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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

function- arteries, veins, cap

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

assessment of venous system- health hx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

assessment of venous system- physical

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

arteriosclerosis- def

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

arteriosclerosis- risk factors

A

non-mod- age, gender, genetics

mod- diab, smoking, obesity, htn, hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

arteriosclerosis- managemnt

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

atherosclerosis and PVD- risk factors-non mod

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

s/s of acute limb ischemia

A
Pain
Pallor
Pulselessness
Paresthesias (numbness/tingling)
Paralysis (unable dorsi/plantar flex)
Poikilothermia (cool)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PAD- interventions

A

if critical

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
example diagnosis for peripheral arterial insuff
Altered peripheral tissue perfusion Chronic pain Risk for impaired skin integrity Knowledge deficient
26
goals for periph arterial insuff
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
27
periph arterial circulation- interventions for improving
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
28
periph arterial circulation- interventions for improving- meds
``` 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) ```
29
impaired tissue integrity- interventions
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 ```
30
post op interventions for arterial surgery (graft or stent)
Pulses, wound (every 15 min), color, edema (isometric exercises), temp
31
aortic artery disease- patho
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
32
aortic artery dis (aneurysm)- manifestations
Asymptomatic until a complication (dissection or rupture) occurs AAA may have a palpable pulsatile abdominal mass Pain (dependent on location)
33
aortic artery dis (aneurysm)- management
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
34
aneurysm- nursing interventions
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
35
venous disorders
Venous thromboembolism Chronic venous insufficiency/postthrombotic syndrome Leg ulcers Varicose veins
36
venous thromboemolism- patho
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
37
venous thromboemolism- causes
Venous stasis Endothelial damage Hypercoagulability (dehydration, genetic dis., oral contraceptive)
38
Venous stasis Endothelial damage Hypercoagulability (dehydration, genetic dis., oral contraceptive)
39
venous thromboemolism- manifestations
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)
40
venous thromboemolism- management
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
41
venous thromboemolism- prevention/ prophylaxis
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)
42
venous thromboemolism- treatment
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
43
contraindications for anticoag
``` 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) ```
44
pt ed- anticoag
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
45
chronic venous insuff- patho
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
46
chronic venous insuff- s/s
Bilateral dependent edema, weeping dermatitis, brown, thick, leathery skin, dependent extremities appear cyanotic
47
chronic venous insuff- prevention
``` 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) ```
48
chronic venous insuff- assessment
``` hx of condition pain, pulses, edema skin assessment infection (risk for ulcers and cellulitis) nutrition ultrasound ```
49
chronic venous insuff-interventions
``` Elevate extremities Encourage ambulation SCD’s Do not cross legs or place pillow under knees I&O Daily weight ```
50
chronic venous insuff v arterial ulcers
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
51
venous insuff v infection
infection has high wbc count check (pain/bilateral assessment)
52
leg ulcer assessment (differentiating btw venous and arterial)
``` 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 ```
53
leg ulcer- management
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)
54
leg ulcer- example diagnosis
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
55
leg ulcer- interventions/ goals
Restoring skin integrity Improving physical mobility Promoting adequate nutrition Promoting home- and community-based care
56
htn- essential v secondary
essential/primary- no known cause | secondary- from another dis (renal dis)
57
htn- requirements for diagnosis
140S or 90D mmHg or higher- 2 tests 1-4 wks apart
58
blood pressure value classifications- norm, prehtn, stage 1 and stage 2 (systolic)
norm- <120 pre- 120-139 1- 140-159 2- >160 or equal to
59
factors that lower bp
Exercise (vasodil to dec PVR), stop nicotine (stop vasoconstriction), dec Na intake
60
htn- manifestations
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
61
TOD (target organ damage)- risk factors
``` Hypertension!!!! Smoking Obesity Physical inactivity Dyslipidemia Diabetes mellitus Microalbuminuria or GFR <60 mL/min Older age Family history ```
62
assessment for htn
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)
63
htn-interventions
``` 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 ```
64
htn- management-DASH diet
Low sodium, high fruits and vegetables, reduce saturated fat | 1600 mg/day Na
65
htn- management
weight loss, moderate exercise, smoking and etoh cessation
66
htn-meds- diuretics
act on kidneys to help eliminate sodium & water, reducing blood volume. Wastes K+ (watch K+ level)
67
htn meds- ca channel blockers
Help relax, dilate muscles of the blood vessels. Some slow the heart rate.
68
htn meds- ace inhib
help relax/dilate blood vessels by blocking the formation of angiotensin II, a vasoconstrictor
69
htn meds- angiotensin II receptor blockers
Help relax/dilate blood vessels by blocking the action, not the formation of angiotensin II
70
htn meds- beta blockers
Reduce afterload on the heart and dilate blood vessels, causing heart to beat more slowly and with less force
71
htn meds- vasodil
relax the muscle tissue in the blood vessel walls | Central agonists: decrease blood vessel ability to contract
72
htn- example goals
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
hypertensive emergency
``` 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
hypertensive urgency
Blood pressure is very elevated but no evidence of immediate or progressive target organ damage
75
htn emergency- goals
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
htn emergency- interventions
Need very frequent monitoring of BP and cardiovascular status Medications IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin
77
htn urgency- interventions
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
htn education
Exercise, Na below 1600mg, BMI 18.5-24.9
79
htn labs (warfarin), and education
``` 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
htn crisis (emergency or urgency) w/ IV vasodil- assessment
I &O’s- diuresis is compensatory mech for htn, w/ vasodil inc diuresis= inc risk hypovolemia
81
ex. situation 180/110 bp w/ NO s/s TOD= hypertensive urgency possible compications include interventions include
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
cardiac output
total amnt blood one vent pumps norm- 4-6 L CO= SV*HR
83
SV
amnt blood from one vent (L) in one heart beat | norm- 60-100mL/beat
84
factors inc CO
infection, exercise, stress, (anything that inc metab demand to tissues)
85
systole v diastole
s- contraction of the heart | d- filling (resting) time where coronary arteries are perfused
86
preload
vol- stretch of ventricle at end diastole
87
afterload
resist needed overcome to eject blood
88
relationship btw afterload and bp
direct- inc a= inc bp
89
EF
end-diastolic vol ejected w/ each heart beat
90
realationship btw sv and contractility
inc contractility= inc SV (great force pushing= more blood leaving vent w/ each beat)
91
Coronary artery disease risk factors- modifiable
``` cigarette- (dec 02 affinity, vasoconstriction- inc bp=inc afterload=dec SV) hyperlipidemia- htn dm type 2 sedentary lifestyle stress excessive alcohol ```
92
Coronary artery disease risk factors- modifiable- hyperlipidemia
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
Coronary artery disease risk factors- nonmodifiable
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
CAD-patho
Characterized by the obstruction of blood flow within the coronary arteries Atherosclerosis is the principal cause of obstruction to blood flow
95
process of plaque rupture
Plaque rupture platelet aggregationclotting cascadethrombus to further decrease blood flowunstable angina, MI, sudden cardiac death asympt. until partial/ fully blocked
96
angina- stable/unstable
Stable angina: chest pain with physical activity | Unstable angina: chest pain occurs with rest less predictable—Precursor to MI
97
relationship btw unstable angina and MI
angina precursor to MI
98
CAD-manifestations
ischemia, angina, epigastric pain, n/v, diaphoresis, syncope, SOB, pain btw shoudlers/jaw, pallor, anxiety and fear
99
CAD- manif- diff btw men and women
Women present less “typically”- more fatigue (often miss actual event)
100
relationship btw categorization of MI and CAD
CAD is the chronic condition | MI is only an acute event of CAD
101
patho of ischemia in CAD
Affected by decrease in coronary perfusion, increased myocardial workload, decrease in blood oxygen content (chest pain)
102
MI- def
Loss of myocardial tissue from lack of oxygenated blood
103
MI- common cause
Most common cause is atherosclerosis Plaque or ruptured plaque w/ attached thrombus 5-12pm, inc adrenaline= inc metab demand
104
MI-manifestations
Obstructed blood flow to heart causes chest pain Angina Symptoms can differ depending on where the blockage is, male vs female
105
R coronary artery blockage- manif
Right sided heart failure | Bradycardia (no trigger for electrical act (SA node
106
L sided heart failure- manif
``` SOB fluid retention (crackles) ```
107
b/ R and L blockage/ heart failure- manif r/t co
dec perfusion= dec pulses/bp= dec CO
108
ways to test for CAD
Coronary angiography, exercise stress test, pharm stress test, ECG, CXR
109
coronary angiography
``` 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
stress test- exercise
test CAD run on treadmill if positive for MI- when Hr high, part of myocardial tissue unresponsive= dec contractility than compared to rest
111
pharm stress test
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
CXR
shows cardiomegaly, or displacement w/in the chest
113
lab tests- CAD- CRP
inflammatory marker | non-specific
114
lab tests- CAD- CK, CK-MB, Troponin
troponin most important! if elevated= active myocardial tissue damage
115
Lipid panel- goal ranges
Hyperlipidemia LDL >160 mg/dl Hypercholesterolemia: >200 mg/dl Hypertriglyceridemia: >200mg/dl Dyslipidemia HDL < 40 mg/dl
116
medications for CAD- statins
statins- stabilize plaque (prevent rupture), reduce LDL (dec total chol) ae-myalgia monitor AST,ALT
117
medications for CAD- aspirin
inhib platelet aggreg (preventative)
118
medications for CAD- beta blockers
Inhib sympathic ns, dec workload myocardium= dec O2 demand s/s dec heart rate and bp
119
meds for CAD- Ca channel blockers
Vasodil (inc perfusion CA), lower bp, dec wrkld
120
meds for CAD- vasodil
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
surgeries for CAD
PTCA (stent or angioplasty) | CABG (CA bypass graft)
122
interventions- generic CAD
EKG (watch for ST depression, Q waves and ST elevation) oxygen assess pulses, cap refill, temp, peripheral perfusion, bp/hr
123
MONA/thrombolytics
used trt CAD MONA- morphine (vasodil), oxygen, nitroglycerin, aspirin
124
EKG signs that are indicative of MI
Q wave before QRS complex ST-elevation (actively infarcting) T wave depression- ischemia
125
chest pain interventions- acute MI
order EKG supplemental O2 assess CO, pulses and bp
126
STEMI (st elevation MI)- management
"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
post-Coronary angiogram management
monitor renal function (Cr, GFR) push fluids check distal perfusion of affected extremity (cap refill and pulses)
128
tele lead places
clouds over grass (pts R) smoke over fire (pt's L) mud in the middle
129
risk factors for HF
CAD (altered contractility), Hypertension (LVH) hypertrophy (structural remodeling, dec vol for blood), DM, Hyperlipidemia, Obesity, Alcohol, Smoking, Sedentary, High Sodium intake
130
patho HF
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
diff btw L and R sided hF
L- lungs | R- systemic
132
causes L sided HF
inc systemic vascular resistance (htn)
133
systolic L sided HF- def and results
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
diastolic L sided HF- def, results and causes
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
L sided HF- s/s
cough (pink frothy, hemoptysis, orthopnea, and pulm edema, paroxysmal PND)
136
how to tell if systolic or diastolic HF
transthoracic echo or heart cath to look at diff P systolic- HFrEF (dec EF) norm 55-70% diastolic- HFpEF (preserved)
137
R sided HF- patho
Right atrium and Right ventricle become distended which impair “pumping action” contractility Blood accumulates in systemic venous system
138
R sided HF- causes
pulmonary artery htn (inc afterload on R vent) | L sided HF
139
R sided HF- s/s
hepatosplenomegaly, edema, ascites, distended jugular veins (HEAD)
140
HF labs
elevated ANP/BNP | if higher than baseline = exacerbation
141
HF- tests- Cxr
eval size and fluid | should be more oblong
142
HF tests- echocardiogram
transducer applied to chest wall: evaluates size, shape, motion of chambers. Calculates Ejection Fraction (% of blood ejected from chambers
143
HF management- pt ed- weight
daily weight same time every day b4 eat and after void (morning) report SOB, dyspnea call if gain >2lb overnight of 5lb wk
144
HF management- pt ed- o2 therapy
Trt high o2 demand- could have pulm edema- assess fall risk
145
HF management- pt ed- low salt diet
< 2g or 1500 mg
146
HF management- pt ed-Positioning
Fowlers (45-60 degrees), Recliner with legs slightly below heart level Promote venous return and o2
147
HF management- med goals
dec afterload, dec preload, inc contractility, dec sympath response
148
HF management- meds- dec afterload
angiotensin converting enzyme inhib (can prevent remodeling) angiotensin recep blockers vasodil
149
HF management- meds- dec preload
vasodil diuretics (furosemide (monitor K and renal function)) aldosterone recep antagonists (spironolactome- risk hyperkal)
150
HF management- meds- contractility
cardiac glycosides
151
HF management- meds- sympath response
beta blockers
152
stage A risk developing HF- management
``` lifestyle mod (exercise, weight loss, diet) trt comorbid (dm, htn, hyperlipidemia) ```
153
stage B asymptomatic w/ structural changes (EKG) HF- management
trt comorbid, lifestyle mod, monitor for dev s/s
154
stage C symptomatic HF- management
educate salt restriction | lifestyle mod and trt comorbid
155
stage D advanced HF- management
refer LVAD discuss end of life goals
156
afib- def
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
afib- causes
htn, pulmonary disease, CAD
158
afib trtment- Meds-anticoag, antiarrhytmics
anticoag- Wafarin dont give if low platelets, fall risk, recent surgery or parkinsons goal w/ antiarrhy is HR <100
159
afib trtment- cardioversion, catheter ablation and pacemaker
shock into normal rhythm check for clots* Transthoracic Echo cath ablation- cauterize alt electrical pathways pacemaker- take out SA node
160
requirements for SIRS- systemic inflamm response
need at least 2 temp > 100.4 < 95 hr 90 RR> 20 or CO2 <32 WBC >12,000 or <4,000
161
SIRS results if untreated
organ dysfunction/ failure- dec CO and perfusion sepsis if 2+ criteria and infection
162
MAP in relation to MODS
MAP <65= organ failure MAP= DBP+ pulse pressure (SBP-DBP)/3 normal is 70-100
163
septic shock patho
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
cause septic shock
pneumonia, sepsis, abdominal sources
165
SOFA assessment
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
spesis- clincial manif- early-late
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
spesis management- prevention
hand washing, meticulous aseptic technique for invasive procedures, and elimination of invasive therapies when possible.
168
sepsis management- w/in 3 hr
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
sepsis management- w/in 6 hr
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
normal serum lactate/Cr levels
lac-0.5-2.2 mmol/L | Cr- <1.2 mg/dL (if inc= dec renal perfusion)