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MedSurg 1 > PVD/ Cardiovasc > Flashcards

PVD/ Cardiovasc Flashcards

1
Q

vascular system pathway- right v left side of heart

A

right- pulmonary- pumps blood through lungs to the pulmonary circ

left- systemic- pumps blood to all other tissues through systemic circulation

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2
Q

function- arteries, veins, cap

A

arteries- carry oxygenated blood (except pulm artery)
veins- deoxygenated blood
cap- filter and absorb

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3
Q

function of the vasc system

A 
circulatory needs of tissues
blood flow
blood pressure
cap filtration/reabsorption
hemodynamic resis
periph vascular regulating mech
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4
Q

factors that affect bp

A

pain, amnt body fluid, protein deficiency (cirrhosis), cap perm, resistance (length and radius of vessel, ex. thickening basemnt mem in diabetic pt inc blood viscosity= inc resistance) inc viscosity presents as inc hct/hgb and clotting/dehydration

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5
Q

conditions where inc metab is present (bp)

A

malignant hyperthermia, febrile states, exercise and infection
all inc metab state= inc o2 demand= inc risk for ischemia (not adeq o2 to tissue d/t dec blood supply)

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6
Q

vascular- age realted changes

A

Physical deconditioning
Result in atrophy of the left ventricle
Decreased elasticity of the aorta
Rigidity of the valves

Changes cause vessels to stiffen
Increased peripheral resistance (inc afterload)
Impaired blood flow
Increased LV workload= hypertrophy of ventricle (cardiomyopathy)

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7
Q

assessment of vasc system- health history

A

Intermittent claudication (cramping pain w/ exercise- stops w rest)
Arterial disorder (ischemia to tissues, dec o2 d/t dec perfusion)- chronic
Not able vasodilate
“Rest pain”
s/s progression
Location of the pain
Calf, throbbing/ sharp

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8
Q

assessment of vasc system- physical assessment

A

Physical assessment
Skin (cool, pale, pallor, rubor, loss of hair, brittle nails, dry or scaling skin, atrophy, and ulcerations)
Pulses
Thready/decreased

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9
Q

assessment of venous system- health hx

A

Dull aching pain- not assoc w/ activity
Swelling/edema
Relieved w/ elevation of feet

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10
Q

assessment of venous system- physical

A

edema, hyperpigmentation bilaterally, ulcers
Rough/scaly skin (elephantitis)
Pulses- present (can be dec d/t edema)

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11
Q

vascular system- diag eval

A 
Doppler ultrasound flow studies
Ankle brachial index (ABI) ratio systolic bp in ankle compared to arm
Exercise testing 
ABI- walking- test b/a
Duplex ultrasonography
Angiography and magnetic resonance angiography
Presence occlusive disease
Labs: LDL, Triglycerides, A1C
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12
Q

arterial disorders

A 
Arteriosclerosis and atherosclerosis
Peripheral arterial occlusive disease
Aortoiliac disease
Aneurysms (thoracic, abdominal, other)
Dissecting aorta
Arterial embolism and arterial thrombosis
Raynaud phenomenon
Hypertension
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13
Q

arteriosclerosis- def

A

(wall thickening)
hardening of arteries
musc fibers and endothelial lining of walls of sm arteries and arterioles become thickened

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14
Q

arteriosclerosis- risk factors

A

non-mod- age, gender, genetics

mod- diab, smoking, obesity, htn, hyperlipidemia

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15
Q

arteriosclerosis- managemnt

A

weight loss, inc exercise, diet, dec na intake, control htn, anti-lipidemia meds (statins)

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16
Q

atherosclerosis

A

accum lipids, Ca, blood components, carbs, and fibrous tissue on intimal layer of the artery
initiates inflamm response that makes plaques unstable, turning them into complicated plaques

(usually happens after arterioscl)(plaque build-up)

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17
Q

common sites of artherosclerotic obstruction

A

*blockage happens after plaques become unstable and travel down vessels

entire span of aorta
left common iliac
femoral and tibial
all carotids, cerebrals, b/ left and right subclavians

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18
Q

atherosclerosis and PVD- risk factors-non mod

A

Age (inc risk after menopause)
Gender
Familial predisposition and genetics

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19
Q

atherosclerosis and PVD- risk factors-modifiable

A 
Nicotine, diet
Stim sympathy ns (inc hr/bp) not accommodate changes w/ stiff arteries, binds o2 to Co2
Hypertension
Continuous damage endothelial tissues (dec elasticity, favorable area for lipid accum)
Diabetes
Work improve A1C, plaque build-up
Obesity 
Stress
Sedentary lifestyle
C-reactive protein
Marker of inflamm
Inc= higher risk for CV disease
Not always specific to CV
All above factors lead to high c-reactive protein levels
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20
Q

peripheral arterial occlusive disease (PAD)- characteristics

A

Hallmark symptom is intermittent claudication described as aching, cramping, or inducing fatigue or weakness
Occurs with some degree of exercise or activity
Relieved with rest
Pain is associated with critical ischemia of the distal extremity and is described as persistent, aching, or boring (rest pain)
Ischemic rest pain is usually worse at night and often wakes the patient (inc urgency)

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21
Q

peripheral arterial occlusive disease (PAD)- interventions

A

DO NOT elevate, keep legs heart level/ neutral position
Heat can inc o2 metab demand (sometimes used bc vasodilates)
Meds- vasodil.

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22
Q

PAD complications

A

Critical limb ischemia***
Acute limb ischemia – thrombus (plaque) forms a narrowed artery progressing to occlusion= emergent situation
Embolism – plaque ruptures and creates a traveling clot
Treat with anticoagulation, thrombolytics, embolectomy

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23
Q

s/s of acute limb ischemia

A 
Pain
Pallor
Pulselessness
Paresthesias (numbness/tingling)
Paralysis (unable dorsi/plantar flex)
Poikilothermia (cool)
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24
Q

PAD- interventions

A

if critical

Angioplasty (clean arteries), atherectomy (remove clots)., surgical revascularization, (graft to bypass thrombus area)

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25
Q

example diagnosis for peripheral arterial insuff

A

Altered peripheral tissue perfusion
Chronic pain
Risk for impaired skin integrity
Knowledge deficient

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26
Q

goals for periph arterial insuff

A

Increased arterial blood supply
Promotion of vasodilatation
Prevention of vascular compression, relief of pain, attainment or maintenance of tissue integrity
Adherence to self-care program

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27
Q

periph arterial circulation- interventions for improving

A

Exercises and activities: walking, graded isometric exercises. Note: consult primary health care provider before prescribing an exercise routine
Create new areas blood flow perfusion to tissues
Positioning strategies
Temperature; effects of heat (w/ caution) and cold (vasoconstrict)
Stop smoking
Stress reduction

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28
Q

periph arterial circulation- interventions for improving- meds

A 
Pentoxifylline (Trental)
“
Cilostazol (Pletal) 
Dec platelet aggregation and blood viscosity 
vasodil
Symptomatic trtmnt 
Aspirin
Clopidogrel (Plavix) 
Prevent thromboemboli
Statins
Stabilize plaques, anti-inflamm, lower LDL (maintain lipid levels)
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29
Q

impaired tissue integrity- interventions

A

complication assoc. w/ arterial insuff

Avoid trauma to extremities
Delayed wound healing
Encourage protective shoes
Inspect feet for signs of injury
Good nutrition
Vitamins (A+C), protein and zinc help w/ healing
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30
Q

post op interventions for arterial surgery (graft or stent)

A

Pulses, wound (every 15 min), color, edema (isometric exercises), temp

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31
Q

aortic artery disease- patho

A

Permanent localized dilation of an artery. Medial layers are weakened, stretching internal and external layers, tension increases
Diameter of artery can be enlarged to at least 2x’s the normal circumference

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32
Q

aortic artery dis (aneurysm)- manifestations

A

Asymptomatic until a complication (dissection or rupture) occurs
AAA may have a palpable pulsatile abdominal mass
Pain (dependent on location)

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33
Q

aortic artery dis (aneurysm)- management

A

Size and location along with presence of symptoms are the determining factors
Treatment is focused on reducing growth rate and preventing complications of aneurysms
Control bp and heart rate (beta blocker)
Surgical repair

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34
Q

aneurysm- nursing interventions

A

VS- Hypertension and tachycardia can further weaken vessel wall
Pulses
Pain
Abdomen auscultation
Anti-hypertensives, Lipid lowering (dec inflamm and stabilizing plaques), Stool softeners (not want straining), macrolides (decrease infection w/ anti-inflamm)
Bed rest, legs flat- restrict blood flow and put extra pressure on aorta
Stress reduction
Monitor size of aneurysm yearly (usually identified incidentally)
Avoid heavy lifting

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35
Q

venous disorders

A

Venous thromboembolism
Chronic venous insufficiency/postthrombotic syndrome
Leg ulcers
Varicose veins

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36
Q

venous thromboemolism- patho

A

Develops in the deep veins of the calf muscles
Less frequently in the proximal deep veins of the lower extremity or upper arm
Assoc w/ line in upper extremities

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37
Q

venous thromboemolism- causes

A

Venous stasis
Endothelial damage
Hypercoagulability (dehydration, genetic dis., oral contraceptive)

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38
Q

Venous stasis
Endothelial damage
Hypercoagulability (dehydration, genetic dis., oral contraceptive)

A
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39
Q

venous thromboemolism- manifestations

A

Patient may be asymptomatic
Might present with Homans’ sign
When nurse dosiflex foot and complain pain in calf
Pain, swelling, Tenderness, discoloration, redness, warmth (RED-HOT-HARD)

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40
Q

venous thromboemolism- management

A

Diagnostics include a combination of a pretest risk assessment, D-dimer testing, and compression ultrasonography
DVT/PE
Surgical management is rarely utilized (thrombectomy)
Anticoagulation 6-8wks

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41
Q

venous thromboemolism- prevention/ prophylaxis

A

SCD’s, ankle pumps, graduated compression stockings –external pressure applied to limbs decreases venous stasis, no pillows under knees, no standing or sitting for prolonged periods
Anticoagulation (ie: enoxaparin, lovenox)

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42
Q

venous thromboemolism- treatment

A

Treatment: Anticoagulation IV or SQ (heparin or LMWH (Lovanox) transitioning to oral anticoagulant like warfarin)
Elevate extremity at rest
Monitor coagulation studies, Hct/Hgb for occult bleeding, signs and symptoms of bleeding
Electric razor
Fluid- dec hypercoagulability
Antiembolic/Compression Stocking

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43
Q

contraindications for anticoag

A 
Intracranial bleed
IVC filter
Laminectomy
Pending surgery
Platelet count < 50,000
Subarachnoid bleed
Aneurysm
*(surgery / active bleeding)
Comfort care
Craniotomy
Epidural 
GI bleed
hemoptysis (blood in sputum)
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44
Q

pt ed- anticoag

A

Report blood in sputum, emesis, stool, urine
Take meds at same time every day
Keep scheduled lab checks
Never skip a dose of medication
Call provider, make sure to take next day
Avoid changes in eating habits (Warfarin)
Vitam K and leafy greens antidote- have in moderation
Consult with provider before also taking aspirin or clopidogrel
Limit physical activities that would increase bleeding risk (ie: contact sports)
Electric razor and soft toothbrush
Monitor for S&S of bleeding

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45
Q

chronic venous insuff- patho

A

Inc risk DVT
Inadequate venous return due to dilated veins and incompetent one way valves over a prolonged period
Venous pressure increases in the lower extremities causing backflow of blood into capillary beds
Serous fluid containing waste products leaks into interstitial space
Venous stasis impairs capillary arteriole circulation

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46
Q

chronic venous insuff- s/s

A

Bilateral dependent edema, weeping dermatitis, brown, thick, leathery skin, dependent extremities appear cyanotic

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47
Q

chronic venous insuff- prevention

A 
Application of graduated compression stockings
Pneumatic compression devices
Early ambulation
Subcutaneous heparin or LMWH
Lifestyle changes
Weight loss (less pressure vasc system)
Smoking cessation
Regular exercise (activation muscles helps return blood through compression)
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48
Q

chronic venous insuff- assessment

A 
hx of condition
pain, pulses, edema
skin assessment
infection (risk for ulcers and cellulitis)
nutrition
ultrasound
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49
Q

chronic venous insuff-interventions

A 
Elevate extremities
Encourage ambulation
SCD’s
Do not cross legs or place pillow under knees
I&O
Daily weight
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50
Q

chronic venous insuff v arterial ulcers

A

venous (ankles)- dull achy pain, lower leg edema, pulse present, DRAINAGE, irregular borders (jagged), yellow slough

arterial (toes and feet)- intermittent claudication pain, no edema, weak pulse, no drainage, round edges, black eschar
*elevating feet makes pain worse
feet cool to the touch

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51
Q

venous insuff v infection

A

infection has high wbc count

check (pain/bilateral assessment)

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52
Q

leg ulcer assessment (differentiating btw venous and arterial)

A 
History of the condition
Assess pain, peripheral pulses, edema
Treatment depends on the type of ulcer
Assess for presence of infection
Assess nutrition
Vitamin A and C, protein and zinc
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53
Q

leg ulcer- management

A

Anti-infective therapy depends on the infecting agent.
Oral antibiotics are usually prescribed
Compression therapy
Debridement of wound
Dressings
Hydrocolloid promote granulation
Hyperbaric, negative pressure (wound vac)

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54
Q

leg ulcer- example diagnosis

A

Impaired skin integrity related to vascular insufficiency
Impaired physical mobility related to activity restrictions of the therapeutic regimen and pain
Imbalanced nutrition: less than body requirements related to increased need for nutrients that promote wound healing

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55
Q

leg ulcer- interventions/ goals

A

Restoring skin integrity
Improving physical mobility
Promoting adequate nutrition
Promoting home- and community-based care

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56
Q

htn- essential v secondary

A

essential/primary- no known cause

secondary- from another dis (renal dis)

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57
Q

htn- requirements for diagnosis

A

140S or 90D mmHg or higher- 2 tests 1-4 wks apart

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58
Q

blood pressure value classifications- norm, prehtn, stage 1 and stage 2 (systolic)

A

norm- <120
pre- 120-139
1- 140-159
2- >160 or equal to

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59
Q

factors that lower bp

A

Exercise (vasodil to dec PVR), stop nicotine (stop vasoconstriction), dec Na intake

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60
Q

htn- manifestations

A

Usually no symptoms other than elevated blood pressure
Symptoms related to target organ damage are seen late and are serious
Retinal and other eye changes
Renal damage
Myocardial infarction (inc PVR = inc wrk load)
Cardiac hypertrophy
Stroke

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61
Q

TOD (target organ damage)- risk factors

A 
Hypertension!!!!
Smoking
Obesity
Physical inactivity
Dyslipidemia
Diabetes mellitus
Microalbuminuria or GFR <60 mL/min
Older age
Family history
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62
Q

assessment for htn

A

signs of TOD
Cardiovascular assessment- pulses, chest pain, SOB, s/s TIA (stroke like), dizziness, headaches
retinal exam
ecg (tell if MI or hypertrophy of ventricle by wave amplitude)
lab tests for renal damage
(urinalysis and blood chem)

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63
Q

htn-interventions

A 
Neuro assessment
BP/HR – assess BP after resting 5 min
BMI
Palpate lower extremities for edema and pulses which may indicate kidney disease/HF
 I&O
Serum Creatinine to eval kidney function
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64
Q

htn- management-DASH diet

A

Low sodium, high fruits and vegetables, reduce saturated fat

1600 mg/day Na

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65
Q

htn- management

A

weight loss, moderate exercise, smoking and etoh cessation

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66
Q

htn-meds- diuretics

A

act on kidneys to help eliminate sodium & water, reducing blood volume. Wastes K+ (watch K+ level)

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67
Q

htn meds- ca channel blockers

A

Help relax, dilate muscles of the blood vessels. Some slow the heart rate.

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68
Q

htn meds- ace inhib

A

help relax/dilate blood vessels by blocking the formation of angiotensin II, a vasoconstrictor

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69
Q

htn meds- angiotensin II receptor blockers

A

Help relax/dilate blood vessels by blocking the action, not the formation of angiotensin II

70
Q

htn meds- beta blockers

A

Reduce afterload on the heart and dilate blood vessels, causing heart to beat more slowly and with less force

71
Q

htn meds- vasodil

A

relax the muscle tissue in the blood vessel walls

Central agonists: decrease blood vessel ability to contract

72
Q

htn- example goals

A

Reports knowledge of disease management sufficient to maintain adequate tissue perfusion
Maintains blood pressure at less than 140/90 mm Hg (less than 150/90 mm Hg for adults older than 60 years of age) with lifestyle modifications, medications, or both
Demonstrates no symptoms of angina (claudication heart), palpitations, or vision changes (TOD)
Has stable BUN and serum creatinine levels
Has palpable peripheral pulses (CO)

73
Q

hypertensive emergency

A 
Blood pressure >180/120 mm Hg and must be lowered immediately to prevent damage to target organs
Severe headaches
Visual disturbance
Severe anxiety
Shortness of breath
Epistaxis
Nausea/Vomiting
Confusion`
74
Q

hypertensive urgency

A

Blood pressure is very elevated but no evidence of immediate or progressive target organ damage

75
Q

htn emergency- goals

A

Reduce blood pressure 20% to 25% in first hour
Reduce to 160/100 mm Hg over 6 hours
Then gradual reduction to normal over a period of days
Exceptions are ischemic stroke and aortic dissection

76
Q

htn emergency- interventions

A

Need very frequent monitoring of BP and cardiovascular status
Medications
IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin

77
Q

htn urgency- interventions

A

Oral agents can be administered with the goal of normalizing blood pressure within 24 to 48 hours
Fast-acting oral agents:
Beta-adrenergic blocker—labetalol
Angiotensin-converting enzyme inhibitor—captopril
Alpha2-agonist—clonidine
Patient requires close monitoring of blood pressure and cardiovascular status
Assess for potential evidence of target organ damage

78
Q

htn education

A

Exercise, Na below 1600mg, BMI 18.5-24.9

79
Q

htn labs (warfarin), and education

A 
vitamin K, Hct/Hgb (occult bleeding),  
PT/INR for therapeutic dosing eval (clotting time) (INR 2-3
s/s bleeding,
avoid contact sports
 fall risk prevention, electric razors
avoid excessive intake of leafy greens
80
Q

htn crisis (emergency or urgency) w/ IV vasodil- assessment

A

I &O’s- diuresis is compensatory mech for htn, w/ vasodil inc diuresis= inc risk hypovolemia

81
Q

ex. situation
180/110 bp w/ NO s/s TOD= hypertensive urgency

possible compications include

interventions include

A

Stroke/TIA, TOD, MI, coronary artery disease, left ventricular hypertrophy (leads to heart failure and MI)

Interventions- meds (beta-blocker), reassess vitals, pulses, assess stroke like s/s

82
Q

cardiac output

A

total amnt blood one vent pumps
norm- 4-6 L
CO= SV*HR

83
Q

SV

A

amnt blood from one vent (L) in one heart beat

norm- 60-100mL/beat

84
Q

factors inc CO

A

infection, exercise, stress, (anything that inc metab demand to tissues)

85
Q

systole v diastole

A

s- contraction of the heart

d- filling (resting) time where coronary arteries are perfused

86
Q

preload

A

vol- stretch of ventricle at end diastole

87
Q

afterload

A

resist needed overcome to eject blood

88
Q

relationship btw afterload and bp

A

direct- inc a= inc bp

89
Q

EF

A

end-diastolic vol ejected w/ each heart beat

90
Q

realationship btw sv and contractility

A

inc contractility= inc SV (great force pushing= more blood leaving vent w/ each beat)

91
Q

Coronary artery disease risk factors- modifiable

A 
cigarette-  (dec 02 affinity, vasoconstriction- inc bp=inc afterload=dec SV)
hyperlipidemia-
htn
dm type 2
sedentary lifestyle
stress 
excessive alcohol
92
Q

Coronary artery disease risk factors- modifiable- hyperlipidemia

A

Can end in build up of plaque
Norm total cholesterol= <200
LDL <100 (high risk < 70)
High risk if have cardiovasc conditions/DM
Lowered w/ genetics, exercise, statins
HDL men >40, women >50
Cardioprotective, increased w/ genetics, exercise!, red wine
Want high levels- directly reflects total (inc HDL= inc total C)
Trig <150 (free fat for caloric consumption of cells)
Exercise, diet, trt w/ fish oil and statins

93
Q

Coronary artery disease risk factors- nonmodifiable

A

Gender
Male inc risk (women at same risk after menopause (estrogen protective factor)
Race
Inc in African americans, natives and pacific islanders
DM Type I
Age older than 65
Dec contractility, endothelial artery damage
Heredity

94
Q

CAD-patho

A

Characterized by the obstruction of blood flow within the coronary arteries
Atherosclerosis is the principal cause of obstruction to blood flow

95
Q

process of plaque rupture

A

Plaque rupture platelet aggregationclotting cascadethrombus to further decrease blood flowunstable angina, MI, sudden cardiac death

asympt. until partial/ fully blocked

96
Q

angina- stable/unstable

A

Stable angina: chest pain with physical activity

Unstable angina: chest pain occurs with rest less predictable—Precursor to MI

97
Q

relationship btw unstable angina and MI

A

angina precursor to MI

98
Q

CAD-manifestations

A

ischemia, angina, epigastric pain, n/v, diaphoresis, syncope, SOB, pain btw shoudlers/jaw, pallor, anxiety and fear

99
Q

CAD- manif- diff btw men and women

A

Women present less “typically”- more fatigue (often miss actual event)

100
Q

relationship btw categorization of MI and CAD

A

CAD is the chronic condition

MI is only an acute event of CAD

101
Q

patho of ischemia in CAD

A

Affected by decrease in coronary perfusion, increased myocardial workload, decrease in blood oxygen content (chest pain)

102
Q

MI- def

A

Loss of myocardial tissue from lack of oxygenated blood

103
Q

MI- common cause

A

Most common cause is atherosclerosis
Plaque or ruptured plaque w/ attached thrombus
5-12pm, inc adrenaline= inc metab demand

104
Q

MI-manifestations

A

Obstructed blood flow to heart causes chest pain
Angina
Symptoms can differ depending on where the blockage is, male vs female

105
Q

R coronary artery blockage- manif

A

Right sided heart failure

Bradycardia (no trigger for electrical act (SA node

106
Q

L sided heart failure- manif

A 
SOB
fluid retention (crackles)
107
Q

b/ R and L blockage/ heart failure- manif r/t co

A

dec perfusion= dec pulses/bp= dec CO

108
Q

ways to test for CAD

A

Coronary angiography, exercise stress test, pharm stress test, ECG, CXR

109
Q

coronary angiography

A 
tests for CAD
invasive (have to have severe symptoms)
usually tested <1h for optimal outcomes
contrast dye- check renal fun
if pt presents w/ blockage >70% w/ no collateral alterations= stent
110
Q

stress test- exercise

A

test CAD
run on treadmill
if positive for MI- when Hr high, part of myocardial tissue unresponsive= dec contractility than compared to rest

111
Q

pharm stress test

A

used test CAD
meds- dobutamine (inc hr/contract)
thallium (tracer tags perfused cardiac tissues)
adenosine (vasodil, norm response is dialation)
if CA blocked= no response

112
Q

CXR

A

shows cardiomegaly, or displacement w/in the chest

113
Q

lab tests- CAD- CRP

A

inflammatory marker

non-specific

114
Q

lab tests- CAD- CK, CK-MB, Troponin

A

troponin most important! if elevated= active myocardial tissue damage

115
Q

Lipid panel- goal ranges

A

Hyperlipidemia LDL >160 mg/dl
Hypercholesterolemia: >200 mg/dl
Hypertriglyceridemia: >200mg/dl
Dyslipidemia HDL < 40 mg/dl

116
Q

medications for CAD- statins

A

statins- stabilize plaque (prevent rupture), reduce LDL (dec total chol)

ae-myalgia
monitor AST,ALT

117
Q

medications for CAD- aspirin

A

inhib platelet aggreg (preventative)

118
Q

medications for CAD- beta blockers

A

Inhib sympathic ns, dec workload myocardium= dec O2 demand

s/s dec heart rate and bp

119
Q

meds for CAD- Ca channel blockers

A

Vasodil (inc perfusion CA), lower bp, dec wrkld

120
Q

meds for CAD- vasodil

A

Improve oxygenation, (nitroglycerin given under tongue)
Can take for unrelieved chest pain w/ rest, not exceed 3 doses, (do not combine w/ vasodil (Viagra)
Feel warm, headache, dec bp

121
Q

surgeries for CAD

A

PTCA (stent or angioplasty)

CABG (CA bypass graft)

122
Q

interventions- generic CAD

A

EKG (watch for ST depression, Q waves and ST elevation)
oxygen
assess pulses, cap refill, temp, peripheral perfusion, bp/hr

123
Q

MONA/thrombolytics

A

used trt CAD

MONA-
morphine (vasodil), oxygen, nitroglycerin, aspirin

124
Q

EKG signs that are indicative of MI

A

Q wave before QRS complex
ST-elevation (actively infarcting)
T wave depression- ischemia

125
Q

chest pain interventions- acute MI

A

order EKG
supplemental O2
assess CO, pulses and bp

126
Q

STEMI (st elevation MI)- management

A

“tombstone” = actively infarcting
MONA- morphine, o2, nitroglycerin, aspirin

door to balloon time- 60 min in order to dec extent of injury
thrombolytics (TPA)- breaks down plaques- w/in 3-6h

127
Q

post-Coronary angiogram management

A

monitor renal function (Cr, GFR)
push fluids
check distal perfusion of affected extremity (cap refill and pulses)

128
Q

tele lead places

A

clouds over grass (pts R)
smoke over fire (pt’s L)
mud in the middle

129
Q

risk factors for HF

A

CAD (altered contractility), Hypertension (LVH) hypertrophy (structural remodeling, dec vol for blood), DM, Hyperlipidemia, Obesity, Alcohol, Smoking, Sedentary, High Sodium intake

130
Q

patho HF

A

Progressive disease characterized by myocardial cell dysfunction
Inability of the heart to pump enough cardiac output to meet the demands of the body
Dec co= dec perfusion

can activate RAAS- vasoconstriction- inc afterload from inc ang 2- inc preload

can activate- SNS- inc hr and contractility- require inc 02 demand

131
Q

diff btw L and R sided hF

A

L- lungs

R- systemic

132
Q

causes L sided HF

A

inc systemic vascular resistance (htn)

133
Q

systolic L sided HF- def and results

A

ventricle fails to contract adequately (decreased contractility) in order to eject blood into arterial system
EF <40%
results in inc preload (bc dec contractility), inc afterload (bc inc resistance) and ventricular remodeling

134
Q

diastolic L sided HF- def, results and causes

A

heart does not completely relax, decreased compliance; ventricle filling is disrupted, inc P pulm system, RV hypertrophy

results- norm SV and CO but pulm congestion

abnormal relaxation fo LV

causes- htn, ischemia

135
Q

L sided HF- s/s

A

cough (pink frothy, hemoptysis, orthopnea, and pulm edema, paroxysmal PND)

136
Q

how to tell if systolic or diastolic HF

A

transthoracic echo or heart cath to look at diff P
systolic- HFrEF (dec EF)
norm 55-70%
diastolic- HFpEF (preserved)

137
Q

R sided HF- patho

A

Right atrium and Right ventricle become distended which impair “pumping action” contractility

Blood accumulates in systemic venous system

138
Q

R sided HF- causes

A

pulmonary artery htn (inc afterload on R vent)

L sided HF

139
Q

R sided HF- s/s

A

hepatosplenomegaly, edema, ascites, distended jugular veins (HEAD)

140
Q

HF labs

A

elevated ANP/BNP

if higher than baseline = exacerbation

141
Q

HF- tests- Cxr

A

eval size and fluid

should be more oblong

142
Q

HF tests- echocardiogram

A

transducer applied to chest wall: evaluates size, shape, motion of chambers. Calculates Ejection Fraction (% of blood ejected from chambers

143
Q

HF management- pt ed- weight

A

daily weight
same time every day b4 eat and after void (morning)
report SOB, dyspnea
call if gain >2lb overnight of 5lb wk

144
Q

HF management- pt ed- o2 therapy

A

Trt high o2 demand- could have pulm edema- assess fall risk

145
Q

HF management- pt ed- low salt diet

A

< 2g or 1500 mg

146
Q

HF management- pt ed-Positioning

A

Fowlers (45-60 degrees), Recliner with legs slightly below heart level
Promote venous return and o2

147
Q

HF management- med goals

A

dec afterload, dec preload, inc contractility, dec sympath response

148
Q

HF management- meds- dec afterload

A

angiotensin converting enzyme inhib (can prevent remodeling)
angiotensin recep blockers
vasodil

149
Q

HF management- meds- dec preload

A

vasodil
diuretics (furosemide (monitor K and renal function))
aldosterone recep antagonists
(spironolactome- risk hyperkal)

150
Q

HF management- meds- contractility

A

cardiac glycosides

151
Q

HF management- meds- sympath response

A

beta blockers

152
Q

stage A risk developing HF- management

A 
lifestyle mod (exercise, weight loss, diet)
trt comorbid (dm, htn, hyperlipidemia)
153
Q

stage B asymptomatic w/ structural changes (EKG) HF- management

A

trt comorbid, lifestyle mod, monitor for dev s/s

154
Q

stage C symptomatic HF- management

A

educate salt restriction

lifestyle mod and trt comorbid

155
Q

stage D advanced HF- management

A

refer
LVAD
discuss end of life goals

156
Q

afib- def

A

Dysrhythmia of heart. Multiple electrical impulses cause chaos in atria of heart.

Can increase risk for HF and Stroke
Loss of CO
Clots: blood pools in atria, clot formation

157
Q

afib- causes

A

htn, pulmonary disease, CAD

158
Q

afib trtment- Meds-anticoag, antiarrhytmics

A

anticoag- Wafarin
dont give if low platelets, fall risk, recent surgery or parkinsons

goal w/ antiarrhy is HR <100

159
Q

afib trtment- cardioversion, catheter ablation and pacemaker

A

shock into normal rhythm check for clots* Transthoracic Echo
cath ablation- cauterize alt electrical pathways
pacemaker- take out SA node

160
Q

requirements for SIRS- systemic inflamm response

A

need at least 2

temp > 100.4 < 95
hr 90
RR> 20 or CO2 <32
WBC >12,000 or <4,000

161
Q

SIRS results if untreated

A

organ dysfunction/ failure- dec CO and perfusion

sepsis if 2+ criteria and infection

162
Q

MAP in relation to MODS

A

MAP <65= organ failure
MAP= DBP+ pulse pressure (SBP-DBP)/3
normal is 70-100

163
Q

septic shock patho

A

Type of Distributive Shock
Result of disease states that cause poor vascular tone and vasodilation
Increased vascular capacity and venous pooling
Even with adequate blood volume, a state of relative hypovolemia exists

164
Q

cause septic shock

A

pneumonia, sepsis, abdominal sources

165
Q

SOFA assessment

A

sequential organ failure assessment
A- rr, mental status, SBP
and
B- coma score, MAP, vasopressor admiin, Cr or urine output, bilirubin ,platelet count, FiO2

166
Q

spesis- clincial manif- early-late

A

Early: tachycardia, bounding pulses, warm flushed skin, febrile, BP may be normal (compensation)
Moderate: Confusion, Decreased UO
Late: cool, pale skin, weak and thread pulses, hypothermia, tachycardia, hypotension, lethargy, coma, anuria

167
Q

spesis management- prevention

A

hand washing, meticulous aseptic technique for invasive procedures, and elimination of invasive therapies when possible.

168
Q

sepsis management- w/in 3 hr

A

VS
Measure lactate levels –elevated levels indicate poor perfusion
Shows conversion to anabolic metabolism (w/out o2)
Obtain blood cultures (b4 antib)
Broad spectrum antibiotics
Fluid resuscitations (crystalloid like NS)

169
Q

sepsis management- w/in 6 hr

A

Vasopressors – if fluid unsuccessful =vasoconstriction, check for circ to periphery, focused on perfusion to organs
Steroids= if comorbidity- adrenal insufficiency
Reassess volume
Reassess lactate

170
Q

normal serum lactate/Cr levels

A

lac-0.5-2.2 mmol/L

Cr- <1.2 mg/dL (if inc= dec renal perfusion)

MedSurg 1 (9 decks)

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