Transcript ACS - Faculty Sites - Metropolitan Community College

ACS
Diana Blum MSN
Metropolitan Community College
1
Statistics
More than 71 million Americans have
cardiovascular disease
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review
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What is cardiac output?
What is Stroke Volume?
What is normal HR?
Why are these important?
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Factors affecting Stroke Volume
Preload: the amount of blood remaining in
the ventricles at the end of diastole or the
pressure generated at the end of diastole
Contractility: is the ability of the cardiac
muscle fibers to shorten and produce a
muscle contraction. (Inotropic, + or -)
Afterload: amount of pressure the Ventricle
must overcome to eject blood volume out
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Autonomic Nervous System
Built in control center of the body
Regulates functions not under conscious control
Blood vessels innervated by sympathetic system
Fight or flight
Nerve endings are adrenergic and
nuerotransmitter is norepinephrine
Increases HR and BP
Parasympathetic is responsible for rest and digest
Cholinergics are the nerve endings and
acetylcholine is the neurotransmitter
Decreases HR and BP
Parasympathetic and sympathetic innervates heart
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Exam
General
appearance
Mentation
Color
Neck Veins
Palpations
Turgor
Cap Refill
Pulses
Auscultation
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Abnormal Heart tones
S3= sounds like
kentucky
(ventricular)
S4= sounds like
tennesee
(atrial)
Gallop=when s3
and 4 heard
Rub= related to
inflammation
high pitched
sweaky yet
muffled like
sandpaper
Murmur=vibrati
ons from
turbulent flow
aka bruit
12
CAD
Arteries have 3 layers: tunica intima,
tunica media, and tunica adventitia
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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Arteriosclerosis: thickening and
calcification of artery
Atherosclerosis: component of
arteriosclerosis that causes reduced
myocardial blood flow
Plaque (cholesterol, lipid, cellular debris)
3 stages of plaque growth:
1:yellow lesion (fatty streak)in intimal layer
2:plaque matures creating a lipid core with
fibrous cap (white in appearance) and are
mostly in bifurcated arteries
3:well established fibrous cap/lipid core
possible rupture
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s/s of CAD
Angina which results from a lack of
0xygen to the heart muscle
4Es=exercise, eating,
emotion, exposure to cold
Weakness, diaphoresis, SOB
N/V
15
Coronary Arteries
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 ventricular
infarction)
*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
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2 branches off the right coronary artery:
a. Right marginal artery:
b. Posterior descending artery:
supplies blood to right atrium, right
ventricle, bottom portion of both ventricles
and back of septum
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2. Left coronary artery begins out of Left
side of ascending aorta and divides into the:
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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Types of Chest Pain:
the myocardial demand for oxygen exceeds the
ability of the coronary vasculature to supply it.
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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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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What can cause angina??
-reduced blood flow =
reduced Hgb, or smoking
-low oxygen content
- excessive O2 demand relative to perfusion
=hypertension, exercise, metabolic rate
-atherosclerosis
-valvular dysfunction
-hypotension
-coronary vasospasm
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Angina S/S
- burning, squeezing “tight band”
- heaviness, pressure in lower sternum
- may radiate to neck, jaws, shoulders, arms,
stomach
OTHER symptoms specific to AfricanAmerican & women:
-fatigue, SOB,indigestion, shoulder/
back discomfort
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Goal in treatment of Angina:
dilate vessels,  O2 availability, ↓
O2 demand
Nitroglycerin
Change lifestyle
IF INCREASING in freq & intensity may need
stress testing, cardiac cath
beta blockers
angioplasty or CABG to  risk of MI
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Angina or MI
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&feat
ure=related
http://www.doctorsecrets.com/yourmedicine/heart-attack-cause-symptomstreatment.html
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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
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Unstable Angina (continued)
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)
31
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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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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Other causes of CP:
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
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MI patterns (as more areas of heart
becomes damaged, the more dangerous the
MI becomes)
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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Anterior STEMI
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Anterior STEMI
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Myocardial Infarction
Pain doesn’t resolve with NTG
s/s: crushing, poorly localized substernal
pain, radiates to shoulder, arm, jaw,
diaphoretic, sense of impending doom,
N/V, tachycardia or bradycardia, dyspnea,
ST elevation, Q waves (occurs after 12 hours
Duration: > 30 minutes with no relief
Not relieved by rest & can even occur @ rest
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MI subdivided into STEMI or
NSTEMI
- 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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Non STEMI
No st segment elevation present
If enzymes are increased it means
severe injury
Higher probability of death
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STEMI
ST segment elevation on EKG
Severe anoxia
Cellular damage present (ex. Complete
blockage)
If blood flow not re-established in 20 min.
cell death occurs
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Diagnostic Tests
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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Diagnostic Tests Continued
Biomarkers:
Troponin I will show elevation 3-12 hrs 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 4 hrs after MI and
normalizes 72 hr after infarct
BNP can be elevated 48 hrs after MI which
indicates heart failure
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Diagnostic Tests Continued
CBC: anemia
CMP: screening K+, etc
PT, INR
PTT
Lipid profile: looks at total cholesterol
(good and bad)
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Diagnostic Tests Continued
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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Complications of MI
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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Treat STEMI Goal: reperfuse the heart
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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Angioplasty with Stent
Procedure done at the time of cardiac cath.
Balloon angioplasty is accomplished to
widen or open specific coronary vesselstent 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=&cac
hedate=&emailId=&affId=&campId=&hideN
av=
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Stents
Holds open the coronary artery where
narrowed
Drug eluding stent (DES) decreases /prevents
endothelial overgrowth
Antiplatelet therapy needed (Plavix)
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NSTEMI and Unstable Angina
Assessment & Treatment
No ST elevation
↓
Draw Troponin I
↓
If elevated
↓
Cardiac cath vs
Management
Medical
↓
Echo, Stress test
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Medical treatment in MI
treatment
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
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Intraaortic Balloon Pump
- reduces afterload of left ventricle AND
increases blood flow to coronary arteries
- used for cardiogenic shock or as cardiac
augmentation until surgery
- usually inserted into femoral artery
- placed in descending thoracic aorta
- is synchronized with pt’s own heart rate
- timed to inflate IMMEDIATELY after aortic
closure (or left ventricle would pump
against great resistance) this is during
ventricular diastole
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Intraaortic balloon pump
(continued)
- forces blood back into coronary arteries
Complications of IABP:
- circulation to leg to insertion site is
compromised
- EXTREMELY IMPORTANT TO MONITOR
AND DOCUMENT PULSES, TEMP,
APPEARANCE OF LEG BELOW INSERITON
SITE.
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Intraaortic balloon (continued)
Must be WEANED off pump;
- the ratio of heart contraction to inflation of
balloon is 1:1
so, then go to 2:1 , then 4:1 (one inflation
for every 4 contractions of hrt)
Some of the pumps, able to wean by
decreasing balloon volume
If balloon ruptures: reason for rapid dissolving
helium
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http://people.brunel.ac.uk/~ems
tawk/IABP.htm
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Contraindications for Balloon
Pump:
Aortic or ventricular aneurysms
Ventricular septal defects
Aortic regurgitation
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Medical support (MI continued)
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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Specifics on Fibrinolytic agents:
must be within 12 hour of
symptoms
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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Nursing Interventions if
fibrinolytic used:
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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Absolute Contraindications to
Thrombolytic Therapy:
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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Monitoring/interventions MI
(continued)
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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Recovery MI
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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Lethal complications of MI that
can occur 5 to 10 days post MI:
Papillary muscle rupture
Ventricular aneurysm
Ventricular rupture
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Treatments
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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Exercise
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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Principles of Exercise
Practice on regular basis
Know how to do own pulse
Strive for target heart rate
Stop if chest pain occurs
Complications: CHF & Dysrhythmias
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Nursing Diagnosis
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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Cardiac Surgery
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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CABG procedure overview:
Pt cooled to reduce O2 demand
Placed on cardiopulmonary bypass – which
diverts blood from heart but oxgenates &
removes CO2
New procedures include working on a beating
heart or the MIDCAB
74
Physiological consequences of
CABG:
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
75
Nursing interventions for CABG
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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Nursing interventions CABG
(continued)
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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Complications of CABG
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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Congestive Heart Failure
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DEFINITION:EF < 35% or
when the myocardium is
no longer able to pump
efficiently and fluid
accumulates in the lungs
and or selected areas of
the body as a result
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Causes of CHF
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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CHF (continued):
Right side failure: (blood backing up
causing congestion in body)
s/s due to blood pooling
JVD, dependent edema, hepatic
congestion, a-fib, fatigue, wt loss,
cyanosis
With a-fib be aware of  risk for
embolization
Echocardiogram: reveals ↓ CO
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S/S of Left Sided CHF (blood
backing up into pulmonary
structures)
Fatigue
Angina
Tachycardia
Cool extremities
Hacking cough
Crackles
Frothy sputum
Gallop
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System Compensation
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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Compensation
Causing S/S of CHF because:
Contractility decreases
Stroke volume and CO continue to
decrease
Afterload (pressure on the other side of
the aorta) increases
Preload ( pressure caused by increase
volume to heart creating an
exaggerated stretch in the muscle)
increases
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Renal Compensation
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
89
Ventricular Hypertrophy
The heart enlarges which results in
strain
The increase in volume causes the
ventricles to dilate
Eventually remodeling will occur
90
Diagnostic Tests
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
91
CHF Management
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
92
Treatment of CHF
Treat underlying cause
Rest and hi Fowlers to reduce work
load and improve ventilation
02 at 2-6 L/min with 02 sats >92% to
increase available 02 and prevent
hypoxemia
Freq VS and cardiac monitoring
93
94
Treatment continued
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_aquaphere
sis_works.html#
95
ULTRAFILTRATION allows for the
production of plasma water from
whole blood across a semipermeable
membrane in response to a
transmembrane pressure gradient
The ensuing fluid or ultrafiltrate is
isotonic to plasma
Ronco et al. Cardiology. 2001;96:155-168.
Fluid Removal by Ultrafiltration
Interstitial
Space (edema)
•
Ultrafiltration can remove fluid
from the blood at the same rate
that fluid can be naturally recruited
from the tissue
Na
P
H2O
Na
UF
K
K
PR
P
Na Vascular
Space
Vascular
Space
1. Lauer et al. Arch Intern Med. 1983;99:455-460.
2. Marenzi et al. J Am Coll Cardiol. 2001;38:4.
Na
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.
Educating the CHF Client
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
99
First line treatment for right side
failure:
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
100
101
102
Treatment with BETA BLOCKERS with heart
failure:
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 Badrenoreceptor antagonist that also blocks α
adrenoreceptors
2. Metoprolol (selective B1 selective
antagonist)
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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.
So what will diuretics really do for CHF?
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
107
When giving ACE inhibitors to
your patient, what should you
remember???
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 !!!!
108
When should Angiotensin-receptor
blockers be used:
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
109
Treatment with direct
vasodilators for heart failure:
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
110
Digoxin
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)
111
Digoxin (continued)
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
112
Dig Toxicity:
Hypokalemia leads to serious arrhythmias
- will see this most in pts on thiazide or loop
diuretics (prevented by using a potassiumsparing diuretic OR supplement with
potassium chloride )
ALSO note that:
Hypercalcemia AND hypomagnesemia
ALSO predispose to dig toxicity !!!!
113
Inflammatory Heart Diseases
114
Rheumatic Heart Disease
Complication of rheumatic fever
Long term damage and scarring of valves
Leading cause of death 100years ago
Occurs mostly in kids 5-15 yrs old
Develops from pharyngitis
Group A beta hemolytic streptococcus
Incubation period= 2-4 days
Valves swell and vegetation occurs on valves
S/S: 1-6wks after strep (murmur, fever,
malaise, HA, swollen tender joints, SOB,
increased WBC, CP, tachycardia, HF signs
115
Rheumatic Heart Disease
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
116
Pericarditis
Inflammation of pericardial sac
3 causes:
Infectious
Coxsackie Virus B
Respiratory diseases
Noninfectious
Uremia
AMI
Surgery
Autoimmune
Rhuematoid
Drug Reactions
Connective Tissue Disorders
117
S/S
Chest pain is hallmark
Friction rub
Effusion
Tamponade (see slides)
Most severe on inspiration, sharp,
stabbing, or dull and burning.
Pain is relieved by sitting up or leaning
forward
Dyspnea, chills and fever
118
Tamponade
119
Tamponade
Medical emergency
Acummulation of pus or blood in
pericardial sac
Pressure increases causing back up of
blood into the venous system
Decreases cardiac output
**key to finding** Beck’s Triad
Decreased bp, muffled heart tones, JVD
Weak pulses also occur
May lose Consciousness
120
Nursing interventions for
pericarditis:
ECG monitoring for dysryhthmias
Supplies ready for emergency
pericardioicentesis
Auscultate cardiac sounds
Meds for pain
Arterial blood gases or pulse ox
Emotional support and explanations
121
Myocarditis
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
122
Endocarditis
Inner layer: tends to affect the valves
(Mitral). Organisms (Bacterial or
fungal) present in blood stream and
collect (colonize) on the valves
Strep
Rheumatic heart disease
May be from IV drug use or invasive
procedures
123
Endocarditis
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
124
S/S
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
125
Treatment and Diagnostics
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
126
Endocarditis treatment:
High doses antimicrobials for extended periods
S. aureus & gram- bacilli most likely
pathogens
Vancomycin IV PLUS gentamicin or
tobramycin IV
For MRSA : Vancomycin
Usually improvement in 3 to 10 days
127
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
128
Valvular Disorders
129
Mitral Stenosis
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
130
Insufficiency
(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
131
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).
132
Mitral Insufficiency
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
133
Aortic Stenosis
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
134
Aortic Insufficiency
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
135
S/S and Treatment
Aortic murmur, tachycardia,
palpitations, CHF with fatigue, SOB,
Ascites
Monitored with echocardiogram
assessing L ventricular dilatation
Chest X-ray-enlargement of heart
May do cardiac cath
May need valve repair or replacement
136
Cardiomyopathies: heart muscle
disease
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
137
138
Dilated cardiomyopathy:
Causes
Idiopathic
Inflammatory
Autoimmune
Toxic (drugs, alcohol)
Hereditary
Ischemic
Metabolic (uremia, vit defic)
Endocrine (thyroid
139
Dilated cardiomyopathy (continued)
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
cardioverter-defibrillator
Need intra-aortic balloon to stabilize pt
NEED HEART TRANSPLANT
140
Hypertrophic cardiomyopathy:
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)
141
Hypertrophic (continued)
B-blockers
Calcium channel blockers
Diuretics
Echocardiogram is key
May need heart transplant
142
Restrictive cardiomyopathy
- very noncompliant ventricular muscle
-diminished LV cavity dimensions
- ventricular volumes decreased
CAUSES:
- idiopathic
- interstitial disease
- radiation
- drug toxicity
143
Restrictive treatment:
Diuretics, afterload reducers
Goal: to improve diastolic function
Eventually hypotension occurs
144
HEMODYNAMIC MONITORING
145
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
146
Components
Monitor
Flush system
Transducer
High pressure tubing
Catheter
147
Setup
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
148
System requires constant flow of sterile
solution in order to maintain patency
Saline bag placed in pressure bag
1-3 ml per hour is common
The transducer converts the pressure at
the tip into electrical signal
This signal is what is seen on monitor
149
Heparin vs No heparin
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
150
Leveling
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
151
positioning
152
Phlebostatic axis
153
Zero referencing
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
154
Square wave test
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
155
Art Line
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
156
CVP
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.
157
Pulmonary Artery Cath
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
158
160
CALCULATING CARDIAC IV DRIPS
http://www.accd.edu/SAC/NURSING/
math/default.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. 9.375 0r 9 cc/hr
B. 1.6 cc/hr
C. 9375 cc/hr
D. 93.75 cc/hr
161
ANSWER
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
162
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
163
ANSWER
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
164
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
165
ANSWER
1.2
166
4. Mr. Rouse is admitted to CCU for
chest pain. A nitroglycerine drip is
started at 12 ml/hr. The label
indicates 100 mcg/ml. How many
mcg/min of nitroglycerin is he
receiving?
A. 10 mcg/min
B. 18 mcg/min
C. 32 mcg/min
D. 20 mcg/min
167
ANSWER
100 x 12 / 60 = 20 mcg/min
168
The Five Rights of Medication
Administration
Right patient
Right medication
Right dose
Right route
Right time
169
The Three Checks of Medication
Administration
1. Read the label of the medication as it is
removed from the shelf, unit dose cart,
refrigerator, or dispensing system
2. Read the label of the medication when
comparing it with the MAR
3. Read the medication label again before
administering the medication to the
patient
170
•LOOK at the label for verification of the
medication name, dosage, route, and
expiration date
CHECK the medication itself, NOT just the
pharmacy label
Be overly cautious with regards to dose,
proper dilution, and administration rate
Watch decimal points
Be aware of the unit
Is the medication dispensed in mcg or
mg?
What is ordered in comparison?
•
•
•
•
•
•
171
COMPLICATIONS OF IV
172
Extravasation
Infiltration
Cardiac Transplant
Criteria
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
174
Cardiac transplant criteria
(continued)
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
175
Cardiac transplant (continued)
Success rate very good
- 1 year survival at 76% and thereafter
approx 4% mortality per year over
11 years
major reason for improving outcome over
years: immunosuppression
Transplanted heart has NO innervation from
the autonomic system, so pt feels no angina
pain
176
The End