PVD/ Cardiovasc Flashcards
vascular system pathway- right v left side of heart
right- pulmonary- pumps blood through lungs to the pulmonary circ
left- systemic- pumps blood to all other tissues through systemic circulation
function- arteries, veins, cap
arteries- carry oxygenated blood (except pulm artery)
veins- deoxygenated blood
cap- filter and absorb
function of the vasc system
circulatory needs of tissues blood flow blood pressure cap filtration/reabsorption hemodynamic resis periph vascular regulating mech
factors that affect bp
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
conditions where inc metab is present (bp)
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)
vascular- age realted changes
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)
assessment of vasc system- health history
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
assessment of vasc system- physical assessment
Physical assessment
Skin (cool, pale, pallor, rubor, loss of hair, brittle nails, dry or scaling skin, atrophy, and ulcerations)
Pulses
Thready/decreased
assessment of venous system- health hx
Dull aching pain- not assoc w/ activity
Swelling/edema
Relieved w/ elevation of feet
assessment of venous system- physical
edema, hyperpigmentation bilaterally, ulcers
Rough/scaly skin (elephantitis)
Pulses- present (can be dec d/t edema)
vascular system- diag eval
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
arterial disorders
Arteriosclerosis and atherosclerosis Peripheral arterial occlusive disease Aortoiliac disease Aneurysms (thoracic, abdominal, other) Dissecting aorta Arterial embolism and arterial thrombosis Raynaud phenomenon Hypertension
arteriosclerosis- def
(wall thickening)
hardening of arteries
musc fibers and endothelial lining of walls of sm arteries and arterioles become thickened
arteriosclerosis- risk factors
non-mod- age, gender, genetics
mod- diab, smoking, obesity, htn, hyperlipidemia
arteriosclerosis- managemnt
weight loss, inc exercise, diet, dec na intake, control htn, anti-lipidemia meds (statins)
atherosclerosis
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)
common sites of artherosclerotic obstruction
*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
atherosclerosis and PVD- risk factors-non mod
Age (inc risk after menopause)
Gender
Familial predisposition and genetics
atherosclerosis and PVD- risk factors-modifiable
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
peripheral arterial occlusive disease (PAD)- characteristics
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)
peripheral arterial occlusive disease (PAD)- interventions
DO NOT elevate, keep legs heart level/ neutral position
Heat can inc o2 metab demand (sometimes used bc vasodilates)
Meds- vasodil.
PAD complications
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
s/s of acute limb ischemia
Pain Pallor Pulselessness Paresthesias (numbness/tingling) Paralysis (unable dorsi/plantar flex) Poikilothermia (cool)
PAD- interventions
if critical
Angioplasty (clean arteries), atherectomy (remove clots)., surgical revascularization, (graft to bypass thrombus area)
example diagnosis for peripheral arterial insuff
Altered peripheral tissue perfusion
Chronic pain
Risk for impaired skin integrity
Knowledge deficient
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
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
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)
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
post op interventions for arterial surgery (graft or stent)
Pulses, wound (every 15 min), color, edema (isometric exercises), temp
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
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)
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
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
venous disorders
Venous thromboembolism
Chronic venous insufficiency/postthrombotic syndrome
Leg ulcers
Varicose veins
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
venous thromboemolism- causes
Venous stasis
Endothelial damage
Hypercoagulability (dehydration, genetic dis., oral contraceptive)
Venous stasis
Endothelial damage
Hypercoagulability (dehydration, genetic dis., oral contraceptive)
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)
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
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)
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
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)
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
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
chronic venous insuff- s/s
Bilateral dependent edema, weeping dermatitis, brown, thick, leathery skin, dependent extremities appear cyanotic
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)
chronic venous insuff- assessment
hx of condition pain, pulses, edema skin assessment infection (risk for ulcers and cellulitis) nutrition ultrasound
chronic venous insuff-interventions
Elevate extremities Encourage ambulation SCD’s Do not cross legs or place pillow under knees I&O Daily weight
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
venous insuff v infection
infection has high wbc count
check (pain/bilateral assessment)
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
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)
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
leg ulcer- interventions/ goals
Restoring skin integrity
Improving physical mobility
Promoting adequate nutrition
Promoting home- and community-based care
htn- essential v secondary
essential/primary- no known cause
secondary- from another dis (renal dis)
htn- requirements for diagnosis
140S or 90D mmHg or higher- 2 tests 1-4 wks apart
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
factors that lower bp
Exercise (vasodil to dec PVR), stop nicotine (stop vasoconstriction), dec Na intake
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
TOD (target organ damage)- risk factors
Hypertension!!!! Smoking Obesity Physical inactivity Dyslipidemia Diabetes mellitus Microalbuminuria or GFR <60 mL/min Older age Family history
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)
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
htn- management-DASH diet
Low sodium, high fruits and vegetables, reduce saturated fat
1600 mg/day Na
htn- management
weight loss, moderate exercise, smoking and etoh cessation
htn-meds- diuretics
act on kidneys to help eliminate sodium & water, reducing blood volume. Wastes K+ (watch K+ level)
htn meds- ca channel blockers
Help relax, dilate muscles of the blood vessels. Some slow the heart rate.
htn meds- ace inhib
help relax/dilate blood vessels by blocking the formation of angiotensin II, a vasoconstrictor
htn meds- angiotensin II receptor blockers
Help relax/dilate blood vessels by blocking the action, not the formation of angiotensin II
htn meds- beta blockers
Reduce afterload on the heart and dilate blood vessels, causing heart to beat more slowly and with less force
htn meds- vasodil
relax the muscle tissue in the blood vessel walls
Central agonists: decrease blood vessel ability to contract
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)
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`
hypertensive urgency
Blood pressure is very elevated but no evidence of immediate or progressive target organ damage
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
htn emergency- interventions
Need very frequent monitoring of BP and cardiovascular status
Medications
IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin
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
htn education
Exercise, Na below 1600mg, BMI 18.5-24.9
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
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
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
cardiac output
total amnt blood one vent pumps
norm- 4-6 L
CO= SV*HR
SV
amnt blood from one vent (L) in one heart beat
norm- 60-100mL/beat
factors inc CO
infection, exercise, stress, (anything that inc metab demand to tissues)
systole v diastole
s- contraction of the heart
d- filling (resting) time where coronary arteries are perfused
preload
vol- stretch of ventricle at end diastole
afterload
resist needed overcome to eject blood
relationship btw afterload and bp
direct- inc a= inc bp
EF
end-diastolic vol ejected w/ each heart beat
realationship btw sv and contractility
inc contractility= inc SV (great force pushing= more blood leaving vent w/ each beat)
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
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
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
CAD-patho
Characterized by the obstruction of blood flow within the coronary arteries
Atherosclerosis is the principal cause of obstruction to blood flow
process of plaque rupture
Plaque rupture platelet aggregationclotting cascadethrombus to further decrease blood flowunstable angina, MI, sudden cardiac death
asympt. until partial/ fully blocked
angina- stable/unstable
Stable angina: chest pain with physical activity
Unstable angina: chest pain occurs with rest less predictable—Precursor to MI
relationship btw unstable angina and MI
angina precursor to MI
CAD-manifestations
ischemia, angina, epigastric pain, n/v, diaphoresis, syncope, SOB, pain btw shoudlers/jaw, pallor, anxiety and fear
CAD- manif- diff btw men and women
Women present less “typically”- more fatigue (often miss actual event)
relationship btw categorization of MI and CAD
CAD is the chronic condition
MI is only an acute event of CAD
patho of ischemia in CAD
Affected by decrease in coronary perfusion, increased myocardial workload, decrease in blood oxygen content (chest pain)
MI- def
Loss of myocardial tissue from lack of oxygenated blood
MI- common cause
Most common cause is atherosclerosis
Plaque or ruptured plaque w/ attached thrombus
5-12pm, inc adrenaline= inc metab demand
MI-manifestations
Obstructed blood flow to heart causes chest pain
Angina
Symptoms can differ depending on where the blockage is, male vs female
R coronary artery blockage- manif
Right sided heart failure
Bradycardia (no trigger for electrical act (SA node
L sided heart failure- manif
SOB fluid retention (crackles)
b/ R and L blockage/ heart failure- manif r/t co
dec perfusion= dec pulses/bp= dec CO
ways to test for CAD
Coronary angiography, exercise stress test, pharm stress test, ECG, CXR
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
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
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
CXR
shows cardiomegaly, or displacement w/in the chest
lab tests- CAD- CRP
inflammatory marker
non-specific
lab tests- CAD- CK, CK-MB, Troponin
troponin most important! if elevated= active myocardial tissue damage
Lipid panel- goal ranges
Hyperlipidemia LDL >160 mg/dl
Hypercholesterolemia: >200 mg/dl
Hypertriglyceridemia: >200mg/dl
Dyslipidemia HDL < 40 mg/dl
medications for CAD- statins
statins- stabilize plaque (prevent rupture), reduce LDL (dec total chol)
ae-myalgia
monitor AST,ALT
medications for CAD- aspirin
inhib platelet aggreg (preventative)
medications for CAD- beta blockers
Inhib sympathic ns, dec workload myocardium= dec O2 demand
s/s dec heart rate and bp
meds for CAD- Ca channel blockers
Vasodil (inc perfusion CA), lower bp, dec wrkld
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
surgeries for CAD
PTCA (stent or angioplasty)
CABG (CA bypass graft)
interventions- generic CAD
EKG (watch for ST depression, Q waves and ST elevation)
oxygen
assess pulses, cap refill, temp, peripheral perfusion, bp/hr
MONA/thrombolytics
used trt CAD
MONA-
morphine (vasodil), oxygen, nitroglycerin, aspirin
EKG signs that are indicative of MI
Q wave before QRS complex
ST-elevation (actively infarcting)
T wave depression- ischemia
chest pain interventions- acute MI
order EKG
supplemental O2
assess CO, pulses and bp
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
post-Coronary angiogram management
monitor renal function (Cr, GFR)
push fluids
check distal perfusion of affected extremity (cap refill and pulses)
tele lead places
clouds over grass (pts R)
smoke over fire (pt’s L)
mud in the middle
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
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
diff btw L and R sided hF
L- lungs
R- systemic
causes L sided HF
inc systemic vascular resistance (htn)
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
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
L sided HF- s/s
cough (pink frothy, hemoptysis, orthopnea, and pulm edema, paroxysmal PND)
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)
R sided HF- patho
Right atrium and Right ventricle become distended which impair “pumping action” contractility
Blood accumulates in systemic venous system
R sided HF- causes
pulmonary artery htn (inc afterload on R vent)
L sided HF
R sided HF- s/s
hepatosplenomegaly, edema, ascites, distended jugular veins (HEAD)
HF labs
elevated ANP/BNP
if higher than baseline = exacerbation
HF- tests- Cxr
eval size and fluid
should be more oblong
HF tests- echocardiogram
transducer applied to chest wall: evaluates size, shape, motion of chambers. Calculates Ejection Fraction (% of blood ejected from chambers
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
HF management- pt ed- o2 therapy
Trt high o2 demand- could have pulm edema- assess fall risk
HF management- pt ed- low salt diet
< 2g or 1500 mg
HF management- pt ed-Positioning
Fowlers (45-60 degrees), Recliner with legs slightly below heart level
Promote venous return and o2
HF management- med goals
dec afterload, dec preload, inc contractility, dec sympath response
HF management- meds- dec afterload
angiotensin converting enzyme inhib (can prevent remodeling)
angiotensin recep blockers
vasodil
HF management- meds- dec preload
vasodil
diuretics (furosemide (monitor K and renal function))
aldosterone recep antagonists
(spironolactome- risk hyperkal)
HF management- meds- contractility
cardiac glycosides
HF management- meds- sympath response
beta blockers
stage A risk developing HF- management
lifestyle mod (exercise, weight loss, diet) trt comorbid (dm, htn, hyperlipidemia)
stage B asymptomatic w/ structural changes (EKG) HF- management
trt comorbid, lifestyle mod, monitor for dev s/s
stage C symptomatic HF- management
educate salt restriction
lifestyle mod and trt comorbid
stage D advanced HF- management
refer
LVAD
discuss end of life goals
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
afib- causes
htn, pulmonary disease, CAD
afib trtment- Meds-anticoag, antiarrhytmics
anticoag- Wafarin
dont give if low platelets, fall risk, recent surgery or parkinsons
goal w/ antiarrhy is HR <100
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
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
SIRS results if untreated
organ dysfunction/ failure- dec CO and perfusion
sepsis if 2+ criteria and infection
MAP in relation to MODS
MAP <65= organ failure
MAP= DBP+ pulse pressure (SBP-DBP)/3
normal is 70-100
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
cause septic shock
pneumonia, sepsis, abdominal sources
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
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
spesis management- prevention
hand washing, meticulous aseptic technique for invasive procedures, and elimination of invasive therapies when possible.
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)
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
normal serum lactate/Cr levels
lac-0.5-2.2 mmol/L
Cr- <1.2 mg/dL (if inc= dec renal perfusion)
