Hypertension Flashcards
risk factors for heart disease
modifiable: diet, smoking, hypercholesterolaemia, diabetes, physical activity, work, stress
non-modifiable: age, gender, race, personality type, family history
symptoms of hypertension
normally, none :)
but people can complain of headache, visual disturbances, chest pain, dyspnoea, palpitations, sweating, lower limb swelling, claudication, loss of consciousness, flushing, anxiety
history of presenting complaint in hypertension. what would you ask?
- have you ever checked your blood pressure?
- do you keep a record of your blood pressure throughout?
- how long have you been diagnosed with hypertension?
- are you on any anti-hypertensive treatment and do you take your medications?
cardiac risk factors
cardiovascular disease, renal disease, family history, glucose intolerance, dyslipidaemia, CVA/TIA, PVD
what is used to assess the risk of hypertension and cardiovascular disease
the European Low Risk Chart
things to evaluate when assessing a person’s lifestyle
social history: smoking, alcohol, recreational drug use, exercise, body weight, diet
- sleep history, erectile dysfunction, gestational hypertension, preeclampsia
- menopause
classifications of hypertension
primary and secondary
causes of secondary hypertension
- endocrine: primary hyperaldosteronism (Conn’s), hyperparathyroidism, phaeochromocytoma, hypercortisolism (Cushing’s), hyperthyroidism, acromegaly, congenital adrenal hyperplasia
- renal: renovascular disease, polycystic kidney disease, renal failure, chronic pyelonephritis, glomerulonephritis, SLE, renal tumours
- others: coarctation of the aorta, OSA, sympathetomimetic drugs, NSAIDs, OCP, recreational drugs like cocaine, meth and phencycline, pregnancy and preeclampsia
what to check for hypertension-mediated organ damage
heart, blood vessels, brain, eyes and kidneys
definition of hypertension
a sustained blood pressure of an SBP higher than 140mmHg and a DBP higher than 90mmHg
investigations for hypertension
bloods, urinanalysis, 12-lead ECG, ABPM/HBPM, echo, CXR, carotid ultrasound, ankle brachial pressure index, cognitive function, CT brain
classes of hypertension
high-normal: SBP >130 DBP >85
Stage I: SBP >140 DBP >90
Stage II: SBP >160 DBP >100
Stage III: SBP >180 DBP >110
management of hypertension
educate on lifestyle changes for every single stage of hypertension
start medicating Stage I patients if you see no hypertension control within 3 months of the diagnosis
start medicating ASAP in Stage II and Stage III patients
lifestyle advice to give
stop smoking, stop drinking, exercise more, eat a balanced diet, reduce salt intake, try to lose weight
drugs used in hypertension
- ACE inhibitors/ ARBs
- Beta blockers
- Calcium channel blockers
- Thiazide-like diuretics
how to give drugs in hypertension
- start with dual-therapy with an ACEi (or ARB) and a CCB/diuretic
- if with step 1 hypertension is not controlled, add on the CCB or diuretic not used in step 1
- add on spironolactone, alpha blocker or another beta blocker
when to consider monotherapy
- Stage I hypertension
- in patients older than 80y or frail patients
device-based therapies for hypertension
- renal denervation
- carotid baroreceptor stimulation
- creation of an atrioventricular fistula
characteristics of malignant hypertension
- severe hypertension
- fundoscopic changes
- microangiopathy
- disseminated intravascular coagulation
- small artery necrosis in the kidney, retina and brain
how are hypertension and obesity linked?
- activation of the sympathetic nervous system
- activation of the RAS
- sodium retention
the link between leptin and hypertension
- contributes through the sympathetic activation via the hypothalamic pro-opiamelanocortin pathway
- relates to the activation of renal nerve traffic and to subsequent alteration of the P-natriuresis relationship
the link between hypertension and the RAAS pathway
the additional adipose tissue deposits will increase the production of renin, angiotensiogen and angiotensin II
the link between insulin and hypertension
insulin causes the tubular reabsorption of sodium
effects of weight loss
- decrease in cholesterol, LDL, triglycerides and total fat content
- decrease in SBP
- decrease in FBG in diabetes
pathogenetic role of hypertension
it stretches the body due to the sodium retention and thus, water retention. this leads to damage of the intima of the vessels and thus, accumulation of fats and cholesterol into the intima, leading to atherosclerosis
what is DASH?
DASH is the dietary approaches to stop hypertension
it consists of a diet which reduces fat intake, added sugars, sweets, sugary drinks and red meats
it is rich in fruits and vegetables, whole grains, seeds, nuts, fish, poultry
levels of sodium needed to reduce blood pressure
2,300mg/day to start lowering it
1,500mg/day to further lower it - recommend this to people who are already hypertensive, have other comorbidities which leave them at risk for HTN, African Americans, middle aged/older adults
electrolytes found in DASH
magnesium, calcium and potassium
potassium has to be supplemented also
diagnosis of hypertension
measure BP multiple times in office and out-of-office
checking for orthostatic hypotension
measure this when:
- sitting
- standing up
- 1 min after standing up
- 3 mins after standing up
populations to check sitting and standing blood pressure
diabetics, people over 80 years or age, people with symptoms of postural hypotension
definition of orthostatic hypotension
a drop in blood pressure of >10mmHg within 3 minutes of standing up
define white coat hypertension
an increase in blood pressure of around 5-15mmHg measured in clinic when compared to an out-of-office measurement
how to take a blood pressure record?
record twice a day, take 2 readings in the morning, 2 at night and keep repeating this pattern for 3-7 days before your next clinic checkup
definition of ambulatory blood pressure monitor
a device which measures BP for a 24hr period of time, takes readings every 15-30 minutes
night time blood pressure dip
10%-20% drop in blood pressure during the night
masked hypertension
when BP measurements are normal in office but are elevated in HBPM readings; these are associated with HMOD; these have a cardiovascular disease risk similar to normal hypertensives
true (sustained) hypertension
when both the office and out-of-office readings are elevated
true (sustained) normotension
when both the office and out-of-office readings are normal
what is hypertension-mediated organ damage?
structural and functional changes in the arteries or end organs caused by an elevated blood pressure
what should be the target BP in controlled hypertension?
- <130/80 in normal patients
- in patients >80yo, target an SBP 130-139
resistant HTN
- BP would not reduce to a value lower than 140/90
- despite the patient being on the correct medications
- it is confirmed that the patient is being compliant with their medications
gestational hypertension
when the woman develops a blood pressure >140/90 when she has completed more than 20 weeks of gestation
management of gestational hypertension
- treat with labetalol
- admit to hospital if the BP >160/110
management of malignant hypertension
- reduce the hypertension slowly to reduce the risk of multiorgan ischaemia whilst lowering the BP
- lower BP to DBP 100-110 using amlodipine; reduce as such in the 1st 24-48hrs
- lower BP to a normal BP in the next 2-3 days
mode of action of ARBs
this blocks the Angiotension II type I receptor
common side effect of ACEi
cough due to the accumulation of bradykinin in the lungs
types of RAS blockers
- direct renin inhibitor (aliskiren)
- ACE inhibitors (perindopril)
- Angiotensin II Type I receptor blocker (valsartan)
mechanism of action of beta-blockers
- decreases the renin release from juxtaglomerular cells
- reduces cardiac contractility
- reduces the heart rate
- vasodilatation
mechanism of action of CCBs
- inhibition of the intracellular calcium influx (reduced LV contractility and decreased myocardial oxygen consumption)
- inhibition of the vascular smooth muscle cell contraction (coronary artery dilatation)
- reduction in the peripheral vascular resistance (decrease the afterload)
mechanism of the thiazide-like diuretic
- block the Na/Cl co-transporter in the distal convoluted tubule
- increases the urinary Na and Cl urinary excretion
effects of thiazide-like diuretics
acute - decrease the extracellular fluid volume and decrease the cardiac output
subacute - decrease the plasma volume and decrease the total peripheral resistance
chronic - decrease the total peripheral resistance
other drugs used in hypertension
- mineralocorticoids eg spironolactone
- alpha-blockers eg doxazosin
- centrally acting agents eg methyldopa
hypertension and chronic kidney disease
- use ACEis with caution
- take a baseline creatinine and eGFR before starting the medication
- diuretics might not work well due to the damage on the kidney
- switch to a loop diuretic if the eGFR drops below 30ml/min/1.72m2
hypertension and heart failure with reduced ejection fraction
- start with triple therapy (ABD)
- use cardioselective beta blockers ideally like carvedilol
contraindications of ACEis and ARBs
- pregnancy
- hyperkalaemia
- bilateral renal artery stenosis
contraindications of beta-blockers
- asthma
- bradycardia
- any high-grade sinoatrial or atrioventricular block
- glucose intolerance
