Transcript ACS *Time Is Muscle

*
MCC NURSING
Diana Blum MSN
2
3
4
5
*S3= sounds like
kentucky (ventricular)
*S4= sounds like
tennesee (atrial)
*Rub= related to
inflammation high
pitched sweaky yet
muffled like sandpaper
*Gallop=when s3 and 4 *Murmur=vibrations
heard
from turbulent flow
aka bruit
*
6
* Arteries have 3 layers: tunica intima, tunica
media, and tunica adventitia (figure 32-1)
* Disease process that occurs over time
* Starts in infancy
* Risk factors: age gender diet sedentary life
smoking
* Atherosclerosis affects medium arteries that
feed heart brain and kidneys as well as aorta
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*
* 2 branches off Aorta: Supplies posterior & inferior
myocardium:
* 1. Right (Longest) coronary artery
*
*occlusion results in inferior MI
*
*
*
*
*
*
(30% of inferior MI’s include right ventricle)
*lower mortality than anterior MI
*more mild AV node dysrhymias
*
(first & second degree blocks)
SYMPTOMS OF INFERIOR MI:
- hypotension from a decrease in preload
available to the LV due to ↓’d RV emptying
*
8
*
*
*
left anterior descending artery(LAD)
= supplies anterior and bottom of Left vent
and front of the septum
* most involved with occlusions
* Blockage here results in anterior MI which has higher
mortality rate AND more serious dysrhythmias !!!!!
* may include 2nd & 3rd degree blocks
* diminished ejection fraction &
symptoms of heart failure !!!!!
* When > 40% of left vent. Is damaged
* mortality is extremely high
*
circumflex= supplies the left atrium & back of left
vent
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10
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*
* 1. Stable Angina:
*
- no or minimal myocardial injury
*
- collateral circulation develops
*
- pain begins with exertion or stress
*
- pain relieved with rest
*
- pain lasts less than 20 minutes
*
- relieved by NTG (may take SL up to
*
3 times every 5 minutes) If not relieved
*
after these 3 doses, pt may be infarcting
*
-ST segment depression with pain then
*
returns to normal with pain subsides
*
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* 2. Unstable Angina:
*
- pain resolves with NTG
*
- similar to stable angina BUT angina
*
occurs more freq with less exertion
*
- often begins at rest with increasing
*
severity
*
- normal cardiac enzymes
*
- ST depression with prolonged CP
13
* 3. variant (Prinzmetal) angina:
* - rare & associated with angina at rest
* - tend to be younger women (smokers)
*
& pain occurs in early am & with menstrual
* - ST elevation (reversible) but cardiac enzymes
norm
* - CAUSE: coronary artery spasm occurs
*
at stenosed area
* Treat: responds to NTG
*
long-term: calcium channel blockers
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* A. reflux or peptic ulcer disease
* B. chest wall pain (pain reproduced on palpation and
localized)
*
- occurs from bruised/ fx ribs
* C. esophageal problems
*
- achalasia, esophageal spasm
* D. pericarditis (will be  sed rate, low-grade
*
fever, viral cause (coxsackievirus)
* E. pneumonia
* F. Aortic dissection (CV EMERGENCY) watch
* for severe pain radiating to back
*
15
* Goal in treatment of Angina:
dilate vessels,  O2 availability, ↓ O2 demand
* HOW?
*
* Angina without MI} often relieved with rest and NTG
* Angina with MI } may be relieved with rest, NTG, 02, MS,
rescue angioplasty, etc.
* Think MONA
* Morphine
* Oxygen
* Nitroglycerin
* Aspirin
*
http://www.youtube.com/watch?v=4GlQmTlP2jE&feature=related
http://www.doctorsecrets.com/yourmedicine/heart-attack-cause-symptomstreatment.html
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*
* - actual necrosis of myocardial tissue
* - most cases, atherosclerotic heart disease
present
* other cases is from artery spasm
*-
IDENTIFICATION OF MI IS MOST IMPORTANT AS
WITHIN 6 hours there is irreversible damage!!!!
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*
* Common patterns:
* Ant/lat
* inf/post
* ant/septal
* 25% of MI are “silent” : presents without
* chest pain (esp in diabetics with neuropathy)
* Patient presents with heart failure, shock,
confusion, delirium (esp in elderly)
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*
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*
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* Depends on which vessel involved & region of the
heart muscle
* Ischemia of condux system, causes arrythmias
* If lg enough area, CHF develops
* Occlusion of Left descending artery: left heart
failure
* Occlusion of Right descending artery: Rt heart
failure
* Infarct of vent wall can result in rupture, heart
hemorrhage into pericardial sac leads to
“tamponade” can be quickly fatal
*
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*
* Symptoms
* ↓
* ECG within 10 minutes
* ↓
* ST elevated
* ↓
* ASA, Troponin, CPK-MB, Morphine, Heparin
* ↓
* Thrombolytic with 30 minutes if PCI not avail
* ↓
↓
* PCI in24 hours
if avail, within 90 min.
*
↓
↓
*
stent
angioplasty
*
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*
* Procedure done at the time of cardiac cath.
* Balloon angioplasty is accomplished to widen or
open specific coronary vessel-stent is inserted to
maintain patency of the vessel.
* pre-procedure Plavix given with follow up Plavix
http://preop.medselfed.com/asp/center.
asp?centerId=heart&partnerId=preop&id=
&cachedate=&emailId=&affId=&campId=&
hideNav=
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*
* No ST elevation
*
↓
* Draw Troponin I
*
↓
* If elevated
*
↓
* Cardiac cath vs
*
*
Medical Management
↓
Echo, Stress test
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*
* Continuous cardiac monitoring
* Oxygen
* IV line
* Hemodynamic monitoring (discuss in a bit)
* Bed rest
* Emotional support
* Need passive & active ROM to reduce risk of
* thromboembolism (immobility)
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*
* For low cardiac output:
*
- dobutamine +inotropic
*
-milrinone +inotropic
* For hypotension:
*
- dopamine ( or at low doses used to
*
improve renal perfusion)
* May need Intraaortic balloon pump
31
*http://people.brunel
.ac.uk/~emstawk/IAB
P.htm
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* Aortic or ventricular aneurysms
* Ventricular septal defects
* Aortic regurgitation
*
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* Begins as soon as MI stop
* Scar tissue dev. at necrotic area (takes 6-8 wks
* May see stages of grief in pt with MI
* - - we need to identify depression as mortality at 1
to 5 years with associated depression !!!!
* MUCH TEACHING NEEDED;
* - MODIFY RISK FACTORS, LIFESTYLE
CHANGES, WORK WITH BOTH FAMILY/PT
*
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*
* Papillary muscle rupture
* Ventricular aneurysm
* Ventricular rupture
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* Precautions with Nitrates and Viagra use:
*
- reports of sudden death, dramatic
*
drop in blood pressure, and further
*
compromising restricted coronary
*
arterial perfusion
*
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*
* Vasodilators to reduce preload/afterload
* - nitroglycern or nitroprusside
* ACE inhibitors:
* - reduce afterload
* Beta blockers:
* - reduce myocardial oxygen consumption
*
- decrease heart rate and BP
* Statins:
* - restrict development of artherosclerosis
* & also have anti-inflammatory effects
* Platelet inhibitors:
* - ASA
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Platelet activation
= treat with GP IIb/IIIa inhibitors
examples:
Abciximab (ReoPro):
0.25mg/kg IV bolus followed by
0.125ug/kg/min for 12 hours
(others: Integrilin, Aggrastat)
* What precaution should we
take with beta blockers ???
* Heart has Beta 1:
so Beta Blockers lower BP
*
slowing heart rate
* Lung has Beta 2: so Beta blockers constrict
*
bronchioles, making it harder to
*
breathe
* Propranolol blocks both types of beta receptors so
SHOULD NOT BE USED IN ASTHMATICS
* Metopolol CAN be used since it is specific for Beta 1 and
DOES NOT CONSTRICT BRONIOLES SO SAFE
WITH ASTHMATICS.
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*
* Streptokinase: depletes fibrinogen to predisposed to
systemic bleeding & allergic reaction possible with
second time use
* Alteplase (tPA, Activase): used most often
* Reteplase (rPA, Retavase) a synthetic, 2nd generation
that works more quickly & lower bleeding
*
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*
* Minimal arterial or venous sticks
* Use finger oximetry
* Avoid automated blood pressure cuffs (bruising
* Assess for signs of bleeding(hypotension, tachycardia,
reduced level of consciousness)
* Reperfusion arrhythmias common
*
- bradycardia and V-tach most common
* IF BLEEDING COMPLICATIONS:
*
-stop fibrinolytic agent, FFP &/or cryoprecipitate
to replenish fibrin & clotting factors, Aminocaproic acid
(Amicar)
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*
* Hx of intracranial hemorrhage
* Known structural cerebrovascular lesion
* Known intracranial tumor
* Ischemic stroke <3 months
* Severe uncontrolled hypertension
* Acute pancreatis
* Aortic dissection
* Hx of hemorrhagic stroke
* pregnancy
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* EKG: rate, rhythm, ischemia (T-inverted), injury
(ST segment elevation), arrhythmias, strain,
infarction (q wave)
* Echocardiogram: (TEE) sound wave test detects
size of chambers, valve integrity, flow, wall
motion, Cardiac Output
*
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Biomarkers:
* Troponin I will show elevation IN 3-48hrs of MI period and
normalizes after 1-2 weeks
<0..06 is negative
0.10-0.60 is intermediate and may indicate injury
>0.60 is positive evidence of MI
Myoglobin normal is 17-106ng/mL
* CPK-MB will show increase 2-12 hrs after MI and normalizes
12-18hr after infarct
BNP can be elevated 48 hrs after MI which indicates heart
failure
*
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*
* CBC: anemia
* CMP: screening K+, etc
* PT, INR
* PTT
* Lipid profile: looks at total cholesterol (good and
bad)
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*
* ABG: assess acid/base levels
* Pulse Oximetry: generally >92%
* Holter monitoring: 24+ hr of EKG + events
* Stress test: treadmill or pharmacological
* Cardiac Catheterization: invasive, NPO 6-8h, consent.
Visualizes chambers, valves, arteries, pressures, CO
* Heart-CT scan: assesses CAD
* Nuclear scans: assess heart muscle viability
* EPS: NPO, consent, IV, assess electrical activity
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*
* Low fat low cholesterol diet
* Prescribed exercise program 5-7 days a week
* Knows correct use of NTG for angina
* Management of DM, HTN
* Stop smoking
* Medications to reduce work load or dilate
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* 5-7 X week is goal to include stretches with
warm-up, progressive walking program, light
weights, stretches with cool down.
* Strengthens heart muscle, reduces BP, BS,
weight, stress, tension, appetite, LDLs.
* Increases HDLs, energy and self esteem and
improves immune system
*
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* Decreased cardiac output r/t Dysrhythmias
* Pain r/t lack of 02 to myocardium
* Anxiety r/t to feeling of doom, lack of
understanding of medical diagnosis
*
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* You are asked to evaluate a 55-year old Caucasian woman who presents to the
Emergency Department with the chief complaint of chest pain for several hours.
* She awoke with the discomfort at 4:00AM today, and it has been a "ten out of ten"
since then. The pain is substernal, radiates to her back, and is associated with
moderate-to-severe shortness of breath and nausea.
* No previous such episodes are reported, but the patient states there is a strong family
history of cardiac disease, and that she has smoked one-half pack of cigarettes daily
for the past thirty-five years.
* Other than that, she denies past medical or surgical conditions, takes only hormone
replacement therapy, and has no known drug allergies.
* Social history reveals that the patient is married, has three children, and works as an
accountant.
* On physical exam, the patient appears to be in mild discomfort due to chest pain, but
otherwise appears normal.
* Temperature is 97.7F, pulse is 110, blood pressure is 150/100, and respirations are 20.
* Head and neck, lung, heart, and abdominal exams are normal.
* An EKG is performed, which shows nonspecific T-wave changes in the lateral leads.
* Other tests, including troponin-I, cardiac enzymes, and chest x-ray have been
performed, but results are still pending.
* What are risk factors?
* What are you concerned with?
* What to do?
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*
* Coronary artery bypass graft- done after
confirmation with cardiac catheterization.
* Re-route blood vessels using mammary or
saphenous v from aorta around block in coronary
artery.
* Valve replacement or repair
* Septal repair and other congenital repairs
* CCU post op, chest tubes
* Pre-op teaching with post op expectations
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*
* 1. damage to blood (platelets, RBCs WBCs &
plasma proteins)
* 2. Incorporation of abnormal substances into
blood (bubbles, fibrin, platelet aggregates)
* 3. a systemic inflammatory response
* 4. increase in systemic vascular resistance
* 5. increase catecholamines
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* 1. fluid status (fluid leaks from vessels)
* 2. O2 sats (indicates excess capillary leaking)
* 3. postop bleeding from anticoagulation for
procedure
* 4. hemodynamic monitoring
* 5. pain relief
* 6. dysrhythmia control
* 7. warming pt may need vasopressors to
maintain BP initially (undesirable to let pt shiver
as  oxygen demands) (use warmed blankets,
warmed blood to infuse, warmed inspired gases)
*
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*
* 8. bleeding not to exceed 300 mL/hour in first
couple hours then 150-200 ml/hour but average
blood loss is 1 L.
* Notify physician if excessive.
* Autotransfusion of medialstinal blood is filtered
& infused
* 9. aggressive suctioning then enc coughing
* 10. monitor electrolytes to prevent dysrhthmias
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* 11. dysrhythmias treated pharmacologically
* 12. pacing wires placed on right atrium and
ventricle before surgical closure.
*
Postop BRADYCARDIA most common
indication for need of pacer.
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* Hemorrhage, cardiac tamponade, MI, ventricular
dysfunction, dysrhythmias, death
* Cardiac tamponade:
* - watch for pts that have bleeding in chest
tube (significant) then suddenly STOPS bleeding
& becomes hypotensive
*
- reopen & immed return to OR
*
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*
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* CAD, advancing age
* HTN is a major factor > CHF x 3
* DM, Smoking, Obesity
* Valvular incompetency, alcohol or other
chemicals, idiopathic,(unknown)
*
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* Inability of either ventricles to pump
effectively
* Both rt and lt failure
* Symptoms are a combo of both
*
* Mediated thru Sympathetic Nervous System: as
CO drops, baroreceptors alert brain>>>signals
adrenal glands to release
catecholamines{norepinephrine and
epinephrine}
* This causes stimulation Beta 1=>>HR
* Stimulation Beta 2= bronchodilation
* Activate Alpha receptors
peripherally=constriction=>>bp
*
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* CO drops initiating renin-angiotensin
mechanism
* Results in powerful vasoconstrictor angiotensin
II,>> aldosterone (hormone) which causes
kidneys to retain Na and H20 which increases
blood volume
*
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* The heart enlarges which results in strain
* The increase in volume causes the ventricles
to dilate
* Eventually remodeling will occur
*
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*
* H&P
* Chest x-ray: see size of heart and fluid in lungs
* EKG: strain, MI
* Echocardiogram: size of heart and CO
* CBC: anemia
* CMP: screening
* Thyroid function
* ABGs
* BNP=B type natriuretic peptide= hormone released in
response to Ventricular stretch ( CHF peptide)
* Nuclear studies to determine heart function, EF, tissue
viability
* Cardiac Cath to determine exact nature of heart
function
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* Directed at: Improving LV function
(Contractility) by decreasing intravascular
volume and decreasing vascular resistance
* Decreasing venous return (Preload)
* Decreasing BP (Afterload)
* Improving gas exchange and 02
* Increasing the CO and reducing anxiety
*
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*
* I & O q shift
* Daily am weights before breakfast and after voiding.
2-3# weight gain in 1-4 days call MD
* Sodium restricted diet
* Medications: to decrease intravascular volume thus
reducing venous return, dilate and reduce BP and
improve contractility
* surgery
* http://chfsolutions.com/zip_how_aquapheresis_work
s.html#
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Ultrafiltration Compared to Loop Diuretics
• Ultrafiltrate is isotonic with plasma, whereas the
diuresis of loop diuretics is virtually always hypotonic
to plasma
• Ultrafiltration removes more sodium than diuretic
therapy
• No electrolyte disturbances
• Ultrafiltration decreases ECF volume more than a
comparable volume of diuretic-induced fluid loss
Schrier. J Am Coll Cardiol. 2006;47:1-8.
*
* ACE inhibitors ( proven to ↓ mortality in CHF
* Beta blockers (proved to ↓ mortality)
* - begin once pt diuresis occurs)
* Diuretics (loop and K+ sparing)
* Spironolactone (proven to ↓ mortality in class IV
CHF)
* Digoxin may be used (doesn’t improve mortality in
CHF BUT improves symptoms, ↓ hosptialization
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*
* Food decreases absorption
* Give on an empty stomach
* Postural hypotension (monitor)
* Watch for hyperkalemia, angioedema,
PERSISTENT DRY COUGH
* NOT TO BE USED WITH PREGNANT WOMEN
AS IT IS FETOTOXIC !!!!
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*
* Prototype: LOSARTAN
* Similar actions to ACE inhibitor
* These meds are a substitute for pts who cannot tolerate
ACE inhibitors (those with severe cough or angioedema)
* - lowers BP
* - reduces morbidity & mortality assoc. with
*
hypertension
* Only need once a day dosing
* Adverse effects similar to ACE inhibitors but without the
cough
* Contraindicated with pregnancy
*
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*
* ABSOLUTE improved systolic functioning &
reverses cardiac remodeling
* Initially may have exacerbation of symptoms
* Decreases heart rate & inhibits release of renin
* Two drugs approved for heart failure:
* 1. Carvedilol (nonselective B-adrenoreceptor
antagonist that also blocks α adrenoreceptors
*
2. Metoprolol (selective B1 selective antagonist)
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*
* By dilating venous blood vessels, leads to decrease in
cardiac preload
* By dilating arterial vessels, leads to reduction of
systemic arteriolar resistance & decrease afterload
* NITRATES
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Diuretics
• The use of loop diuretics in ADHF patients with
dyspnea and shortness of breath is standard
therapy
• In patients with ADHF, diuretics
– May induce a natriuresis
– Decrease extracellular fluid (ECF) volume
– Provide symptomatic relief
Schrier. J Am Coll Cardiol. 2006;47:1-8.
*
Elevated Neurohormones Cause Diuretic
Resistance
Glomerulus
Norepinephrine
(and endothelin) decreases
renal blood flow and GFR
Proximal Tubule
Ang II increases sodium
reabsorption
Collecting Duct
Aldosterone increases
sodium reabsorption
Krämer et al. Am J Med. 1999;106:90.
* Decrease plasma vol.
* ↓
* which will decrease venous return (preload)
* ↓
* which decreases cardiac workload & Oxygen
demand
* ↓
* Which decreases afterload by reducing plasma
volume thus decreasing blood pressure
*
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* Since metabolized by the liver before excreted
in feces, the pt with hepatic disease may
require decreased dosing.
* HYPOKALEMIA PREDISPOSES THIS PATIENT TO
DIGOXIN TOXICITY.
* What can be used to detoxify the body from
dig?
*
DIGOXIN IMMUNE FAB (THIS BINDS AND
INACTIVATES THE DRUG)
*
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* ADVERSE EFFECTS:
* Cardiac: progressively more severe dysrhythmias,
eventually to complete heart block
* That is why is is so important to make sure K+ is
normal !!
* GI: anorexia, n/v
* CNS: headache, fatigue, confusion, blurred vision,
alterations of color perception, HALOS
*
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* Hypokalemia leads to serious arrhythmias
* - will see this most in pts on thiazide or loop
diuretics (prevented by using a potassium-sparing
diuretic OR supplement with potassium chloride )
* ALSO note that:
* Hypercalcemia AND hypomagnesemia ALSO
predispose to dig toxicity !!!!
*
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* Education re: heart failure
* Explanation of heart failure
* Expected S/S and when to call MD
* Self monitoring of daily weights
* Know medications and need to take them
* 2000mg sodium restricted diet
* Importance of low level daily exercise program
(energy conservation)
* Prognosis / advanced directives
*
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*
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* Diagnosis: CBC, Chest X-ray, C reactive
protein, EKG, Heart Cath, blood cultures
* Interventions: PREVENTION is key, PCN like
antibx, NSAIDS for joint pain, Cardiac meds,
Bedrest
* Educate pt and family about prophylactic
Antibx treatment
*
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*
*Inflammation of pericardial sac
*3 causes:
*Infectious
*Coxsackie Virus B
*Respiratory diseases
*Noninfectious
*Uremia
*AMI
*Surgery
*Autoimmune
*Rhuematoid
*Drug Reactions
*Connective Tissue Disorders
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*
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* Uncommon
* Frequently associated with pericarditis
* Usually viral in nature
* S/S: fatigue, malaise, achy joints, GI upset, flu like
symptoms
* Dx: WBC, chest x-ray, heart cath, echo, cardio
enzymes, etc
* Tx: immune therapy, antimicrobials, ACE,
Antidysrhythmics, anticoagulants, antianxiety
*
* Scarring causes permanent damage
93
* Infective endocarditis caused by gram+cocci
* A deformed or damaged valve is usual focus of
infection
* Dental procedures can cause bacteremia
* Diagnosis: cultures, transesophageal
echocardiography
*
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* Fever- (99-105)
* Chills and night sweats may accompany
* Malaise, fatigue and weight loss
* Appearance of petechiae in the mouth, conjunctiva
and legs
* Chest and abdominal pain indicating embolization
*
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* H&P and Lab tests
*
CBC with diff with leukocytosis, > sed rate,
blood cultures
* May have heart murmur
* Echocardiogram to visualize valves and
vegetation
* Chest x-ray: CHF
* Long term antibiotics, rest, limited activity,
prophylactic anticoagulants, valve
replacement after inflammation treated
*
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* Clients with known valvular disease need to be
treated with prophylactic antibiotics prior to
any invasive procedure including dental.
Immunosuppression and any source of
contamination places clients at risk
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*
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* (Also referred to as regurgitation)
* The inability of the valves to close completely.
* Allows the blood to backflow.
* i.e., After the L A has contracted some of the
blood will flow back into the L A
* Mitral valve is the most commonly affected
*
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* Often accompanies mitral stenosis as a result of
rheumatic fever.
* Valve leaflet become rigid and shorten, prevents
closure of valve.
* Hypertrophy of Left Atrium and Ventricle = L sided
heart failure occurs
* Murmur heard. F/U with echocardiogram
* Edema and shock appear quickly
* Afib is common
* TX: vasodilators, same as for stenosis
*
100
*
* Mitral valve leaflets become thickened and
fibrotic.
* Rheumatic heart disease is a common cause
* Affect women age 20-40
* S/S: dyspnea, afib, dry cough, palpitations, angina,
crackles, fatigue, CHF may develop
* TX if failure develops: Digoxin, Lasix, beta
blockers, and anti arrhythmics, lo Na diet, etc
* Will monitor with yearly echocardiogram
* Surgery if worsens
* Prophylactic antibiotics prior to invasive procedure
or dental work
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Cardiac insufficiency can be caused by many factors – by a
swelling of the heart muscle (1), an enlargement of the
hollow chambers in the heart (2), a heart attack (3) or a
blood clot (4).
102
* Occurs when valve cusps become fibrotic and calcify.
* Most commonly caused by aging and atherosclerosis.
* Occurs most predominantly in men
* Untreated will lead to Left sided CHF
* S/S: dyspnea is most common, syncope, angina
*
103
*
* Caused primarily by rheumatic fever
* May also be caused by chronic HTN
* Predominantly in men
* Hypertrophy of the Left ventricle and
eventually to left sided CHF
* Blood may eventually back up into the
pulmonary system and lead to Right Ventricle
failure
* S/S: palpatations, diastolic murmur is classic
sign
104
* Presents with increased ventricular pressures
* 3 common presentations of:
* 1. dilated (most common)
* 2. hypertrophic
* 3. constrictive
* Prognosis is POOR
* NO CURATIVE MEASURES AT THIS TIME
*Cardiomyopathies: heart
muscle disease
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*
* Dilated cardiomyopathy: dilation of cardiac chambers
*
redux of ventricular contractile funx
* Diagnosed: echocardiogram
* TREATMENT:
*
similar to CHF
*
- inotropic agents
*
-diuretics
*
- vasodilators (ACE inhibitors)
*
-beta blockers
* To prevent sudden cardiac death; implant cardioverterdefibrillator
* Need intra-aortic balloon to stabilize pt
* NEED HEART TRANSPLANT
*
107
* Inability of heart to relax during diastole
* Goal: reduce afterload (beta-blockers, diuretics)
* Causes: idiopathic, systemic hypertension, genetic
* -atrial & vent arrhythmias seen in ½ of these pts are
responsible for sudden death
* S/S:
* - dyspnea, angina, arrhythmias cardiac failure,
* very forceful apical impulse
* sudden death (most common in ages 10 to 35 and
occurs during strenuous exertion)
*
108
* - very noncompliant ventricular muscle
* -diminished LV cavity dimensions
* - ventricular volumes decreased
* CAUSES:
* - idiopathic
* - interstitial disease
* - radiation
* - drug toxicity
*
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*
110
* Monitoring of the blood flow and opressures
within the body
* Purposes:
* Aid in diagnosis
* Assist in guiding therapies
* Evaluating response to therapies
* Can be invasive or non invasive
* Consent is needed especially if invasive unless
in ICU when crashing
111
*
* Obtain IV NS 0.9% and transducer system
* Attach the transducer to the IV flush solution and
prime the tubing, removing air bubbles
* Replace all vented caps with non vented sterile
dead end caps
* Inflate pressure bag to 300mmHg
* Assist the patient into supine position with HOB <or
= to 45 degrees
* Measure and mark phlebostatic axis with marker
* Level air fluid interface with that axis
* Zero the system
* Set alarm limits
112
* Heparin influences the patency of the art lines
* Care should be taken so heparin induced
thrombocytopenia is not initiated
* Occurs 4-7 days after heparin exposure
* Client at risk for immune response
* Thrombosis risk increases
*
113
* Means placing transducer at same level as tip
of cath in the patient
* Use the phlebostatic axis (pg 562 osborn)
* *****important to use same
reference each
time is key****
* Positioning above the transducer lowers the
pressure reading
* Positioning below the transducer increases
pressure reading
* Both can lead to incorrect treatment and
fatality
114
*
115
* First make sure system is intact…no air bubbles, no
leaks, and tight connections
* Do Qshift and with each turn
* Zeroing calibrates the system to atmospheric
pressure.
* Procedure:
* Turn stopcock closest to pt to off position
* Remove cap
* Hit zeroing on monitor
* Wait for display to say zero
* Turn stopcock to neutral position
*
116
* Uses built in flush system (pigtail)
* Quickly pull and release
* Perform Q8-12 hours, after blood sampling, or
if accuracy is questioned
* Page 563 osborn
*
117
* Indwelling cath inserted by
*
doctor into artery to monitor
BP
* Allen test prior to is done to
assess circulation
* Systolic pressure is max left
ventricular systolic pressure
* The dicrotic notch represents
closure of aortic valve and
diastolic is pressure at rest
* Complications : hemorrhage,
emboli, spasm, infection
* NSG management: explain
reasons for, assess site
118
* Monitors central venous pressure and reflects
preload
* Right atrium
* Uses: sepsis,
* Obtain consent
* Trendelenburg or Supine position for placement
* DO NOT USE FOR IV infusion or monitoring until
xray placement confirmation
* Reflects BP in vena cava and rt atrium
* 2-6 mmHg is adequate range
* Assess site at least Qshift.
119
*
*
* Multiple lumen
* Can measure temp in pulmonary artery
* Balloon is inflated up to 1.5ml air
* Over inflation can rupture artery and balloon
* Hemoptysis is presenting sign
* Place pt with affected side down to prevent leaking into
unaffected side and call doctor immediately.
* Once inserted leave uninflated a pressure reading is
needed.
* Assess patient (electrolytes, coag., acid base)
* Set up per facility policy or like example earlier
* Complications: infection, air emboli, pneumothorax, artery
rupture, pulmonary infarction, arrythmias
120
122
* http://www.accd.edu/SAC/NURSING/math/de
fault.html
* 1. The physician orders dopamine (Intropin) 400 mg
in 250 mg D5W TRA 5 mcg/kg/min.
For the client who weighs 110 lbs, how many ml
/hr will the pump be set?
* A.
* B.
* C.
* D.
9.375 0r 9 cc/hr
1.6 cc/hr
9375 cc/hr
93.75 cc/hr
*
123
* 9.375 0r 9 cc/hr
* 1) Find concentration. 400 / 250 = 1.6 mg/ cc
= 1600 mcg/cc
* 2) Convert lbs to kg. 110 / 2.2 = 50
* 3) Use formula for rate: Dose (5) x kg (50) x 60
/ concentration (1600)
* 5 x 50 x 60 = 15,000
* 15, 000 / 1600 = 9.375
*
124
* 2. Nitroglycerin is infusing at 16 ml/hr. The
bag has 50 mg NTG in 250 ml D5W. How many
mcg/min is the client receiving?
* A. 5.33 mcg/min
* B. 53.3 mcg /min
* C. 32 mcg/min
* D. 18 mcg/min
125
* 53.3 mcg /min
* 1) Find concentration. 50 / 250 = 0.2 mg/cc =
200 mcg/cc
* 2) Use Dose formula: Rate (16) x
Concentration (200) = 3200 / 60 = 53.33
*
126
* 3. Sodium nitroprusside (Nipride) 50 mg / 250
ml of D5W is hanging. The physician orders
include titrating the Nipride to keep Mr.
Granger's systolic BP <140 mm Hg. The IV is
infusing at 20 ml / hr. Mr. Granger weighs 56
kg. What is the dosage (mcg / kg / min the
client is receiving?
* A. 3.6
* B. 1.2
* C. 2.4
* D. 0.8
127
* 1.2
*
128
* The Five Rights of Medication
Administration
*Right patient
*Right medication
*Right dose
*Right route
*Right time
129
* The Three Checks of Medication
Administration
1.
2.
3.
Read the label of the medication as it is
removed from the shelf, unit dose cart,
refrigerator, or dispensing system
Read the label of the medication when
comparing it with the MAR
Read the medication label again before
administering the medication to the patient
130
*
*
Infiltration
*
* 1. end-stage, ischemic, valvular, or congenital
heart disease with maximum med therapy, not
amendable to surgery
* 2. Class III –IV heart failure with max med
therapy
* 3. prognosis for 1 year survival <75%
* 4. age <65 years
* 5. psychologically stable, compliant
* 6. strong family support system
133
*
* 7. able to adhere to complex med regimen
* 8. absence of the following
*
- systemic disease or infection
*
- serious, irreversible impariment of hepatic,
renal, pulmonary functions
*
- recent CVA or neurologic defects
*
- peptic ulcer disease
*
- active substance abuse
*
- pulmonary vascular resistance >6 wood units
*
- psychological instability
*
- malignancy
* 9. relative contraindications:
*
- diabetes and advanced periph atherosclerosis
134
*