      - Intracoronary Stents
        
        Restenosis: 17% chance
      - Drug eluting Stents
        
        Restenosis: 10% chance
      - indications for CABG
        
        Left main stem stenosis
        
        3 vessel coronary artery disease: LAD, circumflex, RCA
        
        2 vessel disease involving LAD
    - - Imaging
        
        CT:
        
        Image cardiac chambers
        
        Great vessels
        
        Pericardium
        
        Mediastinal structures and masses
        
        Radiation factors
        
        ECHO:
        
        Non-invasive
        
        Well tolerated
        
        Examine structure and function
        
        Xray:
        
        Shape & size of heart
        
        State of pulmonary vessels
        
        State of lung fields
      - Bloods:
        
        FBE,UEC, LFT, coags, ESR, CRP - Inflammatory or infection, Renal function
        
        Cardiac markers: Troponin I or T
        (serial)
      - ECG or stress test
        
        STEMI or NSTEMI, arrythmias, exercise induced
      - CXR
        
        cardiomegaly, pulmonary
        oedema, pneumonia, rib fracture
      - ECHO
        
        heart failure or valvular disease
    - - Moderate reductions in several risk factors may be more effective in risk than major in one factor
      - Clinical decisions based on absolute CVD risk may lead to improved management of CVD risk – early detection of at risk individuals treatment