Flashcards in Cardiovascular disease 1 Deck (72):
What is the definition of ischeamic heart disease?
Inadequate blood supply to the myocardium due to any imbalance in supply vs. demand
For what 2 main reasons could someone have inadequate blood supply to the myocardium?
1) Reduced coronary blood flow - usually atheroma - with or without thrombus
2) Myocardial hypertrophy, usually due to systemic hypertension
Why does diastolic insufficiency occur in IHD?
Most perfusion of the heart occurs during diastole when the aortic valve is closed and there is a degree of back flow into the cusps - in IHD during diastole is when the relative O2 deficit is at its worst
What is loss of autoregulation in IHD, at what percentage of occlusion does it occur?
Autoregulation of the vessels is dilation and constriction according to demand, vessels lose autoregulation when they cannot dilate sufficiently to allow enough blood through - this happens at >75% occlusion
At what percentage of stenosis is blood supply to the heart insufficient at rest?
In which type of IHD is low diastolic flow particularly apparent?
How many seconds of ischemia are possible before function of the myocardium is lost?
What happens to the myocardium if ischaemic for more than 60 secs?
Get myocyte dysfunction and death from ischemia
After how many minutes of ischemia is the damage to the myocardium irreversible?
Name 4 common ischemic heart disease syndromes?
1) Angina pectoris
2) Acute coronary syndrome
3) Sudden cardiac death
4) Chronic ischaemic heart disease
What are the 3 types of angina?
1) Typical/stable - fixed obstruction, predictable relationship to exertion
2) Variant/Prinzmetal - coronary artery spasm
3) Crescendo/ unstable - often due to plaques disruption and small emboli, pain is getting worse and more unpredictable
Which of the 3 types of angina is a red flag and requires urgent treatment?
What classifies a cardiac infarct?
Loss of myocytes
What are the 2 acute coronary syndromes?
1) Acute myocardial infarction (+/- ECG ST elevation)
2) Crescendo/unstable angina
Why does a subendocardial myocardial infarction commonly occur without any acute coronary occlusion?
1) The subendocardial myocardium is relatively poorly perfused in normal conditions (far from coronary vessels and far from heart chamber for direct diffusion)
2) If there is a stable angina or an acute hypotensive episode...
3) The subendocardial myocardium can infarct without any acute coronary occlusion
Subendocardial MIs are different to your typical MIs
What is a transmural myocardial infarction?
Severe occlusion of the coronary vessel leads to death of myocytes across all layers of the myocardium
What would be the gross and microscopic appearance of an infarct less than 24 hours old?
Microscopic - necrosis and neutrophils
Gross - normal/dark
What would be the gross appearance of an infarct which was:
a) 1-2 days old
b) 3-7 days old
c) 1-3 weeks old
d) 3-6 weeks old
1-2 days = yellow infarct center
3-7 days = hyperaemic border, yellow center
1-3 weeks = red/grey
3-6 weeks = scar
What would be the microscopic appearance of an infarct which was:
a) 1-2 days old
b) 3-7 days old
c) 1-3 weeks old
d) 3-6 weeks old
1-2 days = more necrosis and neutrophils (than
What are the 5 blood markers of cardiac myocyte damage?
1) Troponins T and I
2) Creatine kinase MB
4) Lactate dehydrogenase isoenzyme 1
5) Aspartate transaminase
Which blood marker is most commonly used post MI, when does it peak, for how many days is it raised?
Detectable after 2-3 hours, peaks at 12 hours and detectable for up to 7 days
In what 3 other conditions is troponin raised?
1) heart failure
Creatine Kinase MB is detectable how may hours post MI and peaks when, when can you detect it til?
Detectable 2-3 hours post MI for up to 3 days
Peaks at 10-24 hours
Myoglobin peaks when post MI, why is it not the most useful?
Peaks at 2 hours
Less useful as also released from skeletal muscle
Lactate dehydrogenase isoenzyme 1 peaks how many days post MI and is detectable for how many?
Peaks at 3 days, detectable for up to 14 days
Why is aspartate transaminase a less useful blood marker of cardiac myocyte damage?
Because its also present in the liver
What are the 3 subtypes of creatine kinase, where is each mostly found?
1) CK MM - muscle (cardiac and skeletal)
2) CK BB - brain, lung
3) CK MB - mainly cardiac, also skeletal muscle
On the basis of what 3 factors is a diagnosis of MI made?
3) Blood cardiac proteins
What percentage of people die from sudden cardiac death immediately post MI?
What are the 7 common complications of MI?
1) Contractile dysfunction and chronic cardiac failure
3) Infarct extension (free wall, septum, papillary muscle)
4) Myocardial rupture
5) Pericarditis - Dressler's syndrome
6) Mural thrombus
7) Ventricular aneurysm
What is Dressler's syndrome?
Secondary form of pericarditis following damage to the heart or pericardium - believed to be caused by immune response following such injury
What is the term for blood filling the pericardial sac?
What is chronic ischaemic heart disease?
Coronary atheroma produces relative myocardial ischemia and angina pectoris on exertion
What is the main risk with CIHD and what 2 things does it lead to?
Risk of sudden death or MI
Leads to cardiac hypertrophy and dilatation
What is familial hypercholesterolaemia?
Mutations in genes involved in cholesterol metabolism
Which 2 genes are most commonly mutated in familial hypercholesterolaemia?
1) LDL receptor gene
2) Apolipoprotein B
What are the 3 main clinical signs seen in familial hypercholesterolaemia heterozygotes?
1) Xanthomas - cholesterol deposits in tendons
2) Corneal arcus
3) Early atheroscelrosis
What is the treatment for familial hypercholesterolaemia heterozygotes?
How does the treatment for homozygotes for familial hypercholesterolaemia differ to that for heterozygotes?
More complex and less effective
Blood pressure is physiologically regulated to fulfil what 2 functions?
1) Ensure the perfusion of organs is sufficient to maintain function
2) Prevent higher flow that exceeds metabolic demands, increases damage to blood vessels and thus organs
What is considered normal BP?
What is considered abnormal BP?
Sustained systolic 140
What percentage of cases of hypertension are primary ie. idiopathic?
Why is it difficult to identify individuals susceptible to primary hypertension?
Likely caused by many physiological systems interacting over long periods of time with minor dysfunctions
How is the hypothesis that all essential (primary) hypertension share the common pathway of positive sodium balance (ie increased salt intake) explained?
1) Positive sodium balance leads to increased IV volume and volume delivery to the heart augmenting cardiac output and thus pressure
2) Tissue perfusion thus exceeds metabolic demand leading to autoregulation of blood flow to increase vasoconstriction to reduce blood flow
3) This results in a pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output
Name the 4 classes of causes of secondary hypertension?
Name 3 important endocrine causes of secondary hypertension?
1) Cushings syndrome (overproduction of steroids)
2) Primary aldosteronism (excess aldosterone)
3) Phaemochromocytoma (tumour of adrenal glands resulting in overproduction of adrenaline and noradrenaline)
Describe hypertensive heart disease?
- Systemic hypertension leads to increased LV BP
- LV hypertrophy without dilatation initially in response to increased work needed to pump blood
- When the pressure is too great the LV fails to pump blood at normal rate and dilates
- Recognized cause of sudden death
What are the main renal effects of hypertension?
Get vascular changes in primary hypertension:
- arterial intimal fibroelastosis
- Hyaline arteriosclerosis
Slow deterioration in renal function leading to chronic renal failure
What is hypertensive cerebrovascular disease?
Increased risk of rupture to abnormal arteries:
- Atheromatous (circle of Willis)
- berry aneurysms of the circle of willis (SAH)
How is a hypertensive crisis (malignant hypertension) defined?
A hypertensive crisis shows which 3 clinical signs of organ damage?
1) Acute hypertensive encephalopathy
2) Renal failure
3) Retinal haemorrhages
Requires urgent treatment to preserve organ function
What are the 4 main symptoms of and acute hypertensive encephalopathy?
Diffuse cerebral dysfunction:
4) Coma - death
(Rapid intervention is required to reduce the accompanying raised ICP)
What is pulmonary hypertension?
Higher than normal pressure in the pulmonary artery
What are the 4 main causes of pulmonary hypertension?
1) Loss of pulmonary vasculature (COPD, Interstitial lung disease, PE or thrombosis, under ventilated alveoli)
2) Secondary to LV failure
3) Systemic to pulmonary artery shunting
4) Primary or idiopathic
What changes in the heart does pulmonary hypertension lead to?
- Increased right ventricular work to pump blood
- RV myocardial hypertrophy initially without dilation
- Later dilatation and systemic venous congestion as RV failure develops
Which ethnicity is a risk factor for CV disease?
What was the Framingham Heart Study?
Longitudinal population study to identify risk factors for CV disease
What is the Framingham risk score and how can it be calculated?
- Calculates an individuals risk of CV disease based on assessment of multiple risk factors
- Can be calculated using computer algorithms or manually using a table
Name 3 CV risk assessments other than the Framingham risk score?
1) SCORE - European society of cardiology
3) Joint British Societies risk prediction charts
Where is Renin synthesised and stored, what is its role?
- Synthesized, stored in and released from the juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney (in response to low perfusion pressure)
- Cleaves angiotensinogen to angiotensin 1
- Angiotensin 1 is converted to angiotensin 2 in many tissues
What effect does Angiotensin 2 have?
- Potent vasoconstrictor with a very short half life
- Stimulates the adrenal cortex to produce aldosterone
What is aldosterone, what effect does it have?
- Physiological mineralocorticoid
- Renal action causes sodium and thus water retention
- Thus circulating blood volume increases
What is Conn's syndrome caused by?
Excess aldosterone secretion usually due to adrenocortical adenoma, possibly micronodular hyperplasia
What are the 3 endocrine/electrolyte imbalances in Conn's syndrome?
1) Renal sodium and water retention - hypertension
2) Elevated aldosterone, low renin
3) Potassium loss - muscular weakness, arrhythmias, paraesthesia, metabolic alkalosis
How is Conn's syndrome diagnosed?
CT scan of adrenals in presence of metabolic abnormalities of the disease
What is phaeochromocytoma?
Tumour of the adrenal medulla
What leads to the presenting symptoms of phaeochromocytoma?
Secretion of vasoconstrictive catechoamines - adrenaline and noradrenaline
How is phaeochromocytoma diagnosed following presentation with symptoms?
24 hour urine collection for adrenaline metabolites
What are the 5 main presenting symptoms of phaeochromocytoma?
What is Cushings disease?
Overproduction of cortisol by adrenal cortex - cortisol has many metabolic effects including potentiating SNS activity and aldosterone-like effects on the kidneys causing hypertension