Flashcards in Cardiovascular diseases 1 Deck (49)
What is the definition of ischaemic heart disease?
Inadequate blood supply to the myocardium
What are the possible causes of ischaemic heart disease?
- reduced coronary blood flow, almost always due to atheroma +/- thrombus
- myocardial hypertrophy, usually due to systemic hypertension
What is the pathogenesis of IHD?
- acute & chronic ischaemia
- autoregulation of coronary blood flow breaks down if > 75% occlusion
- low diastolic flow especially subendocardial
- active aerobic metabolism of cardiac muscle
- myocyte dysfunction/death from ischaemia
- recovery possible rapid reperfusion (15-20min)
What are the ischaemic heart disease syndromes?
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease
What are the different types of angina?
What is acute coronary syndrome?
- acute myocardial infarction (+/- ecg ST elevation)
- crescendo/unstable angina
What are the features of acute ischaemia?
- atheroma + acute thrombosis/haemorrhage
- lipid rich plaques at most risk
- regional transmural myocardial infarction
- thrombolysis - physiological & drugs
- myocardial stunning
- diagnosis - clinical, ecg, blood cardiac proteins
- subendocardial Mis are different
What is a subendocardial MI?
The subendocardial myocardium is relatively poorly perfused under normal conditions
If there is
- stable athermanous occlusion of the coronary circulation
- an acute hypotensive episode
Then the subendocardial myocardium can infarct without any acute coronary occlusion
What are the blood markers of cardiac myocyte damage?
Creatinine kinase MB
Lactate dehydrogenase isoenzyme 1
What troponin levels would you expect to see in MI?
- detectable 2 – 3h, peaks at 12h, detectable to 7 days
- raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
What creatinine kinase MB levels would you expect to see in MI?
- detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
What myoglobin levels woud you expect to see in MI?
- peak at 2h but also released from damaged skeletal muscle
What lactate dehydrogenase levels would you expect to see in MI?
- peaks at 3days, detectable to 14days
What aspartate transaminase levels would you expect to see in MI?
- Also present in liver so less useful as a marker of myocardial damage
What is the prognosis of MI?
20% 1-2h mortality – sudden cardiac death
What are the possible complications of MI?
- arrhythmias, ventricular fibrillation (75-95%) & sudden death
- ischaemic pain
- left ventricular failure (60%) & shock (10-15%)
- cardiac mural thrombus & emboli
- deep leg vein thrombosis & pulmonary embolus (15-40%)
- myocardial rupture - tamponade, ventricular septal perforation, papillary muscle rupture(1-5%)
- ventricular aneurysm
- autoimmune pericarditis (Dressler’s syndrome) +/- pleurisy 2 weeks to months post MI
What are the features of chronic ischaemic heart disease?
- coronary artery atheroma produces relative myocardial
ischaemia & angina pectoris on exertion
- risk of sudden death or MI
- possible previous occult MIs
- crescendo or unstable angina - evolving plaque
- variant angina - coronary arterial spasm
When is blood pressure considered abnormal?
- Abnormal: Sustained diastolic of 90mmHg
- Abnormal: Sustained systolic of 140mmHg
What causes primary hypertension?
- Cardiac baroreceptors
- Renin-angiotensin- aldosterone system
- Kinin-kallikrekin system
- Naturetic peptides
- Adrenergic receptor system
- Autocrine factors produced by blood vessels
- Autonomic nervous system
What are the 4 groups of causes of secondary hypertension?
What are the key features of the renin-angiotensin-aldosterone system?
- Synthesized, stored in, and released from the juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney
- Cleaves angiotensinogen to angiotensin I
- Angiotensin I is converted to active angiotensin II in many tissues
What are the features of angiotensin II?
- Potent natural vasoconstrictor
- Very short half-life
- Stimulates adrenal cortex to produce aldosterone
What are the features of aldosterone?
- The physiological mineralocorticoid
- Renal action causes sodium and thus water retention
- Circulating blood volume increases
What are the consequences of renal artery stenosis and why is it relevant?
- Reduced blood pressure in kidney
- Reduced blood pressure in renal afferent arterioles
- Juxtaglomerular apparatus stimulated to produce renin
- Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone
- Blood pressure increases
How does coarctation of the aorta result in increased BP?
Hypotension in the kidneys leads to juxtaglomerular apparatus stimulation and renin release.
What is Conn's syndrome?
Caused by excess aldosterone secretion
What are the possible causes of Conn's syndrome?
- Usually due to adrenocortical adenoma
- Possibly micronodular hyperplasia
What are the signs and symptoms of Conn's syndrome?
- Renal sodium and water retention
- Elevated aldosterone, low renin
- Potassium loss
- Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
What diagnostic test can be used in Conn's syndrome?
Diagnose by CT scan of adrenals in presence of these metabolic abnormalities