ACS by changcheng2

VIEWS: 27 PAGES: 178

									          ACS MSN
       Diana Blum
Metropolitan Community College




                                 1
Statistics
More than 71 million Americans have
 cardiovascular disease




                                      2
review




         3
4
5
What is cardiac output?
What is Stroke Volume?

What is normal HR?



Why are these important?




                           6
7
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




                                                 8
9
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




                                                     10
Exam
General      Palpations
appearance   Turgor
Mentation    Cap Refill
Color        Pulses
Neck Veins   Auscultation




                            11
Abnormal Heart tones
S3= sounds like   Rub= related to
kentucky          inflammation
(ventricular)     high pitched
S4= sounds like   sweaky yet
tennesee          muffled like
(atrial)          sandpaper
Gallop=when s3    Murmur=vibrati
and 4 heard       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




                                          13
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



                                                   14
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

                                                 16
17
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




                                                 18
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


                                                        19
20
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



                                                        22
Precautions with Nitrates and Viagra
  use:
      - reports of sudden death,
  dramatic
    drop in blood pressure, and further
    compromising restricted coronary
    arterial perfusion




                                          23
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


                                                 24
Angina S/S
- burning, squeezing “tight band”
- heaviness, pressure in lower sternum
- may radiate to neck, jaws, shoulders, arms,
   stomach
OTHER symptoms specific to African-
   American & women:
        -fatigue, SOB,indigestion, shoulder/
         back discomfort




                                                25
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



                                             26
              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/your-
         medicine/heart-attack-cause-symptoms-
         treatment.html



                                                            27
28
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




                                               30
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.




                                                            32
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


                                              33
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




                                                       34
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)




                                                35
Anterior STEMI




                 36
Anterior STEMI




                 37
38
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




                                                 39
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!!!!




                                              40
Non STEMI
No st segment elevation present
If enzymes are increased it means
   severe injury
Higher probability of death




                                    41
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




                                                42
 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




                                             43
 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




                                                44
    Diagnostic Tests Continued
CBC: anemia
CMP: screening K+, etc
PT, INR
PTT
Lipid profile: looks at total cholesterol
  (good and bad)




                                            45
46
 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




                                               47
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


                                                    48
 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



                                                     49
Angioplasty with Stent
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=&cac
         hedate=&emailId=&affId=&campId=&hideN
         av=



                                                     50
Stents
Holds open the coronary artery where
  narrowed
Drug eluding stent (DES) decreases /prevents
  endothelial overgrowth
Antiplatelet therapy needed (Plavix)




                                               51
52
NSTEMI and Unstable Angina
Assessment & Treatment
No ST elevation
     ↓
Draw Troponin I
     ↓
If elevated
     ↓
Cardiac cath vs   Medical
   Management
                       ↓
                  Echo, Stress test

                                      53
Medical treatment in MI
treatment output:
For low cardiac
    - dobutamine +inotropic
    -milrinone +inotropic
For hypotension:
     - dopamine ( or at low doses used to
          improve renal perfusion)
May need Intraaortic balloon pump




                                            54
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


                                                55
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.



                                              56
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




                                                       57
http://people.brunel.ac.uk/~ems
tawk/IABP.htm




                                  58
Contraindications for Balloon
Pump:
Aortic or ventricular aneurysms
Ventricular septal defects
Aortic regurgitation




                                  59
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


                                               60
 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



                                                 61
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)



                                                            62
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


                                          63
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)



                                              64
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

                                                   65
Lethal complications of MI that
can occur 5 to 10 days post MI:
Papillary muscle rupture
Ventricular aneurysm
Ventricular rupture




                                  66
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




                                         67
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




                                               68
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




                                    69
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




                                          70
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?




                               72
         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


                                             73
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)


                                                  76
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



                                                 77
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.




                                              78
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




                                                  79
Congestive Heart Failure




                           80
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

                            81
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)




                                          82
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



                                          83
84
S/S of Left Sided CHF (blood
backing up into pulmonary
structures)
Fatigue
Angina
Tachycardia
Cool extremities
Hacking cough
Crackles
Frothy sputum
Gallop



                               85
86
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




                                        87
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



                                           88
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                                      Na
     from the blood at the same rate                         P       H2O
     that fluid can be naturally recruited                   Na                      K
     from the tissue                                UF   K

                                                                       PR

                                                                 P



                                                         Na Vascular
                                                            Space
                                                     Vascular                   Na
                                                     Space
1. Lauer et al. Arch Intern Med. 1983;99:455-460.
2. Marenzi et al. J Am Coll Cardiol. 2001;38:4.
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 B-
   adrenoreceptor antagonist that also blocks α
   adrenoreceptors
    2. Metoprolol (selective B1 selective
   antagonist)

                                                   103
104
                    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 potassium-
  sparing 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
Art line




           157
 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.




                                                 158
  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




                                                           159
161
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




                                                 162
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




                                         163
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




                                            164
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




                                        165
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



                                            166
ANSWER
1.2




         167
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



                                          168
ANSWER
100 x 12 / 60 = 20 mcg/min




                             169
  The Five Rights of Medication
         Administration
Right patient
Right medication
Right dose
Right route
Right time

                                  170
      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




                                                171
•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?



                                              172
COMPLICATIONS OF IV




                      173
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



                                                  175
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


                                                             176
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




                                                 177
The End

								
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