Exam 3 Flashcards
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
assessing
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
peripheral artery disease PAD
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
vocab
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
patho of PAD
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
PAD assessment
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
clinical manifestations of PAD
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
pain with PAD
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
chronic S/S of CAD
Palpation tips= Use finger tips Use light touch Symmetry in rate, rhythm, & quality Bilateral & at the same Bruits May be auscultated distal to an arterial stenosis
pulses in PAD
*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
diagnostics for PAD
“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
treatment of intermittent claudication for PAD
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
surgical management of PAD
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
endovascular intervention for PAD
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
post op care for PADS
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
Raynauds Disease
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
Symptoms of Reynaud’s Disease
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
Treatment of Raynaud’s Disease
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
Aneurysms: can occur anywhere
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
abdominal aortic aneurism (AAA)
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
abdominal aortic aneurism (AAA)
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)
Treatment of AAA
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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)
thoracic aortic aneurysm
high in chest
more deadly r/t lack of S/S
*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 & bloody diarrhea r/t clamped vessel effecting mesentery/renal circulation and blood supply to spinal cord (ischemic colitis AMB bloody diarrhea) Paraplegia Organ failure
treatment of thoracic aortic aneurysm
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
Peripheral aneurysms
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Should always put electrodes on clean, dry skin
Change daily
Clip hair/shave - need god connection between patch and skin
monitoring EKG
'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
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
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
ventricle repolarization
T wave
R waves in 6 seconds X 10 = BPM (60 seconds)
30 small boxes = 6 seconds
5 big boxes = 5 seconds
measuring info
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
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
Atrial depolarization
If not there/flat/inverted = automatically know it’s a problem in the atrium
P wave
ventricular depolarization
less than 0.10
QRS complex
ventricular repolarization
when peaked, must assess for hyperkalemia
-if it spikes, means they have hyperkalemia
T wave
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
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)
Electrical impulse through AV node is delayed or stopped
Causes: Medications (beta blockers); previous MI
Treat the patient-not the rhythm
heart block
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
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
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
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
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
Emergencies
Ventricular fibrillation
Ventricular tachycardia
defibrillation
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)
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
