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AH1 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

BP values

A

normal range 100-120/70-90???

pre-hypertension 120-139/80-89

stage 1 140/90

stage 2 160/100

hypertensive crisis 180/120 **Will stroke out if they don’t get to ER** Joint Commision doens’t exclude BB from NPO status, other meds are up to surgeon discretion

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2
Q

Define Hypertension.

A
  1. “The silent killer”
  2. Intermittent or sustained elevation in systolic and/or diastolic pressures
  3. product of cardiac output multiplied by peripheral resistance
  4. A change in either will change the blood pressure

changes way blood flows through body, longer sustained elevation is hypertension

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3
Q

What are some causes of secondary hypertension

A
  1. kidney disease ** most common, chicken or egg? which came first
  2. coarctation of the aorta - increased pressure at entrance of aorta because narrowing of entrance –> automatic increase in BP
  3. endocrine disorders –> hyperthyroidism, Cushing’s - excess fluid, diabetes - more resistance in vasculature - blood viscosity and moves through slower
  4. neurologic disorders - anything that increase intracranial pressure - autonomic nervous response, spinal cord injuries
  5. illegal drug use - cocaine –> associated with hypertensive crisis - can stroke out
  6. pregnancy –> preeclampsia, first trimester more fluid volume
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4
Q

What screening is available for hypertension?

A
  1. Urine - protein ?
  2. HGB A1C - testing for diabetes and how well it is control <5.8 for no diabetest 6.0-6.5 - prediabetes, > 7.0 - diabetes
    1. blood sugar level for past 3 months
  3. Electrolytes - sodium, potassium level
  4. BUN/CR - renal function
  5. Lipid profile - hyperlipidemia? Is it contributing? BB can increase release of triglycerides
  6. GFR
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5
Q

What are tx for HTN?

A
  • DASH - low sodium diet
  • Potassium management - inverse relationship
  • first line defense for HTN is HCTZ - potassium wasting Zestril (lisinopril + HCTZ)
  • Meds
    • diuretic, BB, ACE, ARB, CCB
  • Education
    • wt, ETOH, smoking, exercise, electrolytes
  • BB - blocks s/s of hypoglycemia, can CAUSE hyperglycemia - not good choice for diabetic pt. find something else
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6
Q

What is a hypertensive crisis?

A
  • AKA Malignant HTN, hypertensive emergency
  • BP 180/120 mmHg
  • Manifestations include
    • HA, confusion
    • Papilledema, blurred vision
  • Restlessness
  • motor and sensory defects

**Be careful bringing BP fast, they can stroke out with rapid changes as well**

Goal: Reduce BP by 25% each hour. Could take hours depending on how high the BP is

Labetelol - b/c we can titrate

Nicardipine drip

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7
Q

What is peripheral vascular disease?

A
  • Narrowed peripheral arteries
  • Impaired blood supply to peripheral tissues
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8
Q

What causes Peripheral vascular disease?

A
  • Age
  • DM2
  • Hypercholesterolemia
  • HTN
  • Smoking
  • Elevated homocysteine levels
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9
Q

What are the manifestations of PAD?

A
  • Cramping or aching pain in calves of legs, thighs, and buttocks with a predictable level of activity
  • Rest pain during inactivity
  • Increases with elevation of the legs.
  • Pain decreases when legs are dependent.
  • Skin is thin, shiny, and hairless; discolored areas.
  • Toenails can be thickened.
  • Areas of skin breakdown, edema
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10
Q

What is ABI

A

Ankle-brachial index

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11
Q

What are the complications of PAD?

A
  • Gangrene
  • Rupture of abdominal aortic aneurysms
  • Infection
  • Sepsis
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12
Q

What is the Tx of PAD?

A
  • ASA (Platelet aggregate inhibitors)
  • Clopidogrel (Plavix): platelet inhibitor/vasodilator
  • Pentoxifylline (Trental): dec blood viscosity & inc microcirculation.
  • Foot care-ESSENTIAL!
  • No support hose!
  • Regular, strenuous exercise 30-45 min
  • Control comorbidities: DM, hypercholesteremia, weight control, HTN.
  • Revascularization in severe cases: PTA, endarterectomy with bypass grafts
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13
Q

What is dependent rubor?

A

Pt with dependent rubor. If the patient’s legs were elevated, we would expect them to be pale and possibly painful.

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14
Q

What is chronic venous insufficiency?

A
  • Inadequate venous return over a prolonged period
  • Common cause is deep vein thrombosis.
  • Venous status occurs, impairing arterial circulation.
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15
Q

What does a chronic venous insufficiency wound look like?

A

IRREGULAR BORDERS, SHALLOW

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16
Q

What are the complications of chronic venous insufficiency?

A
  • Deep vein thrombosis
  • Varicose veins
  • Leg trauma
  • WOUNDS=INFECTION
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17
Q

What medications are used in chronic venous insufficiency wounds?

A
  • Corticosteroids
  • Zinc oxide
  • Clotrimazole
  • Miconazole
  • Unna boot
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18
Q

Describe arterial insufficiency

A

Pain: intermittent claudication, relieved by dependent position

Pulses: diminished or absent

Skin: Thickened nails dry, shiny skin; cool temp

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19
Q

Describe ulceration of arterial insufficiency.

A
  • Most common to tips of toes and toe webs, deep and often involving the join; perfectly circular
  • pale fibrotic to black in color to a dry gangrene
  • edema: minimal
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20
Q

Describe venous insufficiency.

A
  • Pain: constant aching, cramping relieved by elevation of extremity
  • pulses: present
  • skin: thickened and tough skin, warm temp
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21
Q

Describe ulceration of venous insufficiency.

A
  • most commonly to medial malleolus
  • can be superficial or shallow
  • base of ulcer is irregular in shape; color is a beefy red to yellow fibrinous to granulation tissue
  • edema: moderate to severe
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22
Q

What is pt education for ulcers? dt venous insufficiency?!

A
  • Most important aspect of education is maintaining/increasing tissue perfusion in the extremeties.
  • Preventing ulceration through careful wound care will help prevent infection.
  • Promote diet for wound healing: protein, Vitamin C,
  • Avoid getting dressings wet
  • Take meds as prescribed (i.e. antibiotics)
  • Walk, walk, walk-rest when needed, but don’t stand for long periods of time.
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23
Q

What is chronic stable angina?

A

There is a temporary imbalance between cardiac muscles’ supply and demand for oxygen.
• This leads to ischemia that is limited in duration and does not cause permanent damage to myocardial tissue.
• The ischemia causes chest discomfort that occurs with moderate to prolonged exertion leading to slight limitation of activity.
• Predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin

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24
Q

What are the causes of chronic stable angina?

A
  • Physical exertion, which precipitates an attack by increasing myocardial oxygen demand
  • Exposure to cold, which causes vasoconstriction and elevated blood pressure, with increased oxygen demand
  • Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle; in a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain
  • Stress or any emotion-provoking situation, causing the release of catecholamines, which increases blood pressure, heart rate, and myocardial workload
25
Q

What are the risk factors for angina?

A

Can be modifiable or non-modifiable

26
Q

Assessment and diagnosis of chronic stable angina

A
  • chest pain radiating to the L arm, worsened by exertion or stress, relieved with rest and nitroglycerin, lasting for less than 15 minutes
  • Labs: Cholesterol (HDL ↓ and LDL ↑), Triglyceride ↑; Homocysteine levels (↑ in atherosclerosis and blood clots); Cardiac enzymes (CK-MB, Troponin) and Myoglobin to r/o MI.
  • Diagnostics: 12-lead EKG (ST depression or T wave inversion)- must be done within 10 minutes of presentation with chest discomfort, Imaging (Thallium scans, CT scans).
27
Q

How is chronic stable angina treated?

A
  • Pain management
  • Oxygen therapy
  • Lipid-lowering medications
  • Nutrition
  • Smoking cessation
  • Exercise – moderate to vigorous, 3-4x/week, 40 minutes/session
  • Anxiety and stress management
  • Address the needs of the family and significant others and provide teaching and information regarding the disease process; clarify any misconceptions.
28
Q

What types of medications are used for angina?

A
  1. Nitrates
  2. Beta-adrenergic blocking agents
  3. Calcium Ion Antagonists (Calcium Channel Blockers
  4. Antiplatelet Meds
  5. Anticoagulants
29
Q

Describe the nitrates used for chronic stable angina.

A
  1. Nitroglycerin (Nitrostat, nitro-bid) - short & long -term reduction of myocardial oxygen consumption through selective vasodilation
  2. Isosorbide mononitrate - long acting
30
Q

What types of beta blockers are used for chronic stable angina?

A

Metoprolol (lopressor) and atenolol (tenormin) - reduction of myocardial oxygen consumption by blocking beta adrenergic stimulation of the heart

31
Q

What calcium channel blockers are used in chronic stable angina?

A
  • Amlodipine (Norvasc)
  • Diltiazem (Cardizem, Tiazac)

Negative inotropic effects, indicated in patients not responsive to beta blockers, used as primary tx of vasospasm

32
Q

What antiplatelet medications are used for chronic stable angina?

A
  • Clopidogrel (Plavix)
  • Prasugrel (Effient)

Prevention of platelet aggregation

33
Q

What anticoagulants are used for chronic stable angina?

A
  • heparin
  • low molecular weight heparins
  • enoxaparin (lovenox)
  • dalteparin (fragmin)

prevention of thrombus formation

34
Q

What is Heart Failure?

A
  • A condition in which the heart cannot pump enough blood to supply the body’s tissues with sufficient oxygen and nutrients; back up of blood in vessels and the lungs causes buildup of fluid (congestion) in the tissues.
35
Q

What causes left-sided HF?

A

Caused by coronary heart disease & HTN.

Results in ↓ CO resulting in ↑ back-pressure to lungs

36
Q

What are the S/S of LS HF?

A
  • Decreased urine output - decreased cardiac output decreases perfussion to renal system
  • Pulmonary congestion - fluid backing up in the lungs - manifests as symptoms of pneumonia, crackles
  • Pulmonary HTN - increased pressure in lungs b/c of backwards flow of fluid
  • Fatigue - inappropriate gas exchange & body tries to compensate
  • Activity intolerance
  • Dizziness
  • Syncope
  • Dyspnea/DOE -
  • Shortness of breath
  • Cough
  • Orthopnea - inability to breathe while asleep (episodes of apnea), pt can sleep in recliner
  • Crackles, Rales, Wheezes
  • Nocturnal dyspnea
37
Q

What causes RS HF?

A
  • restricted pulmonary blood flow from acute/chronic pulmonary disease, cors pulmonale, R sided infarction
    Results in ↓ CO resulting in ↑ back-pressure to abdominal organs and peripheral extremities
38
Q

How does RS HF manifest?

A
  • Lower extremity edema (dependent)
  • Sacral edema (if bedridden)
  • Anorexia
  • Nausea
  • RUQ pain r/t liver engorgement and portal HTN
  • Jugular vein distention
  • Ascites
39
Q

What causes CHF?

A

CAD → HTN → Arrhythmias → Heart valve disease → Myocardial infarction → Cardiomyopathy

Emphysema → Severe Anemia → Thyroid abnormalities (hyper or hypo)

  • HTN - affects how fast blood can travel - causes excess pressure
  • Arrythmias may be preexisting, chronic
    • manage arrythmia to prevent HF
  • Valve disease - in change of one-directional flow, when this is not working properly – clots, damage
    • possible surgical repair
  • MI - whatever side it occurs on causes HF on the affected side
  • emphysema - already have some fluid buildup
40
Q

What are the s/s of heart failure?

A
  1. Edema of extremities and abdomen - RS
  2. cough - LS
  3. SOB - LS
  4. Fatigue/weakness - more common in left
  5. weight gain - both **3 lb in a day or 5 lbs in a week - fluid weight**
  6. tachycardia - both
  7. loss of appetite - RS
41
Q

What kind of testing can be done for CHF?

A
  1. Echocardiogram - sono of heart, follow blood flow
  2. Ejection Fraction: normal 50-70 (less than 35% is looking at heart transplant)
  3. Stress test - treadmill with ECG, run and look for differences, there is a chemical stress test as well
  4. Cardiac Catheterization - go in through groin, inject dye and see how the dye flows through the heart, sometimes can put in a stent at the same time
  5. MRI Cardiac
  6. Nuclear cardiac scan
  7. BUN/Cr
  8. Urine creatinine clearance
  9. CBC
  10. Electrolytes
  11. BNP

*take vitals to establish baseline first*

42
Q

What are the Tx for CHF?

A
  1. ACE inhibitors: ex) enalapril lisinopril, Captopril
  2. vasodilators: decrease workload of the heart
43
Q

What are some other meds for CHF?

A

ARB

  • Losartan and Valsartan
  • Alternative to ACE - if ARBS don’t help, try BB
  • Digoxin - positive inotrope, helps with arrythmias
    • Increased contractility
    • Slows heart rate
    • Reduces symptoms
    • APICAL pulse for a full minute
    • potassium level
    • therapeutic 0.5-2
44
Q

How to beta blockers work for CHF?

A
  • slow the HR
  • Reduce BP
  • Limits/reverses heart damage
  • Lessens chance of unexpected death
45
Q

Describe MOA of loop diuretics.

A
  • Dec fluids in lungs
  • Decreases edema
  • Causes K+ loss
    Ex: Bumetanide and Furosemide
46
Q

Describe aldosterone antagonist (diuretic):

A
  • Diuretic
  • May reverse scarring of heart
  • May increase longevity
  • May increase K+ to dangerous levels
    Ex: Spirolactone

Potassium sparing

Many times combo loop diuretic + aldosterone antagonist to decr risk to potassium level and decr dose of furosemide

47
Q

Name some IV GTTS for CHF

A
  1. Nesirtide: dilates blood vessels and lowers b/p.
  2. Milrinone: Inotrope and vasodilator: inc force of blood flow throughout body.
  3. Dobutamine: Inotropic medication given IV gtt
48
Q

What are the heart failure classifications?

A

New York Heart Association: (quality of life)

*just know it goes from 1-4*

Class I: no symptoms
Class II: can perform everyday activities but SOB on exertion
Class III: Noticeable limitations in activity; comfortable only at rest
Class IV: SOB even at rest

American College of Cardiology (fn and treatment)

A: at risk for HF without heart dysfunction
B: Evidence of heart dysfunction without symptoms
C Evidence of heart dysfunction with symptoms
D: symptoms of heart failure despite maximal therapy

49
Q

What is Acute Pulmonary Edema?

A
  • medical emergency

LEFTSIDED

1 L of fluid = 2.2lbs of weight

*** productive cought with large amounts of pink frothy sputum***

ascites at this point for LS HF

Observe for air hunger, an overwhelming sense of doom, tachypnea, the need to sit straight up in bed, a cough productive of large amounts of pink, frothy sputum.
Measure abdominal girth every shift.
Maintain bed rest, elevate HOB.
Monitor hemodynamic parameters.
Monitor O2 sats and respiratory status

50
Q

What are Nursing Interventions for pulmonary edema?

A
  • VS
  • HOB ↑
  • I&O
  • O2 & O2 sats / Respiratory assess
  • Diuretics
  • Foley
  • Monitor labs - K & Na
  • Safety - fall risk
  • Legs elevated/TED hose
  • Weights

Dusky grey ** fingers and lips**

51
Q

Nursing assessment of HF

A
  • Edema
  • Jugular vein distention
  • Weight
  • Auscultation of lungs
  • Respiratory rate, quality
  • Heart sounds - could have presence of s3 or s4
  • valve problem - swishing sound
52
Q

Nursing considerations for HF

A
  • Elevate extremities
  • Daily weight, report to MD if >5lbs/5 days
  • 1500 cc fluid restrict - give them an idea of how much it really is, teach them other types of fluid, dietary often doesn’t put any fluid on there, this is for the whole 24 hours
  • Low sodium diet - processed foods, canned, smoked, anything with a long shelf life
  • Ted Hose
53
Q

What is the pt education for HF?

A
  1. stop smoking - nicotine patch, remove old, rotate sites, CAN’T smoke with nicotine patch - MI risk and severe tachy
  2. daily weight
  3. sodium restricition
  4. weight control
  5. control other medical conditions
  6. fluid restriction
  7. avoid alcohol
54
Q

What is homocysteine?

A

Homocysteine is a type of amino acid, a chemical your body uses to make proteins. Normally, vitamin B12, vitamin B6, and folic acid break down homocysteine and change it into other substances your body needs. There should be very little homocysteine left in the bloodstream.

55
Q

What causes high homocysteine?

A

Most people who have a high homocysteine level don’t get enough folate (also called folic acid), vitamin B6, or vitamin B12 in their diet. Replacing these vitamins often helps return the homocysteine level to normal. Other possible causes of a high homocysteine level include: Low levels of thyroid hormone.

56
Q

What is the purpose of the heart’s function?

A

Perfuse tissues - oxygenated blood

If this doesn’t happen, then tissue deterioration occurs

57
Q

What is the main issue in heart failure?

A

Can be left or right, but you’re having an issue with your ventricles pumping efficiently

  • heart has to work harder
  • heart knows and tries to compensate (makes it worse & pt deteriorates)
58
Q

What are other treatment options for HF?

A
  • CABG - bypass
  • Heart Valve repair or replacement
  • ICD - internal cardiac - shocks you into sinus rhythm - need to call provider or go to ER if it shocks you
  • Bi-VICD - pacemaker + defibrillator - signal to SA node and maintain a minium HR
  • LVAD -Ventricular assistive device - sounds like enginge
59
Q

What is primary HTN?

A

No other reason that you have it

  • Defined as systolic BP of > 140 mmHg or diastolic >90
  • tx of HA and doesn’t go away

AH1 (6 decks)

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