Exam 3 Flashcards

(80 cards)

1
Q

Purpose looking at joint function? aterial system supplies O2, use muscle to make legs go up and down and muscles need O2
document pulses: 2+/3+, 4+ = bounding/too much pressure/fluid - assess bilaterally to see
ROM motions: STUDY - flexion/extension, external/internal rotation
cap refill: <3 seconds, painted nails = tip of finger

A

assessing

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2
Q

Disease process that affects the arteries
Begins early in adult hood and progresses slowly with age
Risk factors
Family history
20% > than 70
Obesity
Smoking (4X chance increase)
Stress
Preexisting health r/t destruction of vessels (DM12, clotting disorder, thromboemboli, trauma, vasospastic disorder) conditions

A

peripheral artery disease PAD

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3
Q
Dependent: hanging below 
Rubor: purple/blue red
Cyanosis: blue
Contralateral: opposite side
Proximal (=close) vs distal (=far)
Percutaneous: through the skin
Autologous: self (autologous donation)
Bruit: swish/turbulent blood flow - use bell side
Excision: cut it out
Angio- artery
Veno- vein
-graphy: picture
-oscopy: view with camera through scope
A

vocab

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4
Q

Narrow lumen-> ischemia-> infarct
Obstructive lesions usually occur from aorta below the renal arteries to the popliteal arteries
Arteriosclerosis is the most common artery disease affecting muscle fibers and endothelial lining of the small arteries and arterioles (become thickened)
– affects fibers in vessel, stenosis (narrowing) of artery
Atherosclerosis-> arterial stenosis->obstruction by thrombus->aneurysm-> ulceration-> rupture of vessel

Vessel gets smaller, decreases O2 in blood, leads to ischemia/tissue death/infarction
Can occur where arteries go
Affect brain (AMB stroke) and heart (AMB MI), lungs and kidneys

A

patho of PAD

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5
Q

Structural changes from lack of oxygen & nutrients
Skin color changes: temp = cool, Color = pale/rubor, Elevate = harder for body in PAD, Drop = easier for PAD (*position = lay flat to decrease need on heart)
Pulse changes: Diminished = 1 occlusion in 1 leg
Sensation changes: nail buds = thick/cloudy/clubbed, ROM to check muscle use; no O2 to muscle = atrophy
- numbness/tingly (like SS DM12)
Ulceration/gangrene: PAD = pour wound healing r/t lack of O2 to blood; pain at rest = late stage
Edema: very rare with PAD

A

PAD assessment

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6
Q

Most have no symptoms
1- 5% have critical limb ischemia: pain at night waking them up. Progresses to gangrenous ulcers/poor wound healing

Acute limb ischemia: r/t embolus: immediate blocking (ex: cocaine)
- upper limbs are acute AMB more pain with hands above heal, like doing hair. Numbness/tingling is less common

Atherosclerosis- systemic disease that affects arteries of the brain, heart, kidneys, mesentery and limbs.
Manifestations happen in the end organ supplied by arterial blood flow
Increased risk of mortality, MI, and CVD

A

clinical manifestations of PAD

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7
Q

Intermittent Claudication- very common
Muscle pain cramp caused by exercise or activity
Relieved by stopping muscle use
Arteries cannot provide blood flow with increased demand
Pain in muscles distal to diseased vessel
Exercise demands oxygen and nutrients->Tissues complete energy cycle without nutrients-> metabolites and lactic acid
-Treat: walking into pain = increasing blood flow to areas; lose weight, stop smoking, eat better

Rest Pain- Severe
Critical degree of arterial insufficiency
Pain worse at night
Interferes with sleep

A

pain with PAD

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8
Q
Hair loss: lower leg/ smooth/shiny skin
Brittle nails: curve up
Dry or scaling skin: lack of nutrients
Atrophy: inability to do ROM
Ulcerations
Gangrene
A

chronic S/S of CAD

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9
Q
Palpation tips=
Use finger tips 
Use light touch
Symmetry in rate, rhythm, &amp; quality 
Bilateral &amp; at the same 
Bruits 
May be auscultated distal to an arterial stenosis
A

pulses in PAD

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10
Q

*Doppler: look at arterial signals; BP in limbs, vessels, size and compressibility
- look for thrombus/valve function
Exercise Testing: ankle BP while on tread mill. look for drop in ankle pressure which indicates claudication
Duplex Ultrasound: look for vascular obstruction, stenosis, vascular with reflux, image and audible sign
CTA: spiral looks for AA, graft rejections or occlusion, hemorrhage (computed tomorgraphy angiography)
MRA (magnetic resonance angiography): angiography-MRA scan with software to isolate blood vessels and give 3 d images - Looks for changes, aneurysms, DVT
Air Plethysmography: measurement of volume, ejection fraction, residual volume, venous reflex, calf muscle pump ejection
Venous Duplex
Angiography: look for occlusive artery disease with dye
Venography: use radiopaque contrast into venous system for image
Angioscopy

A

diagnostics for PAD

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11
Q

“Walk into Pain”
Cilostazola-vasodilator that interferes with platelet aggregation: dilate to get blood out, can’t use with low BP because you will pass out due to lack of perfusion everywhere else
Antiplatelet agents: aspirin, Plavix - make platelets slippery so clots are harder to form (this is prevention)
Thrombolysis: destroy

A

treatment of intermittent claudication for PAD

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12
Q

Revascularization or arterial bypass first-line intervention (most common) - cut vessel via autonomous donation and reroute blood to get same benefit of blood flow
Type of surgery depends on health of patient
Bypass grafts are done to reroute blood flow around occlusion
Doppler evaluation done on grafts post-op to ensure patency
Post op - worried about bleeding, pts BP goes up and pops open graft
- lots of care post op. pulses will be normal

A

surgical management of PAD

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13
Q

Angioplasty (percutaneous transluminal balloon angioplasty (PTA) w/ or w/o stent: into vascular system, find clot, squeeze out with balloon by force and leave stent. The sent is foreign object, so risk for clot. It will secrete anti-platelets meds to prevent that
Decreased hospital stay
Less trauma
Outpatient setting
– to get clot go through femoral artery, make hole and go in with camera.
— post op: monitor femoral artery, manual pressure, peusdoaneurism = swelling/hematoma/decrease BP/pain

Risks:
Hematoma
Embolization
Dissection (rips open)
Bleeding
Stent migration
A

endovascular intervention for PAD

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14
Q

MAINTAIN ADEQUATE CIRCULATION: circulation issue, so prevent future/potential circulation risk
Activity level-get patient moving
Anticoagulation: increase clotting factors - lovenox to prevent clot
Monitor for compartment syndrome & renal failure
Monitor for local complications: bleeding, hemorrhage, swelling
Monitor for systemic complications (organ fails, kidney/heart/brain issue)
Pain management: opioids, narcotics, Tylenol
Maintain tissue integrity
- When sensation is lost, at risk for impaired tissue integrity (watch incision line and loss of sensation)
Postop teaching (take BP meds, notify for infection, stop smoking, no ice/heat, no tight clothing, no crossing legs

A

post op care for PADS

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15
Q

Inflammatory disorder->granulation formation->vessel destruction
Vasospasms that occurs with cold or stress
–Cold/stress trigger spasm/inflammatory response, so avoid cold/stress
Raynaud’s phenomenon is common with patients who have lupus or scleroderma (those with a weak immune system)
Etiology-unknown
Affects women age 16-40 years old who live in cold climates
Causes skin and muscle atrophy

A

Raynauds Disease

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16
Q
Skin color cyanotic (vasospasm)
Then vasodilation causes redness (rubor)
Numbness
Tingling 
Burning pain 
-progresses/cuts circulation - leads to atrophy, chronic lack of O2 to tissues
A

Symptoms of Reynaud’s Disease

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17
Q

Avoid stimuli that causes vasoconstriction (Usually cold or smoking)
Calcium channel blocker (pain) (best treatment)
acute conditions: corticosteriods
Sympathectomy
wear special gloves to keep warm, smoking cessation and increase activity

A

Treatment of Raynaud’s Disease

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18
Q

Is a localized out-pouching sac or dilation formed at a weak point in the artery wall
-disruption is loss of elastic fibers/collagen (ex: HTN increases pressure/creates pouch)–> degeneration of medial layer of vessel wall thought to be an inflammatory response (wall becomes thin/ulceration forms)
Types:
Abdominal aortic aneurysm
Thoracic aortic aneurysm
Peripheral aneurysms
Dissecting aneurysms

A

Aneurysms: can occur anywhere

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19
Q

Most common type (it’s below renal arteries (kidneys) and above iliac)
80% morality due to rupture and hemorrhage
Caused by:
Congenital weakness - vessel formed incorrectly –> trauma –> weakness of vessel or genetics
Trauma
Disease: Chronic increase in BP, atherosclerosis
Treatment: for rupture, only treatment is surgery to clamp vessel

A

abdominal aortic aneurism (AAA)

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20
Q

Risk factors/causes:
If symptoms occur
-Heart beating in abdomen when lying flat
-Abdominal mass
-If associated with thrombus, may cause cyanosis in the toes
Prior to rupture
-Severe back or abdominal pain r/t pressure on spinal cord
– increase heart rate, diaphoresis, back pain indicate rupture aneurysm
-NO deep palpation in abdomen
Best diagnostic indication of AAA- pulsatile mass in abdomen - if skinny
-Palpable if not obese
-Bruit: swoosh heard with bell
-CT to determine the size
– 3 cm wide: not high risk, no surgery, picture q 6 months
– > 5.5 cm: fix it r/t increased risk for dissection/rupture

A

abdominal aortic aneurism (AAA)

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21
Q

Ultrasound Q 6 months
- Stop smoking,

Antihypertensives: control BP withany one

  • diuretics,
  • Beta blockers
  • Ace inhibitors
  • Ca channel blockers

Surgical Treatment
> 5.5 cm (or enlarging)
Endovascular grafting
1. Open procedure for rupture: cut out vessel & close them up
–Major issue: weaken area, susceptible to blow out/hemorrhage, traumatic
–The vessel feeds everything, kidney, liver, heart, brain, spinal cord
–Clamping stops blood flow to all the organs
–Longer surgery/longer clamped = increased risk
2. Prior to dissection/endovascular grafting: don’ cut, leave in diseased part, put polyester pant in
–risks: clotting, platelet aggregation on stents so give antiplatelet meds (Plavix to reduce clotting), body doesn’t like polyester stent = fever/decrease in WBC/lysis of WBC, give NSAID/steroids and resolves in a week, stent migration, polyester stent leaks (occurs when BP is high, fluid in aneurysm = failed graft)

A

Treatment of AAA

TEGRITY THIS SLIDE 23

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22
Q

Caused by atherosclerosis
Symptoms
Boring pain when supine
Dyspnea- pressure on airway (esophagus/trachea) from mass)
Cough (pressure on airway (esophagus/trachea) from mass)
Hoarseness (pressure on airway (esophagus/trachea) from mass)
Stridor: harsh high pitch sound in upper airway r/t thoracic issues
Dilated veins in chest, neck and arms r/t increased pressure
Unequal pupils r/t pressure dilating

Diagnosed by chest xray, TEE (Trans-esophageal echocardiogram: look at back of heart with camera to find clots/aneurysm) , and CT (most common)

A

thoracic aortic aneurysm
high in chest
more deadly r/t lack of S/S

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23
Q
*BP control - 1st thing
Pain control
Close monitoring
Open surgical repair
- ICU post op  w/ vent until body/organs compensate - vessel is clamped during surgery, no O2 blood, do coagulation tests after
Endovascular graft 
-Less invasive 
Post-op assessment 
Mentation: slow to arouse but arousal 
Vision: PERRLA
Speech
Strength: could come out paraplegic: test by squeezing hands/pushing foot - see if spinal cord was affected
Abd pain/ flank pain: S/S of rupture and still leaking; can go through retroparitenium to look for bruising-manifests as back pain
Vomiting &amp; bloody diarrhea r/t clamped vessel effecting mesentery/renal circulation and blood supply to spinal cord (ischemic colitis AMB bloody diarrhea)
Paraplegia 
Organ failure
A

treatment of thoracic aortic aneurysm

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24
Q
Location-
Renal artery - most common
Femoral artery - most common
Popliteal artery - most common
Caused from atherosclerosis

Symptoms-
Pulsating mass and lack of circulation distal to aneurysm - may hear bruit directly below
Pain & Swelling

A

Peripheral aneurysms

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25
Aorta diseased by arteriosclerosis will tear resulting in dissection Causes: HTN: want a low BP Blunt force trauma: fast way to push open Cocaine use: constricts/vasodilator & make it more narrow most common in aortic arch may be confused with MI ``` Symptoms Sudden onset: goes from intermittent back pain to severe; abdominal swells, increase BP/heart rate/ dyspnea, tachypnea, diaphoresis --If BP has >15 mm difference, that's a sign Severe pain Pale Sweating Tachycardia Increased BP Change in BP in contralateral arm ```
dissecting aneurysm
26
Vitals: check often heart rate and BP I/O: don't want fluid overload --> increase pressure in venous system that can raise BP Bilateral upper arm BP Bilateral peripheral pulses (Take ALL pulses - could have PAD everywhere) Sensory function (spinal cord injury) Temp of extremity Color changes (hematomas), cap refill Signs of embolization Monitor access site (Endo)* Lie flat (Endo)* - 0 degree to prevent changes in pressure in femoral artery Monitor temp - blood flow/perfusion to extremities/infection - vascular reaction to graft within 1 week Call MD w/ persistent coughing, vomiting, sneezing, BP greater than 180 - increase interthoracic pressure in femoral artery Running IV fluids if not adequate po intake Monitor for complications: MI, ARDS, acute renal failure, GI complications
post op nursing care for aneurysm
27
Venous blood flow reduced by thrombus or embolus, incompetent valves, or reduction of circulation to surrounding muscles Decreased venous blood flow-> Increased venous pressure-> increased capillary pressure-> filtration of fluid into the interstitial space-> tissue edema Edematous tissue gets lack of nutrients-> breakdown, injury, infection -Tissue is mostly fluid - gets stretched and can break - increased risk of ulceration
venous disorders
28
Thrombosis, deep vein thrombosis (DVT), thrombophlebitis, and phlebothrombosis Cause (DVT is combo of causes) Virchow’s Triad -Stasis blood: blood not moving -Vessel wall injury (or external factor of clotting - body responds by clotting factors) -Altered coagulation r/t alteration in hormones -- Heparin works on those disorders
Venous Thrombosis
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Swelling, pain, and warmth in area with clot + Homans sign Pulmonary Embolism (PE) Assessment of hx + of d-dimer if unsure: compare to contralateral side and/or measure it if untreated: body will break down the clot in know known DCT: treat with heparin (short 1/2 life so wears off fast - too sliperry with no clotting can lead to hemorrhage) NO SCD'S
DVT symptoms
30
SCD’s Ted hose Medication Heparin: measure PTT; antidote = protamine sulfate - start on heparin for 2-3 days until therapeutic (INR = 2-3) -complication: heparin induced thrombocytopenia: massive clotting/bleeding Lovenox: type of heparin; give subq; longer 1/2 life Coumadin: measure PTT/INR; antidote = vitamin K
prevention of DVTs | use SCDs to prevent not treat
31
``` Monitor Drug Therapy -aPTT (PTT) -PT (prothrombin time) -INR -ACT (Activated Coagulation Therapy) School of thought on DVTs: Reposition patient frequently (elevation): elevate from venous stasis return Bedrest vs early ambulation Watch for bleeding complications Comfort (warm packs): careful in PAD r/t decreased sensation Apply compression devices ```
nursing management of DVT
32
``` Thrombolytic therapy: inject to dissolve -Dissolves clots If given within 3 days after acute thrombosis: poor candidates are elder, high pulse pressure, low weight, recent stroke/operation, CHF Long term damage less likely Coumadin PO INR monitored Given before heparin discontinued due to 3-5 day delay Vena cava filter ```
treatment of DVT
33
Common drugs: Alteplase (catheter directed infusion), Reteplase (used off label), and Urokinase (bolus and infusion) Lysis can happen between 6-72 hours (Alteplase) Advantages: avoid surgical intervention, can be repeated, works fairly quickly Disadvantages: long infusion times, hemorrhagic complications, allergic reactions, embolism, stroke, reperfusion arrhythmias Risks factors: older age, lower body weight, elevated pulse pressures, uncontrolled HTN, recent stroke, recent operation, bleeding disorders, CHF
Arterial and Venous Thrombolysis
34
Chronic venous insufficiency-> ischemia-> ulceration Occur in lower extremities near ankle Dry cracked, itchy skin Fibrotic sub Q tissue Color: beefy red - see in ankle/calf r/t skin being stretched the most
vascular ulcers | TEGRITY 36
35
``` Treatment based on etiology Wound cleansing and debridement Surgical Wet to dry Enzymatic debridement Autolytic debridement (tissue/colloids that eat it away, so no scraping) Dressings: Stimulated human skin HBO therapy Compression to return blood back and reduce pooling Maggots ```
treatment for venous thrombolysis
36
``` Arterial: no blood to distal tips Buildup of plaque and stenosis->Blocks the flow of blood through the arteries-> HTN Kidney failure Stroke Intermittent claudication Ulcerations and pallor/rubor Shiny skin, loss of hair, cool skin ``` Venous: Weakening of walls and valves in the veins-> Pooling of blood in the legs Varicose veins, spider veins r/t long term standing Stasis dermatitis, cellulitis - pooled blood --> infection/cellulitis DVTs Edema, brown thickened skin Cyanotic and dark colored
arterial vs venous problem
37
What is the purpose of the lymphatic system? Filtration, remove waste especially interstitial fluid and plasma Dumps by TEGRITY What is the lymphatic system made of? Spleen, lymphatic nodes and vessels
lymphatic disorders
38
Primary or secondary -Tissue swelling occurs in the extremities because of an increase in lymph that obstructs the lymphatic vessels -Starts with edema that is soft and pitting -Becomes firm and non-pitting, unresponsive to treatment -Worse with dependent positions -Chronic: leads to thickening of SQ, hypertrophy of skin (elephantitis) Diagnosed -Assessment and exclusion of other causes Prevent reoccurrences: lifelong vigilance, elevate TEGRITY and take care of tissue
lymphedema
39
Reduce edema Prevent infection and tissue damage Avoid break in skin Diuretics or antibiotics Surgical management- excision and grafting Keep moisturized skin, dry skin well, no tight shoes Diuretics don't work well on interstitial fluid -Can amputate but not effective treatment
treatment of lymphedema
40
Keep skin clean and dry Wear compression support garments as prescribed: lymphatic compression devices Avoid BP cuffs and needle sticks in affected limb Report new selling, redness, pain, heat, rash, or cracks in skin Avoid tight clothing r/t restraint movements Check feet for sores, rashes, cracks in skin Avoid trauma, bruising, insect bites (path for bacteria) Elevate limb whenever possible
patient teaching for lymphedema
41
Most common cause of infectious limb swelling -Single or reoccurring event -Often misdiagnosed as recurrent thrombophlebitis or chronic venous insufficiency -Happens after bacteria entered and is common with lymphedema S/S -Redness, pain, swelling, fever, chills, and sweating -Not uniform, dimpling in hair follicles Treatment: -Elevate -Warm, moist packs: head increases blood flow/circulation; encourage blood r/t antibiotics and increase in healing -Oral or IV antibiotics
cellulitis
42
Smoking: vasoconstriction --> stenosis of artery --> ischemia --> tissue death - BP and heart rate, increase risk of clot formation HTN: increase in pressure damages vessel walls --> issues DM: increase risk of infection --> poor wound healing -higher risk of amputations with DM and PAD - excess sugar damanges vessel and with PAD vessels already suck
Risks for PAD
43
EKG: Electrical impulse that travels through the heart can be viewed via ECG Electrodes-’patches’ that are placed on the skin Wires-electrode is connected to recording device via a set of wires-many are color coded Leads-images the nurse sees on paper or monitor. Direction of ecg complex varies depending on which lead is viewed Depolarization-contraction Repolarization-resting
Vocab for EKG
44
Should always put electrodes on clean, dry skin Change daily Clip hair/shave - need god connection between patch and skin
monitoring EKG
45
``` 'Pacemaker of the heart’ Causes atrial contraction node fires causing atrial depolarization All electrical impulses start 60-100 BPM P wave on the EKG ```
SA node | Atrial depolarization
46
Gatekeeper of the heart Takes over if the SA node fails Allows blood to empty from the atrium into the ventricle (no blood backs up) 40-60 BPM
AV nodes
47
``` In the intraventricular septum Branches off into right & left bundle branches Branches spread out into purkinje fibers Depolarization of the ventricles QRS complex on EKG 20-40 BPM ```
Bundle of His | ventricle depolarization
48
ventricle repolarization
T wave
49
R waves in 6 seconds X 10 = BPM (60 seconds) 30 small boxes = 6 seconds 5 big boxes = 5 seconds
measuring info
50
``` Heart rate Rhythm - regular vs irregular Interpretation - sinus rhythm, a fib., etc. PR interval ORS interval QT interval ``` PR, QRS, QT tell us what interpretation it is
what we measure in EKG
51
count number of large boxes between 2 consecutive r waves and divide into 300. Example……if there are four large boxes the heart rate is 300/4=75. *Can only be used in regular rhythms*
large box method
52
Atrial depolarization | If not there/flat/inverted = automatically know it's a problem in the atrium
P wave
53
ventricular depolarization | less than 0.10
QRS complex
54
ventricular repolarization when peaked, must assess for hyperkalemia -if it spikes, means they have hyperkalemia
T wave
55
Isoelectric line-baseline - base where impulse is at PR interval: beginning of the P wave to the beginning of the QRS complex - Normal: .12-.20 seconds - Anything over .20 seconds is a 1st degree heart block QRS: beginning of the Q wave to end of S wave -Normal
what you measure in EKG
56
``` Standard - we judge all strips to this Impulse starts in SA node Regular rhythm Heart rate 60-100 P wave before every QRS ```
normal sinus rhythm
57
Irregular rhythm P wave in front of every QRS complex Respiratory - can change heart rate pattern Not dangerous - could be r/t respiratory change
sinus arrhythmia
58
Regular rhythm Heart rate >100 P wave in front of each QRS ``` Causes: Bleeding - huge cause Hypovolemia Fever - can drive up heart rate Anxiety Meds *Decreased cardiac output! - 1st thing we look for - S/S of decrease CO = low BP, dyspnea, low urine output, diminished peripheral pulse, altered mental status, pallor/cool/clammy Treat underlying cause of tachycardia - if fever, give Tylenol; bleeding, give blood to fill tank back up ```
sinus tachycardia
59
Regular rhythm Heart rate <60 P wave in front of each QRS causes: Vagal stimulation - bearing down/pooping/vomit/suction r/t vagal response Meds - beta blockers Athletes - ex: runners - this is their normal Watch for: Altered mental status if decrease perfusion and CO Hypotension Chest pain Treat underlying cause of bradycardia Other treatments/meds used - surgery = pacemaker - meds: dopamine (vasoconstrictor that increases HR and BP) - symptomatic (not in athletic) = feel fatigue/crappy
sinus bradycardia
60
Always Irregular rhythm No P waves; “fibrillation waves” Heart rate is variable - can be 40 or 140 QRS normal since ventricle is fine problem with atrium - atrium quivers, blood pools and pt at risk for clot - need to assess lungs (for PE), stroke (clot in brain) and heart (for MI)
atrial fibrillation
61
Blood pools - pt at risk for clot/PE/stroke/MI/DVT At risk patients: heart failure, chronic lung disease, cardiovascular disease, caffeine, infection r/t body fighting Intermittent or continuous Signs and symptoms: can be asymptomatic, chest pain, SOB, fatigue Rapid ventricular response (RVR): ventricle responds, pumps very fast so with have high heart rate - this can decrease cardiac output --> hypotension, altered mental status, low urine output
atrial fibrillation
62
``` Treatment -Control heart rate -Medications --Antiarrhythmics --Amiodorone --Beta blockers- Metoprolol --Calcium channel blockers --Diltiazem --Anticoagulants-Warfarin r/t risk of blood clot. if not on anticoag could be r/t GI bleed, surgery, fall risk (risk vs benefit) --Oxygen r/t poor C.O. -Cardioversion -Stable vs unstable IV Adenosine: slow heart all the way down and restart it Ablation: surgery: cardiologist freeze/burns it if reoccurring ``` with clot: do TEE to look for clot - ok to shock if no clot is found Also, pt comes in with SOB, tachycardia and a fib started 25 mins ago, its ok to shock
a fib
63
Usually regular-can also be irregular! No P waves; saw tooth pattern/flutter waves QRS normal Atria contracts but impulse goes so fast through AV node Risk for stroke and clot issues Causes: heart disease, surgery, core pulmonale (right ventricle fails) Signs & symptoms: can be asymptomatic, chest pain, SOB, fatigue Treatment -Cardioversion -IV adenosine - Medications: antiarrhythmic
atrial flutter
64
Not a rhythm is irregular Electrical impulse starts in atrium-other than in the SA node P wave looks different Early beat Normal QRS SA starts somewhere but not in P wave r/t early beat Causes: caffeine, nicotine, anxiety, hypervolemia, hypokalemia (cardiac arrhythmias) Signs and symptoms: feels heart skip beat*, palpitations, dyspnea* Treatment: lay off triggers NC: no caffeine, draw blood to check potassium level Can lead to atrial fibrillation if frequent
premature atrial complex (PAC) not something you have ex: sinus rhythm with PAC
65
Not a rhythm Impulse starts in ventricle-conducted through before next sinus impulse P wave is hidden because it's conducted through before the next impulse QRS >.12 and will be wide since ventricle is weird Causes: caffeine, nicotine, patients with previous MI, hypervolemia, hypokalemia* Signs & symptoms: heart skips beat, SOB like in PAC, can be asymptomatic Treatment: Correct the cause - give potassium, no coffee, no smoking
premature ventricular complex (PVC)
66
What does ‘paroxysmal’ mean? - intermittent, from time to time, sudden* Electrical problem in the AV node - AV node causes heart beat to be in circular motion and atrium beats very fast - sudden onset Atrium beats too quickly/re-entry tachycardia prolonged episode and HR > 180 BPM may cause decrease C.O. (palpitations, hypotension, dyspnea, angina) Treat: vagal stimulation* (blow through straw, suction if on trach/vent, headstand, ice to face) -adenosine (stops heart/resets), beta blockers, CA channel blockers, digoxin, amiodarone -cardioversion: if unstable like BP in 60s do what will work fastest
paroxysmal supraventricular tachycardia
67
Regular rhythm No P wave QRS >.12 and wide Pulse vs pulseless fatal arrhythmia so run 1st thing: assess to check if they have pulse and check responsiveness - if not then life saving techniques Causes: heart disease, hyperkalemia Signs & symptoms: hypotension, syncope (pass out) Treatment -Medications-Amiodorone -Cardioversion: if pt is still alive (alive but need to get out of rhythm) R on T phenomenon: can cause this - ventricles depolarize on T wave instead out repolarize and sends into v tach
ventricular tachycardia
68
``` Polymorphic-varying QRS shapes and rates Causes: -Drug interactions -*Hypokalemia/hypomagnesium - especially mag with torsades -Heart disease Treat immediately!! r/t pulseless Give Magnesium during code Prepare for defibrillation because they don't have a pulse ```
torsades de pointes
69
``` No atrial activity No pulse/responsiveness Ventricles quiver Chaotic/disorganized Coarse vs fine Fatal Causes: heart disease, electrolyte abnormalities Signs & symptoms: no pulse, syncope, no breathing, unresponsive, basically dead Treatment -Immediate defibrillation is a must -CPR ```
ventricular fibrillation
70
P wave absent QRS absent No electrical activity No perfusion 1st: check pulse (leads can come off and that looks exactly like this) BLA: <10 secs Causes: hypoxia, electrolyte imbalance, drug OD, hypovolemia, tension pneumothorax, thrombosis (PE/astoyle), trauma, hypothermia Treatment: CPR to get perfusion then think of causes (if hypoxia, give O2) -cannot shock them r/t no electrical activity to shock - not very treatable or good outcome
asystole | run super fast
71
Electrical activity on monitor No pulse, not breathing Treatment: CPR to get perfusion Can't nurse from desk - can look fine on monitor but not have a pulse
pulseless electrical activity (PEA)
72
Electrical impulse through AV node is delayed or stopped Causes: Medications (beta blockers); previous MI Treat the patient-not the rhythm
heart block
73
``` When Conduction delayed through AV node Prolonged PR interval PR >.20 Regular rhythm QRS normal Causes: Idiopathic (Runner); Medications (Beta blockers) Signs and symptoms: asymptomatic Treatment: none unless caused by medication and you can change dose ```
first degree heart block
74
Due to gradual conduction abnormality/delay in AV node PR interval gradually gets longer and longer before a dropped QRS occurs Ventricular rhythm irregular Causes: Vagal response; Medications-beta blockers, calcium channel blockers, digoxin Manifestations: Chest pain Dyspnea Hypotension Fatigue Treatment: Only if symptomatic - Atropine and Transcutaneous pacing
second degree heart block type 1 (wenckebach) if your PR gets longer longer longer and then drops then you will have
75
Only some of the impulses go through AV node and to ventricles QRS will drop P waves normal PR interval will stay normal-NOT PROGRESSIVE QRS-normal (will spontaneously drop) More severe: increases chance to progress to 3rd degree heart block Causes: Ischemia Manifestations: Chest pain Hypotension Dyspnea Treatment: Symptomatic - give- Atropine and Transcutaneous pacing
second degree heart block type 2
76
``` No atrial impulse conducted through the AV node into ventricles One impulse stimulates the atria One impulse stimulates the ventricles No relationship between them! Cardiac output will decrease and pt feels crappy Rhythm: each are regular/no relationship Rate-ventricular rate 20-40 Causes: Interruption in the conduction system Manifestations: Syncope Chest pain Hypotension Dyspnea Treatments: Pacemaker ```
third degree heart block
77
Put sync on What happens if the nurse defibrillates the patient during the repolarization period? What is the repolarization period?? - resting (t wave) send into R on T phenomenon and send into v tach Sedation Monitor Document: important number of joules/shocks Anticoagulation meds - don't want to send shock systemically
cardioversion
78
Emergencies Ventricular fibrillation Ventricular tachycardia
defibrillation
79
Placed in the chest Detects arrhythmias. If arrhythmia is detected, shock is delivered Can serve as a pacemaker/defibrillator Who needs an ICD? - Hx of Vfib or Vtach AND CHF or cardiomyopathy Used for prevetion Nursing care after insertion: Monitor site for infection Complications: Infection and Dislodged leads
implantable cardioverter defibrillator (ICD)
80
Placed in the chest Treats arrhythmias-often tachycardia or bradycardia rhythms Who needs a pacemaker? - CHF (heart doesn't pump right and gets bigger and doesn't contract right, gets stretched) andThird degree heart block Temporary or permanent Nursing care: Monitor site for infection and Activity restrictions (no lifting arm above shoulder) Complications: Infection Pneumothorax Bleeding Chest x-ray post op cardiac output will go back to normal - normal BP, pulse, U.O, LOC
pacemaker