Hypertension and Myocardial Infarction Flashcards
how many litres of blood are pumped each day
6000L
composition of blood vessel walls
tunica intima, tunica media and
adventitia
risk factors for hypertension
Stroke
Cardiac disease
Renal disease
BP in systolic and diastolic state that constitutes as hypertension
systolic BP > 140mm Hg
diastolic BP > 90mm Hg
classification of hypertension
95% essential - idiopathic
5% secondary - underlying identifiable cause
what %age of hypertension is malignant
5% rapidly rising BP that leads to death in 1-2 years if untreated
how is malignant hypertension characterised
high BP (200/120mm Hg) with renal failure & retinal haemorrhage +/- papilloedema
secondary hypertension
Renal
Endocrine
CVS
Neurologic
conditions that cause renal hypertension
(polycystic disease, renal artery
stenosis, vasculitis, renovascular
disease.)
conditions that cause endocrine hypertension
(phaeochromocytoma,
Cushing’s, acromegaly, Conn’s
syndrome)
conditions that cause CVS hypertension
(coarctation aorta, increased
intravascular volume etc.)
conditions that cause neurologic hypertension
(acute stress, increased
intracranial pressure)
renin-angiotensin aldosterone system
angiotensinogen released from liver and combines w/ renin from kidney
converted to angiotensin I
angiotensin converting enzyme from lungs and renal endothelium converts Angiotensin I to Angiotensin II
Inc. SNS activity
Inc. Na+, Cl-, H2O reabsorption and K excretion
Inc. Aldosterone secretion from kidney
arteriolar vasoconstriction inc. BP
Inc. ADH secretion
cardiac output
heart rate x stroke volume
blood pressure
Cardiac output x Peripheral
resistance
peripheral resistance
to resistance to blood flow at the level of the arterioles – this will increase due to vasocontraction
what does kidney responds to and how
hypertension by eliminating salt & water
what may initiate essential hypertension
reduced renal sodium excretion
leads to increased fluid volume and cardiac output
what triggers renin-angiotensin aldosterone system
low blood pressure
low renin
low Na and Cl
causes of secondary hypertension
mineralocorticoid excess
corticosteroid excess
mineralocorticoid
type of steroid hormone that regulate salt and water retention in blood
example of mineralocorticoid
aldosterone
causes of mineralocorticoid excess
aldosterone producing adenoma
bilateral adrenal hyperplasia
aldosterone adrenal carcinoma
ectopic aldosterone secretion
cortisol
stress hormone
inc. blood sugar levels,
increase use of glucose etc
causes of corticosteroid excess
exogenous or endogenous increase in cortisol
cushing disease
hypertension
cushing disease
pituitary tumour leading to excessive production of ACTH (adrenocorticotropic hormone). – Excessive ACTH stimulates the adrenal cortex to produce high levels of cortisol
cushing syndrome symptoms
weight gain
glucose intolerance
moon face
acne
cause of cushing syndrome
adrenal gland tumours,
adrenal hyperplasia,
ectopic/paraneoplastic
acromegaly
growth hormone excess
pituitary gland
produces too much growth hormone during adulthood
expansion of extracellular fluid volume & increased
peripheral vascular resistance
catecholamines examples
– epinephrine
and norepinephrine
what response are catecholamines involved in
fight of flight response
epinephrine
and norepinephrine cause
increase heart rate,
vasoconstriction
Phaeochromocytoma
Tumors of Chromaffin tissue of adrenal medulla
Paraganglioma
Tumors of Chromaffin tissue of extra adrenal medulla
symptoms of Paraganglioma and Phaeochromocytoma
can be functioning or non functioning - may or may not release catecholamines
symptoms can vary from asymptomatic to hypertension
management of excess catecholamines
Initial management relies upon
blockade by medications
(alpha and beta blockers)
symptpms of thyrotoxicosis
Increased contractile activity of heart increased stroke volume
• Increased sympathetic activity -> vasocontraction
• Increased angiotensinogen levels
• Increased systolic BP
symptoms of hypothyroidism
- Impaired endothelial function (in the tunica intima)
- Increased vascular resistance
- Extracellular volume expansion
- Increased diastolic blood pressure
causes of hypertension
sleep apnoea syndrome
oral contraceptive use
vascular effects of hypertension
Accelerates atherosclerosis
• hardening of arteries
• Cause degenerative effects in vessel wall
leading to dissection
• Small vessel disease: hyaline arteriolosclerosis
and hyperplastic arteriolosclerosis
left sided cardiac effects of hypertension
concentric left ventricular
hypertrophy (weight ~ 500g, LV > 1.5cm).
Response to systemic hypertension.
right sided cardiac effects of hypertension
right ventricular hypertrophy
caused by disorders of pulmonary vasculature
causing pulmonary hypertension.
end organ effects of hypertension
Due to ↓ blood flow or rupture of artery/arteriole • Stroke • Heart failure • Angina/MI • Retinopathy • Aortic dissection • Renal failure • Peripheral vascular disease
arteries that supply blood to the heart
left anterior descending artery
left circumflex artery
right coronary artery
ischaemia
• Imbalance between supply (perfusion) and
demand of oxygenated blood to a tissue
ischaemia is characterised by
insufficient O2 and nutrients and inadequate removal of metabolites
difference between ischaemia and infarction
Ischaemia - reduced oxygenation of tissue.
• Infarction - necrotic tissue due to Ischaemia
modifiable risk factors for ischaemic heart disease
Hypertension Smoking Diabetes Hyperlipidaemia Obesity
non-modifiable risk factors for ischaemic heart disease
Family history
Genetics
Age
Sex
clinical manifestation of ischaemic heart disease
Angina pectoris (stable and unstable) • Myocardial infarction • Non- STEMI • STEMI • Chronic IHD with heart failure • Sudden cardiac death
what cells respond to atherosclerotic plaque in blood vessels
macrophages
macrophage derived foam cells
CD4+T cells infiltrate lipid core
what cells respond to ruptured lining of blood vessel due to plaque build up
platelets
stable angina
fixed luminal narrowing with
reduced distal perfusion
lack of oxygen and build up of metabolites = chest pain
unstable angina
sudden change in
atherosclerotic plaque = severe and transient
reduction in coronary blood flow
acute coronary syndrome
Unstable angina, acute Myocardial Infarction (MI) and sudden death
Ischaemia due to abrupt plaque change
(rupture, erosion, haemorrhage) with
superimposed thrombus
Myocardial Infarction - MI
Sudden change in plaque morphology
• Platelets aggregate and adhere to plaque
• Vasospasm occurs
• Coagulation pathway activated
• Thrombus develops on atheromatous plaque
and evolves to occlude lumen
Symptoms of myocardial infarction
- Chest pain +/- arm pain
- Short of breath
- Sweaty
- Dizzy
- Rapid, weak pulse
- “silent”- elderly, diabetics
how is myocardial diagnosed
History
• ECG changes
• Cardiac enzymes (troponin, CK-MB, LDH)
myocardial changes that occur in first 12 hours of MI
some haemorrhage
myocardial changes that occur in 12-24 hours of MI
necrosis and acute inflammation
myocardial changes that occur in 1-3 days of MI
more necrosis and neutrophils
myocardial changes that occur in 3-7 days of MI
disintegration of myocytes and macrophages
myocardial changes that occur in 7-10 days of MI
granulation tissue
myocardial changes that occur after 10 days of MI
early scar formation
complications of myocardial infarction
- Heart failure (acute, chronic)
- Arrhythmias
- Rupture (wall, septum, papillary muscle)
- Pericarditis
- Ventricular aneurysm
- Mural thrombus
prevention of MI
- Stop smoking
- Control BP
- Reduce cholesterol & weight
- Control of diabetes
Treatment of MI
- Medication
- Thrombolysis
- Percutaneous Coronary Angioplasty and stents
- CABG
