Transcript Cardiac - Community College of Philadelphia

Cardiac
Community College of Philadelphia
Nursing 132 Spring 2007
Anatomy and Physiology Review
 Structures
 Chambers
 Valves
 Arteries
 Physiology
 Direction of flow
 Preload
 Afterload
Coronary Circulation
 Structure
 Epicardium
 Myocardium
 Endocardium
 Chambers
 Right and Left Atria
 Right and left Ventricles
 Valves
 Atrioventricular
 Tricuspid - Separates RA from RV
 Mitral - Separates LA from the LV
 Semilunar
 Pulmonic – Separates RV from the Pulmonary Arteries
 Aortic – Separates LV from the Aorta
Physiology
 Blood flow through the heart
 http://wwwmedlib.med.utah.edu/kw/pharm/hyper_heart1.h
tml
 Cardiac conduction
Automaticity
 Electrophysiology
 Nodes
 Pathway
 Automaticity
Cardiac conduction
Basic EKG Interpretation
 What is an EKG and what does it measure/record?
 PQRST
 Measuring boxes
 Horizontal measure time: small box 0.04 seconds
Large box 0.20 seconds
 Vertical voltage: small box 1mm or 0.1 mV
large box 5mm or 0.5 mV
P wave
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Atrial depolarization
Small, smooth, rounded
No taller than 2.5 mm
No wider than 0.11 sec
Q wave
 First downward deflection
 Should be less than 0.03 seconds in duration
and less than 25% of the R wave
 Indicates myocardial infarction
QRS Complex
 Represents ventricular depolarization
T wave
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Ventricular repolarization
Usually rounded
Should be same direction as QRS
Inverted T waves can be a sign of ischemia
Peaked T waves can be a sign of
hyperkalemia
U wave
 Small rounded wave not always present,
thought to be part of ventricular
repolarization
PQRST
Chronic Stable Angina
Angina (Stable Chronic)
 Most common sign of ischemic heart disease
 Myocardial oxygen demand is increased by
exercise, smoking, eating heavy foods, weather
extremes, emotional distress, etc…
 Atherosclerosis causes progressive fixed
narrowing of the arterial lumen
 Relieved by rest or pharmacological interventions
 Goal is to prolong survival, reduce disease
progression
Acute Coronary Syndrome
(ACS)
 Unstable Angina (UA)
 Non-ST Elevated Myocardial Infarction
(NSTEMI)
 ST Elevation Myocardial Infarction
(STEMI)
Penumbra
Unstable Angina (UA) / Non-ST Elevated
Myocardial Infarction (NSTEMI)
 Imbalance between myocardial oxygen
supply and demand
 UA occurs at rest without exertion
 Reduced myocardial perfusion
 Release of biochemical markers vs. no
release of biochemical markers
Evaluation and management
 Stratification
High risk
Intermediate
Low risk
Immediate Management
 History, PE, 12 – Lead EKG, initial cardiac
markers
 Assign to 1 of 4 categories
 Definite or Possible
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Cont. EKG monitoring
Cardiac markers
In facility observation
Repeat EKG and cardiac markers 6-12 hours
 EKG and cardiac markers normal follow up stress
test as outpatient acceptable
 Definite ACS admit to hospital – Chest pain unit if
available
 Hospital Care
 Nursing Management
 Minimize or eliminate ischemia
 Administer meds
 Educate
 Discharge teaching
ST Elevation Myocardial
Infarction (STEMI)
 MI occurs as a result of thrombotic occlusion of
one or more of the coronary arteries
 *******
 CP is most common symptom, severe, doesn’t go
away
 Diagnosis
 EKG
 Cardiac markers
 PE, History
 Ventricular Remodeling – Changes in the
size, shape, and thickness of the left
ventricle involving both the infarcted and
non-infarcted segments of the ventricle.
 Penumbra
 1.68 million unique discharges for ACS in
2001, 30% estimate to have STEMI
Management
 Pt contact with healthcare system
 Initiation of fibrinolytic therapy – < 30 minutes
 Balloon inflation for PCI - < 90 minutes
 Choice of treatment decided by EM
physician and resources of institution and
surrounding institutions
 Contraindications to fibrinolytics
 12 lead EKG completed and shown to
experienced emergency physician WITHIN
10 minutes
 Cardiac Markers
 Troponin
 CK-MB
 Myoglobin
 Lab results should not delay treatment
Cardiac Enzymes – Troponin,
Myoglobin, CK-MB, Total CK
What should be done?
 EKG
 Lab work
 Portable CXR
 Oxygen
 Nitroglycerin: 3 sublingual 0.04mg, IV if needed
**** Phosphodiesterase inhibitor ****
 Morphine Sulfate: 2 – 4mg IV
 ASA chewed
 Beta blocker if not contraindicated
 ACE orally within 24 hours of STEMI for anterior
infarct, pulm. congestion, LV EF < 40%
Patient Education Before Discharge
 Lifestyle changes
 Recognizing cardiac symptoms: calling 911
if symptoms not improving
 Family education about AED, CPR
 Lipid Management
 Weight Management
 Smoking cessation
Cont.
 Antiplatelet Therapy: ASA, Plavix
 ACE inhibitor if without contraindications
 Beta blockers: except low risk and
contraindications
 Hypertension Control
 Diabetes Management
 No Hormone therapy
Cont.
 Warfarin Therapy
 Physical activity: should be encouraged and
prescribed appropriately / Rehab
 Follow up care with medical provider
See flow chart
Questions????
Cardiac Catheterization
Percutaneous Coronary
Interventions (PCI)
 “Cardiac Catheterization”
 PTCA (Percutaneous Transluminal
Coronary Angioplasty / Angiography)
 PCI - Angioplasty, atherectomy,
intracoronary stenting
 Web site
 http://www.heartsite.com/html/cath_4.html
Who undergoes PCI?
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Stable CAD
Unstable angina
NSTEMI
STEMI
What is a stent?
 http://www.cnn.com/2007/HEALTH/03/23/
stents.vs.drugs.ap/index.html
Preprocedural Management
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What do you think?
Informed consent
Consent for CABG
Education
Hold Metformin (Glucophage), insulin
etc… NPO status
 Lab values - Which ones, and why??
Postprocedural Managment
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What do you think?
12-Lead EKG
Labs - Will CE be elevated?
Hydrate
Anticoagulation per institution
Sheath removal
Femstop
Manual pressure
Vascular closure devices
Angioseal
SANDBAG Study
 Nurse to patient ratio of 1:1.5 or less maintained
during sheath removal
 Sheaths removed within 4-6 hours
 Medicate for comfort, HOB can be 30 degrees
 Allowed to ambulate 8 hours after removal
 SANDBAGS ARE NOT EFFECTIVE TO
MINIMIZE BLEEDING AND CAUSE
DISCOMFOT
*****Evidence-Based Practice*******
Complications of PCI
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Abrupt Closure
Acute Stent Thrombosis < 1%
Vascular Spasm
NSTEMI
STEMI <1%
Coronary Vessel Perforation
Arrhythmias
Equipment Failure
Contrast-Related Complications
Cerebrovascular Complications
CABG Emergently
Groin Complications
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Hematoma
Retroperitoneal bleeding
Arterial thrombosis
Pseudoaneurysm
Arteriovenous fistula
Nursing Management / Diagnosis
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Anxiety
Risk of altered myocardial tissue perfusion
Risk of decreased cardiac output
Risk of altered cerebral tissue perfusion
Extracellular fluid volume deficit
Risk of extracellular fluid volume deficit:
hemorrhage
Take Home Points !
 PTCA / PCI: What do they stand for?
 Reasons for PCI: Evaluate and possibly
provide an intervention
 Stent, Atherectomy, Angioplasty
 Groin complications !!!
Chronic Heart Failure
Heart Failure (HF)
 Complex clinical syndrome
 HF is not a stand alone diagnosis - it has a
cause
 What are the causes of HF?
 What is HF?
 HF is a complex clinical syndrome that can result
from any structural or functional cardiac disorder
that impairs the ability of the ventricle to fill or
eject blood
 CAD is the underlying cause of HF in two thirds
of patients with LV systolic dysfunction
 2-Dimensional Echo is the single most useful
diagnostic tool in the evaluation of patients with
HF
 Systolic Dysfunction
 Diastolic Dysfunction
Important Concepts
 Myocardial Damage
 Questions
 Neurohormonal Effects
 Hemodynamic Defense Reaction
 Sympathetic response
 Inflammatory Reaction
 Hypertrophy or growth Reaction
 Remodeling
 Questions
 Left ventricular dysfunction begins with some injury to the
myocardium and is usually a progressive process, even in the
absence of a new identifiable insult to the myocardium. The
principal manifestation of such progression is a process known
as remodeling, which occurs in association with homeostatic
attempts to decrease wall stress through increases in wall
thickness. This ultimately results in a change in the geometry of
the left ventricle such that the chamber dilates, hypertrophies,
and becomes more spherical. The process of cardiac
remodeling generally precedes the development of symptoms,
occasionally by months or even years. The process of
remodeling continues after the appearance of symptoms and
may contribute importantly to worsening of symptoms despite
treatment.
Signs and Symptoms
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Elevated pulmonary venous pressures
Decreased cardiac output
Pulmonary congestion - Breath sounds?
Breathlessness
Weakness
Fatigue
Dizziness
Confusion
Hypotension
Death - HF sometimes develop sudden cardiac death
Signs and Symptoms
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Increased systemic venous pressure
Jugular venous distention
Hepatomegaly
Dependent peripheral edema
Ascites
Weight gain
ACC / AHA Guidelines for the
Evaluation and Management
of Chronic Heart Failure in
the Adult
 Nearly 5 million patients have HF
 Nearly 500,000 patients diagnosed with HF
for first time yearly
 12 - 15 million office visits
 6.5 million hospital days each year
4 Stages
Stage A:
Patients at high risk of developing HF because of
the presence of conditions that are strongly
associated with the development of HF. Such
patients have no identified structural or functional
abnormalities of the pericardium, myocardium, or
cardiac valves and have never shown signs or
symptoms of HF.
Stage A Examples
 Systemic hypertension, CAD, DM, hx of
cardiotoxic drug therapy or alcohol abuse,
personal history of rheumatic fever, family
history of cardiomyopathy
Stage A Therapy
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Treat HTN
Encourage smoking cessation
Treat lipid disorders
Encourage regular exercise
Discourage alcohol intake, illicit drug use
ACE inhibition in appropriate patients
(atherosclerotic vascular disease, DM,
HTN)
Stage B:
Patients who have developed structural
heart disease that is strongly associated with
the development of HF but who have never
shown signs or symptoms of HF.
Stage B Examples
 Left ventricular hypertrophy or fibrosis, left
ventricular dilatation or hypocontractility,
asymptomatic valvular heart disease,
previous myocardial infarction
Stage B Therapy
 All measures under Stage A
 ACE inhibitor in appropriate patients (recent or
remote MI history, regardless of ejection fraction
and patients with reduced ejection fraction
whether or not they have experienced a MI)
 Beta blocker in patients with recent MI
 Valve repair if needed
 Regular evaluation
Stage C:
Patients who have current or prior
symptoms of HF associated with underlying
structural heart disease.
Stage C Examples
 Dyspnea or fatigue due to left ventricular
systolic dysfunction; asymptomatic patients
who are undergoing treatment for prior
symptoms of HF.
Stage C Therapy
 All measure under A
 Drugs for routine use
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Diuretics
ACE inhibitors
Beta blockers
Digitalis
 Dietary salt restriction
Stage D:
Patients with advanced structural heart
disease and marked symptoms of HF at rest
despite maximal medical therapy and who
require specialized interventions.
Stage D Examples
 Patients who are frequently hospitalized for
HF or cannot be safely discharged from the
hospital; patients in the hospital awaiting
heart transplantation; patients at home
receiving continuous intravenous support
for symptom relief or being supported with
mechanical circulatory assist device;
patients in a hospice setting for the
management of HF.
Stage D Therapy
 All measures under A, B, and C
 Meticulous identification and control of fluid
retention
 Referral to a HF program
 Mechanical assist devices
 Heart transplant
 Continuous IV inotropic infusions for palliation
 Hospice care
New York Heart Association
Classification
 Class I:
No limitation of physical activity. Ordinary physical
activity does not cause undue fatigue, palpitation, or
dyspnea (shortness of breath).
 Class II:
Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in fatigue, palpitation, or
dyspnea.
 Class III:
Marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity causes fatigue,
palpitation, or dyspnea.
 Class IV:
Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency at
rest. If any physical activity is undertaken,
discomfort is increased.
Susan is a 63 yo, Caucasian women who
presented to the ED, c/o: N/V, fatigue,
shortness of breath, and heart burn. She has
a history of DM and HTN. Her VS were
stable and a 12 lead EKG showed the
following:
What is Susan experiencing?
What do you, as the nurse need to
do, remember, consider?
 What causes HF?
 What Stage is Susan?
 What medications should Susan receive
now and at discharge?
Ten years later Susan has noticed she can no
longer walk to the mailbox without getting
very short of breath, and feeling very
fatigued. She sleeps on 3-4 pillows, and has
significant leg swelling. Her Nurse told her
at her last appointment that her heart is,
“enlarged and not pumping enough blood”
 What Stage is Susan at now?
 What Class is Susan at now?
 What mediations should she be on and
why?
Five years later, Susan is in the ICU and is
rapidly deteriorating. Her family is present,
and they are deciding what, if anything
should be done next.
 What Stage is Susan in now?
 What Class is Susan in now?
 What are Susan’s options?
Nursing Management / Diagnosis
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Decreased cardiac output
Extracellular fluid volume excess
Knowledge deficit
Altered respiratory function:
 ineffective breathing patterns
 Ineffective airway clearance
 Impaired gas exchange
Cardiovascular Drugs
 See online contents
 Some test questions will come from the
online pharmacology content
 Know these drugs:
 ACEI, Beta blockers, Nitrates, Digoxin,
Diuretics, ASA, Heparin, Lovenox, Plavix,
Calcium Channel Blockers
Questions
How to study for the test?
 Use the power point slides to direct your studies then read in your text
 If something is not in your text study the power
point slides
 Review notes from class
 Review pharmacology on Webstudy - understand
how the pharmacology impacts the disease states,
Angina, ACS, HF