Hypertension Cheat Sheet

J
Justin BerkStudent em Texas Tech University Health Sciences Center - School of Medicine

This student "cheat sheet" is designed to provide medical students with basic information regarding the diagnosis and treatment of Hypertension. It includes Questions to Ask, what to look for on a Physical Exam, Labs to Order, and basic Treatment Plans. These guides are particularly designed for first and second-year medical students as an introduction to primary care and ambulatory care medicine and attempts to tie in the basic pathophysiology that is high-yield for USMLE Step 1. Any and all feedback is very welcomed.

Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback.
HYPERTENSION CHEAT SHEET
 A chronic disease of elevated arterial pressure- a measurement of how hard the heart has to work.
 “Primary” hypertension accounts for 95% of hypertension –mechanism is not understood.
Systolic – arterial pressure when heart contracts | Diastolic – arterial pressure when heart relaxes
How to take an ideal blood pressure
- No nicotine/caffeine for 30 minutes
- Patient should be sitting for 5 minutes
- Free of restrictive clothing
- Appropriate cuff size
Other factors that BP: full bladder, unsupported back/feet, crossed legs, cuff over clothing, unsupported arm, conversation.
Risk factors for hypertension
- Ethnicity (Black)
- Family history
- Excess sodium intake
- Sedentary lifestyle
- Obesity
- High cholesterol
Classification and Treatment Guidelines
Classification of HTN is based on the average of 2 or more properly measured readings after an initial BP
screening. Treatment is then based on the classification.
Hypertension Stage BP Reading Treatment
Systolic Diastolic
Normal < 120 < 80 No treatment.
Pre-HTN 120-139 80-89 Lifestyle Modification
Stage 1 140-159 90-99
Add 1 anti-HTN medication
+ lifestyle modifications
Stage 2 160-200 100+
Start 2 anti-hypertension
medications + lifestyle
modification
Hypertensive emergency 200+ with symptoms Call ER (labetalol, nitroprusside)
*If patients remain hypertensive, resistant to multiple oral treatments, consider secondary causes of HTN
Questions to Ask
Elevated pressures, over time, wear down organs that have smaller vasculature e.g. eyes & kidneys
The heart is also forced to work harder and can therefore become overworked, leading to heart failure.
Some of the primary concerns of chronic HTN are stroke, heart attack, retinopathy, nephropathy
 Vision changes
 Chest pain
 Shortness of breath
 Headache
Physical Exam Findings
 AV nicking on eye exam
 Displaced PMI (point of maximal impact)
 Carotid bruit (if atherosclerosis)
 Peripheral edema
 Pulmonary edema (if heart failure)
Secondary causes of hypertension
 Cushing’s disease
(hypercortisolism)
 Hyperthyroidism
 Renal artery stenosis
 Pheochromocytoma
 Aortic coarctation
 Conn’s syndrome
(hyperaldosteronism)
 “White coat hypertension”
 Oral Contraceptive Pills
 Sympathomimetics (e.g
decongestants)
Laboratory / Diagnostics
Initial: CBC, CMP, TSH, urinalysis, microalbumin, EKG
EKG Findings: LVH, past MI
Follow-up: BMP (bi-annually)
Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback.
TREATMENT
PHARMACOTHERAPY - FIRST LINE MEDS: diuretics, ACEI/ARBs, CCBs
Class Example Mechanism Notes
ACE-Inhibitor Lisinopril
Block Angiotensin
converting enzyme
Dry cough, angioedema
(2/2 inhibition of
bradykinin). Cr , K+
Angiotensin 2 receptor
blockers (ARBs)
Losartan Blocks AT2 receptors K+
Renin is secreted
by kidneys when
they perceive
hypoperfusion.
Renin stimulates
AT1 which is
converted to AT2
by ACE in the lung.
AT2 is a
vasoconstrictor
and stimulates
formation of
aldosterone
(which increases
BP through sodium
retention).
Calcium Channel
Blocker (CCB)*
Nifedipine
Blocks smooth muscle
vasoconstriction
Edema
Thiazide Diuretic
Hydrochlorothiazide
(HCTZ)
Increases natriuresis
Good in AA population –
salt sensitive. Lose K.
Beta Blockers** Atenolol, Metoprolol
MAP = CO x TPR
Decrease CO via HR
and inotropy
Can mask hypoglycemia
Alpha antagonists Doxasozin
Block a1 receptors
which vasoconstrict
Used for co-morbid BPH
Others: hydralazine, nitroprusside, methyldopa, clonidine
*Heart selective vs. vessel selective: Dihydropyridines (Amlodipine, Nifedipine) work preferentially on the vessels. (Thus, they can cause
rebound tachycardia.) Non-dihydropyridines (Verapamil, Diltiazem) work preferentially on the myocardium of the heart
**Selective vs. non-selective: e.g carvedilol (non-selective alpha and beta blockade)
LIFESTYLE MODIFICATION:
DASH Diet: Rich in fruits, vegetables, low-fat. Limit carbs. Eat whole grains.
Exercise: 40 minutes a day. Can include 3 bouts of 10 minutes walking
Smoking cessation: Reduces CVD risk associated with HTN. Consider pharmacotherapy.
Reduce salt intake: Choose “no salt added” foods, do not add salt.
Increase potassium intake: through fruits and nuts (only if renal function is normal)
Limit alcohol to 1 drink (women) or 2 drinks (men) per day
Maintain normal weight: Every 1% weight loss can decrease BP by 1mmHg.
Stress reduction / Good sleep: Consider yoga, meditation, prayer. Encourage good sleep habits.
Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback.

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Hypertension Cheat Sheet

  • 1. Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback. HYPERTENSION CHEAT SHEET  A chronic disease of elevated arterial pressure- a measurement of how hard the heart has to work.  “Primary” hypertension accounts for 95% of hypertension –mechanism is not understood. Systolic – arterial pressure when heart contracts | Diastolic – arterial pressure when heart relaxes How to take an ideal blood pressure - No nicotine/caffeine for 30 minutes - Patient should be sitting for 5 minutes - Free of restrictive clothing - Appropriate cuff size Other factors that BP: full bladder, unsupported back/feet, crossed legs, cuff over clothing, unsupported arm, conversation. Risk factors for hypertension - Ethnicity (Black) - Family history - Excess sodium intake - Sedentary lifestyle - Obesity - High cholesterol Classification and Treatment Guidelines Classification of HTN is based on the average of 2 or more properly measured readings after an initial BP screening. Treatment is then based on the classification. Hypertension Stage BP Reading Treatment Systolic Diastolic Normal < 120 < 80 No treatment. Pre-HTN 120-139 80-89 Lifestyle Modification Stage 1 140-159 90-99 Add 1 anti-HTN medication + lifestyle modifications Stage 2 160-200 100+ Start 2 anti-hypertension medications + lifestyle modification Hypertensive emergency 200+ with symptoms Call ER (labetalol, nitroprusside) *If patients remain hypertensive, resistant to multiple oral treatments, consider secondary causes of HTN Questions to Ask Elevated pressures, over time, wear down organs that have smaller vasculature e.g. eyes & kidneys The heart is also forced to work harder and can therefore become overworked, leading to heart failure. Some of the primary concerns of chronic HTN are stroke, heart attack, retinopathy, nephropathy  Vision changes  Chest pain  Shortness of breath  Headache Physical Exam Findings  AV nicking on eye exam  Displaced PMI (point of maximal impact)  Carotid bruit (if atherosclerosis)  Peripheral edema  Pulmonary edema (if heart failure) Secondary causes of hypertension  Cushing’s disease (hypercortisolism)  Hyperthyroidism  Renal artery stenosis  Pheochromocytoma  Aortic coarctation  Conn’s syndrome (hyperaldosteronism)  “White coat hypertension”  Oral Contraceptive Pills  Sympathomimetics (e.g decongestants) Laboratory / Diagnostics Initial: CBC, CMP, TSH, urinalysis, microalbumin, EKG EKG Findings: LVH, past MI Follow-up: BMP (bi-annually)
  • 2. Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback. TREATMENT PHARMACOTHERAPY - FIRST LINE MEDS: diuretics, ACEI/ARBs, CCBs Class Example Mechanism Notes ACE-Inhibitor Lisinopril Block Angiotensin converting enzyme Dry cough, angioedema (2/2 inhibition of bradykinin). Cr , K+ Angiotensin 2 receptor blockers (ARBs) Losartan Blocks AT2 receptors K+ Renin is secreted by kidneys when they perceive hypoperfusion. Renin stimulates AT1 which is converted to AT2 by ACE in the lung. AT2 is a vasoconstrictor and stimulates formation of aldosterone (which increases BP through sodium retention). Calcium Channel Blocker (CCB)* Nifedipine Blocks smooth muscle vasoconstriction Edema Thiazide Diuretic Hydrochlorothiazide (HCTZ) Increases natriuresis Good in AA population – salt sensitive. Lose K. Beta Blockers** Atenolol, Metoprolol MAP = CO x TPR Decrease CO via HR and inotropy Can mask hypoglycemia Alpha antagonists Doxasozin Block a1 receptors which vasoconstrict Used for co-morbid BPH Others: hydralazine, nitroprusside, methyldopa, clonidine *Heart selective vs. vessel selective: Dihydropyridines (Amlodipine, Nifedipine) work preferentially on the vessels. (Thus, they can cause rebound tachycardia.) Non-dihydropyridines (Verapamil, Diltiazem) work preferentially on the myocardium of the heart **Selective vs. non-selective: e.g carvedilol (non-selective alpha and beta blockade) LIFESTYLE MODIFICATION: DASH Diet: Rich in fruits, vegetables, low-fat. Limit carbs. Eat whole grains. Exercise: 40 minutes a day. Can include 3 bouts of 10 minutes walking Smoking cessation: Reduces CVD risk associated with HTN. Consider pharmacotherapy. Reduce salt intake: Choose “no salt added” foods, do not add salt. Increase potassium intake: through fruits and nuts (only if renal function is normal) Limit alcohol to 1 drink (women) or 2 drinks (men) per day Maintain normal weight: Every 1% weight loss can decrease BP by 1mmHg. Stress reduction / Good sleep: Consider yoga, meditation, prayer. Encourage good sleep habits.
  • 3. Revised 8/17/14. Email justin.berk@ttuhsc.edu with any feedback.