Structural heart disease Flashcards

Question

what is mitral regurgitation ? pathophysiology? complications

Answer 1

: backflow of blood from L ventricle to aorta during systole Pathophysiology Infectious endocarditis leads to abscess formation, vegetations, rupture of chordae tendineae and leaflet perforation Complications Chronic MR progression leads to eccentric hypertrophy leading to elongation of myocardial fibres Increases left end diastolic volume Increase in preload & a decrease in afterload Increase in end- diastolic volume and a decrease in end-systolic volume Eventually prolonged volume overload leads to left ventricular dysfunction and increased left ventricular end-systolic diameter Can lead to heart failure

Answer 2

``` Causes Acute : Mitral valve prolapse Rheumatic heart disease Infective endocarditis Following valvular surgery Prosthetic mitral valve dysfunction ``` ``` Chronic: Rheumatic heart disease SLE Scleroderma Hypertrophic cardiomyopathy Drug related ```

Answer 3

``` Presentation: Dyspnea diminished S1, murmur high pitched , blowing sound Fatigue Orthopnea Chest pain Atrial fibrillation Due to backflow of blood into left atrium ```

Answer 4

Management Acute MR Emergency Surgery adjunct preoperative diuretics adjunct intra-aortic balloon counterpulsation Chronic asymptomatic 1st ACE inhibitors or Beta blockers If left ventricular ejection fraction is less than 60% 1st line is surgery Chronic symptomatic 1st surgery plus medical treatment If left ventricular ejection fraction is less than 30% 1st line is Intra-aortic balloon counterpulsation

Answer 5

``` ECG Transthoracic echocardiography Chest X ray Cardiac catheterisation Cardiac MRI/CT Scan ```

Answer 6

Disease of heart muscle making it harder to pump blood to rest of body Can lead to heart failure 3 main types : dilated , hypertrophic , restrictive

Answer 7

Pathophysiology Ventricular chamber enlargement + systolic dysfunction with normal LV wall thickness Complications Enlargement of the left ventricle ↓ejection fraction , ↑ ventricular wall stress, ↑ end systolic volumes. Due to Left ventricle not able to contract fully Early compensatory mechanisms ↑ heart rate and tone of the peripheral vascular system. Due to neurohumoral activation of the renin-angiotensin aldosterone system → ↑ circulating levels of catecholamines. ↑ levels of natriuretic peptides Help increase contraction Eventually these compensatory mechanisms become overwhelmed and the heart fails.

Answer 8

``` Primary 25% Idiopathic (without family history) Familial Rare autosomal dominant inheritance patterns Secondary Heart valve disease After childbirth Thyroid disease Myocarditis Alcoholism Autoimmune disorders Ingestion of drugs Mitochondrial disorders ```

Answer 9

``` Dyspnoea, displaced apex beat, S3 or systolic murmur fatigue, angina, pulmonary congestion low cardiac output ```

Answer 10

1) diet modifications ie fluid restriction 2) treatment of underlying problems 3) treating symptoms of heart failure ie ACE / B blockers w / wo diuretics --> if medication ineffective move onto surgery 4) Treatment for arrhinias 5) anticoagulants for thrombolytic events see google docs please

Answer 11

``` Investigations: Genetic Testing Viral serology Rule out infection ECG Chest X ray Cardiac catheterisation Cardiac MRI/CT Scan Exercise stress test Echocardiograph ```

Answer 12

Hallmark finding : In autopsy LV dilation > 4mm

Answer 13

Pathophysiology Increase in LV wall thickness ( hypertrophy) that is inappropriate, often asymmetrical + occurs in absence of hypertrophy stimulus LV hypertrophy often occurs in interventricular septum → obstruction of flow through the LV outflow tract Complication Most patients with HCM have abnormal diastolic function, impairs ventricular filling ↑ filling pressure, despite a normal or small ventricular cavity. These patients have abnormal calcium kinetics and subendocardial ischemia, which are related to the profound hypertrophy and myopathic process.

Answer 14

Familial | Autosomal dominant Mendelian inherited disease

Answer 15

Presentation Most patents are asymptomatic . Usual first clinical manifestation is sudden death due to ventricular tachycardia / fibrillation ``` Sudden cardiac death Double carotid artery impulse, S3 gallop, Syncope ejection systolic murmur Presyncope Congestive heart failure Dizziness Palpitations Angina ```

Answer 16

HCM with symptoms : B blockers --> verapamil if B blockers don't work add disopyramide surgery if all else fails Please see insendi

Answer 17

Investigations Hemoglobin level: Anemia exacerbates chest pain and dyspnea Brain natriuretic peptide (BNP) troponin T levels: Elevated BNP, NT-proBNP, and troponin T levels are associated with a higher risk of cardiovascular events, heart failure, and death Echocardiography Chest Xray Cardiac MRI

Answer 18

Pathophysiology Increased stiffness of myocardium : Infiltrative cardiomopathies due to deposition of abnormal substances ie, amyloid proteins, noncaseating granulomas, iron) within the heart tissue. → stiffening of ventricular walls → leading to diastolic dysfunction. Restrictive physiology predominates in the early stages: causing conduction abnormalities and diastolic heart failure. Normal systolic function Adverse remodelling may lead to systolic dysfunction and ventricular arrhythmias in advanced cases. Complications Increased stiffness of the myocardium → ↑ ventricular pressures with small increases in volume. Thus, accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase. Patients typically have: ↓compliance ( ↑ diastolic stiffness), Inadequate left ventricle filling at normal pressure → ↓cardiac output. Atrial enlargement due to impaired ventricular filling during diastole but volume + thickness of ventricles are normal

Answer 19

Causes Primary causes Idiopathic familial (has been related to troponin I or desmin mutations, the latter often in association with a skeletal myopathy) various systemic disorders/ secondary causes : ``` ie haemochromatosis Amyloidosis Sarcoidosis Fabry's disease carcinoid syndrome Scleroderma anthracycline toxicity previous radiation. ```

Answer 20

``` Presentation comfortable in the sitting position Due to fluid in the abdomen or lungs Frequently have ascites and pitting edema of the lower extremities Due to fluid not being pumped property Enlarged liver Due to fluid Can be painful Weight loss cardiac cachexia ↑ jugular venous pressure ↓ pulse volume is decreased consistent with decreased stroke volume and cardiac output. ``` ``` Amyloidosis symptoms Easy bruising periorbital purpura Macroglossia systemic findings: carpal tunnel syndrome, ```

Answer 21

Management Heart failure medication Guideline-directed medical therapy for heart failure, including angiotensin-converting enzyme inhibitors or angiotensin receptor II blockers, diuretics and aldosterone inhibitors should be initiated in patients with reduced LV Antiarrhythmic Therapy ``` Immunosuppression Steroids ( for amyloidosis or other immune problems) ``` Pacemaker Cardiac transplantation

Answer 22

``` Investigations CBC Serology Amyloidosis check Chest Xray ECG Echocardiography Catheterisation MRI/Biopsy ```

Answer 23

on google docs

Structural heart disease Flashcards

(55 cards)