Upgrade to remove ads
Only $2.99/month

Week 2 - HTN

Terms in this set (57)

Describe the categorization of normal, elevated, Stage 1 and Stage 2 hypertension per the AHA guidelines.
Describe the categorization of normal, elevated (pre-hypertension), Stage I and Stage 2 hypertension for pediatric patients
What are some recommended antihypertensives and their general MOA?
Thiazide Diuretics
- Decreases Na+ reabsorption by inhibiting Na+/C- cotransporter
- Lowers BP by increasing sodium and water excretion
- Lowers CO and renal blood flow; lowers peripheral resistance with long term us

ACE inhibitors
- ACE inhibitors lower your blood pressure by reducing angiotensin II in your body. This allows your blood vessels to relax and widen, making it easier for blood to flow through. It also lowers the amount of water your body retains, which lowers your blood pressure.

Angiotensin receptor blockers
- Angiotensin receptor blockers (ARBs) lower your blood pressure by blocking the actions of angiotensin II. This allows your blood vessels to relax and widen, making it easier for blood to flow through. It also reduces the amount of water your body retains, which lowers your blood pressure.

Calcium channel blockers
- Vasodilate arterial smooth muscle to decrease systemic BP
- Vasodilate coronaries to increase blood supply to cardiac muscles
- Decreases rate of SA node discharge (slows HR) and decreases myocardial contractility. Aka, heart doesn't have to work as hard.

Beta blockers
- These are adrenergic receptor blockers, meaning they lower BP by reducing binding of adrenaline and noradrenaline to slow HR
- This allows left ventricle to fill completely
- Also dilates peripheral arteries to lower BP
- This decreases afterload for the LV
- less effective in preventing stroke, though
What are some common substances that can affect the productivity of antihypertensives?
Alcohol, amphetamines, antidepressants, antipsychotics, caffeine, decongestants, immunosuppressants, NSAIDs, oral contraceptives, TK inhibitors, corticosteroids
What are some non-pharmacologic treatments to lower blood pressure in kids/adults?
- Dietary Approaches to Stop Hypertension (DASH) diet (rich in fruits, veggies, whole grains, and low-fat dairy

- Reduce sodium intake and increase potassium (although contraindicated in some patients, such as those with kidney disease)

- Expect a 1 mmHg BP reduction for every 1 kg reduction in body weight

- 90 to 150 minutes of aerobic and/or dynamic resistance exercise a week; or 3 sessions per week

- Alcohol; less than 2 drinks/day for men and 1 drink/day for women
What is the difference between the two forms of hypertensive crises?
Hypertensive urgency: severe BP of 180/20 of above without target organ damage Intensify antihypertensive drugs

Hypertensive emergency: severe BP of higher than 180/120 mmHg with new or worsening target organ damage
- 1 year mortality rate 79% with life expectancy at 10.4 months
- Needs immediate BP reduction to prevent further damage
What are the general recommendations for treatment and follow up of the different categories of hypertensive patients?
What are the two branches of the autonomic nervous system and the NTs involved.
sympathetic
- preganglionic axon secretes Ach, but the post ganglionic axon secretes Norepinephrine (N-epi)
- The receptors for norepinephrine are called adrenergic receptors (called B1 receptors in the heart)
- The arterial (alpha1) receptors in the arteries constrict arteries, increasing BP and flow; these are more responsibe to NE than Epi
- serves to increase SA Node pacing, rate of conduction, force of contraction, and irritability of foci (excitatory responses)

parasympathetic
- preganglionic and postganglionic axon NTs are acetylcholic (ACh)
- Ach activates cholinergic receptors
- Acts on the heart to decrease SA Node pacing, decrease rate of conduction, decrease contractility, and decrease irritability of atrial and junctional foci (inhibitory cardiac effect)
- The vagus nerve also stimulates the GI tract
- activation of arterial cholinergic receptors dilates arterial vessels (reduces BP and blood flow)
What is the process of merciful syncope?
severe pain and/or seeing one's own blood often initiates a reflex PSNS response that causes syncope (loss of consciousness) when the blood supply to the brain decreases
- this slows the SA node pacing (bradycardia)
- also dilates systemic arteries and leads to hypotension (BP falls)
- This is sometimes called "vaso-vagal syncope"
What are the layers of the heart?
Fibrous pericardium: The most superficial; thickest

Serous layer: formed of two layers, parietal most external and bound to the fibrous pericardium >>> pericardial cavity with serous fluid >>> visceral pericardium (epicardium) >>> myocardium (muscle) >>> thin layer termed the endocardium
What is cardiac tamponade?
Usually blood accumulating in the pericardial cavity.

It can either be more acute/emergent (such as penetrating injuries) or it can be more gradual (eg CHF, renal disease, etc)

Increased fluid inside cavity increases pressure on heart, impairs its ability to relax and fill, decreasing CO

aspirate fluid w/ a needle
Tell me about pericarditis?
inflammation of pericardial sac

retrosternal pain is how it presents; can lead to cardiac tamponade if fluid accumulates quickly

idiopathic usually

The opposing serous layers become rough from friction (parietal and visceral)
What is the venous drainage for the heart?
What is the definition of cardiac output?
CO = SV x HR

- SV determined by ventricular inotropy and preload
- cardiac index: CO divided by body surface area
- Preload is the ventricular end-diastolic volume (degree of tension on the muscle when it begins to contract; affected by blood volume and vessel compliance
- afterload is the sum of all forces against the EF of blood from the heart
What is the Frank-Starling Law?
Description of cardiac hemodynamics as it relates to myocyte stretch and contractility
- SV of LV will increase with increase in LV volume
- the ability of the heart to adapt to changing volumes of inflowing blood
- more stretch of the ventricle = higher contractility of the heart muscle
- only more effective up to a certain point: can't stretch the sarcomeres too far!
What are some examples of vagal maneuvers?
vagal maneuvers may be employed to produce a reflex parasympathetic response for both diagnostic and therapeutic purposes
- induced gagging
- carotid sinus massage
What is the autonomic response that occurs when a person stands? What is orthostatic hypotension?
Autonomic response
- SA Node stimulation increases
- leads to compensatory vasoconstriction of peripheral arteries to prevent distal blood pooling
- if someone stands too long the normal sympathetic response can be impaired, diminishing flow to the brain
- orthostatic hypotension: abrupt fall in BP caused by a failure of these compensatory mechanisms upon standing
What is neuro-cardiogenic syncope?
In some elderly patients, when blood pools in the legs they have a reflex sympathetic increase in HR, but the arteries in the extremities do not constrict (as they should)

Thus, parasympathetic mechanoreceptors in the left ventricle are stimulated, and you have a reflex slowing of SA node pacing (bradycardia) and hypotension --> syncope
Describe the regulation of vascular tone, including vasopressin, catecholamines (epinephrine and norepinephrine),alpha 1, beta 1, and beta 2
What is the difference between inotropy and chronotropy?
inotropy: the force of contraction (SV)

Chronotropy: speed/bmp (HR)
How are the vessels adjusted both locally and globally? How is volume controlled?
VESSELS
- local: adjust the vascular resistance
- global: change the preload

VOLUME/BP
- kidneys: renin-angiotensin-aldosterone system (RAAS) for blood volume
- brain: chemoreceptors in the vasomotor center (the short term regulation of BP. Neuronal... due to receptors, vessel diameter, rate and contractility aka CO, adjusting blood distribution)
What are the functions and hormones involved with SNS and PSNS?
SYMPATHETIC
- vasoconstricts the arterioles and veins
- increases HR
- increases contractility
- Epinephrine
- Norepinephrine
- Vasopressin (ADH)
- Angiotensin

PARASYMPATHETIC
- slows the HR
- acetylcholine
Tell me about baroreceptors and chemoreceptors?
BARORECEPTORS
- these are stretch receptors; neuronal, fast reflex responses that respond to the rapid BP changes (both high and low pressures)
- receptors in arteries in carotid aa. and aortic arch wall.
- when stretched, they are stimulated, increasing firing rate during high BP. This activates the PSNS to decrease HR and contractility, vasodilate; when not stretched/times of low BP, they decrease firing rate of CNIX (glossopharnygeal) to the vasomotor brain stem, increasing SNS and decreasing PSNS

CHEMORECEPTORS
- primary respond to lower pressures
- sense a lack of oxygen and excess of CO2/H+ ions
- located in small organs, carotid, aortic bodies
- activation of these receptors excites the vasomotor center (SNS)
Tell me about the RAAS system?
Lower blood perfusion and catecholamines present at the kidneys signal renin release;
- this is an enzyme that converts angiotensinogen produced by the liver to Angiotensin I
- Angiotensin I travels to the lungs and is converted to AII by ACE
- AII leads to increased thirst, vasoconstriction, Na+ reabsorption
- AII stimulates aldosterone release from the adrenal cortex, which acts at the kidney to increase Na+ reabsorption and K+ excretion (leads to water retention)
- this system acts in the long term (when BP has really started to be affected)
Tell me about the functions of renin, AII, ADH, aldosterone.
ADH/Vasopressin
- involved with hemorrhage; aka respondsto decrease in BP and causes release of vasopressing from the posterior pituitary
- this is a potent vasoconstrictor, which increases TPR by activating V1 receptors in arterioles
- increases water reabsorption at the kidney level by inserting aquaporin channels
Pharmacology: how does epinephrine (catecholamine) affect vascular tone?
EPINEPHRINE (released during SNS stimulation)
- Alpha-1 cardiac receptor stimulation: increased HR and contractility, vasoconstriction, increased myocardial O2 consumption (epi binds these receptors when it is in high concentration. aka dose dependent)

- Beta2 receptor stimulation: smooth muscle relaxation of bronchioles, dilation of skeletal muscle vasculature (works at lower doses of epinephrine to result in vasodilation)
What is sinus rhythm? What is sinus bradycardia? What is sinus tachycardia? (Rapid EKG)
sinus rhythm: The SA node generates a sinus rhythm, pacing the heart at a rate range of 60-100 bpm

This regular pacemaking stimuli is termed "automaticity"

sinus bradycardia: HR less than 60 bpm

sinus tachycardia: the sinus node (SA node) paces at a rhythm greater than 100 bpm; usually from sympathetic stimulation of the SA node (eg exercise)
What are automaticity foci? Where are they located and what are they called? What is the inherent rate for each? (Rapid EKG)
these are potential pacemakers termed automaticity foci that come into play if SA Node pacemaking fails

these foci pace at an inherent rate

there are a few atrial automaticity foci (inherent rate of 60-80 bpm)

There are not any foci at the proximal end of the AV Node, but rather in the middle and distal end of the node called the AV junction (junctional automaticity foci) (Inherent rate of 40-60 bpm)

In the ventricles, there are foci in the His bundle and the Bundle Branches and their subdivisions, termed the ventricular automaticity foci (inherent rate of 20-40 bpm)

**note, any specific automaticity foci has its own inherent rate, but it usually falls within a certain range (see above)
What is overdrive suppression? (Rapid EKG)
OVERDRIVE SUPPRESSION
- rapid automaticity suppresses slower automaticity (eg the SA Node suppresses atrial and junctional foci)
- if there is a failure of a certain level, there are emergency backups at three separate levels
What is happening with conduction block at the junctional automaticity focus?
IF there is a conduction block, then the AV junctional foci are no longer overdrive-suppressed, allowing it to become the active pacemaker for the ventricles

This would pace the ventricles at 40-60 bpm
What is a good method for rapidly determining HR on an EKG strip? What if they are under 50 bpm?
Find an R wave that falls right on a heavy black line. Then go every five boxes (to the next thick line) and count in this order:
300 ... 150 ... 100 ... 75 ... 60 ... 50

wherever the next R wave falls gives the rate (if between the lines you know it is between the two numbers; eg between 75-100)


If under 50 bpm:
- small marks on the top of the rhythm strip indicate the "three second intervals"
- two of these intervals represent a 6 second strip
- count the number of complete cardiac cycles within the 6 second strip
- take the number of cycles per 6 strip and multiply by 10 to give you a HR (put a zero next to the number of cycles per 6 second strip)
- this method is also helpful for determining rates of irregular rhythms!
Describe the appropriate method for determining a diagnosis of hypertension ini adults. H&P, lab data to order, what are some lifestyle mods
H&P
- make sure it really is HTN (recheck after seated calmly for 5 min)
- make sure it is elevated over 2-3 visits over more than 2 weeks
- Rule out secondary causes (you are concerned about a young patient with not much FH, or try to treat pt and BP isn't coming down; are they on Venlafaxine antidepressant, obese pt with snoring? Evaluate thyroid for hypo- hyper- thyroidism; heavy EtOH use/SNS activating substances)
- Risk-stratification: other CV risks besides HTN?
- Prior Hx, prior meds tried for elevated BP, complete med/herbal list
- Past medical Hx (CV risks: smoking, FH, etc)
- Physical: do a full CVP exam, including checking 4 pulses @ extremities

LABS (for anyone you might Dx with HTN)
- BMP
- Creatinine (rule out kidney disease)
- TSH (hypo- hyper- thyroidism)
- Lipid panel (to define CV risk profile)
- EKG (to look for LV hypertrophy)

LIFESTYLE MODS
- every 2 lbs (1kg) lowers BP by ~1 mmHg
- DASH diet: lowers BP by 10 mm Hg (definitely helpful)
- Low sodium diet (lowers 5 mmHg)
- Limit alcohol
- quit smoking
Identify secondary causes of hypertension and describe appropriate evaluation to rule out secondary hypertension.
Secondary causes of HTN by hx
- obese with snoring and daytime somnolence
- onset of HTN before puberty
- recently started NSAIDs OR birth control containing estrogen OR venlafaxine (antidepressant) OR steroids
- social hx for heavy alcohol use
- fatigue, unintentional weight gain, cold intolerance, constipation
- 5 Ps of pheochromocytoma (palpitations, perspiration, pallor, pounding headache, increased BP); this is a tumor of the adrenal gland --> too much epi and norepi
- FH of secondary cause of HTN

Secondary causes of HTN by PE
- decreased/delayed femoral pulses or decreased femoral BP
- abdominal bruit
- cushingoid features
- acute rise in BP over prior stable values
- refractory HTN to therapy
- fluctuating high/normal BP
Describe an appropriate approach to the initial evaluation of the patient with hypertension, assessing for target organ damage and risk-stratification.
...
Apply principles of management for hypertension, including risk factor and lifestyle modification, and medications.
...
1. Describe the following drug classes in terms of mechanism of action and side effects: Thiazide and loop diuretics, aldosterone antagonists, ACE-Inhibitors, ARBs, beta-blockers, and calcium-channel blockers.
THIAZIDE AND LOOP DIURETICS
- MOA: decrease total body salt and water (Decreased blood volume)
- Side effects: dehydration (MUCH more common with loop diuretics eg furosemide), hypokalemia, worsens insulin resistance
- containdicated in pregnancy

ALDOSTERONE ANTAGONISTS
- MOA: competes w/ aldosterone at distal renal tubule, conserves potassium while causing excretion of Na+/water
- Side effects: hyperkalemia and dehydration''

ACE INHIBITORS (ACE-I)
- usually the first-line therapy
- MOA: inhibits RAAS system (prevents A1 >>> A2 conversion at lungs), leading to decreased salt & water retention and decreased PVR
- Side effects: hyperkalemia, dry cough 20-30% patients, hyperkalemia, urticaria/angioedema
- NOT recommended during pregnancy
- can significantly decrease incidence of DM in HTNive individuals
- Meds: Benazepril, Lisinopril, Ramipril

ANGIOTENSIN-RECEPTOR BLOCKERS
- MOA: Inhibits AII binding to receptor, as well as aldosterone secretion
- side effects: hyperkalemia, angioedema
- decreases insulin resistance, similar to ACE-I

CALCIUM-CHANNEL BLOCKERS
- MOA: Dihydropyridine (DHP) vasodilate the peripheral blood vessels and decrease PVR; non-DHP lowers HR, as it has lesser peripheral dialtion properties
- Side effects: Edema, Bradycardia (non-DHP), CHF exacerbation (non-DHP)

BETA BLOCKERS
- MOA: lowers HR (and thus CO), as well as decreases PVR via SNS
- Side effects: containdicated in asthma, bradycardia, CHF exacerbation, can mask hypoglycemia in diabetes
Given a patient with a hypertension diagnosis, recommend the appropriate target blood pressure and anti-hypertensive agent, after considering patient age and comorbidities.
...
Discriminate between hypertensive urgency and hypertensive emergency in terms of diagnosis and treatment
HYPERTENSIVE URGENCY
- blood pressure greater than or equal to 180/120 WITHOUT end-organ damage
- must rule out end-organ damage
- Tx: oral meds to lower BP to less than 160/100 over 3 hours; initiate 1 medication with close follow-up to add a second. Have a preference for diuretic class.

HYPERTENSIVE EMERGENCY
- Elevated BP greater than or equal to 180/120 mmHg AND end-organ damage (neuro: hemorrhagic stroke, retinal exudates/hemorrhages. Cardiovascular: unstable angina/MI, heart failure with pulmonary edema, aortic dissection. Renal damage: proteinuria, hematuria, acute renal disease. pregnancy: preeclampsia/eclampsia
- triage the patient to the ED if positive for symptoms or exam findings are concerning for end-organ damage
- Tx: in ED/ICU, IV meds used to lower diastolic by MAX of 25% in 2-6 hours; goal is to reduce DBP to 100-105 mmHg within minutes to 2 hours
- See picture for meds
Design a treatment plan for a patient with hypertension based on individual risk factors
- in general, aim for a BP less than 130/80
- Exception: if they have a low ASCVD risk (<10%) then lifestyle mods are okay w/ a BP goal of <140/90
- Exceptions: <150/90 would be elderly pt with high fall risk, orthostatic hypotension, terminally ill patients
what is the definition of essential hypertension?
A systolic BP greater than or equal to 130 mmHg OR diastolic BP greater than or equal to 80 mmHg

The elevated BP is consistent over time in a patient's usual state of health

there is no evident secondary cause

THUS essential hypertension = primary hypertension

there must be elevated BP over 2-3 visits OVER GREATER THAN OR EQUAL TO 2 weeks; a diagnosis can be made if 2+ readings of >130/80 mmHg is measured, spaced at least 2 weeks apart
What is the pathophysiology of essential hypertension?
The two main components are an increased cardiac output (CO) OR an increased Peripheral vascular resistance (PVR)

INCREASED CO
- CO = SV x HR
- Increase in SV is due to an increased extra-cellular volume, usually from higher sodium levels
- Increased sodium due to: increased sodium intake, RAAS activation, impaired renal sodium excretion

INCREASED PVR
- increase in SNS vasoconstriction
- increased due to higher AII levels (RAAS) and/or lower kallikrein-kinin levels
- impaired local vasodilation (impaired local NO production
Describe MOA and Side effects of thiazide and loop diuretics
THIAZIDE AND LOOP DIURETICS
- first line for most patients; effective therapy for black patients especially or non-black patients >60 yo
- Thiazide: better for decreasing PVR.
- Loop diuretics: a better fluid mobilizer.
- MOA: decrease total body salt and water (Decreased blood volume); by inhibiting renal absorption of salt and water; decreases PVR to reduce BP (thiazides)
- Side effects: dehydration (MUCH more common with loop diuretics eg furosemide), electrolyte depletion, worsens insulin resistance
- contraindicated in pregnancy
- see picture for the drug examples
- significant edema? use the loop diuretic
- there are certain potassium sparing diuretics that do not provide BP lowering but simply mitigate serum potassium lowering with thiazides
Describe MOA and side effects of aldosterone antagonists for hypertension
ALDOSTERONE ANTAGONISTS
- MOA: competes w/ aldosterone at distal renal tubule, conserves potassium while causing excretion of Na+/water
- Side effects: hyperkalemia and dehydration''
Describe MOA and side effects of ACE Inhibitors for hypertension
ACE INHIBITORS (ACE-I)
- usually the first-line therapy (non-black patients)
- MOA: inhibits RAAS system (prevents A1 >>> A2 conversion at lungs), leading to decreased salt & water retention and decreased PVR
- Side effects: hyperkalemia, dry cough 20-30% patients, hyperkalemia, urticaria/angioedema, potential renal failure w/ renal a stenosis
- Drug increases lithium concentrations
- NOT recommended during pregnancy
- Added benefit: can significantly decrease incidence of DM in HTNive individuals
- Meds: Benazepril, Lisinopril, Ramipril "Ben will prolly (pril) ram his head into the wall if he doesnt ACE this exam"
Describe MOA and side effects of angiotensin receptor blockers (ARBs) for hypertension
ANGIOTENSIN-RECEPTOR BLOCKERS
- a good alternative to ACE-I, first-line for most patients (non-black)
- don't lower BP as well as ACE-I
- MOA: Inhibits AII binding to AT1 receptor, as well as aldosterone secretion
- side effects: hyperkalemia, angioedema but not as much as ACE-I (no dry cough here! Can increase creatinine values (same as ACE-I)
- contraindicated in pregnancy, bilateral renal artery stenosis
- decreases insulin resistance, similar to ACE-I
- drug examples: Irbesartan, valsartan, losartan (-artan is after every drug!) --- "I had to take a SHART in ARBys"
Describe MOA and side effects for beta blockers for hypertension
BETA BLOCKERS
- unless the patient has a compelling indication (heart failure with reduced EF, post MI, CAD, stable ischemic heart disease) beta blockers should not be first line therapy
- MOA: inhibits the action of endogenous catecholamines (epi and norepi) to lowers HR (and thus CO), lower afterload, lower contractility
- Side effects: contraindicated in asthma, bradycardia, CHF exacerbation, can mask hypoglycemia in diabetes, exercise intolerance (due to decreased contractility), HR and possible heart block
- contraindications: heart block, acute heart failure, severe asthma
- can have rebound hypertension if discontinued quickly, need to taper off
- Meds: see picture "-olol" is a common suffix! "I always -lol whenever I see a tri beta...."
Describe MOA and side effects of calcium channel blockers for hypertension
CALCIUM-CHANNEL BLOCKERS
- first-line med for most patients; Especially effective in black or non-black patients > 60 years
- MOA: Dihydropyridine (DHP) vasodilate the peripheral blood vessels and decrease PVR (can lead to headache and peripheral edema); non-DHP lowers HR (hemodynamics), as it has lesser peripheral dilation properties
- Overall effect: increases O2 supply (DHP > nonDHP); decreases O2 demand (non-DHP>DHP)
- Side effects: Edema, Bradycardia (non-DHP), CHF exacerbation (non-DHP)
- Meds: see picture (highlighted examples)
- DHP is used more commonly for hypertension
- NEVER USE DHP ON PATIENT WITH HEART FAILURE AND REDUCED EF
Describe the practical approach to diagnosing HTN in children and adolescents
...
Describe the pathophysiology of HTN
BP = CO x PVR

When we have a lot of sodium present in circulation, a lot is reabsorbed and water follows with it. This increases the volume of blood (stroke volume)
design a systematic approach to the evaluation for a peds patient with hypertension. Inspecting the patient, taking a hx, ordering diagnostic tests...
HIGH BP (for the history)

H: high risk factors (MONSTER - Meds, Obesity/OSA, Neonatal hx, signs/sx, trends in family, endocrine, renal)
I: integumentary (sweating, rash, skin changes)
G: Gu complaints (hematuria, edema, enuresis)
H: hyper/hypothyroid sx (weight loss, gain, growth failure, diarrhea, constiaption, fevers)

B: brain (blurred vision, gait changes)
P: pain (dyspnea, palpitations, chest pain)


LOOK at them: EDEMA

Endocrine disorders (thyroid enlargement for hyperthyroidism, ambiguous genitalia)
Defects in heart/vasculature (renal bruit for renal vascular disease, 4 extremity BP and brachiofemoral lag for CoA, mumurs and edema for CHD)
End organ damage (focal neurologic deficits, papilledema)
Multipe syndromic findings (neurofibromatosis, growth faltering and syndromic appearance-- Turner syndrome)
Abdominal mass (neuroblastoma, Wilms tumor, pheochromocytoma)



Diagnostics: **note, those >6 yo with FH of HTN or are obese or have a negative hx and PE suggestive of secondary HTN do not need extensive work-up (aka, you are pretty certain it is primary/essential HTN)
- Level 1: electrolytes, BUN/cr, lipid profile, TSH, CBC, UA with microscopy (for glomerular or tubule problems), HgbA1c if obese, ALT and AST for hyperlipidemia (if BMI >95th percentile), renal US, echocardiogram
- Level 2: plasma renin activity, serum aldosterone and cortisol (points us to primary aldosteronism or/and congenital adrenal hyperplasia), a sleep study to detect obstructive sleep apnea (if Level 1 didn't help)
Prepare a treatment plan for peds patients with essential or secondary hypertension. Include lifestyle mods, pharmacotherapeutics, and appropriate referrals.
LIFESTYLE MODS
- Reduce sodium intake (DASH Diet); limit grocery purchases of salt-added foods, limit meals from fast-food restaurants, not adding salt to cooking
- Increase activity to reduce obesity (ask more about exercise-associated syncope, light headedness, chest pain, dyspnea; FH of sudden death, HOCM); 30-60 minutes activity/session, 3-5 days/week; those with stage 2 HTN should avoid static exercise (as PVR is high and systolic pressure increases, recipe for disaster)
- Quit smoking/tobacco
- Reduce alcohol

MEDS
- main med for kids is an ACE-I, ARBs are fine too
- give meds only with symptomatic HTN, Stage 2 HTN without a modifiable factor, HTN with LVH, persistent HTN despite 6 mo trial lifestyle mods
What BP meds are first line for those with chronic kidney disease. How about black/african american? All other races? Diabetics?
CKD
- give ACE-I or ARB (protect kidneys)

BLACK/AA:
- thiazide diuretic or CCB first line

OTHER RACES
- diuretic or ACE-I/ARB or CCB preferred

DIABETICS
- ACE-I or ARB. Tend to decrease incidence of DM in HTNive individuals!
What are the definitions/equations for cardiac output and blood pressure?
CO = SV x HR




BP = CO x PVR
What are the most common etiologies of HTN in neonates, children 1-12 yo, and adolescents 12 yo+?
NEONATES
- Bronchopulmonary dysplasia
- Coarctation of aorta
- Renal disease (congenital renal anomalies, renal artery stenosis)

CHILDREN (1-12 yo)
- Renal disease (renal parenchymal disease)
- Coarctation of aorta (usually after CoA repair)
- Primary/essential hypertension (especially if +FHx and obese)

ADOLESCENTS (>12 yo)
- primary/essential hypertension (the #1 cause)
- drug-induced
What are the types of prevention? (this is a LO)
primary prevention
- avoidance of disease or injury; immunizations
- "Primary Prevention"

secondary prevention
- early detection (screening) and treatment
- mammography
- eg colon cancer screening
- "Secondary Screening"

tertiary prevention
- reduction of disability and prompt rehab
- management of existing conditions
Tell me about the USPSTF screening recommendation grading
- the screens are graded A, B, C, D , E, or I
- under the ACA, private insurers must cover A and B level recommendations at no cost to patients
- A and B means grade means the USPSTF recommends the service (net benefit!)
- C: selectively offer the service to individual patients based on professional judgment (moderate certainty the net benefit is small)
- D: USPSTF recommends against this service
What do you assess for in target organ damage via HTN?
Neuro
- headaches, transient neurologic sx (blindness and weakness)
- rule out prior CVA with CN, strength, sensation, and cerebellar testing

CV
- chest pain (angina)
- claudication (Peripheral artery disease)

Ophthalmology
- cotton-wool spots (tiny eye hemorrhages)
- Arteriovenous nicking (elevated bp in eye causes indentation when it crosses a vein)

Pulmonary
- rales (CHF exacerbation)
- DOE (CHF)
Sets found in the same folder