Cardiac Flashcards
Complications of Myocardial Infarction - Mechanical
Mechanical:
- cardiogenic shock
- CCF
- mitral regurg. (if LV infarct and papillary muscle rupture) - cardiac rupture: wall (tamponade) or septum (shunt)
- ventricular aneurysm a month later
Complications of Myocardial Infarction - Arrhythmias
- VF that day (most common cause of sudden death)
- 90%(!) have other arrhythmia
Complications of Myocardial Infarction - Pericardial
- Early pericarditis (dusky tissue)
- Pericardial effusion (?tamponade)
- Dressler’s Dyndrome: CP, fever, effusion, weeks/months later (autoimmune response)
- Fibrinous Pericarditis: if infarct reaches pericardium
Histological evolution of MI
Normal for first 6 hours;
6-24 hours: necrosis and loss of nuclei;
1-4 days: polymorphs then macrophages;
5-10 days: debris removal;
1-2 weeks: granulation tissue, new vessels, myofibroblasts, collagen synthesis;
4+ weeks: scar tissue.
Causes of heart failure (6)
- IHD
- Hypertension
- Valve disease
- Dilated cardiomyopathy
- Myocarditis
- Arrhythmias
Complications of heart failure
- Sudden death
- Systemic emboli
- DVT/PE
- Arrhythmias
- Pulmonary oedema (pink transudate) (+ infection)
- Hepatic cirrhosis (nutmeg liver)
Three types of cardiomyopathy,
and do they cause systolic or diastolic dysfunction?
Dilated - Systolic (doesn’t stretch)
Hypertrophic - Diastolic (doesn’t fill)
Restrictive - Diastolic
Causes of dilated cardiomyopathy
Idiopathic, Alcohol, Giving birth, Gentic, Sarcoid, Myocarditis.
Causes of hypertrophic cardiomyopathy
Genetic,
Inborn errors of metabolism.
Causes of restrictive cardiomyopathy
Sarcoid,
Amyloid,
Radiation-induced fibrosis.
Genetics of hypertrophic cardiomyopathy
Autosomal Dominant,
Sarcomeric protein genes,
beta-MHC (myosin heavy chain) most common,
also MYBP-C and Trop-T.
What does acute rheumatic fever affect?
Heart: pancarditis;
Joints: arthritis and synovitis;
Skin: erythema marginatum, subcutaneous nodules;
Neuro: Encephalopathy, Sydenham’s chorea.
Steps of atherosclerosis
- Endothelial injury
- LDL accumulation
- LDL oxidised (foreign, so inflam)
- Macr use scavenger R, become foam cells
- Apoptosis: more inflam and more chol
- Adhesion molecules, so more macr
- Fibrous cap by smooth muscle
Modifiable atherosclerosis RFs
T2DM,
Hypertension,
Hyperchol,
Smoking.
Non-modifiable atherosclerosis RFs
Male,
Old,
FHx.