CARE OF PATIENTS WITH HYPERTENSION & VTE Flashcards by Kelsey Klipfel

Most common health problem seen in primary care settings
AHA 2017 Guidelines recommended BP below 130/80
Continuous BP elevation results in damage to organs
HTN is a major risk factor for:

HTN

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Desired BP below 150/90 (60 years and older)
Desired BP below 140/90 (younger than 60 years old)
Desired BP below 130/90 (patients with DM and heart disease)

AHA 2017 Guidelines recommended BP below 130/80

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Continued high pressure over time Causes thickening of the arterioles/blood vessels
As the blood vessels thicken, perfusion decreases and perfusion decreases to body organs are damaged

Continuous BP elevation results in damage to organs

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Stroke
Myocardial infarction
Kidney failure
Death

HTN is a major risk factor for:

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Primary (essential)
Secondary

Classifications and etiology/causes of HTN

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Most common type of HTN
Not caused by an existing health problem; can develop when a patient has any one or more of the risk factors:

Primary (essential)

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Family history - lot have this
African-American ethnicity
Hyperlipidemia
Smoking
Older than 60 or postmenopausal
Excessive sodium and caffeine intake
Overweight/obesity
Physical inactivity
Excessive alcohol intake
Low potassium, calcium, or magnesium intake
Excessive and continuous stress
Some modifiable and not; teaching about modifiable and seeing diff risk factors have

Not caused by an existing health problem; can develop when a patient has any one or more of the risk factors:

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Results from specific diseases and some drugs
Kidney disease is one the most common causes of secondary hypertension

Secondary

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Physical assessment/clinical manifestations
Orthostatic hypotension
Psychosocial
Diagnostic assessment

Assessment of HTN

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Most people have no symptoms oftentimes - not getting screened for HTN no idea unless really bad
Some patients experience esp when really bad and high headaches, facial flushing (redness), dizziness, fainting
No idea unless annual phys/screenings - imp places have BP cuffs to check BP
Blood pressure screenings

Physical assessment/clinical manifestations

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Best prac in screenings to Take in both arms
Two or more readings at a visit
Use appropriate size cuff to arm - wrong size cuff can cause falsely high/low reading

Blood pressure screenings

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Decrease in BP with changes in position - take in supine, take in sitting, take in standing
Sig: 20 mmHg for systolic and/or 10mmHg for diastolic BP

Orthostatic hypotension

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Assess for stressors that can worsen hypertension - stress is risk factor that can make HTN worse

Psychosocial

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No specific lab or x-rays are diagnostic of primary hypertension - relying on BP readings
Secondary hypertension can be screened with labs specific to the underlying disease: Ex. kidney disease

Diagnostic assessment

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Major interventions - direct therapy: meds
Lifestyle changes
Complementary and alternative therapies
Drug Therapy
Avoid OTC medications (NSAIDs and decongestants - educate on this)

Interventions for HTN

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Helps with risk factors
Dietary sodium restriction to less than 2 grams/daily - very hard to do this
Reduce weight
Use alcohol sparingly
Exercise 3-4 days a week for 40 minutes and moving
Use relaxation techniques to decrease stress - stress can exacerbate HTN
Avoid tobacco and caffeine

Lifestyle changes

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Biofeedback
Meditation - use to decrease stress and relax

Complementary and alternative therapies

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Biggest intervention for pats with HTN
Diuretics:
Calcium channel blockers:
Angiotensin-Converting Enzyme (ACE) Inhibitors:
Angiotensin II Receptor Blockers (ARBs):
Aldosterone Receptor Antagonists:
Beta-Adrenergic Blockers:

Drug therapy for HTN

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First line of medications used for HTN and very effective
Decrease blood volume in order to lower blood pressure
EX: Thiazides: Hydrochlorothiazide (HCTZ)
EX: Loop diuretics: Furosemide (Lasix); Torsemide (Demadex) - cause excrete K
EX: Potassium-sparing: Spironolactone (Aldactone) - not cause excrete K
Monitor for hypokalemia with thiazide and loop diuretics - Check electrolytes and often on electrolyte protocols that prior to giving med not need K replacement therapy
Monitor for hyperkalemia with potassium-sparing diuretics - not getting to high
Sometimes get loop and K-sparing
Educate patients about frequent voiding - voiding lot more with diuretics; imp educate about; not before bed; think if fall risk - get more often to void: using bedside commode
Monitor for dehydration (urinating a lot) and orthostatic hypotension with diuretics

Diuretics:

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Interferes with calcium ions causing vasodilation to lower blood pressure
Check HR and BP prior to admin and keep monitoring post-admin so not giving opp effect where too low
Ends in -pine except Verapamil (Calan)
Amlodipine (Norvasc)

Calcium channel blockers:

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Blocks angiotension conversion which inhibits vasoconstriction- vasodilation occurs and blood pressure is lowered
Inhibit ACE from lungs and blocks/inhibits ACE - not able convert angiotensin I to II - result is vasodilation and lower BP
Affects RAAS sys - decreased renal blood flow kidneys release renin which goes to angiotensin I which converted to angiotensin II which causes vasoconstriction increasing BP
Commonly given
First line - not as effective in African American pop
-pril ending
Captopril (Capoten)
Lisinopril (Prinivil, Zestril)
Enalapril (Vasotec)
Common side effect: nagging, dry cough - sometimes go away and sometimes have switch to another anti-hypertensive drug if too annoying; monitor BP before giving meds - causes vasodilation - not too hypotensive before; also monitor for hypokalemia; blocking RAAS reducing excretion of K which puts at higher risk of hyperkalemia

Angiotensin-Converting Enzyme (ACE) Inhibitors:

Blocks binding of angiotension to receptor sites which inhibits vasoconstriction-vasodilation occurs and blood pressure is lowered
Blocks binding of angiotensin to receptor sites which inhibits it from causing vasoconstriction which then causes vasodilation decreasing BP
Affects RAAS sys - decreased renal blood flow kidneys release renin which goes to angiotensin I which converted to angiotensin II which causes vasoconstriction increasing BP
monitor BP before giving meds - causes vasodilation - not too hypotensive before; also monitor for hypokalemia; blocking RAAS reducing excretion of K which puts at higher risk of hyperkalemia
Commonly given
-artan ending
Candesartan (Atacand)
Valsartan (Diovan)
Losartan (Cozaar)
Azilsartan (Edarbi)
Monitor for hyperkalemia

Angiotensin II Receptor Blockers (ARBs):

Blocks binding of aldosterone at receptors which inhibits sodium reabsorption and fluid reabsorption
Kidneys retain water and Na - not reabsorb that lowers BP because lowering blood volume
Affects RAAS sys - decreased renal blood flow kidneys release renin which goes to angiotensin I which converted to angiotensin II which causes vasoconstriction increasing BP
Eplerenone (Inspra)
Monitor for hyperkalemia - blocking receptor sites because reducing excretion of K
Can interact with many other drugs and grapefruit - imp edu

Aldosterone Receptor Antagonists:

Drug of choice for hypertensive patients with ischemic heart disease
Blocks beta receptors which decrease heart rate and myocardial contractility
Affect SNS; Sympathetic nervous system is blocked
-lol ending
Metoprolol (Toprol, Lopressor)
Atenolol (Tenormin)
Bisoprolol (Zebeta)
Monitor for orthostatic hypotension (AE of it), HR, BP
Start and stop slowly; can cause rebound HTN if stopped abruptly
Can cause fatigue, depression and sexual dysfunction - not taking meds talk to them about this - hard stay on drugs esp having these AE and not having symp prior with HTN; provide edu on staying meds and talk about moving to diff drug if possible; let know about talk about these
Angioedema can be side effect - monitor for these; after on for awhile; if develop: emergent and need be taken off drug
Use with caution in patients with diabetes because glucose production may be affected - make harder recongnize symp of hypoglycemia: rapid HR and with beta blockers lowering HR may not recognize hypoglycemia as readily

Beta-Adrenergic Blockers:

Includes both Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) Thrombus - clot in one spot Embolus - moved from one spot to another VTE huge in healthcare settings and prevention big and want interventions in place; not want VTE esp PE because decomp quickly - need prevent Risk Factors: Prevention: SCDs

Venous thromboemolism (VTE)

Virchow’s Triad

Risk Factors:

Stasis of blood - blood not moving/pooling in places Vessel wall injury - damage to vessel; inflammatory response does occur to fix it; platelets and other coag properties trying to stabilize injury - will have more clotting with injury Altered blood coagulation - history certain disease/meds: hypercoagability

Virchow’s Triad

PREVENTION IS KEY TO ADDRESS THIS CHALLENGE IN HEATLH CARE - prevention is very imp; measure as quality/core measure in acute care because not want clot develop for pats while in acute care setting Patient education - edu about prevention and why interventions in place; education increases compliance Leg exercises - if cannot get out of bad to increase circulation Early ambulation - post-op/while sick; very imp Adequate hydration - encourage this; increases blood volume Graduated compression stockings Intermittent pneumatic compression, such as sequential compression devices (SCDs) - helps move blood around Venous plexus foot pump - helps move blood around Avoid certain meds: oral contraceptives Use Anticoagulant therapy - prevent; many in hospital on prophyalictic anticoag therapy because not up and moving as norm

VTE prevention

Assess first always Symptoms Preferred diagnostic test: Lab testing:

Symp and diagnostic assessments of DVT

May be symptomatic or asymptomatic Classic sign/symptom DVT: Induration (hardening) along the blood vessel Warmth, edema, redness in extremity Checking a Homans’ sign is not advised because it is an unreliable tool/test - do other things to confirm diagnosis Physical exam findings may be adequate for diagnosis

Symptoms

Venous duplex ultrasonography Assesses flow of blood through the veins of the arms and legs Definitive diagnosis

Preferred diagnostic test:

Calf or groin tenderness and pain depending on DVT location Sudden onset of unilateral swelling of the leg - look and assess both extremities

Classic sign/symptom DVT:

Negative D-Dimer test can exclude a DVT - do lab test for D-Dimer; if high move on to US/venous duplex; if - not have DVT Used for the diagnosis DVT when the patient has few clinical signs

Lab testing:

Goals for treatment: Observe/monitor for symptoms of pulmonary emboli: Elevate legs when in bed and up in chair Do not massage the affected extremity - no SCD on extremity Drug Therapy for pats

DVT interventions

Prevent pulmonary emboli, further thrombus formation, or an increase in size of the thrombus Want prevent DVT but not want it move to cause PE

Goals for treatment:

Sudden Shortness of breath, Sudden chest pain, acute confusion - when getting hypoxic: confusion early sign of hypoxia Suspect PE: CT chest best diagnostic tool; also V/Q scan and if mismatch - good vent and not perfusion know is clot; often do CT angiograms down

Observe/monitor for symptoms of pulmonary emboli:

Anticoagulants Start on IV and want on PO because not want home on IV med; if not therapeutic bridge using SQ until therapeutic

Drug Therapy for pats

IV Heparin SQ Enoxaparin (Lovenox) PO Warfarin (Coumadin)

Anticoagulants

Prevent clot from extending and more from forming then clot dissolved and reabsorbed on own Giving anticoag - not allowing clot as normally would do lot monitoring Baseline labs to see how doing prior to giving meds: PT, aPTT, INR, CBC with platelet count Anti-factor Xa assay - better monitoring tool than PTT - 6 hours after initiation and every day once two consecutive esults are within therapeutic range Assess therapeutic action of heparin; start heparin and monitor lab results q6h; look at it and see result; if blood too thin then lower heparin but if too thick increase drip - want in therapeutic range - thin enough so no more clots but not too thin where bleeding Get to point where 2 of 6 hour results in therapeutic range then doing labs daily Platelet count 24 hours after initiation and then every other day IV bolus heparin (based on body weight) followed by IV infusion drip and monitoring - watch for bleeding: urine, stool, bruising, altered LOC: bleeding in brain, pain esp abd: peritoneal bleeding Notify provider for: Heparin-induced thrombocytopenia (HIT) – life-threatening complication of heparin therapy; sig comp and need change to diff anticoag Have antidote available for excessive bleeding for hep To prevent DVT, unfractionated heparin may be given in low doses SQ for high-risk patients

Drug therapy: Unfractionated heparin therapy (UFH)

Suspected or confirmed bleeding: hematuria, frank or occult blood in stool, ecchymosis, petechiae, altered LOC, or pain (especially abdominal pain) Decrease of 50% from initial platelet count anytime during therapy Decrease in hemoglobin of greater than 2 grams/dL anytime during therapy

Notify provider for:

Protamine Sulfate - need have available if need reverse effects and have excess bleeding

Have antidote available for excessive bleeding for hep

Preferred for prevention (lower dose) and treatment (higher dose) of VTE Ex. Enoxaparin (Lovenox) given SQ: Prevent clot from extending and more from forming then clot dissolved and reabsorbed on own Dosed based on weight (1mg/kg) Monitor PT,INR (per textbook) Monitor anti-factor Xa assay (per Saint Luke’s) Serum creatinine (kidney func) and platelet counts are also monitored Assess for signs of bleeding: hematuria, frank or occult blood in stool, ecchymosis, petechiae, altered LOC, or pain Have antidote available for excessive bleeding If treating acute DVT or PE, may see overlap of Enoxaparin and Warfarin given - ready go home and getting warfarin but not therapeutic; not have IV drip but give LMWH SQ that give at home - sending home requires nurse and pharmacist to provide education to pat - need able admin at home Patient can self administer at home

Drug therapy: Low-molecular-weight heparin (LMWH)

Protamine Sulfate

Have antidote available for excessive bleeding

Warfarin (Coumadin) given po - give when going home for long-term treatments DVT/PE on anticoag for at least 6 months but varies on pat and provider Monitor with PT, INR Prevent clot from extending and more from forming then clot dissolved and reabsorbed on own Assess for signs of bleeding: hematuria, frank or occult blood in stool, ecchymosis, petechiae, altered LOC, or pain Have antidote available for excessive bleeding HCP specifies the desired INR level to obtain Teach patients to avoid foods with high concentrations of vitamin K

Drug therapy: Warfarin

INR is more reliable - monitored regularly; vary on pat and provider; normalized number regardless of location; therapeutic range: 2-3; not norm range but therapeutic for pats who need blood thinner PT - based on lab going run lab tests Need to adjust medication based on INR to achieve desired range

Monitor with PT, INR

Vitamin K - must be available

Have antidote available for excessive bleeding

Dark green leafy vegetables - eat consistent amount; not avoid completely More difficult to achieved desired levels

Teach patients to avoid foods with high concentrations of vitamin K

Other medications are available for clot prevention Thrombolytics Surgical management:

DVT - other interventions

Ex. rivaroxaban (Xarelto) - PO but no monitoring like warfarin No labs are required no antidote is available for meds - like because no lab required and have good results with it

Other medications are available for clot prevention

Tissue plasminogen activators (TPA) Administered directly into clot through a catheter Not used very often since have High risk for bleeding Breaks up clot

Thrombolytics

Thrombectomy - remove clot Inferior vena cava filtration: Very common for recurrent DVT and other risk factors that high risk for anticoag meds: frequent falls; stops DVT from moving and progressing to PE

Surgical management: