HTN Flashcards
What is the impact of HTN in society:
Nearly 1000 deaths/day; 67 M americans ahve HTN; 1-3 ration; incidence in children increases risk of HTN d/t obesity
Why is HTN known as the “silent Killer’?
HTN is not associated w/symptoms that would prompt individuals to seek medical help; severe target organ damage will be the result of un-tx HTN
What are the goals of HEALTHY PEOPLE in the reduction of HTN:
healthy weight, reduce NA intake, increase exercise, limit EtOH, know/monitor bld pressure, take medications if ordered
What are the types of comorbidities that are a MAJOR contributor to HTN:
heart attack, stroke, HF, kidney failure, cardiovascular disease
What ethnicites have the highest HTN incidences:
African/ mexican, Native Americans
What area of the US has the highest incidence of HTN regardless of race:
Stroke Belt or southeastern US
A persistent/sustained elevation of BP at >140/90 mmHg is defined as:
HTN
The classification of HTN is based on what:
The average of two or more office visit occasions
Stage 2 HTN is:
> 160/100
PreHTN is:
120-39/80-89
What is the elderly impact of HTN:
Not considered a normal part of aging, but common among pts >60 yo; increases w/age; prone to drug overdosing d/t decreased renal function; Isolated systolic HTN is more common in older adults
The force exerted by the blood against the walls of the bld vessels is defined as:
BP
The total bld flow through the systemic or pulmonary circulation per min is defined as:
CO (also described as the stroke volume of blood pumped out by L ventricle per beat)
The force that opposes the movement of blood within the blood vessels is defined as:
systemic vascular resistance (SVR)
What is the principal factor in determining vascular resistance:
The radius of the small arteries and arterioles
What happens if the systemic vascular resistance is increased but the CO is the same or increases:
arterial BP increases
An elevated BP w/specific causes that can be identified and corrected: narrowing of the aorta, renal disease, endocrine disorders, neurological disorders, sleep apnea, medications, PIH (pregnancy-induced HTN), and pheochromocytoma (adrenal tumor) is defined as what type of HTN:
Secondary HTN
An elevated BP w/out identified causes (accounts for 90% of cases) such as: increased activity of the SNS, overproduction of Na retaining hormone, increased Na intake, obesity, excessive EtOH intake, and DM is what type of HTN:
Primary/Essential HTN
How does heredity affect HTN:
strongly familial d/t activities/dietary factors; 30 % genetic factor in some populations
How does water and NA affect HTN:
Increased Na intake causes water retention; in some degree, NA intake triggers the development of HTN according to studies done on primitive vs. industeralized and salt loading studies
Arterial BP increases with the increase of what:
CO or systemic/peripheral vascular resistance
How does the renin-angiotensin-aldosterone system affect BP
Decreased BP/SNS stimulation causes renin to to be secreted from the JA of the kidneys–>Renin converts A-1 to A-2–>A-2 increases BP as a vasoconstrictor (increasing SVR), and causes adrenal glands to secrete aldosterone which cause NA and water retention increasing blood volume=increasing CO=increasing BP
How does Stress affect HTN:
stress increases the SNS activity–>increased SNS activity causes vasoconstriction, increased HR, and increased renin release
How does insulin resistance/hyperinsulinemia affect HTN:
present in PRIMARY HTN (DM); high insulin stimulates SNS activity, impairs nitric oxide mediated vasodilation, vascular hypertrophy, increased Na retention
How does endothelial cell dysfunction affect HTN:
contributes to atherosclerosis, High levels of endothelin prolongs vasoconstriction, decreased vasodilator response to nitric oxide
How does gender and age play a role in HTN:
HTN is prevalent in males young/middle-age; prevalent in women after 55 yo; BP rises progressively w/increasing age, but HTN is not a normal aging process
What are the major target organ complications of HTN:
Cerebrovascular disease, retinopathy; hypertensive heart disease (CAD, LVH, HF); aortic aneurysm; nephrosclerosis, PVD, neuropathy
Transient ischemic attack (neurological dysfunction d/t bld loss) or stroke (commonly d/t atherosclerosis); intracranial pressure is a manifestation of what target organ disease:
cerebrovascular disease
Narrowing of the retinal arterioles; arteriovenous nicking (arteriole crossing over vein), or hemorrhagic/exudate w/or w/o papiledema (all causing vision blurred/loss of vision/retinal hemorrhage) are manifestations of what target organ complication of HTN:
retinopathy
EKG/clinical/radiologic evidence of CAD d/t MI…; LVF/HF; left ventricular dysfunction are manifestations of what target organ complication of HTN:
hypertensive heart disease/cardiac disease
One/more pulses in extremities that are reduced or absent; intermittent abd bruits/thrills; abd aneurysm (all sped up by atherosclerosis) are manifestations of what target organ complication of HTN:
PVD (peripheral vascular disease)
Atrophy of renal tubules, destruction of glomeruli, eventual death of nephrons all indicated by proteinuria, microalbuminuria, heaturia, nocturia are manifestations of what target organ complication of HTN:
Nephrosclerosis
Atherosclerosis contributes to what major complications of HTN:
ischemic stroke, heart attack, peripheral arterial disease
What’s the difference between atherosclerosis and arteriosclerosis:
Atherosclerosis has plaque; arteriosclerosis is hardening of the vessels
What is the subjective assessment for HTN:
PMHx, medications (birth control increases BP), functional health patterns
Objective assessment of HTN include:
physical exam-neurological, CV, musculoskeletal, renal; most people have no S/S of HTN; accurate BP taking (measured w/arm at heart level)
Diagnostic assessment include:
assessing the risk/comorbidities; determine identifiable cause of HTN; assess presence of target organ damage; obtain lab tests: CBC, K/Ca, glucose, BUN, Creat
What is the normal level of K:
3.5-5.1
What is the normal level of Ca:
8.5-10.3
What is the normal level of glucose:
65-99
What is the normal level of BUN:
8-22
What is the normal level of creat:
0.5-1.3
What dx study may show evidence of an ischemic heart disease and LVF:
ECG
What dx study may show STRUCTURAL heart disease and LVF:
echocardiogram
Common nsg dx include:
sexual dysfunction, ineffective health maintenance; ineffective therapeutic regimen management, disturbed body image
The collaborative intervention for primary HTN is:
To RETAIN wellness via stratification and tx; independent nsg intervention includes screening and teaching
The collaborative intervention for secondary HTN is:
To ATTAIN wellness via drug therapy: monitor effectiveness of drugs/side effects/contraindications
Drugs that promote the excretion of water and electrolytes by the kidneys to reduce BP/edema; first line of drugs to tx HTN are defined:
diuretics
Most commonly Rx diuretic that works on the distal convoluted tube; has 3 hypers/2hypos (hyper:calcemia/glycemia/uricemia; hypos:kalemia/natremia; inhibits Na, h2O, Cl, K reabsorption
thaizides (HCTZ)
When taking thiazides, considerations would be:
DO not give in Renal pts (use Loops) monitor K level in the elderly, NSAIDs reduce effect; avoid sulfonamide allergies
This diuretic works on the ascending Henle to cause rapid diuresis of Na, Cl, H20; considered to be the most potent of diuretics (except osmotics); potent K-wasting diuretic; can cause orthostatic hypotension:
Loop diuretics (Bumex or Lasix)
What are some important considerations in the taking of loop diuretics:
hypokalemia especially if taking digoxin can cause toxicity; electrolytes should be monitored d/t rapid diuresis effect
This diuretic acts on the collecting ducts; promotes Na and H2O excretion and RETAINS K; can cause hyperkalemia:
Potassium-sparing diuretics (spironolactone (aldactone)
What are some important considerations of taking K-sparing diuretics:
Hyperkalemia (especially if taking ACE inhibitors)
Beta-blockers decrease HR/contractility/renin release; NSAIDs decrease effectiveness of BBs; widely used for stage 1 and 2 HTN; what are the names of the common ones:
Propanolol (B1 &2), metoprolol/atenolol (B1)
When are BBs contraindicated:
COPD, bradycardia, asthma (d/t bronchospasm)
This type of BB will inhibit B1 and B2 to decrease HR, and bronchoconstriction:
propanolol (non-selective BB)
This type of BB inhibits B! to decrease HR, contractility, renin release w/o affection bronchoconstriction:
Cardioselective BBs: metroprolol/atenolol
This type of anti-HTN drug blocks angio 1 from converting to angio-2=prevents vasoconstriction; is recommended fro pts when BBs are contraindicated or ineffective; hyperkalemia (don’t use w/k-sparing diuretic); chronic cough
ACE inhibitors (prils)
This anti-HTN med blocks the chemical receptors for angi-2 on the arterioles to prevent the relase of aldoserone:
Angi-2 inhibitors (tans)
Centrally acting alpha 2 agents have the three c’s to inhibit the SNS causing dilations of Peripheral vessels; comes in a patch; decreaed PVR=increased vasodilation=diuretics need to be given
Catapress decreases cascade (nori-epi-renin release)
Direct acting vasodilators reduce SVR and BP, used in HTN crisis, severe hypotension; tachycardia can occur d/t nervous system stimulation; what type of drugs are they:
Nipride and aprelosine
A severe and abrupt elevation in BP >180/120 that can trigger endothelial damage=release of vasoconstriction substance=can lead to target organ failure; common in non-compliant pts or cocaine users is defined as:
HTN crisis
What are the manifestations of HTN crisis:
depends on organ damage: S/S of neurological dysfunction, retinal damage, HF, pulmonary edema, renal failure
What is used to measure HTN crisis to guide drug therapy:
mean arterial pressure (MAP = DBP = 1/3 of pulse pressure)
What is the normal MAP:
70-100 mmHg
How is HTN crisis treated:
Decrease MAP by 1-20% in the first 2 hrs, then GRADUALLY over the next 24 hrs; Direct acting Vasodilators are used (titration to prevent hypotension) intra-arterial line or automated BP monitoring machine is used; hourly urine output/neuro checks
What are some common HTN misconceptions:
pt feels sick when he’s HTN; pt has a hyper personality; Elevated DBP is more important than SBP; HTN can be cured; pt cannot live a normal life; increased cholesterol means HTN
What are some important teaching guidelines when taking meds:
avoid hot baths/strenous exercise/intake of EtOH within 3 hrs of taking meds to promote vasodilation
A dietary approach to stop HTN is called DASH:
Eat fish/plenty of fruits/veggies/increase whole grains/increase K, mg, CHON, fibers;
DASH wants you to decrease what:
saturated fats and cholesterol, less than 2.4 grams of NA/day; avoid processed foods
What are the components of lifestyle modifications:
DASH, weight reduction; Na reduction, aerobic activity, moderation of EtOH
BMI should be between:
18.5-24.9
