Hypertension & Afib Flashcards

1
Q

Hypertension

A

As BP increases, so does the risk of
MI
Heart failure
Stroke
Renal disease

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2
Q

BPs

A

Normal: less than 120/ less than 80
Elevated: 120-129/ less than 80
HTN stage 1: 130-139/ 80-89
HTN stage 2: 140+/ 90+
HTN crisis: 180+/ 120+

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3
Q

Primary HTN

A

no identified cause

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4
Q

Secondary HTN

A

Specific cause can be identified and corrected
Suspect with: Unexplained hypokalemia, Abdominal bruit over renal arteries, Variable B/P with history of tachycardia, sweating, tremor, Family Hx of renal disease

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5
Q

Risk Factors for Primary Hypertension

A

Age
Alcohol
Tobacco use
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
Family history
Obesity
Ethnicity
Sedentary lifestyle
Socioeconomic status
Stress

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6
Q

Pathophysiology of Primary Hypertension

A

Genetic Links
Water and sodium retention
Stress and increase sympathetic nervous system activity
Altered renin-angiotensin-aldosterone system (RAAS)
Insulin resistance and hyperinsulinemia
Endothelial dysfunction

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7
Q

Clinical Manifestations HTN

A

“silent killer”
Symptoms of severe hypertension
Fatigue
Dizziness
Palpitations
Angina
Dyspnea

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8
Q

Target Organ Diseases

A

Heart
-Coronary artery disease (CAD)
-Left ventricular hypertrophy (LVH)
-Congestive heart failure (CHF)
Peripheral vascular disease (PVD)
Kidneys (Nephrosclerosis)
Eyes (Retinal damage)

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9
Q

Goals HTN

A

Goal:
< 140 / 90 mm Hg
< 130 / 80 mm Hg for those at high risk for / with CAD
Medications
Decrease circulating blood volume
Reduce SVR – systemic vascular resistance (“After-load”)

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10
Q

Medication Therapy

A

Diuretics
Adrenergic inhibitors
Vasodilators
Angiotensin & renin inhibitors
Ca+ channel blockers

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11
Q

Drug Therapy action

A

Decrease the volume of circulating blood
Reduce systemic vascular resistance

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12
Q

Diuretics

A

promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines

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13
Q

Adrenergic-inhibiting agents (Beta blockers)

A

act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels.

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14
Q

Direct vasodilators

A

decrease the BP by relaxing vascular smooth muscle and reducing SVR

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15
Q

Calcium channel blockers

A

increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells.

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16
Q

Angiotensin-converting enzyme (ACE) inhibitors

A

inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)–mediated vasoconstriction and sodium and water retention.

17
Q

A-II receptor blockers (ARBs)

A

) prevent angiotensin II from binding to its receptors in the walls of the blood vessels.

18
Q

Lifestyle Modification

A

Weight reduction – weight loss of 22 lb may decrease SBP by ~ 5 – 20 mm Hg
Dietary sodium reduction - HEALTHY ADULTS <2300 mg per day
Moderation of alcohol intake
Physical activity – moderate or vigorous aerobic activity, muscle-strength training, flexibility and balance exercises
Avoidance of tobacco products

19
Q

Dietary Approaches to Stop Hypertension (DASH)

A

K+ rich foods (4700 mg/day)
Ca+ rich foods (1200 mg/day)
Decrease Na+ (2400 mg/day [1 tsp])
Limit fat calories to 27%
Fruits (6 – 8 daily)
Vegetables (4 – 5 daily)
Fat-free or low fat dairy (2 – 3 daily)
Whole grains (6 – 8 daily)
Lean meat, fish, poultry (6 oz or less daily)
Beans, seeds, nuts (4 – 5 per week)
Low fat sweets (5 or less per week)

20
Q

Psychosocial Risk Factors

A

Low socioeconomic status
Social isolation
Lack of support
Stress
Negative emotions

These activate the SNS and stress hormones

21
Q

BP Measurement in Older Adult

A

Take in both arms initially
Proper size and placement f cuff

Auscultatory Gap: Wide gap between 1st Korotkoff sound & subsequent beats
Failure to inflate cuff high enough may cause serious under-estimation of B/P
Avoid by palpating brachial / radial artery during inflation
Sensitivity to B/P changes: Reducing SBP < 120 mm Hg in those with long-standing HTN can lead to inadequate cerebral blood flow
Postprandial hypotension: Greatest drop occurs approximately 1 hour after eating
Avoid giving vaso-active medications with meals

22
Q

Hypertensive Crisis

A

SBP >180 mmHg and/or DBP >120 mmHg
Hypertensive urgency
Develops over hours to days
May not require hospitalization
Hypertensive emergency
Very severe problems can result if prompt treatment is not obtained
Rate of rise more important than absolute value

23
Q

Managing Hypertensive Crisis in the Acute Care Setting

A

Labetolol (Normodyne
Hydralazine (Apresoline

24
Q

Labetolol (Normodyne)

A

Antihypertensive, anti-anginal
Mixed alpha/beta effects
Decreases B/P without reflex tachycardia or significant reduction in HR
Reduces CO, SVR & BP
20 mg IV over 2 minutes
Usually ordered every 6 - 8 hours PRN

25
Q

Hydralazine (Apresoline)

A

Direct peripheral artery vasodilator
Reduces B/P with reflex increase in
HR
Stroke volume
Cardiac output
10 – 20 mg IV every 4 to 6 hours PRN
Contraindication CAD
Caution > 40 years old

26
Q

Atrial Fibrillation

A

Paroxysmal or persistent
Most common dysrhythmia
Prevalence increases with age
Usually occurs in patients with underlying heart disease
Can also occur with other disease states

27
Q

atrial flutter

A

causes a decrease in cardiac output and an increased risk of stroke

28
Q

Medications AFib

A

Long term anti-coagulation therapy:
Eliquis
Xarelto
Pradaxa
Savaysa
Aspirin (on rarer occasions)

29
Q

Warfarin (Coumadin)

A

Inhibits activation of Vitamin K-dependent coagulation factors
II, IX, X, Proteins C & S
48 – 72 hours to affect PT
Several days for maximum effect
Rationale for parenteral anticoagulant for five (5) days while therapy started
Contraindicated
Aspirin
NSAIDS
Phenytoin (Dilantin) – Use cautiously
Barbiturates
Vitamin, mineral, herbal supplements
Wide gap of individual response to dosage
Age
Weight
Cardiac or liver impairment
Diet (Vitamin K intake?)
Drug interactions
Must be closely monitored & titrated
Monthly PT/INR
Major bleeding 1–2%
Intracranial bleeding 0.1–0.5%

30
Q

Coumadin v heparin

A

Coumadin
Prothrombin Time (PT)
Used to monitor Warfarin
Extrinsic system
Slow onset, persists for 7 – 14 days
11 – 12.5 seconds
INR 0.8 – 1.1 (normal range)
Therapeutic range = 1.5 – 2 times control
2.0 – 3.0
Warfarin reversal agents
Vitamin K: 12 – 24 hours
FFP more rapid
Hepato-cellular liver disease
Obstructive biliary disease

Heparin
Partial Thromboplastin Time (PTT)
Used to monitor Heparin
Intrinsic system
aPTT: 30 – 40 seconds
PTT 60 – 70 seconds
Therapeutic range = 1.5 – 2.5 times control
Heparin reversal agent
Protamine sulfate 1 mg : 100 units Heparin
Altered very little by small doses of Heparin (5000 units SQ every 12 hours) or Enoxaparin (Lovenox)
Not monitored
Minimal risk of spontaneous bleeding

31
Q

Dietary Sources of Vitamin K

A

Green, leafy, vegetables
Kale
Collards
Spinach
Turnip greens
Asparagus, Beet greens, Broccoli, Brussels sprouts, Cabbage, Cabbage, Celery, Cucumber, Dandelion greens, Endive, Lettuce, Mustard greens, Okra, Onions, Parsley, Peas, Rhubarb, Sauerkraut

OTHERS:
Bread crumbs, dry, grated, seasoned
Coleslaw
Noodles, spinach
Prunes
Pie crust, graham cracker