Exam #1 Flashcards
(161 cards)
1
Q
<p>CCUs/ICUs</p>
A
<p>* RRTs: rapid response teams
- pts exhibit subtle changes 6-8 hours before a cardiac or respiratory arrest
- critical care nurse, RT, MD, APN
- help diminish codes
* PCUs: transition between ICU and general care
- telemetry monitoring
* critically ill patient:
- physiologically unstable
- at risk for serious complication
- requires intesnsive and complicated nursing support
* ONLY for patients who are expected to recover </p>
2
Q
<p>Common ICU problems</p>
A
<p>- venous thromboembolism due to immobility
- skin problems d/t immobolity
- hospital aquired infection HAI: many IV lines, vents, etc
- sepsis
- multiple organ dysfunction syndrome (MODS): systemic inflammation response
- nutritional deficiencies related to hypermetaolic or catabolic states: use enteral (GI system) route first, then parenteral if they have an illius, start nutrition within 3 days
- anxiety related to threat of physical health, foreign environment, pain, sleeplessness, immobilization, loss of control, impaired communication: work with pts, families, caregivers; encourage bringing personal items and photos; use antianxiety drugs (ativan); use massage/guided imagry
- pain due to medical conditions, immobilization, invasive monitoring devices and procedures: continuous IV sedation and analgesics; balanced anesthesia = neuromuscular blocking drugs and analgesics done every 1-2 hours in the ICU
- impaired communication due to use of sedative or paralyzing drugs, ET tube: always explain what is happening to pt, use picture boards, notepads, look directly at pt, use hand gestures, use interpreter, provide comforting touch, decrease meds when doing a neuro assessment
- sensory/perception prolems d/t delirium: assess for delirium with confusion assessment method for ICU an the intensive care delirium screening checklies; address physiologic factors (noises, decreased rest may cause delirium); encourage presence of caregiver; may need haloperidol
- sensory perceptual problems realted to sensory overload: be cautious with conversations, mute phones, set alarms appropriate to pts condition, limit overhead paging, limit unnecessary noises
- sleep problems d/t noise, anxiety, pain, frequent monitoring, treatment procedures: interrupted q 30-1hr for vitals and checks; structure the enviro to promote sleep wake cycle; cluster activities; schedule rest periods; limit noise; provide comfort measures; use benzodiazepines or zolpidem (ambien, be careful with this)</p>
3
Q
<p>caregivers in the ICU</p>
A
<p>- give them guidance and support
- actively listen
- provide them with opportunity to participate in decision making
- involve durable power of attorney for health care if pt is incapable of making decisions
- give convenient access to the pt
- prepare caregivers for the ICU and the pts appearance
- provide option for caregivers presence during invasive procedures and CPR
- be culturally aware esp with death and dying</p>
4
Q
<p>hemodynamic monitoring in the ICU</p>
A
<p>* measurement of blood pressure in veins, arteries, and heart, also measures blood flow and amount of ocygen in the blood
- invasive or non invasive monitoring
- can include: systemic and pulmonary arterial pressures, CVP (central venouse pressure), PAWP (pulmonary artery wedge pressure), CO/CI (cardiac output and index), SV/SVI (stoke volume and index), SaO2/SvO2, 02 sat
* integrating all this data together and trending provides a picture of how well the heart is working and how well tissues are being perfused
* very important to be technically accurate to prevent unnecessary or inappropriate treatment</p>
5
Q
<p>preload</p>
A
<p>* preload = amount of blood in ventricle right before contraction; end of diastole
- PAWP: pulmonary artery wedge pressure, amount of blood in left side of heart; left ventricular end-diastolic pressure, left vent preload
- CVP: central venous pressure, right ventricular preload or right ventricular end diastolic pressure , amount of fluid in right side of heart, right vent preload
- PAWP &amp; CVP
- increased with: fluid overload
- decreased with: hypovolemia and vasodilation</p>
6
Q
<p>invasive vs non invasive </p>
A
<p>- non invasive monitoring: Bp cuff, SpO2 monitor
| - invasive: arterial pressryres, CVP, PAWP</p>
7
Q
<p>cardiac output &amp; cardiac index</p>
A
<p>* CO: volume of blood in liters pumped by the heart in 1 minute
* CI: measurement of the CO adjusted for body surface area; more specific to person; more precise measurement of efficiency of the heart's pumping action
- CO and the forces opposing blood flow determine BP
- increased with = high circulating volume, hypermetabolism with hypoxia
- decreased with = low circulating volume or decrease in strength of ventricular contraction (trauma, shock, sepsis, burns, massive vasodilation); 3rd spacing happens with decreased CO, decreased preload; massive MI causes decreased CO</p>
8
Q
<p>stroke volume &amp; stroke volume index</p>
A
<p>- SV: volume of blood (MLs) ejected with each heartbeat; determined by preload, afterload, and contractility
- SVI: SV adjusted for BSA
- preload, afterload, and contractility determine SV (and thus CO and BP)</p>
9
Q
<p>systemic vascular resistance &amp; pulmonary vascular resistance</p>
A
<p>- SVR: opposition encountered by the left ventricle
- PVR: opposition encountered by the right ventricle
- resistance of blood flow by the vessels</p>
10
Q
<p>frank starlings law</p>
A
<p>- explains the effects of preload and state that the more a myocardial fiber is stretched during filling the more it shortens during systole and the greater force of the contraction
- increased preload = increased SV and CO = increased O2 demand to the myocardium</p>
11
Q
<p>afterload</p>
A
<p>* afterload = forces opposing ventricular ejection, resistance the ventricle has to overcome to send blood to the body (SVR) or the lungs (PVR)
- resistence to properly circulate blood to entire body
- Systemic Vascular Resistance (left heart) or Pulmonary (right heart) = afterload
- when afterload is increased, CO is decreased
- increased SVR with: HTN, hardened arteries, CAD, low volume, catecholemines (fight or flight)
- increased PVR with: pulmonary HTN, right sided heart failure, hypoxia, PE
- decreased SVR with: vasodilators (morphine, nitrates), acidosis (blocks alpha and beta 1)
- decreased PVR with: oxygen, calcium channel blockers, aminophylline, isoproteronol</p>
12
Q
<p>Sa02</p>
A
<p>- amt of 02 in arterial blood</p>
- normal: 93-100%
13
Q
<p>Sv02</p>
A
<p>- how much 02 left in bood when it returns to the heart
- tells us if the body is using enough or too much 02</p>
- increased with: late sepsis (body alkolitic and wont release 02 to body), 02 improving in a patient, hemobloginb has tight grip on 02 and wont release
- decreased with: acidosis, hemoblobin has weak grip on 02 and it floats off, increased metabolic state, fever
- normal: 60-80%
14
Q
<p>Sp02</p>
A
<p>- oxygen saturation
- % of hemoglobin with 02 on it</p>
- normal: 95-100%
15
Q
<p>goals of hemodynamic monitoring</p>
A
<p>- maintain adequate tissue perfusion: early detection of changes, titration of therapy in unstable patients, determine what organ is causing a problem
- uses: shock, sepsis, any loss of cardiac function, burns, surgeries, hemorrhage, dehydration</p>
16
Q
<p>PAWP</p>
A
<p>- pulmonary artery wedge pressure
- low PAWP = low volume/preload (fluid bolus, lopressors, helps titrate therapy)
- high PAWP = fluid overload (slow fluids even if low BP, vasopressors)</p>
17
Q
<p>CO = HR X SV</p>
A
<p>- SV = preload, afterload, contractility
- preload: filling of ventricles
- afterload: resistance to properly circulate blood to body
- contractility: heart beat</p>
18
Q
<p>ejection fraction</p>
A
<p>- measurement of the percentage of blood leaving your heart each time it contracts
- normal is 60-75%</p>
19
Q
<p>CHF patients, example</p>
A
<p>- left sided systolic and diastolic issues
- systolic: problem with ventricles pumping = poor echocardiograms
- diastolic: preload, fluid issue, can't hold enough fluid but pumping is working fine = echo looks normal </p>
20
Q
<p>contractility</p>
A
<p>* contractility = strength of contraction
- when increased: SV and o2 demand are increased
- increased with: positive inotropes (epi, norepi, isoproteronol, dopamine, dobutamine, digitalis), make heart fire off harder which increases contraction power
- deceased with: heart failure, alcohol, negative inotropes (calcium channel blockers, beta blockers), acidosis; slow HR and decreaesd BP cause decreased contractility </p>
21
Q
<p>equipment needed for hemodynamic monitoring</p>
A
<p>* Intraarterial Catheter: 1 lumen, arterial
* central venous catheter: venous, single or multi lumen
* pulmonary artery catheter: venous, 4 or 5 lumens
- pressure bag: 1000 ml NS with a BP cuff around it; pump BP cuff up to 300 mmhg; 3-6mls/hr through art line
- 3-way stopcock: use this for "zeroing" to atmospheric pressure
- transducer: converts electrical activity into numbers on the monitor
- fast flush device: allows bolus of NS to go into atery and flush the line; makes sure you get accurate results</p>
22
Q
<p>principles of hemodynamic monitoring</p>
A
<p>* at initiation and with every reading:
1) position pt supine or up to 45 degrees
2) leveling (to the heart) - positioning the zero reference point (stopcock nearest the transducer) to the phlebostatic axis (level at the right atrium), mark on the pt with a permanent marker (4th ICS, midaxillary line)
3) zeroing the transducer (to atmospheric pressure) - opening the reference stopcock to air, set the monitor to 0, close the stopcock to air and open to the patient
- obtain results at end expiration (respirations affect the reading)
* every shift:
- fast flush square wave test (dynamic response test) to ensure accurate wave forms
- ensure pressure bag is inflated to 300mmhg and infusing at 3-6ml/hr
* every 3 days: change pressure tubing, flush bag, and transducer</p>
23
Q
arterial wave form
A
- systolic: uphill, depolarization, increased pressure
- dicrotic notch: aortic valve closes
- diastolic: downhill, repolarization, heart relaxes
- bolus dose, fast flush wave test
24
Q
arterial lines
A
- purpose: continuous measurement of BP (systolic, diastolic, MAP), also allows frequent ABG/Blood sampling
- before insertion, ensure pt has positive allen test (shows proper circulation between radial and ulnar arteries)
- look for normal waveform: dicrotic notch (systolic pressure) shuld be after QRS on EKG
- complications: infection, impaired circulation, hemorrhage, emboli = monitor q 1 hr at least
25
Mean Arterial Pressure
- normal = 70-105
- most often used to assess perfusion
- more accurate than Bp alone since systolic BBP is affected by cent function and diastolic BP is affected by peripheral vasoconstriction
- tells us about blood flow to organs and tissues
- (diastolic x 2) + (systolic) divided by 3: 120/80 = 93 MAP
- needs to be greater than 60 to perfuse organs
26
central venous pressure monitoring
- CVP = right sided preload (filling) measure
- purpose: for pts with significant alteration in fluid volume, measures filling pressures of right side of heart
- placed in the subclavian vein, IJ, or femoral while in trendelberg position, may be asked to hold their breath, CVC is threated so that the tip rests in the superior vena cava
- single or multi lumen
- can give IV fluids and draw venous blood
- complications: tension pneumothorax, air embolus, thrombus, infection
27
CVP or right arterial pressure
- normal 2-8mmhg
- approximates right ventricle filling pressure (blood in right artium)
- tells us about right vent function and general fluid status
- increased with: fluid overload, right sided heart failure, pulmonary HTN
- decreased with: hypovolemia, decreased venous return (vasodilation, shock)
28
pulmonary artery catheter, Swan-Ganz
- tells us PAWP and PAP
- multiple ports
- right atrium/ventricle
* purposes:
- CVP/RAP monitoring (2-8mmhg)
- medication/ fluid admin
- blood sampling
- Sv02 (returned blood 02 sat)
- blood temp (increases with MI)
- CO thermo monitoring
*
- pulmonary arterial pressures
- pulmonary arterial wedge pressures (6-12mmhg)
- right atrium --> right ventricle --> pulmonary artery --> PAWP (upon inflation) and PAP (uninflated)
29
circulatory assist devices
- used temporarily or permanently to decrease vent work and improve end-organ perfusion
- used as: bridge to transplant (most common), destination thearpy for those who are ineligable for transplant, bridge to recovery
- requires no immunosuppression, but does require anticoags
- goal is to improve CO without increasing work of a failing heart
1) intraaortic balloon pump IABP: most common
2) ventricular assist device VAD
30
CAD, Intraaortic balloon pump IABP
- balloon is placed in descending thoracic aorta above the renal arteries
- balloon fills with helium at start of disatole and deflates before systole (triggered by close EKG monitoring), counterpulsation (inflates opposite to vent contraction, inflates with every heartbeat
- nursing care: heparain/anticoags, HOB
31
CAD, ventricular assistive decice (VAD)
- allows more mobility than IABP
- placed internally or externally
- takes blood from left artium or vent to the device and then to the aorta, may also be used to provide right heart support or biventricular support
- nursing care: has an external controller, odd heart sounds are normal, BP usually only by doppler, pulse ox may be inaccurate, CPR is often not sage, may need to be disconnected for defibrillation
- deccreases workload to the heart, blood is taken out of the body and flows through a machine
- cx: anemia, cirulatory issues
32
resting hemodynamic parameters
* Preload*
- central venous pressure/right atrial pressure: 2-8
- pulmonary artery wedge pressure/left arterial pressure: 6-12
- pulmonary artery diastolic pressure: 4-12
* afterload*
- MAP: 70-105
- PAMP: 10-20
* other*
- SV: 60-150
- SVI: 30-65
- HR: 60-100
- CO: 4-8L/min
- arterial hemoglobin 02 sat: 95-100%
- mixed venous hemoglobin 02 sat Sv02: 60-80%
- venous hemoblobin 02 sat: 70%
33
Coronary Artery Disease CAD
- a blood vessel disorder caused by atherosclerosis = hardening of plaque and arteries
- CAD is the most common type of CV disease
- other names: arteriosclerotic heart disease, CV heart disease, ischemic heart disease, coronoary heart disease
- usually rakes a long time to develop so impt to focus on people at risk and start treatment early
34
Acute Coronary Syndrome
- s/s of severe coronary artery disease CAD and includes unstable angina and myocardial infarction
35
atherosclerosis
- increased BP damages tissues, tears in the vessel wall form and inflammation cascade begins (increased plaque formaion in area of tear)
- foam cells build up, fibrin builds up but inflamm response is still going on underneath the fibrin buildup
- increased 02 demand will cause angina, MIs
- heart attack is when the clot breaks off and released throughout the body
36
collateral circulation
- influenced by genetic predisposition to angiogenesis and the presence of chornic ischemia
- it is helpful to the body
- no time for development of collateral circulation with rapid-onset CAD or coronary spasm leading to a big risk for MIs
- blockage forms but vessels grow around it to help increase blood flow
- may help when there is a blockage in the heart but wont prevent it
37
CAD risk factors
- non-modifiable: age, genger (higher incidence in males but more women die from it), ethinicity, family history, genetic
- modifiable: HTN > 160, tobacco use (1+ ppd), diabetes type II, high cholesterol > 200, physical inactivity, obesity, metabolic syndrome (HTN, other factors leading to insulin resistence), physiologic states (anxiety, stress increase HR and cause vessel damage), substance abuse
38
proper physical activity guidelines for CAD
- FITT
- frequency: most days of the week
- intensity: moderate, brisk walking, hiking, biking, swimming
- type: isotonic, increase healthy proteins and decrease insulin resistence
- time: 30 minutes
- adding resistence 2 days/week helps
39
Nutrition for CAD
- fat intake: 30% of calories (monounsaturated fats - decrease red meats, eggs, whole milk products)
- reduce or eliminiate alcohol and simple sugars
- take EPA and DHA supplements (turn to fatty acides which decrease cholesterol, omega 3s)
- increase omega 3 fatty acids (tofu, soybeans, fish, flax, walnut, canola)
- therapeutic lifestyle changes diet: low sat fat, low cholesterola, calories controlled by activity level, no absolute restrictions, no rules for coffee
40
cholesterol lowering therapy
- complete lipid profile q 5 years (start at age 20)
- diet therapy first: restrict calories to decrease weight, decrease dietary fat and cholesterol, increase physical activity
- reassess cholesterol levels after 6 weeks of diet therapy
- drugs are used concurrently with diet modification
- drugs are often needed for lifetime
- increased HDL = good, healthy
- decreased LDL = good, bad/increase cholesterol
41
cholesterol lowering drugs
* statins: inhibit cholesterol synthesis in the liver
- simvastatin - take meds at night when cholesterol peaks
- do not drink grapefruit juice!
- monitor AST and ALT for liver damage, side effect
- increase receptors in liver to breakdown cholesterol
* niacin: inhibits cholesterol synthesis
- many adverse effects: severe flushing, itching, GI problems, orthostatis hypotension
- take NSAID with this med to decrease side effects
* Lopid: fibric acid derivative, won't affect LDLs
- affects vLDLs, targets coronary arteries
- may cause GI problems, interacts with many drugs
* Questran: welchol (bile acid sequestrants - increase conversion of cholesterol to bile acids
- bile acid is the product of cholesterol breakdown
- don't give with any other meds, it will inhibit their effects
- give 2 hours apart from other meds
* zetia: inhibits absorption of dietary and bilary cholesterol
- often used with diet changes for primary hypercholesterolemia, works really well when combined with statins
42
antiplatelet therapy
- most people with cad should be on low-dose ASA (81mg): stops aggirgation of platelets in people with increased BP and atherosclerosis; side effects = GI bleeds; not as effective for women until >65
- for high risk women intolerant of ASA use plavix/clopidrogrel
- beware of GI bleeding and hemorrhagic stroke symptoms
43
gerontologic considerations, CAD
- although the incidence is high, risk reduction and CAD tx are worthwhile
- aggressively treat HTN, hyperliopidemia, and stop smoking
- planned physical activity: longer warm ups, longer peropds of low level activity, longer rest periods between sessions, avoid extreme temperatures (thinner skin, risk for dehydration)
44
Angina
- strangling of the chest
- temporary imbalance of 02 supple to the heart's demand
- usually caused by stable, atherosclerotic plaque (people with high BP and cholesterol)
- doesn't caused permanent change if unstable
- unstable: blockage getting worse and worse but some blood flow
- stable: MI
45
precipitating factors with angina
- physical exertion: with compromised supply of 02
- temperatue extremes
- strong emotions: stress, mad, excitement = increased work on heart and 02 demand
- eating a heavy meal: lots of blood needed in GI system and decreased 02 to heart
- tobacco use: catecholemines increase HR
- sexual activity: catecholemines
- stimulents: cocaine, amphetamines
- circadian rhythm patterns: more angina in the morning, body increase activy thgoughout the day
46
chronic stable angina
- chest pain that occur intermittently over a long period of time with the same pattern of onset, duration and intensity
- pressure, ache, constribitve, squeezing, NOT sharp or stabbing
- pain does NOT change with potiioning or breathing
- pain lasts 5-15 minutes
- may also have indigestion
- pain can radiate: around neck, back, mid chest
- usually controlled with rest of meds: nitro (vasodilator) can be take prophylatically before activity
47
other types of angina
- silent ischemia: ischemia without symptoms (diabetics can't feel), will have shortness of breath and fatigue insteak, EKG diagnosis
- nocturnal angina: occurs only at night and they're not sure why, not dependent on laying or standing
- prinzmetal's angina: often occurs at rest, seen with migraines and raynaud's syndrome, coronary spasms, need calcium channel blockers and/or nitrates - massive increase in calcium in vessels
- decubitus angina: only when laying down
48
Angina Diagnostic Tests
- 12 lead EKG: compare with previous testing, old MIs will show on current tests
- CXR: look for heart enlargement, calcifications, pulmonary problems
- labs: confirm CAD (triglyceride panel, protein levels (increased inflamm), HDL, LDL, vLDL, homocystine levels , look for risk factors
- if known CAD: echocardiogram (to see if drop in ejection fraction or not), exercise stress test (stable or unstable angina, blockage, EKG with exercise), cardiac cath (go in, look at arteries, stent if needed)
- chemical stress test: for elderly
- adenosine (small dose) stress test = increases HR
49
angina drug therapy, short acting nitrates
- short acting nitrates: 1st line tx
- SL, patch, spray, PO
- Glyceryl trinitrate (GTN) tablets or sprays, Isosorbide dinitrate
- should relieve pain in 3 mins and lasts 30-60 mins
- check BP, don't give if less than 100
- 1 tab SL or 1 spray under tongue - may cause tingling, increased HR, headache, dizziness, flushing (vasodilation with increased ICP)
- if symptoms unchanged after 5 mins call EMS
- if symptoms improved after 5 mins, give max of 3 doesse and if not totally resolved after that then call EMS
- NEVER give if pt taking viagra
- monitor for ortho hypotension
- store away from light and heat
- replace q 6 months
- can take prophylacitcly before activity 5-10 mins
50
angina drug therapy, long acting nitrates
- isordil, Imdur
- used to reduce angina attacks
- caused headache, ortho hypotension, can cause tolerance
- nitropaste is dosed per inch on a flat muscular area with no hair or scars (works 3-6hrs, good for nocturnal and unstable angina)
- transdermal controlled-release by resevoir or matrix to maintain levels for 24 hours
- still take rapid/short acting for acute pain
- to decrease tolerance, on during day off at night
51
angina drug therapy
* bet blockers: preferred drug of choice for stable angina and following an MI
- metropolol, betalol, propanolol
- slows HR, heart works less, less 02 demand, less preload = decrease in heart demand
- side effects: low HR, low BP, wheezing, GI problems, wt gain, depression
- do NOT give if: HR
52
Angina treatment summary (ABCDEF)
- A = antiplatelet/anticoagulant, antianginal, ACE, ARB
- B = beta blocker, BP control
- C = cigarette smoking cessation, calcium channel blockers, cholesterol mngmt, cardiac rehab
- D = diet, diabetes, depression screening
- E = education, exercise
- F = flu vaccination (weakens heart muscle)
53
acute coronary syndrome ACS
- associated with deterioration of a plaque causing partial (UA, NSTEMI) or total (STEMI) occlusion by thrombus
- coronary arter disease --> chronic stable angina (slow) OR acute coronary syndrome (fast) --> Unstable angina/NSTEMI MI (small blood flow) OR STEMI (full occlusion)
54
unstable angina UA
- new chest pain, pain that occurs at rest, or pain that has a worsening pattern
- emergency!!
- unpredictable
- oftentimes women have prodromal (non-typical, no chest pain) symptoms (fatigue, dyspnea, indigestion, anxiety, back pain)
- men: more common to have big main artery blockages
- women: more common to have smaller vessel blockages
55
chest pain comparrison
- angina: onset/duration = sudden,
56
acute MI patho
- sustained ischemia >20mins causing irreversible myocardial cell death (4-6 hrs to necrose entire thickness of heart)
- due to thrombus
- most involve some portion of the left ventricle
- degree of preexisting collateral circulation influences the severity of the infarction
- 20+ mins = tissue death
- 4-6hrs = whole heart necrosis
- heart dies inside out
- collateral circulation may delay heart death
57
heart vessels
- left anterior descending artery LAD: widow maker, feed anterior portiono f heart
- circumflex artery: feed lateral and posterior portion of heart
- Right Coronary Artery RCA: feeds inferior portion of the heart
58
AMI s/s
- severe, immobilizing chest pain not relieved by rest, position change, nitrates or antacids
- more common in early AM, lasts > 20 mins, can be atypical
- sweating, ashen, clammy
- increased BP and HR (Drops later on)
- crackles (fluid in lungs backs up from heart)
- low MAP
- JVD, hepatic engorgement, edema, mimicks CHF
- n/v - stress response to pain
- tempt up to 100.4 (inflamm response)
- high glucose levels: fight or flight response from cortisol
- denial
- distant hearts ounds s3/s4
- dysrhythmias - sinus tachy with PVCs, T wave inversion, ST elevation or depression, abnormal q waves
- holosystolic murmor: interpapillary muscles die and valves malfunction
59
AMI healing process
- dead cardiac cells release enzymes: toponins, CKMG, norepi, epi
- leukocytes infiltrate, thinning the cardiac wall: inflamm process takes away dead tissue
- glucose and free fatty acids are released: cortisol release, increased glucose to supply ATP to heart
- can see the necrotic zone by ECG changes (st elevation, pathological q waves)
- 10-14 days later a weak scar develops, but the heart is very vulnerable
- 6 weeks after they are healed, but the scarred area is less compliant
- normal cells will hypertophy and dilate (vent remodeling) which can lead to heart failure
- ACE inhibitors help with prevention of ventricular remodeling by decreasing heart's workload
60
dx studies for ACS
- serial ECGs (q 2-4hrs)
- change in QRS, ST segment and t wave
- distinguish between STEMIM (pathological Q wave) and NSTEMI or UA (incomplete occlusion without a pathological Q wave)
- look at pattern among the 12 leads to find the coronary artery involved
- ischemia causes ST depression, T wave inversion
- injury (still reversible) causes ST elevation
- infarction causes pathological Q wave and T wave inversion (occurs within hours, may be present for months0
- full blown occlusion/MI = STEMI with or without angina
- partial occlusion/MI = NSTEMI
61
normal EKG
* P wave: SA nodal depolarization; atrial depolarization
* PR interval: Depolarization travels from SA node through AV node via internodal pathway (getting to the AV node is quick!).
* QRS complex: ventricular depolarization (includes bundle branches & purkinje fibers)
* T wave: ventricular repolarization
* QT interval: total time the ventricles spend depolarized. Measured from beginning of QRS complex to end of T wave. (not shown).
* ST segment: The time between the end of the QRS complex and the beginning of the T wave. Along with the QRS complex, during this time the ventricle is in the absolute refractory period.
62
STEMI and NSTEMI
* STEMI: ST-segment elevation MI
- ST elevation, Pathological Q wave, T inversion
- complete occlusion of major coronary artery
- full-thickness damage to heart muscle
* NSTEMI: non-ST segment elevation MI
- ST depression, T inversion, NO pathological Q wave
- full occlusion of minor coronary artery or partial occlusion of major coronary artery
- partial thickness damage to heart muscle
* pathological Q wave: sign of a pervious MI, takes hours to develop
63
diagnostic cardiac markers
- all signify muscle death, CKMG and Troponin are cardiac muscle specific
- myoglobin is realeased earliest but not heart specific
- lab draws every 4-6 hours to keep track of levels
- if ECG and cardiac markers are non-diagnostic: exercise or pharm stress test, echo, stress echo
1) CKMG: increases within 4-6 hours of MI, peaks within 18 hours, normal within 24-36 hours
2) troponin: increases 4-6 hours within MI, highest specificity to MI, peaks within 10-24 hours, takes 2 weeks to normalize
3) myoglobin: released very fast, not cardiac specific but muscle death in general
64
AMI tx
- establish an IV
- give 02 (2-4 liters by NC), position upright, heart has increased 02 demands
- 12 lead EKG, continuous monitoring
- aspirin, SL nitro (decreased preload, decrease workload of heart, vasodilate)
- morphine IV is pain not relieved by nitro
- treat dysrhythmias
- VS with pulse ox frequently
- bedrest for 12-24 hours
- SPO except sips of water (potential testing)
65
tx for STEMI vs NSTEMI
* UA or NSTEMI without cardiac markers: aspirin, heparin, integrillin (antiplatelet), coronary angiogram with stent once stabalized
- stents, antiplatelet therapy to prevent clots
* STEMI or NSTEMI with cardiac markers: reperfusion therapy (emergent stent, fibrinolytics, coronary surgical revascularization)
66
percutaneous transluminal coronary angioplasty PTCA
- 1st line tx with confirmed MI
- goal is to open the artery within 90 mins of arrival to the hospital
- usually do with drug-eluting stent
- local anesthesia, walking within 24 hours, home in 1-3 days, work in 1 wk
- requires antiplatelet drugs
- nursing care is like cardiac cath
- cx: abrupt closure, vascular injury, AMI, stent embolization, coronary spasm, dysrhythmias
- nursing care: sheath in place, remove sheath and provide 20 + mins of pressure to site, give atropine when removing sheath, VS q 15, neurovascular checks
67
Fibrinolytics
- criteria: s/s within 6 hours, no bleeding issues, no recent surgeries
- used if facility doesnt have a cath lab
- goal is to stop the infarction process by dissolving the thrombus and reperfusing the myocardium
- Give ASAP (within 1 hr of symptoms, no later than 6hrs)
- only give IV
- cx: reocclusion of the artery (prevent with IV heparin), bleeding ( minor surface bleeding and from gums is ok), hemorrhage/shock
68
Fibrinolytics Nursing Care
- baseline lab values: H&H, coag PT INR, Platelet ct
- start 2-3 iv lines before, in case of transfusion
- get all invasive procedures done first if possible
- give IV volus over 30-90 minutes
- closely monitor EKG, VS, pulse ox, neuro assessments
- signs of reperfusion: return of ST segment to baseline, abrupt cessation of chest pain, early/rapid rise of CKMB within 3 hrs, peaking at 12 hrs, may have sudden onset of reperfusion dysrhythmias
69
coronary surgery revascularization
- MIDCAB, OPCAB, Robot-assisted cardithoracic surgery, TMR
- CABG = coronary artery bypass graft = most common
- CABG is done for pts who fail medical mngmt, have left main coronary artery or 3-vessel disease, are not candidates for PTCA, failed PTCA with ongoing chest pain or have diabetes
- requires sternotomy with cardiopulmonary bypass
- use internal mammary artery the most, can also use radial artery and aphenous vein
- palliative tx, not a cure
70
nursing care after CABG
- in ICU for 24-36 hours with PA catheter, arterial line, chest tubes, continuous ECG monitoring, ETT, epicardial pacing writes, urianry catheter, NGT
- usually extubated within 6 hours and to step down unity in 24 hours
- many post op cs due to CPB (cardiopulmonary bypass machine) : systemic inflammation, F&E imbalance, hypothermia, bleeding
- postop dysrhythmias in first 3 days
- care for surgical sites, esp donor site
- may have postop congnitive dysfunction - can be acute or forever after use of CPB
71
MI medications
- intially: IV nitro (titrate to stop MI cycle), morphine (vasodilator, pain med), dual antiplatlet therapy (apsirin, clopidrogrel/plavix), LMWH or IV heparin
- Within 24 hours: oral beta adrenergic blockers, ACE inhibirors (prevents vent remodeling), antidysrhythmics (only if life-threatening), lipid lowering drugs, stool softeners (prevent bearing down)
72
CX after MIs
- dysrhythmias: very common esp with ischemia, electrlyte imbalances, SNS stimulation (tachy); occur more with anterior wall infarction, heart failure, or stroke
- heart failure: subtle s/s (mild dyspnea, agitation, mild tachy); pulmonary congestion, s3/s4, crackles, JVD
- Cardiogenic shock: less likely now taht we use PTCA/fibrinolytics; requires tx with meds, IABP (heart famages so much that it cant supply enough blood to the body)
- papillary musclye dysfunction: occurs if infarction is near the mitral valve; papillary muscles mess up the valves; new systolic murmor can be heard; muscle can rupture and cause mitral valve regurgiation which causes pulm edema, decreased CO; tx with mitral valve replacement, IABP, nipride
- ventricular aneurysm: heart failure, dysrhythmias, agnna; leades to thrombi or rupture or death; ventricle ruptures
- pericarditis: common 2-3 days post MI; chest pain worse with inspiration, cough, upper body movement, friction rub, fever; diagnosis with 12 lead; tx: pain relief with ASA, NSAIDS, corticosteroids
- dressler syndrome: body attacks scar tissue formed in heart
73
home care after acute coronary syndrome
- CAD is chornic, not curable
- focus on modifiable risk factors
- physical activity is impt, stop exer if chest pain or dyspnea, treat depression, mantain contact with pt
- resume normal sex activity within 7-10 days after uncompolicated IM, no more strenuous than climbing 2 flights of stairs, may have some sex dysfunction, take nitro prophylactically, avoid sex after heavy meals
74
Sudden cardiac death
- may or may not have know CAD
- young, male, athletes
- death usu occurs within 1hr of symptoms, most have no warning signs
- cause: acute ventricular dysrhythmias, sometimes a vent obstruction or extreme bradycardia
- if they survive: diagnostic workup for MI, cardiac cath, 24 hour holter monitoring, Internal cardio defribrilatio to prevent recurrence, lidocaine
75
adrenergic blocking drugs, alpha blockers effects and indications
- cause both arterial and venous dilation, reducing peripheral vascular resistance and BP
- used to treat HTN
- effect on receptors on prostate gland and bladder deceases resistance to urinary outflow, thus reducing urinary obstruction and relieveing effecgs of benign prostatic hyperplasia (BPH)
used to control and prevent HTN in pts with pheochromocytoma
76
alpha blockers adverse effects
- cardiovascular: palpitations, orthostatic hypotension, tachycardia, edema, chest pain
- CNS: dizziness, headache, anxiety, depression, weakness, numbness, fatigue
77
alpha blockers
- phenoxybenzamine HCL (dibenzyline)
- phentolamine (regitine)
- prazosin (minipress)
- terazosin (hytrin)
- alfuzosin (uroxatral)
- tamsulosin (flomax)
* phentolamine (regitine): alpha 1 blocker used to treat HTN, tx for HTN caused by pheochromocytoma, tx for extravasation of vasoconstricting drugs (epi, dobutamine), SQ injection in circular fasion around extravasation
78
Beta blockers: indications
- angina: decreases demand for MI o2
- cardioprotective: inhibits stimulation from circulating catecholamines
- dysrhythmias: calss II antidysrhythmic
- migaine headaches: lipophilicty allows entry into CNS
- antihypertensive
- heart failure
79
Beta Blockers: adverse effects
- blood: agranylocytosis, thrombocytopenia
- cardio: av block, bradycardia, heart failure
- CNS: dizziness, depression, unusual dreams, drowsiness
- GI: n/n, constipation, diarrhea
- other: impotence, alopecia, wheezing, bronchospasms, dry mouth
- nonselevtive beta blockers may interefere with normal responses to hypoglucemia (tremor, tachy, nervousness) -- may mask s/s of hypoglycemia, use in caution with DM pts
80
Beta Blockers
- atenolol (tenormin)
- carvedilol (coreg)
- esmolol (brevibloc)
- labetalol (normodyne)
- metoprolol (lopressor)
- propanolol (inderal)
- sotalol (detapace)
* atenolol (tenormin): cardioselective beta blocker, PO, prevent MI in pts with history, TX of HTN, angina thyrotoxicosis
* Esmolol (brevibloc): very shrot acting beta 1 blocker, acute situations to provide rapid temporary control of the vent rate in pts with SVT, short half life, continous IV infusion, titarted to achieve serum levels
* propanolol (inderal): prototypical nonselevetive beta1 and beta 2 lblocker, po/iv, shown to increase survival in pts experiening MI, tx for tachy dysrhythmias associated with glycoside toxicity, hypertophic subaortic stenosis, pheochromocytoma, thryoticisosis, migraines, containdicated in ots with asthma/resp disorders
* metopolol (lopressor): beta 1 blocker, PO/IVP, shown to increase survival in pts experiencing MI, tx for tachydysrhythmias, migraines, contra in pts with resp disprderes/asthma
81
adrenergic blocking drugs: nursing implications
- assess for allergies and history of COPD, hypotension, cardiac dysrhythmias, bradycardia, heart failure, other cardio problems
- may precipitate hypotension
- some beta blockers may precipitate brady, hypotension, heart block, heart failure, bronchoconstriction
- avoid OTCs for interactions
- drug interactions: atnimuscarinics, anticholinergics, dieuretics, neuromuscular blocking drugs, oral hypoglycemic drugs
- never stop abruptly
- report constipation and/or bladder issues
- change positions slowly
- avoid caffeine
- avoid alcohol
- notify if new dysrhythmias
- Therapeutic Effects = decreased chest pain, return to normal BP and HR, other effects depending on use
82
nursing implications: beta blockers
- rebound HTN or chest pain may occur if this med is discontinued abruptly
- may notice decreased tolerance for exercise (Dizziness, fainting)
- report to physician: weight gain of more than 2 lbs in 1 day or 5lbs in 1 week, edema of the feet or anckles, SOB, fatigue weakness, sycope
83
antianginal drugs
1) nitrates/nitrities
2) beta blockers
3) calcium channel blockers
- therapeutic objectives: minimize frequency of attacks and decrease duration and intesity of anginal pain , improve functioning with as few adverse effects as possible, prevent or delay the worst possible outcome, MI
84
nitrates/nitrites
- available forms: SL, chew tabs, PO tabs, IV, patches, ointments, translingual sprays
- rapid acting: used to treat acute angina, SL, IV
- long acting: used to prevent anginal episodes, patch
85
nitrates
* nitroglycerin (nitro-Bid, nitrostat)
- prototypical nitrate, NTG, large first pass affect if PO
- sublingual/meter dose used for tx of acute chest pain, angina
- symtomaic treatment of angina
- IV form used for BP control in perioperative HTN, treatment of HF, ischemic pain, pulm edema, hypertensive emergencies
* isosorbide dinitrate (isordil)
- extended release with 2 active metabolites
- PO 5-20mg BID/TID
- PO 40-80 MG
- same effect as other nitrates
- both nitrates cause vasodilation
* isosorbice mononirtate (imdur)
- long acting with 1 active metabolite
- PO 20mg BID given 7 hours apart
- PO 30-120 mg/day for SR
- produce consistent, steady htearpuetic response, less varaition between patients
86
nitrates adverse effects
- headaches: increased ICP, usually diminish in intensity and frequency with continued use
- relfex tachy
- postural hypotention
- give tylenol for headaches
- tolerance may develop: nitrates around the clock or with long acting forms, prevent by making times when there is not nitro (at night)
87
beta blockers
- atenolol (tenormin)
- metoprolol (lopressor)
- propanolol (inderal)
- nadolol (corgard)
* atenolol (tenormin)
- cardio selective beta 1 adrenergic blocker
- PO
- PRevent MI in pts with history, decrease HR, decrease work of heart
- tx: HTN, angina, thyrotoxicosis (which speeds up your HR)
* metoprolol (lopressor, toprol XL)
- cardioselective beta 1 adrenergic blocker
- PO, IVP
- prophylatic treatment of angina
- shown to increase survival in pts experiencing MI
- tx: HTN
- contraindicated in asthmatics
88
beta blocker indications
- angina
- antihypertensive
- cardiac dysrhythmias
- cardioprotective effects, esp after MI
- some used for migraines, essential tremors, stage fright
89
beta blocker adverse effects
- Cardiovascular: bradycardia, hypotension, atrioventricular block, dysrhythmias
- metabolic: hyperglycemia and/or hypoglycemia
- CNS: dizziness, fatigue, depression, lethargy
- other: wheezing, impotence, dyspnea
90
calcium channel blockers
- verapamil (calan, Isoptin)
- diltiazem (cardizem)
- nifedipine (procardia)
- amlodipine (norvasc)
- nicardipine (cardene)
* diltizem (cardizem)
- high affinity for cardiac conduction system
- effective in tx of angina pectoris resulting from HTN and coronoary infusufficiency
- one of the few CCB available in arenteral form
- used for afib, aflutter, PSVT
91
calcium channel blocker indicatiosn
- angina
- HTN
- Supraventricular tachy
- coronary artery spasms (prinzmetal angina)
- short term managemente of atrial fib and flutter
92
calcium channel blockers adverse effects
- limited
- primarily related to overexpression of their therapeutic effects
- Hypotension, palpitations, tachy or brady, constipation, nausea, dyspnea, other adverse effects
93
antianginal meds nursing implications
- priro to admin, perform complete health history to determine presence of conditions that may be contraindicated
- obtain baseline VS, include resp patterns and rate
- assess drug interactions
hr > 60
BP > 100
- limit caffeine intake
- pts report: blurred vision, persistent headaches, dry mouth, edema, fainting episodes, weight gain of 1lbs or 5lbs, pulse rates less than 60, dyspnea
- avoid alcohol and hot baths
- change position slowly
- record anginal attacks and precipitating factors
- monitor adverse rxns: allergic, headache, lightheadedness, hypotension, dizziness
- monitor therapeutic effects: relief of angina, decreased BP
94
nitroglycerin nursing implications
- teach proper techniques for taking and administering SL nitro for anginal pain
- never chew or swallow SL form
- burning felt with SL indicates the drug is still potent
- replace after 3-6 months
- store in airtight, dark area
- rotate and remove old patches as needed
- monitor VS during angina
- after taking SL lie down to decrease dizziness
- in anginal pain occurs: stop, sti, talk SL, take one q 5 mins 3 times, if doesnt stop then call EMS
- ive given in special tubing
- discard parenteral solution that is blue, green or dark red
95
beta blocker nursing implications
- monitor pulse daily and report
96
calcium channel blocker nursing implications
- abrupt withdrawl can precipirate rebound HTN and worsening tissue ischemia
- monitor weight, edema, SOB
- instruct pt to change positions slowly/cautiously to prevent syncope
- constipation may occur, eat high fiber and drink fluids
- NO GRAPEFRUIT JUICE
97
normal heart conduction
1) SA node
2) atrial contraction
3) AV node
4) bundle of his
5) left and right bundle branches
6) purkinje fibers
7) ventrical contraction
* p wave: atrial depolarization, contraction
* PR interval: SA node -> AV node travel, 0.20 = 1st degree block
* QRS complex: ventrical depolarization, fire of AV node (atrial repo also) .12 = bundle branch block
* ST: ventrical contract and pump; any increase is bad
* T: ventrical repolarization/diastole
* QT: .44 = abnormal tachy
- depolarization: causes action potential, contraction of heart
- repoloarization: return of ions to resting state, relax/diastole of heart
98
QT
.44 = abnormal tachy
99
PR
.20 = 1st degree block
100
QRS
.12 = bundle branch block
101
peaked T wave
- hyperkalemia
102
u wave
- hypokalemia
103
STEMI
- fully occluded MI
- pathological Q wave
- ST elevation
- possible u wave
104
12 lead placement
- 10 leads with 12 views
- 2 arms
- 2 abs/legs
- v1 = 4th right intercostal space at sternal border
- v2 = 4th left intercostal at sternal border
- v3 = halfway b/n v2 and v4
- v4 = 5th intercostal space midclavicular line
- v5 = anteroaxillary line same plane as v4
- v6 = midaxillary line horizontal to v4
105
5 lead placement
- Right arm = white
- left arm = black
- right leg = green
- left leg = red
- chest = brown
106
ECG paper
- small square = 0.04 seconds
- large square = 0.20 seconds
- 1 second = 5 large squares
- 1 minute = 300 large squares
- 1mm height = 1 small box
- every 3 seconds there is a marker on the ECG
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calculating HR
- count number of QRS complexes in 1 minute
- 6 second strip method: count # of QRS complexes in 6 seconds and multiple that number by 10
- small block method: count # of small squares between one RR interval, divide by 1500
- big block methods: count # of large squares between one RR interval, divide by 300
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P wave
- represents atrial contracton
- smooth and rounded, no peaks or notches
- 0.06-0.12 seconds
- upright in leades 1, II a VF
- suggestions problems with conduction in the atria
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junctional rhythm
- normal SA = 60-100
- normal AV = 40-60
- AV node has become the main pacemaker of the heart and the SA node isn't working or isn't working correctly
1) no SA node: no p wave with a QRS (atria not working but vents are)
2) inverted P wave: junctional rhythm, sick SA node, no PR interval
3) P wave after the QRS: Sa node very slow, AV node took over
- junctional rhythm: 40-60 BMP (give atropeine)
- junctional brady: 60 BPM (adrenergic response)
- junctional tachy: > 100 BPM (adrenergic response to promote blood flow)
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PR interval
- from beginning of P wave to end of PR segment
- 0.12-0.20 seconds
- represents the time it takes the electrical impulse to travel from the SA node to the ventricle
- at the end of the PR interval, the ventricles are starting to contract while the atria relaxes
- > .20 = delay in atrial filling, suggests heart block
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QRS complex
- ventricular contraction/depolarization
- 0.04-0.12 seconds
- if it is wider it is concerning: suggests old MI or possible ischemia
- problems are usually from bundle branches or in the ventricles
* digoxin and metropolol can delay the QRS complex
- pathological Q wave = wide and/or deep = MI ischemia, STEMI
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ST segment
- measured at the end of the QRS through the beginning of the T wave
- 0.12 seconds
- ST segment indicates the period of time between the end of ventricular contraction/depo and the start of ventricular relaxation/repo
- ST is usually on baseline (should be no elect activity), deviation may be indicative of myocardial ischemia, injury or infarction
- increased/elevated ST segment = STEMI
- decreased/depressed ST segment = NSTEMI
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T wave
- ventricular relaxation/repolarization
- 0.16 seconds
- T wave usually follows the QRS complex and deflects in the same direction, should be smooth and rounded
- problems usually from F&E imbalances, ischemia, or infarction
- increased T = hyperkalemia
- decreased T = ischemia, NSTEMI
- decreased T with U wave = hypokalemia
114
QT interval
- measured from beginning of QRS complex to end of T wave
- represents the total time for ventricular contraction and relaxation
- problems are usually from something affecting repolarization (drugs, F&E imbalances, changes in HR)
115
U waves
- not very common and easy to overlook
- associated with electrolyte imbalances, heart disease, HTN
- most prominant in HYPOkalemia
116
causes of dysrhythmias
- problem with impulse formation:
* SA node: main pacemaker of the heart, 60-100
* AV node: secondary pacemaker, 40-60 BPM
* purkinje fibers: tertiary pacemaker, 20-40 BPM
* ectopic foci from atria AV node, or ventricles (Afib, Aflutter)
- problem with conduction of beats:
* delays: bundle branch block > .12, AV block > .20
* blocks
- Combination of above issues
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cardiac dysrhythmias
- always cause a risk of decreased perfusion, decreased cardiac output
- always assess the pt, not just the EKG
- how it pt tolerating rhythm?
- causes include: CAD, electorlyte imbalances, changes in heart muscle (cardiomypoathy), injury from MI, healing process after cardiac surgery (Scar tissue), dig toxicity (slow HR, affects SA node)
* nursing diagnosis: impaired cardiac output r/t cardioelectric abnormality 2nd to junctional rhythm AEB HR
118
stable vs unstable
- stable: asymptomatic or mild symptoms (palpitations)
| - unstable (decreased perfusion/CO): pulselessness, dizziness, syncope, hypotensions, chest pain, SOB
119
syncope
- fainting
- not always caused by CV problems but can be vasovagal response or dysrhythmias
- must consider hypoglycemia, hysteria, seiure, stroke, TIA
- if we do think it is cardiac: diagnostic tests = echocardiogram, stress testing (adenosine, dobutemine), may need EPS (can induce dysrhythmias and stop Afib, A flutter), head up tilt test (lay flat stapped to table and check BP and HR, then raise it up and check for ortho hypo issues), holter monitor (pts prone to sudden cardiac death), event monitor/loop recorder
120
dysrhythmias diagnostic tests
- continuous ECG monitoring
- transesophageal echocardiogram (TEE): sedate pts and p put it down the throat, can see better without chest bones in the way
- electrophysiologic study (EPS): may incude electrical dysrhythmias to see if they're prone to the
- holter monitoring
- event monitoring
- exercise treadmill testing
- signal-averages ECG
121
antidysrhythmic drugs
* for ACLS best route is IV or IO, endotraceal route is least desired
* for ACLS, all meds need 20ml NS flush and CPR to circulate the meds
1) atropine
- for bradycardia
- 0.5 mg every 3-5 minutes, up to 3mg total
2) adenosine
- for tachycardia, SVT, VT
- 6mg rapid IVP, 2nd dose of 12 mg
- causes brief period of asystole then hopefully creates normal heart rate
3) epinephrine
- for cardiac arrest to stimulate the heart
- 1mg every 3-5 minutes or 2-10mcg/min
4) amiodarone
- 300 mg IV, 2nd dose of 150 mg
- very toxic, very long half life (180 days)
- not used routinely for oral management of dysrythmias; vfib, unstable VT
5) procainamide, sotalol, lidocaine
122
vagal Stimulation
- slows conduction of electrical impulses decreasing heart rate in SVT
- valsalva, coughing, immersing the face into ice water, carotid massage, digital finger up rectum
123
pacemakers
- includes a power source and one or more pacing leads
- permanent - placed like the ICD
- temporary - power source is outside the body
- synchronous or asynchronous
124
pacemaker lead wire
- atrial pacing: forces artias to fire off
- ventricular pacing: forces the vents to fire off at a certain rate (70 ish)
- AV sequential pacing: both atrial and ventricular pacing
- ventricular pacing on demand: only shocks when heart falls below a certain BPM
125
pacemaker monitoring
- patient needs to check their apical pulse often
- failure to captures: pacemaker goes off ok but isnt strong enough to cause a rxn. may see spikes but no action after it
- failure to sense: pacemaker goes off at the wrong time but strong enough
126
pacemaker teaching
- no sudden jerky movements for 8 weeks post op
- limit driving
- baths are fine after incision heals
- avoid direct blows to the site
- avoid large magnets, MRIs, security devices at the airport
- dnt use cell phone close to pacemaker site
- monitor pulse daily
- check pacemaker function every 3 months
- battery life span is 10 years
- wear a medic ID bracelet
127
CPR
- restores blood flow to body but won't restore an organized rhythm (wont help VT, VF)
- circulates blood and meds, push hard and fast
- 100 compressions/minute, 2 inches deep
- switch providers q 2 minutes or 5 rounds
- cx: sternumn and rib fractures, spleen and liver lacerations. pneumothorax, cardiac tamponade
128
AEDs
- for each minute that defibrilation is delayed 10% survival rate reduced
- defibrilation = used ONLY for PULSELESS pts (VT or VF) nonsyncronized delivery of energy during any phase of the cardiac cycle
- cardioversion = delivery of energy synchronized to the QRS complex, used for SVT, Afib, aflutter, VT
129
defibrillation
- select proper energy level: biphasic = 2 energy levels 200, mnophasic = 1 energy level 360
- turn off synchronizer switch, no QRS complex
- ONLY pulseless Vtach or V fib
130
synchronized cardioversion
- delivers countershock on the R wave of the QRS complex
- start at lowest energy and increase as needed
- if non-emergent then sedate with versed first
- if patient becomes pulseless or develops vfib, turn off synchronized and begin defibrillation
131
implanted cardioverter-defibrillator ICD
- used for pts who survive sudden cardiac death, have spontaneous sustainted VT, have syncope with VT/VF, are at high risk for life-threatening dysrhythmias
- if the system senses Vtach or VF, it will send a 25 joulse shock
- can have a combo pacemaker with ICD
132
ICD patient teaching
- same as pacemaker plus:
- discharge will feel like a blow to the chest
- sit or lie down immediately if feeling faint
- if it fires more than once, call EMS
- caregivers should learn CPR
- if device is beeping then call doctor
133
radiofrequency catheter ablation therapy
- electrical energy is used to "burn" ectopic areas
- EPS is done first to identiy the source of the dysrhythmia
- low cx rate
134
immediate post cardiac arrest
- after return of spontaneous circulation:
- transport pt to higher level of care
- identify and treat the cause to prevent recurrence
- use therapeutic hypothermia if pt remains comatose -- decreasing temp decreases cell metabolism which decreases 02 demand which decreases the Sv02
135
normal sinus rhythm
- regular PQRST cycles
- rate 6-100
- P wave BEFORE QRS complex
- narrow QRS (
136
sinus bradycardia
- caused by: valsalva, gagging, carotid sinus massage, vomiting, suctioning ( can cause valscalva and bear down), hypoxia, meds (BBs, CCBs), can be normal for athletes, sleeping
- ECG:
137
sinus tachycardia
- caused by: exercise, fever, pain, hypovolemia, meds
- ECG: 101-200 BPM, regular, everything else normal (narrow QRS)
- S/S: dizziness, dyspnea, hypotension, decreased urine output, restlessness (decreased CO)
- tx: treat underlying cause (fever, pain, hypovolemia)
138
sinus arrhythmia
- normal phenomenon of mild acceleration (with inspiration) and slowing of the heart (with expiration) c/b more blood filling the heart during inspiration causing acceleration
- ECG: irregular, everything else normal
- S/S: none
- tx: none
- increased HR = inspiration
- decreased HR = expiration
139
premature atrial complex (PAC)
- caused by: emotional stress, fatigue, caffeine, tobacco, alcohol, meds
- ECG: can be irregular, P wave is early and different from the other P waves (notched, downward, hidden)
- S/S: asymptomatic or palpitations, states heart "skipped a beat"
- tx: decrease sources of stimulation (caffeine, meds)
- SA node is not the one to fire, an electrical impulse fires randomly instead
- occassional = ok, more than occasional = not ok
140
cardio terminology
- tachydysrhythmias: > 100 BPM, increase work of the heart, increases 02 demand, decreases coronary perfusion time (diastole); initially increases CO and BP but then it falls; can cause palpitations, chest pain, restlessness, anxiety, pale/cool skin
- dysrhythmias: aflutter, afib, SVT, VT
- cx: heart failure
- tx: if stable, vagal maneuvers, adenosine, if unstable then cardioversion
- adenosine = decreases HR
- atropine = increases HR
141
atrial dysrhythmias
- atrial tissue acts as an ectopic pacemaker for 1-2 beats
- p waves don't all look the same
- premature atrial complexes (PACs)
- SVT (supraventricular tachy, atria issue)
- atrial flutter
- atrial fibrillation
142
atrial fibrillation
- common but rarely occurs in a healthy heart, c/b underlying heart disease, can develop acutely with thyrotoxicosis, alcohol intoxication, caffeine, stress, electrolyte imbalances, transient after cardiac surgery, aging
- ECG: atrial rate of 350-600 BPM, vent rate of 110-140, irregular QRS narrow
- S/S: 90% are asymptomatic, decreased CO, thrombi due to blood stasis, risk of stroke
- tx: treat like atrial flutter, warfarin for 3 weeks before if lasting > 48 hours, may have elective cardioversion, if unstable then needs urgent cardioversion
143
atrial flutter
- rarel occurs in health heart, increases risk of blood clots, stroke, common after heart surgery
- ECG: recurring, regular, sawtooth-shaped flutter waves, narrow QRS complex
- S/S: decreased CO, heart failure, increased risk of stroke
- Tx: coumadin, oxygen, digoxin, CCBs, BBs, cardioverson if unstable, radiofrequency catheter ablasion may be needed
- irregularly regular rhythm, more organized than Afib
144
supraventricular tachycardia (SVT) or Paroxysmal SVT (PSVT)
- abrupt onset and termination of tachycardia followed by a brief period of asystole
- ECG: 150-220 BPM, regular, P wave may be hidden, narrow QRS
- S/S: if prolonged can cause decreased CO
- Tx: vagal stimulation, IV adensoine, unstable then cardioversion, may need radiofrequency catheter ablation
145
dysrhythmias terminology
- premature complexes: caused by ectopic focus after there is one there is usually a pause between complexes, can cause skipping or palpitations which cause decreased CO
- couplets: paris of PVCs
- bigeminry: every other beat PVCs
- trigeminy: every third beat PVCs
- quadrigeminy: every fourth beat PVCs
146
permature ventricular contraction (PVC)
- caused by potassium imbalance, caffeiene, hypoxia, fever, stress, heart disease
- ECG: HR varies, irregular bizarre shaped QRS without a P wave before it, T wave large and opposite in direction to QRS
- S/S: asymptomatic or feel skipped beat, may cuase chest pain
- tx: usually dont have to treat untless becomes V tach
- 3 or more PVCs in a row = nonsustained Vtach
147
Bigeminy/Trigeminy
- bigeminy = every 2nd beat
| - trigeminy = every 3rd beat
148
ventricular dysrhythmias
- will lead to wide > .12 QRS complexes because the impulse originates and depolarizes first one veintricle then the other
- usually atrial rhythm remains regular
- Premature ventricular contraction
- ventricular tachy
- ventricular fibrillation
- ventricular standstill (asystole)
- pulseless electrical activity (PEA)
149
ventricular tachycardia
- ominous/threatening rhythm
- 3 or more PVCs
- sustained = > 30 seconds
- unsustained =
150
ventricular fibrillation
- associated with AMI, heart failure, cardiomyopathy, can happen during pacing or after fibrinloytics
- ECG: nothing measurable
- S/S: unresponsive, pulseless, apneic
- tx: rapid defibrillation, if no conversion give epi or vasopressin, then move to amiodarone
- the pt is clinically dead and will die unless the rhythm is quickly stopped
- pulseless = CPR, rapid defibrillation, followed by vasopressors (epi) and antidysrhythmics (eamiodarone)
151
terminology
-bradydysrhythmias:
152
atrioventricular (AV) blocks or heart block
- delay or interruption in impulse conduction between the atria and the ventricles
- affects the PR interval
- can be transietn or permanent
- SA node continue to function normally, but WRS complexes are delayed or blocked
- one of the primary causes of bradycardia
- 1st degree = all sinue impuilses reach the ventricles >.20 (not a problem)
- 2nd degree = some sinue impulses reach the ventricles (sometimes a problem)
- 3rd degree = no sinus impulses reach the ventricles (always a problem)
153
first degree AV heart block
- delay
- every impulse is conducted to the ventricles but the duration of the AV conduction is prolonged (PRI)
- ECG: everything is normal except for a prolonge (PRI)
- S/s: asymptomatic
- tx: none unless causative meds need to be changed, monitor for new changes in rhythm
154
2nd degree AV block type I
- gradual lengthening of the PRI until an atrial impulse is not conducted and a QRS is dropped
- ECG: atrial rate is normal but ventrical rate is slowed and irregular b/c of dropped QRS complexes, repeated cycles with progressive lengthening of the PRI, P wave, and WRS normal
- s/s: usually transient and well-tolerated, but can be a warning of more serious problems
- tx: if symptomatic give oxygen, atropine, may need a temporary pacemaker if asymptomatic closely ovserve with a transcutatnous pacemaker
- PR intervals get longer and longer until eventually QRS drops
155
2nd degree AV block type 2
- associate with rheymatic heart disease, CAD, MI
- long PR internval, stays the same length
- ECG: atrial rate is normal but ventricular rate is slowed and irregular b/c of dropped QRS complees, PRI is normal or prlonged but constant, P wave is normal, QRS is wide
156
3rd degree AV block, complete heart block
- no impulses from the atria are coducted to ventricles, atria contract independently, associated with severe heart diease and some systemic diseases
- ECG: atrial rate is normal but ventrical rate is slowed, regular, PRI is variable, more Ps than QRS
- s/s: decreased CO
- rtx: oxygen, atropine, pacemaker, drugs to increasrs HR and support BP
- p wave and QRS are going at regular rates but not at the right time
157
asystole
- no ventricular activity, LETHAL
- caused by hypoxia, high potassium, hypokalemia, hypothermia, acidosis, drug overdose
- ECG: occasional P waves
- s/s: unresponsive, pulseless, apneix
- tx: CPR, epi or vasopressin, temporary pacemakder, NO defibrillation
158
pulseless electrical activity
- electrical actibity is seen on the ECG, but the pt has no pulse
- must treat the cause (hypovolemia, hypoxia)
- tx: CPR, epi
```
Tensionpneumothorax
Emboli
Aacidosis/alkalosis
Cardiac tamponade
Hypo/hyper elextrolytes/volemia
MI
Drug overdose
```
159
prodysrhythmias
- sometimes antidysrhytmic drugs will cause life-threatning dysrhythmias
- more common with a pt with left vent dysfunction
- more common with digoxin and certain classes of antidysrhythmia drugs
- more common in the first few days of drug therapy
160
rhythms summary
IRREGULAR
- sinus arhythmia
- PACs, PVCs
- atrial fibrillation
- 2nd degree AV block, type 1 and 2
TACHYCARDIAS
- SVT
- VT
- Aflutter
- Afib
BRADYCARDIAS
-heart blocks
PULSELESSNESS
- VT
- VF
- PEA
- Asystole
161
ACLS meds summary
VF/PULSELESS VT
- shock
- epi/vasopressin
- shock
- amiodarone
- sometimes lidocaine or magnersium sulfate
PEA/ASYSTOLE
- CPR
- Epi
BRADY
- atropine
- TCP or epi
TACHY
- adensosine
- diltizem
- amiodarone
- mag sulfate
ACUTE CORONARY SYNDROME
- ASA
- nitro
- morphine
- heparin
- beta blockers
- fibrinolytics
