HTN Flashcards
What is the most modifiable risk factor of cardiovascular disease?
HTN
What risks increase when BP increases?
Risk for: MI, CVA, HF, Renal disease
Definition of HTN
persistent elevation:
- systolic BP greater than or equal to 130 mm Hg OR
- diastolic BP greater than or equal to 80 mm Hg OR
- current use of anti-HTN medications
- could be persistent elevation of both systolic and diastolic BP but needs to be at least one.
Types of HTN
- primary (essential or idiopathic) = >90% of all cases
- no known cause
- secondary= 5-10% of cases in adults, 80% of cases in children
- usually from underlying causes such as renal failure, heart failure, or adrenal tumor (once you fix underlying cause, BP will normalize)
- isolated systolic hypertension (ISH): average SBP >130 with average DBP <80
- good DBP but systolic is high (systolic is only thing that changes). occurs mostly with elderly pts due to lack of elasticity in arteries (goal is to decrease systolic without dropping diastolic too far). Systolic naturally increases with age, diastolic also increases with age, but at around 55yo it starts to go down because of loss of elasticity.
Normal BP Values
SBP: <120 mm Hg
AND
DBP: <80 mm Hg
Elevated BP Values
SBP: 120-129 mm Hg
AND
DBP: <80 mm Hg
Stage 1 HTN Values
SBP: 130-139 mm Hg
OR
DBP: 80-89 mm Hg
Stage 2 HTN Values
SBP: greater than or equal to 140 mm Hg
OR
DBP: greater than or equal to 90 mm Hg
1 Cause of Death in US
Heart disease
*HTN contributes to heart disease
HTN leads to:
- CAD (coronary artery disease) leading to MI
- heart failure - left ventricular hypertrophy (super enlarged left ventricle)
- worsening atherosclerosis
- PVD (peripheral venous disease)
- Renovascular disease (not enough blood to the kidneys)
- Aortic aneurysms
- Retinal damage
*HTN doesn’t necessarily kill you, it’s the other things it leads to such as those listed above
CO
total blood flow with systemic or pulmonary circulation per minute
CO = SV x HR
SV = amount of blood pumped out of the left ventricle per beat
SVR
systemic vascular resistance
- the force opposing the movement of blood within the vessels (force pushing back on the ❤️ )
- combo of arteries and arterioles and whether they are constricted or dilated
- if vessels are constricted in the feet for example, it’s harder for the heart to pump blood into those vs if they were dilated
- so it’s radius difference of arteries and arterioles that is the primary factor determining SVR
Primary HTN: Pathophysiology
- increased SVR and/or increased CO leading to elevated BP
- may have normal CO, or it may return to NL, but you have consistently elevated SVR which is the hallmark sign of HTN
- altered plasma renin activity leads to vasoconstriction, vascular hypertrophy, increase in aldosterone
- stress causes increase in SNS activity leading to vasoconstriction, increased HR and increased renin (the altered plasma renin pathway)
- insulin resistance
- endothelial cell dysfunction
HTN: Non Modifiable Risk Factors
- Age (usually appears at 30-50yo)
- poorer prognosis the younger the dx
- Male (greater risk in men than women)
- new genetic links found
HTN: Modifiable Risk Factors
- Stress: causes increase in SVR, increased CO, stimulation of SNS
- 60-90% of visits to HCP r/t stress
- Obesity: apple-shaped associated with HTN, pear-shaped associated with decreased risk of HTN
- Diet (increased Na+ intake)
- Substance abuse: Nicotine, cocaine, ETOH, caffeine
TOD
target organ disease
often asymptomatic until TOD
you are going to see the effects of HTN on other organs which is how you figure out pt has HTN, not necessarily through HTN itself.
Severe HTN
pt c/o persistent HA, fatigue, vertigo, palpations, flushing, blurred or double vision, epistaxis.
severe HTN is emergent situation
symptoms will resolve when severe HTN is treated
HTN and Weight
BMI is usually higher in those with HTN
HTN and VS
BP: measure in both arms and use the higher reading.
Dx requires 2-3 measurements on 2-3 separate occasions
Pt should sit for 5 min prior to BP with feet on floor and back supported (no crossed legs, constrictive clothing). No caffeine or tobacco 30 min prior to BP taken. Arm at heart level.
Appropriate BP cuff needs to be used
- too small cuff gives high reading
- too large cuff gives low reading
HTN and Funduscopic Exam
eye exam that looks at blood vessels in back of eye
look for microhemorrhages or papilledema (minute swelling in back of eye), indicators of heart conditions, brain conditions, kidney/vessel issues, but mostly point back to HTN
HTN and Neck
Distended neck veins, carotid bruits, enlarged thyroid.
common area for plaque to break apart and travel to cerebral circulation
HTN and Heart
increased HR, location of PM is shifted, heart murmurs, extra heart sounds
CAD: found in heart failure pt’s, body’s normal reaction to HTN that leads to left ventricular hypertrophy
Left ventricular hypertrophy: the heart is working super hard against pressure pumping blood to extremities that it gets big and bulky which makes it ineffective and can cause heart failure
HTN and Abdomen
- bruits
- aortic dilation: occurs b/c it’s trying to respond to pressure from HTN and normalize it out and aorta is quickest to respond to that
- enlarged kidneys
- AAA: aorta is working hard to hold in pressure and the wall weakens and balloons out
- Renovascular disease (nephrosclerosis): renal ischemia d/t narrowing of renal blood vessels
- nocturia: indicates issues with kidneys that can often be traced back to HTN
HTN and Extremities
pulses are usually absent or very diminished and un equal in lower extremities
edema d/t inadequate BP from heart (CO is pushing blood down to extremities, but it’s inadequate to push that back up to the heart)
intermittent claudication (pain in lower extremities)
HTN and Neuro
with HTN can have cerebral thrombus or hemorrhage that leads to CVA or TIA.
HTN and neuro s/sx are highly linked
a neuro exam is done with any changes in mental status
mild HTN increases risk of stroke 4x
HTN and Lab studies
lab values can tell us how bad the vascular disease is, about TOD, possible causes of the HTN
secondary HTN will need more workup to evaluate what is causing the HTN
- bloodwork: CBC, CMP, CRP, lipid profile
- urinalysis: test for microalbuminuria, proteinuria, hematuria, increased BUN and/or creatinine, decreased GFR
ECG- provide baseline, can show cardiac death (ischemia) through certain rhythms, can show LVH
Chest x-ray: can show if position of heart has shifted and if heart is enlarged
HTN: Goal of Management
Elevated BP: associated with increased risk of developing stage 1 or stage 2 HTN
- if pt has elevated BP in addition to other risk factors they are 2x as likely to develop HTN
- address lifestyle modifications with them
Decrease BP <140 and <90, optimally to <120 and <80 if tolerated
HTN and Lifestyle Modifications
- Stop smoking: educate about cessation techniques, resources, info and support to quit
- Dietary changes: decrease Na+, dash diet, adequate amounts of K+, Ca+, Vitamin D
- Weight reduction: each 10lbs lost will reflect in decrease of SBP by 5-10 mm Hg
- ETOH: decreasing alcohol will decrease weight
- Stress management: temporarily reduces BP, no evidence of long term effects
- Physical activity: 30 min of moderate activity as often as possible leads to decreased BP and weight, lowers stress, lowers systolic BP by 4-9 mm Hg
HTN and Interventions/Meds
Anti-hypertensive Drug Therapy:
- ACE Inhibitors: check K+ levels as they cause increase in K+ levels, common with meds ending in “pril” like lisinopril for dry cough to develop in which case you need to take pt of med and try something else
- ARBs: don’t effect K+ levels
- Thiazide diuretic: check K+ levels
- CCB (Calcium channel blockers)
- Diuretics: check K+ levels
- Beta Blockers: common in HTN pts, meds always end in “lol” like labetalol, can effect both BP and HR so you need to monitor both
- Vasodilators: monitor BP as it can drop drastically so you start with small doses then increase as you go as needed.
HTN and Antihypertensive Drug Therapy Stats
- over 50% of pts with stage 1 and creeping into stage 2 HTN are controlled with 1-2 meds (usually 2 meds b/c they work on different receptors)
- most will require 2 or more meds
- start them out slow w/low dose and slowly increase until manageable BP is reached where BP is under control on single dose of multiple meds. Once at correct dosage for all meds and stay on that for 1 year without changes, you can slowly decrease meds until you have change of BP that starts going up, then you keep at dose where it is most effective. This is done b/c with increased dose there is increased chance of side effects occurring. with more meds you’re taking at lower doses, the better the tx plan, the better the outcomes.
Lasix: Side Effects
increased voiding frequency
dry mouth
hypotension
sexual dysfunction (which can lead to noncompliance w/ meds)
- instruct pt’s to drink lots of fluids, change positions slowly
- *take into account ADL’s and normal lifestyle
Benefits of Lowering BP
Reduction of:
- stroke incidence (35-40%)
- MI (20-25%)
- Heart Failure (50%)
HTN in Older Adults
- Increased variability in BP
- Auscultory gap: period of diminished or absent sounds when taking BP that can lead to incorrect diastolic BP as you may not be able to hear this. When listening for diastolic, let needle fall 20 mm Hg after last sound heard to ensure you haven’t missed something.
- Decrease BP even more slowly in elderly population
- more likely to experience adverse effects from meds
- if decreased too rapidly may lead to cerebral hypoperfusion (dizziness, mental status change, weakness)
