Cardio lecture 2 Flashcards
Normal BP is 120/80mmHg. After a certain point, high blood pressure causes damage to blood vessels and heart. How is hypertension categorised into stages?
Stage 1 hypertension: BP persistently between 135/85mmHg and 149/94mmHg.
Stage 2 hypertension: BP persistently >150/95mmHg.
Stage 1 and 2 – needs to be a persistently high BP measured at home. Pts may get white coat effect from doctor / dentist.
Stage 3 hypertension: causes organ damage. Systolic BP > 180mmHg or diastolic >120mmHg.
Call 111!
Malignant hypertension - medical emergency. Systolic BP > 220mmHg. Call 999!
What are the consequences of hypertension on the body?
Chronic kidney disease
Hypertensive retinopathy
Aneurysms
Atheroma
Peripheral Vascular Disease
Heart Failure
In hypertension, blood vessel walls are damaged and thickened e.g. thickened walls in arterioles leading to smaller diameter lumen with increased peripheral resistance = increase BP. What effect does this have on organs with smaller blood vessels? And what are the longer term effects?
Organs with a lot of tiny blood vessels e.g. kidneys and eyes are particularly at risk of damage in hypertension.
Chronically, this may lead to Chronic kidney disease and Hypertensive retinopathy.
How does hypertension causes thickening of artery walls?
Increased tough collagen and calcium deposits in the artery walls due to hypertension, which makes them stiffer and less able to stretch with each pulse of blood. This in turn causes more damage to artery walls increasing risk of atheroma, aneurysms and peripheral vascular disease.
The heart has to work harder to create a higher pressure in the left ventricle than the pressure is in the aorta. The high BP in the aorta needs a higher pressure in the ventricle to push blood into it. This leads to ventricular hypertrophy – the muscle in the left ventricle becomes thickened and stiffer. Ultimately leading to heart failure.
When atheromas develop in the vessels of the brain or heart, what happens?
Brain – stroke, seizures
Heart – acute cardiac ischaemia
Most of the time, the cause of hypertension is unknown – essential hypertension. However, there are non-modifiable risk factors such as _____.
Genetics
Age
Ethnicity
What are the modifiable risk factors of hypertension?
Obesity – modifiable through diet and exercise. Risks of being overweight – also linked to diabetes which also increases risk of hypertension.
Alcohol.
Sodium intake- Normally, the body removes salt through kidneys and water from blood follows. This would reduce the venous return and cardiac output & BP. High salt diet causes you to retain more water = hypertension.
Smoking (Chemicals in cigarette smoke impair vasodilation, and cause atherosclerosis (stiffening of blood vessels = hypertension).
Stress (sympathetic fight or flight response which increases BP)
Kidney and endocrine disease - Long term control of BP: salt excretion and hormones are controlled by kidneys. Kidney disease can cause hypertension. Other endocrine disorders such as those causing an increase in catecholamines (hormones / neurotransmitters) in sympathetic NS like adrenaline.
Drugs – increases BP either deliberate or as a side effect. Some medications may interact, preventing an anti-hypertensive from being effective.
How does Conn’s syndrome affect BP?
Conn’s syndrome – where adrenal glands make excess aldosterone; which controls salt and potassium in the blood = hypertension.
How does Phaeochromocytoma affect BP?
small vascular tumour of adrenal medulla leading to irregular secretion of adrenaline and noradrenaline = hypertension, palpitations, headaches.
Drugs for hypertension typically act on the pathways controlling the long-term BP control mechanisms. What are diuretics?
Drug that increases urine production.
*Increases excretion of fluid via kidneys = reduce circulating volume and lower the BP.
What are ACE inhibitors?
ACE-Inhibitors – end in ‘opiril’ - inhibit the ACE enzyme.
Prevent formation of angiotensin-2 (which increases BP), and prevents bradykinin (a vasodilator) from being broken down.
Side effect of stopping bradykinin causes dry cough or angioedema (facial swelling).
How do angiotensin-receptor blockers work?
Angiotensin-Receptor Blockers – end in ‘sartan’ alternative to ACE inhibitors. Blocks angiotensin at the site of its’ action = reduces BP.
Block the arteriolar contraction and sodium retention effects of renin–angiotensin system.
Calcium-channel blockers – prevent _________, and reduce rate & force of heart beat which is all dependent on Ca. These channels are blocked to reduce muscle contraction.
vasoconstriction
Beta-Blockers – end in ‘olol’
Prevent HR and stroke volume from rising too high by blocking _________ pathways. Also decrease _______ release which is a component of blood pressure rising mechanism.
sympathetic
renin
Alpha-Blockers- cause ________ to reduce BP. Clonidine & Methyldopa- rarely used. Block the sympathetic NS centrally in the brain.
vasodilation
Patients who are on anti-hypertensive drugs may be more prone to _________________
postural hypotension (standing up after laying down = feel dizzy. Ask pt to get up slowly). Better to perform tx under LA rather than sedation.
How does atherosclerosis occur?
Initially, a fatty streak in vessel wall due to lipids building up in the inner-most layer of the arterial wall (tunica intima).
Collagen deposition follows, making the vessel stiffer. A fibrotic cap forms over the fatty streak creating a fibrolipid plaque. This plaque can become damaged by the high BP or blood flowing past it e.g. in hypertension. Typically happens at bifurcations of arteries- where blood flow is more turbulent.
When the cap becomes damaged, a complicated fibrolipid plaque occurs.
What is the link between atherosclerosis and periodontal disease?
Atherosclerosis and its’ outcomes such as coronary HD is shown to be correlated with periodontal disease. This may be due to pts propensity for inflammation or periodontal disease causing cytokine / endotoxin release = exacerbating atherosclerosis formation.
Complicated plaques are a great place for thrombosis to occur. What is thrombosis?
A mass of platelets, RBC, and fibrin that sits in the vessel wall.
A thrombus formation is predisposed by which factors of the Virchow’s triad?
the blood, the vessel and blood flow
e.g. the blood constituents themselves becoming sticky, or by the way the blood flows (turbulence, areas like bifurcations of arteries, or hypertension in stiff vessel walls), or damage to vessel wall itself e.g. fibrolipid plaque.
Describe the effect of a thrombus on the vessel and subsequently on the structures the vessel leads to.
Thrombosis reduces the size of the lumen of the blood vessel. This reduces blood flow to the organ. After a certain point, this causes stress to the tissue leading to ischaemia (reduced/restricted blood flow) – eventually the tissue dies due to inadequate blood supply, leading to an infarction (tissue death).
