Hypertension Flashcards
The cardiovascular system comprises __ circulations in series
2 circulations in series
Left heart pumps to the body, blood from the body returns to the right heart
The right heart pumps to the lungs, and blood from the lungs return to the left heart
The site in the circulatory system where nutrient and waste metabolic products is exchanged
Capillaries
Define perfusion
Rate of flow of blood through tissue
Arterial Pressure refers to pressure in that compartment of the circulation between __ and __
Aortic valves and arterioles
Mean arterial pressure (blood pressure) = ?
Cardiac Output (CO) X Peripheral Resistance (TPR)
What is pulse pressure?
It is the difference between systolic and diastolic pressures
Which receptors are responsible for detecting acute changes in blood pressure? And where are they located respectively?
Carotid and aortic baroreceptors
Aortic baroreceptors: in the walls of the aorta
Carotid: in one of the major arteries supplying the brain
How are acute changes in blood pressure corrected in the body?
Via the autonomic nervous system (has 2 arms- sympathetic and parasympathetic)
Sympathetic nervous system acts to increase BP, contractility etc.
Which organ in the body plays a key role in the longer-term regulation of BP?
Kidney
How is blood pressure regulated in the long term?
Through volume regulation via the renin-angiotensin-aldosterone system
Which of the following produced by the juxtaglomerular apparatus plays a key role in regulating blood pressure?
Renin
What is the key component of the Renin-Angiotensin-Aldosterone System?
Juxtaglomerular apparatus
When does circulatory shock occur?
When arterial pressure is insufficient to maintain perfusion
- usually systolic BP < 80mmHg or mean BP < 60mmHg
What are the components of the juxtaglomerular apparatus?
JG Apparatus:
- JG cells
- Macula Densa
Sensors:
- JG cells
-Macula Densa
Effector:
- Renin in JG cells
What are juxtaglomerular (JG) cells and what is their role?
Modified cells of afferent arterioles
Role: Sense pressure in afferent arterioles; contains renin which is released when BP decreases
Where is the Macula Densa located and what is their role?
Location: next to JG cells
Role:
1) signals to the JG cells when there is not enough filtrate for JG cells to release renin
2) Sense Na and Cl presence in the filtrate to determine if there is a sufficient amount
What is primary hypertension?
Hypertension that has no known cause; also known as essential hypertension
What predisposes to primary hypertension?
Involves a dysregulation of BP:
1) Heart: sympathetic overdrive
2) Blood vessels: sympathetic overdrive, dysregulation of vascular smooth muscle tone (smoking, age), smooth muscle hypertrophy due to insulin resistance
3) Kidneys: insensitivity of the RAAS; with age, balance in RAAS is no longer sensitive, kidneys keep reabsorbing Na even though the body does not need it -> volume expansion -> HTN
4) Obesity:
- angiotensinogen released from adipocytes -> increased angiotensin II -> increased resistance -> increased BP;
- increased blood volume
- increased blood viscosity due to dysregulation of the clotting system
Define isolated systolic hypertension
Wide pulse pressure (SBP - DBP > 80 mmHg) + SBP >/= 140mmHg and DBP </= 90 mmHg
Function of aging and arteriolar stiffness
When treating ISH, may lead to orthostatic hypotension. Start low, go slow
What is the definition of orthostatic hypotension?
Defined as a decrease in systolic blood pressure of 20 mmHg or a decrease in diastolic BP of 10 mmHg within 3 minutes of standing when compared to BP from sitting/ supine position
List 2 classes of medications that could lead to secondary causes of hypertension
1) Corticosteroids (cortisone, dexamethasone, hydrocortisone, prednisolone etc.)
2) NSAIDs: Cox-2 selective (celecoxib) and non-selective
- as inhibition of COX in kidneys leads to constriction of afferent arterioles
Other classes:
- Calcineurin inhibitors (e.g. tacrolimus, cyclosporine)
- Decongestants (e.g. pseudoephedrine, oculr phenylephrine)
- Testosterone
- Anti-depressants: desvenlafaxine, venlafaxine, buproprion
- Erythropoiesis-stimulating agents (erythropoietin, darbepoetin)
- Estrogen-containing oral contraceptives
Increased sympathetic activation of beta-1 adrenergic receptors of heart leads to?
Increased cardiac output -> increased preload
Increased sympathetic activation of alpha-1 adrenergic receptors in the smooth muscles leads to?
increased peripheral resistance -> increased afterload
Explain the RAAS cascade in the event of decreased blood pressure
1) Reduced BP -> reduced renal blood flow. This leads to increased secretion of renin which converts angiotensinogen to angiotensin I, which leads to increased production of angiotensin II. Increased angiotensin II leads to increased secretion of aldosterone, leading to increased Na and water retention, leading to increased blood volume
2) Reduced renal blood flow also leads to reduced glomerular filtration rate, which also contributes to increased Na and water retention, hence increasing blood volume
Explain how activation of calcium channels can lead to increased vascular tone & cardiac contractility
Opening of Ca channel -> increased conc of Ca in cell -> Ca combines with calmodulin (in cells) -> ca-calmodulin complex -> activates myosin light chain kinase (MLCK) -> activated MLCK phosphorylates myosin-light chain -> phosphorylated myosin- light chain acts together with actin -> contraction
Explain how beta agonists can lead to activation of Ca channels
Beta agonists activates adenylyl cyclase -> adenylyl cyclase converts ATP to cAMP, which indirectly activates Ca channels
Explain how nitric oxide can lead to relaxation of vascular tone
Nitric oxide activates guanylyl cyclase, which converts GTP to cGMP. Increased cGMP causes actin to disengage from myosin-light chain, and dephosphorylation of myosin-light chain -> relaxation
What is the determinants of BP
BP = CO x TPRCO = Stroke Volume x HR (Stroke Vol is determined by contractility and fill of the heart)
Pathogenesis of HTN
RF: Ageing, Na+ intake (increase CO), Dehydration/Heat stroke (decrease CO)
Why is HTN often called the “Silent Killer”
typically no smx, usually presents as complications eg. target organ damage -> HF, kidney impairment
Smx of severe HTN
- headaches, pulsating behind the eyes, usually early in mornings- visual changes, blurred vision- N&V
Correlation btw SBP and CV risk
5mmHG SBP decrease = 10% CV risk decrease (17% CHD, 27% Stroke, 28% HF)
BP Categories
Normal: <120 and <80Elevated: 120-129 and <80HTN stage 1: 130-139 or 80-89HTN Stage 2: >=140 or >=90Hypertensive crisis (emergency): >180 and/or >120
Risk factors for CVD
- age- smoking-fam Hx of premature CVD- dyslipidemia- DMobesity- cerebrovascular disease (stroke, ischemic attack)- heart disease- renal disease- vascular disease- atherosclerosis
When to treat HTN?
Usually high BP: 130-139/85-89mmHg can start lifestyles changes first then monitor 3-6months, if not working then start drug therapy.If BP >140/90 usually drug tx is started but can still offer lifestyle changes first to pt and see what they prefer.Esp if have comorbidities or high ASCVD/DM/kidney risk, btr to start drug tx earlier
What are some non-pharm management for HTN?
- Weight loss: every 10kg loss, remove 1 drug, every 1kg loss, 1mmHg decrease. Aim BMI <23kg/m2 and waist circumference <90cm (M) and <80cm (W)2. Exercise: at least 30mins moderate exercise 5-7days/wk, >=150mins/wk. decrease -5/8 mmHg3. DASH diet: low Na, higher K. More veg, fruit, fish, putry, nuts. Less diary, red meats, sweets4. Quit smoking: decrease 5mmHg5. Decrease caffeine, alcohol consumption: decrease 4mmHg6. Reduce stress7. Low salt diet/salt substitutes 8. Monitor own BP at home regularly
Problem of inappropriate BP monitor cuff size
Undersized: raises BP -> too tightOversize: lowers BP -> too looseNormal Adult cuff size: - width 37-50% of limb’s length (length to width ratio 2:1)- bladder 75-100% (wrap ard arm >75% of circumference)- OTC usually sells 22-26cm arm circumferenceObese: consider wrist meters, place at lvl of heart. below heart- over reads, above heart- under readspaediatrics: right arm BP unless coarctation of aorta + limb BP (supine)
What to take note of when monitoring BP at home
- Take BP twice a day: Before breakfast, administration of meds, or exercise and then in evening. Measure at the same time every day.- Avoid food, caffeine, alcohol 30mins prior to measurement- Sit quietly during monitoring. Sit for 5 mins with legs and ankles uncrossed, back supported against a chair. Stay calm and don’t talk while taking BP. Dont talk and move. - Position arm at rest, at level of your heart on a table or chair arm. Use a pillow or cushion as needed to elevate it.- Place cuff on bare skin, not over clothing. Avoid rolling long sleeves up. For muslim women: make sure they wear loose clothing to allow rolling up of sleeves but sometimes no choice so home BP is impt. - Wait for at least 1 minute before repeating. Write down the readings, average them -> give them BP chart to record. - Ideally, 7 consecutive days readings. Min 3 days consecutively prior to the next apptm. - Calibrate against clinic BP meter
What is the recommended antihypertensive agent/standard therapy for patients with heart failure with congestive history?
Beta blockers + ACE-i/ARB/ARNi
For patients with heart failure with congestive history, what antihypertensive agents can be considered as an add-on?
Aldosterone antagonist, diuretics
What is the recommended antihypertensive agent/standard therapy for patients with post myocardial infarction or Atrial Fibrillation?
Beta blockers
For patients with post myocardial infarction or atrial fibrillation, what antihypertensive agents can be considered as an add-on?
ACE-i/ ARBs;
ARB may prevent recurrence of AF (class IIa)
What is the recommended antihypertensive agent/standard therapy for patients with coronary artery disease, especially if angina?
Beta-blockers
For patients with coronary artery disease, especially if angina, what antihypertensive agents can be considered as an add-on?
1) ACE-i / ARBs
2) DHP CCB or diuretic
*for left ventricular hypertrophy, use of ACE-i/ARB/CCB associated with more effective regression than BB or diuretics
What is the recommended antihypertensive agent/standard therapy for patients with diabetes mellitus, especially if they are proteinuric?
1) Any first-line antihypertensives
2) ACEi if proteinuric
For patients with diabetes mellitus, what antihypertensive agents can be considered as an add-on?
1) CCB
2) Diuretics
What is the recommended antihypertensive agent/standard therapy for patients with CKD (Stage 3 and greater) or stage 1/2 CKD with albuminuria?
1) ACE-i/ARB especially if proteinuric
For patients with CKD (Stage 3 and greater) or stage 1/2 CKD with albuminuria, what antihypertensive agents can be considered as alternatives?
Consider other BP drugs if issues with RASi arise
What is the recommended antihypertensive agent/standard therapy for patients on recurrent stroke prevention? And what needs to be ensured if patient has AF?
1) Thiazide-like diuretic + ACE-i
2) If patient has Atrial fibrillation, ensure strict anticoagulant control
What is the recommended antihypertensive agent/standard therapy for pregnant women?
1) Nifedipine (usually first-line)
2) Methyldopa
3) Labetalol
Which antihypertensive agents are contraindicated in pregnant women?
ACE-i, ARBs, direct renin inhibitors
What is the recommended antihypertensive agent/standard therapy for patients with BPH?
Alpha blockers
What is the BP treatment target for patients with concomitant conditions?
<130/80
What is the BP treatment target in general?
120-130/70-80 mmHg
What is the BP treatment target for adults >65 - 80 years old?
Proceed in stepwise approach, as much as patient can tolerate:
1) <150 mmHg, if tolerated and achievable,
2) < 140 mmHg; and ideally, if tolerated and achievable,
3) <130 mmHg
What is the BP treatment approach for elderly >80y/o?
Titrate cautiously
What needs to be monitored when ACEi/ARB is initiated when treating for hypertension?
1) Effectiveness (BP Control), adherence, relevant ADRs
2) Renal panel (Cr, K) in 1-2 weeks
3) Check for cough (ACE-i)
4) Look out for ADR cross reactivity
What needs to be monitored when beta-blockers are initiated for treatment of hypertension?
1) Effectiveness (BP Control), adherence, relevant ADRs
2) Follow up in 2-4 weeks, PRN
3) Pulse rate control
What needs to be monitored when CCBs are initiated for treatment of hypertension?
1) Effectiveness (BP Control), adherence, relevant ADRs
2) Follow up in 2-4 wks, call in PRN
3) Pulse rate control (for non-DHPs)
What needs to be monitored when diuretics are initiated for treatment of hypertension?
1) Effectiveness (BP Control), adherence, relevant ADRs
2) Renal panel (Cr, K), in 1-2 weeks
3) For some patients (e.g. elderly- at risk of hyponatremia), monitor Na as well
Are beta-blockers generally considered as first-line treatment options for hypertension?
No. Usually considered when there is a specific indication for their use
