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RNSG 1533 > Perfusion > Flashcards

Perfusion Flashcards

1
Q

Electrical Conduction of the Heart

A 
"action potential"=electrical impulse
SA (sinoatrial) node (P wave)
Internodal Tract
Right and Left Atria (contract)
AV (atrioventricular) Node
Bundle of HIS
Bundle Branches
Purkinje Fibers
Ventricle (Contract)
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2
Q

Absolute Refractory Period

A

Cardiac muscle does not respond to any stimuli during ventricular contraction

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3
Q

Relative refractory period

A

After absolute refractory when cardiac muscle gradually recovers its excitability (by early distole)

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4
Q

ECG Waves

A

P-1st, firing of SA node, depolarization of the atria
QRS-2nd, depolarization from AV throughout ventricles
T-3rd, repolarization of the ventricles
U-4th repolarization of Purkinje fibers, or hypokalemia
Intervals between each wave reflect the time it takes for the impulse to travel from one area to another.

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5
Q

ECG lead placement

5 Lead

A 
RA-right arm, on cx where arm/torso meet
RL-Left arm, on cx where arm/torso meet
RL-Right leg, on abd near hip
LL-Left leg, on abd near hip
C1-(for V1) 4th IC, rt sternal border
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6
Q

P wave normal

A

0.06-0.12
firing of SA node, depolarization of atria (contract)
longer: conduction problem within atria or SA node

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7
Q

QRS wave normal

A

0.04-0.12
depolarization of AV through ventricles (contract)
longer-conduction problem in branches

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8
Q

T wave normal

A

0.16
repolarization of ventricles
longer: MI or ischemia
inverted: old MI injury

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9
Q

MAP formula

A

MAP = (SBP + 2(DBP)) / 3

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10
Q

depolarization

A

contraction

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11
Q

repolarization

A

rest

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12
Q

ST interval

A

0.12

MI
elevated = STEMI

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13
Q

PR interval

A

0.12-0.20

conduction problem AV, bundle of his, bundle of branches, atria

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14
Q

QT interval

A

0.34-0.44

ventricular Repolarization disturbances

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15
Q

Sinus Bradycardia

A
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16
Q

Sinus Tachycardia

A

> 100 bpm
Causes: normal response to increased activity, anxiety, pain, stress, fear, fever, anemia, hypoxemia, hyperthyroidism, pulmonary embolism, decrease cardiac ouput/hypotension, hypovolemic shock, MI, heart failure
caffeine, drugs, alcohol, nicotine

Sx: Decreased blood pressure, Decreased Cerebral perfusion=restlessness, anxiety, confusion, Decreased oxygen saturation, Weakness, Fatigue, Shortness of breath, Decreased urine output, Pain, Palpitations, Orthopnea

Tx: fix the cause!

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17
Q

Sinus Arrhythmia

A

Ps and Rs irregular
breathing and meds: Morphine, digoxin
asymptomatic

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18
Q

Cardiac output formula

A

HR x stroke volume = CO

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19
Q

Pathophysiology of PVD

A

leading cause is atherosclerosis, gradual thickening of intima (innermost layer) and media (middle layer) of the arterial wall from deposit of cholesterol and lipids. also: inflammation and endothelial injury.
collateral circulation develops
mostly affects parts of arterial tree and lower extremity arteries
Plaque develops arterial bifurcations
Symptoms develop when the vessel is occluded by 60% or more

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20
Q

PVD risk factors

A

tobacco, DM, hyperlipidemia, elevated C-reactive protein, uncontrolled HTN
other factors: family hx, age, gender, hypertriglyceridemia, obesity, sedentary lifestyle, stress, men, cholesterol >240

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21
Q

S/Sx of PVD

A 
Intermittent pain/ cramping with activity [claudication]
Rest pain – burning sensation in legs
Numbness, decreased sensation
Diminished or absent peripheral pulses
Extremity pallor with elevation
Extremity dark red when dependent
Thin, shiny and lack of hair on skin
Thickened toenails
Skin areas of discoloration 
Skin breakdown
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22
Q

Treatment for PVD

A 
Clinical therapies:
       Smoking cessation
       Meticulous foot care
       Support hose
       Exercise [walk 30-60m, 3-5x week; walk until pain, rest, then walk again until pain for 30min]
       Rest for pain
       BMI
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23
Q

2 priority education topics for PVD

A

Smoking cessation
DM control, foot care
lipid mgt -statins [lipid-lowering agent; lowers LDL & triglycerides]
HTN [thiazides, ACE-inhibitors, lifestyle changes]

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24
Q

two priority nursing diagnoses for PVD

A

ineffective tissue perfusion
impaired skin integrity
risk for falls

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25
Q

atropine

A

–

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26
Q

beta blockers

A 
-olol
slows HR, reduces workload
angina, BP, HF, heart attack
drowsy, fainting, swelling, bradycardia
blocks negative effects of SNS
watch BP
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27
Q

Ca channel blockers

A

-VND (vera nifed dilti)
decreases demand for O2 by lowering contractility and conductivity of the heart//relaxes blood vessels
bradycardia, constipation, edema

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28
Q

lipid-lowering agents

A

–

muscle pain, soreness, GI upset

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29
Q

complications with PVD

A

gangrene, limb amputation, infection, sepsis

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30
Q

Types of PVD

A

asymptomatic [found at dr]
intermittent claudication [pain upon activity]
critical limb ischemia [rest pain, tissue loss]

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31
Q

anticoagulants

A

warfarin, heparin

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32
Q

antihypertensives

A

–

orthostatic hypoTN, don’t stop abruptly!

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33
Q

antiplatelets

A

aspirin, clopidogrel

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34
Q

segmented BP

A

used to check peripheral pulses with doppler
thigh, below knee, ankle
drop in segBP >30 suggests PVD

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35
Q

Ankle Brachial Index

A

ABI
uses doppler
divides the ankle Systolic BP by the higher of the Lt and Rt brachial Systolic BPs
NOTE: elderly and DM pts-falsely elevated ABIs due to calcification of arteries
DON’T do immediately after revascularization or on distall bypass grafts [risk of graft thrombosis]

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36
Q

ACE-inhibitors

A

-pril
BP, HF, MI
relaxes blood vessels, reduces heart workload
dry COUGH, dizzy, drowsy, sunburn

37
Q

digoxin

A

affects strength, contractility of heart
K+ high or low
early toxicity: anorexia, N/V, fatigue, headache, vision changes
late toxicity: dysrhythmias (brady, AV block)
HOLD if HR

38
Q

PVD post op care

A

walk!
no knee flex, or prolonged sitting
if edema, lay with feet above heart level

39
Q

Acute arterial ischemia

A

sudden interruption to blood supply
6 Ps: pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia
tissue necrosis and gangrene
paralysis = nerve death
start IV heparin, remove thrombus (meds: tPA, urokinase0 through femoral artery to site of clot (24-48hrs)

40
Q

a-adrengergic receptors

A

vasoconstriction

41
Q

b-adrenergic receptors

A

vasodilation

42
Q

classifications of HTN

A

normal 160/>100

43
Q

cause of secondary HTN

A 
cirrhosis
narrowing of aorta
drugs: estrogen, NSAIDs, sympathetic stimulants
endocrine disorders
neuro disorders
pregnancy
renal disease
sleep apnea
44
Q

Risk factors for primary HTN

A 
Age
alcohol (limit to 1oz)
smoking
DM (higher risk for organ disease (heart, kidneys))
elevated lipids (atherosclerosis)
excess sodium intake 
gender (men)
family hx
obesity
ethnicity
sedentary lifestyle
socioeconomic status
stress
45
Q

HTN concept correlation

A 
Altered antecedents: Cardiopulmonary System
Fluid Volume
Blockages
Altered Atrributes: Blood Pressure
Capillary Refill
Pulses
MAP
Negative Consequences: Ischemic Pain
Loss of Fine Tactile Sensation
Confusion
↓ Organ Function
46
Q

HTN S/Sx

A

fatigue, dizziness, palpitations, angina, dyspnea

HTNsive crisis: nosebleeds, headache, anxiety, dyspnea

47
Q

HTN Complications

A

Heart: CAD (atherosclerosis)
Lt Ventricle Hypertrophy: increase cardiac workload
Heart failure: when heart can’t pump enough blood to meet demand (SOB on exertion, paroxysmal nocturnal dyspnea, fatigue
Brain: CV disease (atherosclerosis -> ischemic attacks, stroke, brain damage bc vessels aren’t able to control blood flow in brain causing cerebral edema)
PVD
Nephrosclerosis: chronic kidney disease (early sign is nocturia)
Renal damage: blurred vision, retinal hemorrhage, loss of vision

48
Q

Collaborative Care HTN

A

Lifestyle mod: weight loss, DASH plan, Na reduction, moderate alcohol, physical activity, avoid tobacco, Mgt psychosocial risk factors

49
Q

HTN diagnostic tools

A

Thorough H & P
Eye exam – assess retinal damage
Check EKG
UA – check protein
Check labs – BUN, creatinine, lipids, K+,
Renal eval. – IVP, renal arteriogram
Assess BP- for each check - √ BP x 2 at least 2 minutes apart

50
Q

HTN emergency v. urgency

A

Hypertensive emergency - BP > 200/150
Evidence of organ damage
Most times d/t patients d/c meds abruptly

Hypertensive urgency- BP > 180/120
BP ↑ but no organ damage

Note: both require quick assessment and initiation of treatment

51
Q

HTN drugs

A 
Diuretics
2nd drug from other antihypertensive drug classifications 
All work as vasodilators in some way
ACE inhibitors
angiotensin receptor blockers
beta blockers
calcium channel blockers
52
Q

CHF Patho (systolic)

A

inability to pump blood effectibely
impaired contractile function (MI), increased afterload (HTN), cardiomyopathy, and mechanical abnormalities (valvular disease)
loses ability to get enough pressure because it’s dilated and hypertrophied.
Ejection Fraction (EF)

53
Q

CHF patho (diastolic)

A

inability for vetricles to relax and fill during diastole
“HF with normal EF”
decreased stroke volume and CO
veinous engorgement
result of Lt ventricular hypertrophy from HTN, MI, valve disease, cardiomyopathy

54
Q

CHF patho (mixed)

A

dilated lt ventricular walls unable to relax

EF

55
Q

Compensatory Mechanisms (CHF)

A
  1. SNS activation-1st (triggered in low CO states); least effective; releases epi and norepi; increases HR, contractility, vasoconstriction
  2. Neurohormonal-starts renin-angiotensin-aldosterone system (kidneys, hold water/salt, increase BP and vasoconstrict) ADH released holds more water-all of this leads to increased cardiac workload, myocardial dysfunction, and ventricular remodeling
  3. Dilation-enlargement of chambers of heart; caused by increased pressure in chambers over time; eventually overstretches
  4. Hypertrophy-increase in muscle mass and cardiac wall thickness in response to overwork and strain; leads to poor contractility, needs more O2, poor coronary artery circulation (ischemic more easily), prone to dysrhythmia
56
Q

Left Sided HF

A

most common
causes blood to back up into lt atrium and pulmonary veins
pulmonary congestion and edema
frothy pink sputum

57
Q

Right Sided HF

A

Rt ventricle fails to contract effectively
causes: lt sided HF, rt ventricular infarction, pulmonary embolism, “cor pulmonale”=rt ventricular dilation and hypertrophy from pulmonary disease
JVD, hepatomegaly, splenomegaly, vascular congestion of GI tract and peripheral edema

58
Q

S/Sx Right Side HF

A

JVD, edema, weight gain, increased HR, ascites, body edema, hepatomegaly

Fatigue, anxiety, dependent edema, RUQ pain, anorexia, GI bloating, nausea

59
Q

S/Sx Left Side HF

A

increased HR, alternating pulses, low PaO2, crackles, S3/S4 heart sounds, pleural effusion, change in mental status, restless/confused

Weakness/fatigue, dyspnea, shallow breaths @ 32-40/min, paroxysmal nocturnal dyspnea, orthopnea, dry hacking cough, nocturia, frothy pink sputum

60
Q

FACES (CHF)

A 
Fatigue
limitations of Activity
chest Congestion/cough (dry, nonproductive)
Edema
Shortness of Breath
61
Q

Clinical Manifestations CHF

A

Fatigue, dyspnea, tachycardia (compesation), edema, nocturia, skin changes (dusky, shiny, swollen, X hair growth, brown/brawny), behavioral changes, chest pain (low coronary perfusion), weight changes (edema, muscle waisting)

62
Q

Complications of CHF

A

Pleural effusion, dysrhythmias (atrial fibrillation, ventricular tachycardia (VT), ventricular fibrillation (VF)), lt ventricular thrombus (formed in LV), Hepatomegaly (liver congested with venous blood: fibrosis, cirrhosis, cell death), Renal failure

63
Q

CHF Risk Factors

A 
Hypertension
Ischemic Heart Disease
Age
Obesity
Diabetes
Renal Failure
Valvular Heart Disease
Cardiomyopathies
Myocarditis
Congenital Heart Disease
Excessive Alcohol Use
Genetics
64
Q

angiotensin blockers

A

-sartan

65
Q

CHF Treatments

A

Drugs, supp O2, high fowler’s, ultrafiltration or aquapheresis, intraaortic balloon pump (increases coronary blood flow to heart), Ventricular Assist devices, diet, exercise with rest periods, lifestyle change, fluid intake (lowered)

66
Q

Mitral Valve Prolapse Clinical Manifestations

A 
A mid-systolic click & a late systolic murmur
Atypical chest pain; tightness
Dizziness; syncope
Tachycardia
Palpitations r/t dysrhythmias
Fatigue; weakness
Dyspnea; hyperventilation
Anxiety; depression; panic attacks
chest pain during emotional stress-nitrates don't work
67
Q

MVP patient teaching

A

Take meds as prescribed
avoid caffeine (may exacerbate Sx)
Check OTC drugs for stimulants that may exacerbate Sx
Begin/maintain exercise program
Contact HP if palpitations, fatigue, SoB or anxiety develop or worsen

68
Q

MVP nursing interventions

A 
stay hydrated, exercise regularly, avoid caffeine
Associated Risks
Arrhythmias
Infective Endocarditis
Smoking Cessation
Control Blood Pressure
Diagnostic/Surgical Procedures
Medication Therapy
69
Q

MVP Collaborative Care

A

Diagnostics:
Echocardiogram; EKG; CXR; Stress Test; Coronary Angiogram and Cardiac Catheterization
Pharmacological Tx:
Beta Blockers; Diuretics; Vasodilators; Digoxin; Antidysrhythmics; Aspirin; Anticoagulants
Surgical Tx:
Valve Repair
Valve Replacement

70
Q

Gestational HTN

A

onset of HTN without proteinuria without proteinuria

doesn’t persist longer than 12 weeks postpartum

71
Q

Preeclampsia defined

A

HTN and proteinuria after 20weeks
MAP >105
proteinuria >0.3

72
Q

Eclampsia defined

A 
Onset of seizure activity or coma in a woman with preeclampsia with no Hx of preexisting condition that causes seizures (seizures usually occur within 48hrs after birth)
MAP >105
DTRs +3
headache
Urinary OP
73
Q

Chronic HTN defined

A

HTN present before 20wks pregnancy, and/or lasts 12wks postpartum

74
Q

HELLP Syndrome

A

H-hemolysis
EL- elevated liver enzymes
LP- low platelet count
Sx-malaise, flu-like Sx, Rt upper epigastric pain

75
Q

Patho Gestational HTN

A

Uterine arteries don’t widen
decreased placental perfusion and hypoxia
placental ischemia causes endothelial cell dysfunction
generalized vasospasm
poor tissue perfusion to all organs, increased peripheral resistance and increased BP

76
Q

Labs for preeclampsia & HELLP

A

H&H up down
platelets normal to down 70 and up
Uric Acid >5.9 >10
bilirubin normal or up up >1.2

77
Q

Mild Gestational HTN and Preeclampsia Treatment

A

Activity Restrictions
Diet (protein, Ca, Folic Acid, Zinc) with 48-64oz water
Limit excessive salt, eat roughage, avoid alcohol, tobacco, caffeine

78
Q

Preeclampsia Pt Teaching

A

Take BP as directed in right arm, sitting (report increase)
Dipstick clean-catch urine (report >+2)
Assess baby’s activity (report

79
Q

Sever Gest HTN and Preeclampsia

A

immediate Mag sulfate (4-6g load dose over 15-30min, 1-2g in LR maintenance)
monitor BP, UO, cerebral status, epigastic pain, labor, vaginal bleeding
after 34 wks, risk of continuing are greater than preterm birth (get baby and placenta out!
Hospital Precautions: Quiet, non-stimulating
Seizure precautions (suction, O2, call light)
Emergency Meds: hydralazine, labetalol, nifedipine, Mag sulfate, Ca gluconate or Ca chloride
Emergency birth pack

80
Q

Mag Sulfate mild toxicity

A

normal s/sx: flushed, feels hot, sedated, nauseous, burning at IV site

toxicity: lethargy, muscle weakness, decreased/absent DTRs, double vision, slurred speech

81
Q

Mag sulfate high toxicity

A

maternal hypotension, bradycardia, bradypnea, cardiac arrest

antidote! d/c immediately, admin calcium gluconate IV

82
Q

HTN drugs intrapartum

A

hydralazine-decreases peripheral resistance
headache, flushing, tachycardia, N/V

labetalol-vasodilator
flushing, orthostatic hypoTN, tremulousness

Methyldopa-CNS suppression
sedation, sleeepiness, constipation

Nifedipine-relaxes smooth muscle (Ca blocker)
headache, flushing
DON’T give with Mag Sulfate-paralysis!!

83
Q

Seizure care

A

turn head to one side, side rails up, place pillows/blankets around to avoid injury, call for assistance, document time of onset and duration
after: assess airway, suction if needed, admin O2 in non rebreather @ 10L, check cervix

84
Q

pathophysiology of CAD

A

atherosclerosis!
CRP increased
1. fatty streak-earliest lesions of atherosclerosis, characterized by lipid filled smooth muscle cells (tx includes lowering LDLs)
2. fibrous plaque-progessive change in artery wall; narrowing of the vessel wall and reduction in flow to distal tissues
3. Complicated lesion-final stage (most dangerous) inflammation causes rupture, leading to thrombus that further narrows (glycoproteins and fibrinogen cause more clotting) or occludes the artery (plaque is now referred to as a complicated lesion)

85
Q

Risk Factors for CAD

A

age, gender, ethnicity, family hx, serum lipids, BP >140/90, DM, tobacco, inactivity, obesity

86
Q

CAD diet

A

low saturated fat and cholesterol, high complex carbs (whole grains, fruits, veggies)
Fat 30% of diet
reduce red meat, egg yolks, whole milk
eat omega-3s (salmon or tuna 2x/week)

87
Q

CAD Treatment

A 
stress-lowers SNS response
cholesterol-keeps from buildup
BP control-kees from injury
angina-
coronary angiograms-xray with contrast
percutaneous transluminal cornoary angioplasty (PTCA) - balloon/stent
stints-holds open vein
coronary artery bypass grafts (CABG) -grafts new vein around obstruction
88
Q

chronic stable angina

A

reproducible, goes away with rest
notify immediately if ups in frequency or length!
higher demand for O2=angina

89
Q

Unstable Angina

A

can happen at rest

plaque rupture

RNSG 1533 (12 decks)

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