BP control Flashcards
What is BP? What is it a balance between?
- Driving force propelling blood to tissues
- Balance between organ perfusion and vascular damage (too much blood)
- Closely autoregulated
What is the equation for CO?
Cardiac output (L/min) = heart rate x stroke volume
What is the equation for mean systemic arterial pressure?
Mean systematic arterial pressure = cardiac output x total peripheral resistance
What is the equation for Total peripheral resistance?
R = resistance to blood flow L = length of vessel η = viscosity of blood flow r = radius of the blood vessel
R= 8nl/ Pi x r^4
How is the ANS regulated?
- Baroreceptors- found in aortic arch and carotid bodies/ sinus
- Local e.g. renal juxtaglomerular apparatus
Where are baroreceptors located?
Located: Carotid sinuses, Aortic Arch
How does baroreceptor increased/ decreased firing affect sympathetic and parasympathetic tone?
• ↑Baroreceptor firing – Decreases Sympathetic Tone – Increases Parasympathetic Tone • ↓Baroreceptor firing – Increases Sympathetic Tone – Decreases Parasympathetic Tone
If mean systemic arterial pressure decreased, how would that affect baroreceptor firing, sympathetic and parasympathetic tone?
If mean systemic arterial pressure decreased, baroreceptor firing would decrease, sympathetic tone would increase and parasympathetic tone would decrease.
If mean systemic arterial pressure increased, how would that affect baroreceptor firing, sympathetic and parasympathetic tone?
If mean systemic arterial pressure increases, baroreceptors fire more, sympathetic tone will decrease and parasympathetic tone will increase.
What are direct sympathetic actions?
① Positive chronotropy-SA node regulates- speeds up the HR acting on sinus node- changing the rythm
② Positive dromotropy (conduction)-AV node
③ Positive inotropy (contraction)-Ventricles and atria
④ Positive lusitropy (relaxation)-Ventricles and atria
What are systemic sympathetic actions?
① Activation of Renin-Angiotensin-Aldosterone-System (RAAS)
② Suprarenal stimulation- Catecholamines
How does the RAAS system work?
Liver to Angiotensinogen to Renin converts angiotensinogen to angiotensin I to Angiotensin converting enzyme converts AgI to AgII to Ag II leads to pituitary glands secreting aldosterone and AgII leads to vasopressin.
What is blood pressure regulated in the long term?
Natriuretic peptides
- Induce excretion of Na+ in the urine
- ANP = atrial natriuretic peptide
- BNP = brain natriuretic peptide
- Released when myocytes are mechanically stretched by increased plasma volume
What are the results of hypertension?
High BP- able to compensate for stresses in the body Ischemia Heart Disease (IHD) Cerebrovascular accident/ stroke (CVA) Cardiovascular Disease (CVD) Atrial Fibrillation (AF) Peripheral Vascular Disease (PVD)
How to classify hypertension?- Primary
Primary (Essential):
90% of cases
• Over-activation of physiological mechanisms
• Age-related decrease in baroreceptor sensitivity
• Age-related vascular calcification- causes vessels to be more stiff
• No identifiable cause
Primary- don’t know why someone has high BP- over activation of mechanisms
How to classify hypertension?- Secondary
10% of cases
• Renal – Renovascular disease, parenchymal disease
• Endocrine – Conn’s syndrome, Cushing’s syndrome, Cardiovascular – Coarctation of aorta
• Tumour – Phaeochromocytoma
• Pregnancy – Pre-eclampsia, eclampsia
Secondary- not that common- related to something else that is causing high
What is pheochromocytoma?
Pheochromocytoma is a rare tumour of adrenal gland tissue. is a rare tumour of adrenal gland tissue.
What is Conn’s syndrome?
Conn’s syndrome is a rare health problem that occurs when the adrenal glands make too much aldosterone.
What is pre-eclampsia?
Pre-eclampsia (PE) is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine.
What is white coat syndrome?
White coat syndrome- people exhibit a blood pressure level above the normal range, in a clinical setting, although they do not exhibit it in other settings
What are complications of hypertension to the heart?- LVH
Heart- LVH- left ventricular hypertrophy
High BP
No valve barrier but blood is trying to get out of an area at a higher pressure- more difficult
So muscle has to get stronger in order for this to happen.
LVH increases LV thickness, reduces LV cavity radius and therefore reduces wall stress.
What is the law of Laplace for LV cavity P?
for any given LV cavity pressure (P), the wall stress will be directly proportional to the LV cavity size or radius (R) and inversely proportional to the LV thickness (T)
What are complications of hypertension to the heart?- Diastolic dysfunction?
Heart- Diastolic dysfunction- thickens too much- if ventricle too stiff and thick won’t relax enough for blood to move.
What are complications of hypertension to the heart?- Hypertensive heart failure
LVH to Increased stiffness to Increase LV End diastolic pressure to Increase LA pressure to Pulmonary congestion/ oedema (fluid in the lungs) to Heart failure
Diastolic dysfunction to Impaired relaxation to Increase LV End diastolic pressure to Increase LA pressure to Pulmonary congestion/ oedema (fluid in the lungs) to Heart failure
What are complications of hypertension?- vasculature
Prolonged HTN → vascular remodelling
Any organ is affected by it. Affects the BV itself. BV get thicker and bigger to reduce stress.
What is eutrophic remodelling?
Small arteries
↑SVR → ↑DBP
Eutrophic remodeling- Increase in media to lumen ratio but cross sectional same
What is hypertrophic remodelling?
Large arteries
↑Wall stiffness → ↑SBP
Hypertrophic remodeling- Increase media to lumen ratio increase in cross sectional area
What does vasculature lead to?
– More prone to atherosclerosis
– More prone to large vessel structural damage
What are the manifestations of atherosclerotic disease to the head, heart, kidneys, lower limbs and other?
Head:
• Brain- stoke
• TIA
• Carotid disease
Heart: • Heart Failure • Arrhythmia • Angina • MI
Kidneys:
• Renal Failure
Lower limbs: • Mesenteric ischaemia/infarction • Peripheral Vascular Disease: • Intermittent Claudication • Gangrene
Other:
- Impotence
- Aortic aneurysm
What are complications of hypertension?- kidneys
– Hypertensive nephropathy
- Renal arteriole thickening → luminal narrowing
- Resulting ischaemia → tubular atrophy & interstitial fibrosis- build up of fibrotic tissues
- Damage to glomeruli → haemoproteinuria (protein and blood in urine)
What are complications of hypertension?- eyes
– Hypertensive retinopathy
Investigations for secondary causes of hypertension?
- To look for cause (Secondary HTN)
* Assess end-organ damage
What are blood tests done for secondary hypertension?
- FBC: Hb (blood viscosity)
- U&Es (urea and electrolytes: Renal impairment, hypernatraemia
- Lipids & glucose: Other CVD risk factors
What is hypernatraemia?
Hypernatraemia is defined as a serum sodium concentration exceeding 145 mmol/L.
What further test other than bloods is done for secondary hypertension?
Urinalysis:
-Haemo/proteinuria
Metabolic syndrome- high BP, dyslipidemia and high glucose
What investigations for the eyes is there?
Fundoscopy- Grade 1-4 hypertensive retinopathy
What tests are there for the kidneys?
Renal tract USS: RVD, APKD, CKD- find if kidneys aren’t working well- have an US
-MRI renal/adrenals: RVD, phaeochromocytoma- shows better detail blood flow to kidney
What is pheochromocytoma?
Pheochromocytoma is a rare tumour of adrenal gland tissue.
What are other investigations for hypertension?
- 24 hour urinary catecholamines: phaeochromocytoma
- Plasma renin-aldosterone: Conn’s syndrome
How to manage hypertension- lifestyle and support?
• Smoking cessation • Lipid control • Diet +/- wt loss • Exercise • Education – Specialist nurses – Leaflets – Support groups – Websites e.g. BHF
What are pharmacological treatments to manage hypertension?
A-ACEI, ARB
C-Calcium-Channel Blockers (CCB’s)
D-Diuretics
ACEi and A2RBs- E.g. Ramipril, Candesartan ACEI end in priol. A2RBs end in artan.
RAAS Blockade- ACEI stops ACE stops production of AgII lose all the effects of AgII
If AgII isn’t produced what does that effect in the RAAS?
• Angiotensin II – Vasoconstriction – Increased Na+ and H2O retention • Aldosterone – Increased Na+ and H2O retention • Vasopressin (Antidiuretic Hormone) – Promotes H2O retention
What do calcium channel blockers do and what are the different types?
- Disrupt movement of Ca2+ through channels
- Dihydropyridine and non-dihydropyridine
- E.g. Amlodipine and Diltiazem
CCB’s cause HR and SV to decrease, CO decreases, TPR decreases so mean systemic arterial pressure decreases.
What do dihydropyridines and non-dihydropyridines do?
• Dihydropyridines vasodilate • Non-Dihydropyridines also: – Negatively Inotropic – Negatively Chronotropic All will cause vasodilation causes BV to relax.
What do diuretics do?
- Induce diuresis → reduced circulating volume
- Thiazide and loop
- E.g. Bendroflumethiazide and furosemide
Indapamide affects sodium absorption.
Spironolactone- works against aldosterone- causes more diuresis and affects RAAS.
What are other agents for reducing hypertension?
- Beta-blockers e.g. bisoprolol- Beta blockers get rid of the sympathetic actions
- Alpha-blockers e.g. doxazosin
- Moxonidine: centrally acting to ↓SNS activity
- Spironolactone: aldosterone antagonist
What are the drugs preferred in heart failure, angina, diabetes and proteinuria?
– Heart Failure → ACEi/A2RB or Beta-blocker
– Angina → Beta-blocker
– Diabetes → ACEi/A2RB
– Proteinuria → ACEi/A2RB
What are the problems with ACEI/A2RBs, Beta Blockers, CCBs and diuretics?
ACEi/A2RBs → pregnancy, B/L RAS, hyperkalaemia
B blockers → asthma, 2nd/3rd degree AVB
CCBs → 2nd/3rd degree AVB (NDHPs)
Diuretics → hypokalaemia, gout (thiazides)
AVB= atrioventricular block CCB= Calcium channel blocker
How is hypertension defined (values)?
HTN defined as SBP ≥ 140 and/or DBP ≥ 90
