Oxygen Needs Interference with O2 Transport
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Transcript Oxygen Needs Interference with O2 Transport
Oxygen Needs
Interference
with
O2 Transport
Case Study
Oxygen Needs
Interference with O2 Transport
Coronary Artery Disease
Complications
Dysrhythmias
Pulmonary Embolism
Hypertension
Complication
Congestive Heart Failure
Peripheral Vascular / Arterial Disease
Oxygen Needs
Interference with O2 Transport
Care
of Patients with:
Coronary Artery Disease
Risk Factors
Myocardial Infarction
Alterations in:
Rate & Rhythm (Cardiac Conduction)
Effect on Cardiac Output
Content Approach
Anatomy
& Physiology Review
Demographics/occurrence
Pathophysiology
Clinical Manifestation
Medical / Surgical Management
Nursing Process (APIE)
Assessment - Nursing Actions - Education
Anatomy & Physiology
Right
Heart
Left Heart
Systole
Valve Closure:
Diastole
Valve Closure:
Cardiac Circulation
Myocardium
Anterior
Posterior
Cardiac Cycle
1.
2.
3.
4.
5.
Passive Filling – preload
Atrial contraction – Aortic & Pulmonic
semilunar valves close – S2
Isovolumetric ventricular contraction – all
valves closed
Ejection – ventricular systole – Mitral &
Tricuspid valves close – S1 - afterload
Isovolumetric ventricular relaxation – all valves
closed
Cardiac Cycle Phases
Heart Sounds & Stethoscope
Placement
Coronary Arterial System
Physiology: Oxygen Supply
to the Cardiac Muscle during
the Cardiac Cycle
Coronary artery oxygen deficit
during ventricular contraction & ejection (systole)
Coronary artery filling
during ventricular filling (diastole)
What is the impact of heart rate on coronary
artery filling?
Oxygen Supply to the Cardiac
Muscle during the Cardiac Cycle
The actual time available for diastole shortens significantly as the
heart rate increase
% of a Minute
70%
50%
33%
Heart Rate
60
120
188
Results: Less time for ventricular filling & coronary artery filling +
as HR increases, increased oxygen is needed each minute to eject
the same volume of blood.
Stroke volume: volume ejected in one heart beat
Cardiac Output: volume ejected in one minute
Cardiac Output = Stroke Volume x Heart Rate
Factors
Determining Myocardial Oxygen
Needs
Decreased Oxygen Supply:
Noncardiac: Anemia, hypoxemia, pneumonia, asthma, COPD, low
blood volume
Cardiac: Arrhythmias/dysrhythmias, congestive heart failure (CHF),
coronary artery spasm, coronary artery thrombosis, valve disorders
Increased Oxygen Demand or Consumption:
Noncardiac: anxiety, cocaine use, hypertension, hyperthermia,
hyperthyroidism, physical exertion
Cardiac: aortic stenosis, arrhythmias, cardiomyopathy, hypertension,
tachycardia
CAD - Demographics
CAD - Demographics
Comparison of death by CV Disease
and Breast Cancer – by Women’s Age
400
300
Cardiovascular
Disease
Breast Cancer
200
100
0
35-54
55-74
>=75
Coronary Artery Disease (CAD)
Pathophysiology
ASHD, IHD, CVHD = CAD
AHA
1.1 mil Americans will have an MI in 2003
460,000 will die
About half of those deaths occur within 1 hour of the
start of symptoms and before the person reaches the
hospital.
Major cause: Atherosclerosis—focal deposit of
cholesterol & lipids
CAD – Risk Factors
Unmodifiable: Age, Gender, Ethnicity, Genetic
predisposition/family history
Modifiable Major: Dyslipidemia--Elevated serum
lipids*, hypertension*, cigarette smoking,
obesity—visceral/central obesity
Modifiable Contributing: Diabetes Mellitus*,
stressful lifestyle
* may have genetic predisposition
CAD – Risk Factors
Metabolic Syndrome:
–
–
–
–
–
–
Insulin Resistance
Hyperglycemia >110mg/dL
Hypertension - > 130/85
Increased triglycerides >110mg/dL
Decrease HDL <40 men; < 50 women
Central Obesity
men: waist > 40” women: waist > 35”
Risk Factors
One of the Major Modifiable
Physical Inactivity
Types of Plasma Lipoproteins
HDL –
Contain more protein and less lipid
Carry lipids away from arteries to liver for metabolism
This process prevents lipid accumulation within arterial walls
Higher levels are desirable
LDL –
Contain more lipids than any other lipoproteins
Affinity for arterial walls
Increased levels correlate closely with an increased
incidence of atherosclerosis
Lower levels are desirable
VLDL
Contain of triglycerides
Correlation with heart disease is uncertain
Plasma Lipoproteins
Atherosclerosis
Elevated serum lipids
Cholesterol > 200mg/dl
Triglyceride > 200mg/dl
HDL
< 35 mg/dl – major risk
45-59 mg/dl – average risk
> 60 mg/dl – negative risk
LDL
< 130 – desirable
130 – 159 mg/dl – borderline risk
> 160 mg/dl – high risk
Progressive Atherosclerosis
Drug Therapy for Dyslipidemia
Bile Acid Sequestrants (Questran) - Binds with bile salts
Niacin - Inhibits synthesis of VLDL & LDL
Fibric Acid Derivatives (Atromid)– Decrease VLDL
HMG CoA Reductase Inhibitors (Statins - Lipitor,
Pravachol, Zocor) – Block synthesis of cholesterol
Cholesterol Absorption Inhibitor (Zetia)– Inhibits
intestinal absorption of cholesterol
Natural Lipid Lowering Agents
Niacin - < LDL levels
Omega-3 fatty acids – fish/flaxseed oil <Triglycerides & > HDL levels
Milk thistle – Silymarin - > HDL levels
Fiber - < Cholesterol
Phytosterols - < Cholesterol
Soy - < Cholesterol absorption from GI tract
CoEnzyme Q10 – HMG CoA reductase inhibitors
– natural statins
Coronary Thrombogenesis
During an Acute Coronary
Syndrome
Angina
Clinical Manifestations
Angina – Chest Pain
Stable Angina Pectoris – intermittent, same pattern of onset,
duration, intensity of symptoms - 3-5 mins.
Silent Ischemia – 80% of patients with ischemia are asymptomatic
Prinzmetal’s Angina – variant – not precipitated by physical activity
– may be due to spasm
Nocturnal Angina – occurs at night but not necessarily during sleep
or in recumbent position
Angina Decubitis – recumbent position – relieved by standing
Unstable Angina – Unpredictable or may evolve from stable angina
– increasing frequency, duration, intensity
CAD
Clinical Manifestation – Diagnostics
History & Physical Examination
EKG / Echocardiogram / Stress Echocardiogram
Thallium Stress Test (perfusion scanning) cold spots where tissue is
inadequately perfused cardiac tissue
CAT scan- calcium score/CT coronary angiogram
MUGA (Multiple gated radioisotope scan) – left ventricular function
MRI of the heart
PET (Positron emission computed tomography) – evaluate coronary
artery patency
Normal Thallium Stress Test
Abnormal Thallium-Stress Test
CAD - Clinical Manifestation
Invasive Diagnostics
Cardiac Catheterization
Right sided:
Catheter through the femoral vein through the vena cava into
right atrium and right ventricle – pulmonary artery – wedge
pressure
Left sided:
Catheter through the femoral artery through the aorta into the
left atrium and left ventricle / openings of the coronary arteries
Coronary arteriography: Injected dye with video & x-rays
CAD - Clinical Manifestation
Invasive Diagnostics
Cardiac Catheterization
Potential Complications
Catheter looping/breaking, dysrhythmias, allergic
reaction to contrast medium, arterial thrombosis,
myocardial infarction, hemorrhage, infection.
Patient Preparation
Informed consent; allergies – shellfish/iodine;
NPO x 6 hrs; explanation “flushed/tingling”; supine
– absolutely still
Postprocedure Care
Right Heart Catherization
Left Heart Catheterization
Coronary Angiography
Coronary Blockage - LAD
Cardiac Catheterization
Post Procedure Care
Assess:
VS q15 mins. x 2 hrs; q30 min x 2 hrs
Monitor cardiac rate and rhythm
Check site for bleeding
Extremity: Peripheral pulse check, temperature, color, sensation, mobility
Assess for chest pain, dizziness, dyspnea
Nursing Action:
Straight at groin x 24 hours; pressure at site x 30 mins.
Maintain IV KVO for 2 hrs; IV capped x 2 hrs; then d/c
Encourage oral fluids
Patient/Family Education:
Rationale for all nursing actions
No squatting, sitting, lifting for 24 – 48 hours++
Report bleeding, swelling, discoloration, drainage
Change dressing after 24 hours – small dressing to bandaid
Clinical Manifestation
Myocardial Infarction
Lab Diagnostics
Cardiac Protein – Troponin T
More sensitive than CK
Elevates 3 hr – peak 24-48 hrs; normal 5-14 days
Cardiac Enzyme – Creatine kinase (CK-MB)
Released when cardiac cells die
Elevates 3 hrs – peak 12-24 hrs; normal 2-3 days
Cardiac Marker - Myoglobin
First to elevate
Lacks cardiac specificity
Normal range within 24 hours
Serum Cardiac Markers after MI
CAD – Angina Relationship
Coronary Artery Disease
/
\
Stable Angina Acute coronary syndrome
/
/
\
Unstable Angina > Myocardial Infarction
ST-elevated MI
Non-ST-elevated MI
CAD & Acute Coronary Syndrome
Heart With Muscle Damage and a
Blocked Artery
Myocardial Infarction
Myocardial Infarction
Acute Coronary Syndrome
Location correlates with coronary circulation
involved
Inferior Wall – Right coronary artery
Anterior Wall – Left anterior descending
Lateral, posterior or inferior – left circumflex
Healing Process
Within 24 hours – leukocytes & enzymes
Third day – collateral circulation developing
10-14 days – scar tissue is still weak
Vulnerable time – unstable state of healing + increased
activity
6 weeks – scar tissue replaces necrotic tissue
Normal myocardial tissue may compensate – ventricular
remodeling – can cause late congestive heart failure
Coronary Artery
Collateral Circulation
Angina
Medical Management
A
Aspirin / Antianginal therapy / ACE Inhibitor
B b-Adrenergic blocker / blood pressure
C
D Diet / Diabetes
E Education / Exercise
Cigarette smoking / Cholesterol
Angina- MI
Medical Management
B-Adrenergic Blockers – decreases rate, contractility,
afterload
Nitrates – peripheral vasodilation decreasing preload and
afterload / coronary artery vasodilation
Calcium Channel Blockers – Coronary & peripheral
vasodilation, decreases AV conduction and myocardial
contractility
Morphine – analgesic – reduces preload & myocardial
oxygen consumption
Angiotensin-Converting Enzyme Inhibitors – Vasotec /
Capoten - prevents Angiotensin I conversion to Angiotensin
II – HTN, CHF
Antiplatelet and Anticoagulant Agents in
unstable angina and NSTEMI
Oral anti-platelet agent
Aspirin Initially 300 mg p.o. then 75 - 150 mg daily
Clopidogrel (Plavix) Initial loading dose of 300 mg then 75 mg daily
• Increased bleeding risk
Heparins
Heparin Sodium: Bolus: 60 U/kg IV bolus to a maximum of 4,000 units
Drip: 12 units/kg/h infusion to a maximum of 1 000 units/h
• Monitor PTT: keep at 50 - 70 seconds
Low-molecular-weight heparin - Enoxaparin 1 mg/kg subcut q12 hr
Precautions: • Peptic ulceration • Aspirin allergy • GI bleeding
Antiplatelet Drugs
used in unstable angina and NSTEMI
Intravenous
– tirofiban (Aggrastat), eptifibatide (Integrilin)
New class, GP IIb/IIIa inhibitors
– Abciximab (ReoPro) 0.25 mg/kg IV bolus 10 - 60 min
before PCI, than 10 μg/min IV - Infusion for 12 h
Precautions:
• Thrombocytopenia • Bleeding disorder • Surgery < 6 weeks
• Abnormal bleed < 30 d • Active GI ulceration
• Puncture of a non-compressible • Prior stroke, organic CNS pathology
• Any systolic BP > 180 mmHg during the acute event
Thrombolytic Drugs
Drugs that break down, or lyse, preformed clots
Tissue plasminogen activator
– plasminogen-streptokinase activator complex
(APSAC)
– streptokinase (Streptase)
– alteplase (t-PA, Activase)
– reteplase (Retavase)
Angina - MI
Invasive Medical Management
Percutaneous Coronary Intervention –
PCTA – Percutaneous transluminal
coronary angioplasty
Balloon-tipped catheter passed through just beyond
the lesion – balloon inflated – atherosclerotic plaque
is compressed
Reduction in lesion size by >50% in 90% of patients
Used in conjunction with thrombin inhibitors
Angina- MI
Invasive Medical Management
Stent Placement – may be placed during PCTA
– expandable meshlike structures to maintain
vessel patency – placed over the angioplasty site
to hold the vessel open
* Stents are thrombogenic –
IV antiplatelet agents
ASA/Plavix
Atherectomy – plaque is shaved away from
the coronary artery wall
Limited to use in larger portions of vessels
Laser Angioplasty – “cool” laser – no heat
Coronary Artery Stent Placement
Coronary Atherectomy
Angina - MI
Invasive Medical Management
Complications
Abrupt closure of angioplasty site
Stent thrombosis / embolization
Hemorrhage / vascular damage
Coronary spasm, Acute MI
Need for emergent coronary artery bypass
graft (CABG)
Fibrinolytic Contraindications
Absolute Contraindications
Active internal bleeding, active inflammatory bowel
disease, active peptic ulcer disease, acute pericarditis,
GI/GU bleeding within 6 months, Hx of hemorrhage
CVA, Neurosurgical procedure within 2 months,
Pregnancy, Suspected aortic dissection, Uncontrolled
HTN, >180/110
Relative Contraindications
Bacterial endocarditis, chronic Coumadin Therapy,
Diabetic hemorrhagic retinopathy, Poorly controlled
HTN
Angina - MI
Surgical Management
Coronary Artery Bypass Graft
(CABG)
construction of new vessels between the aorta to
beyond the obstructed coronary artery
(or arteries)
Saphenous vein or internal mammary artery
Palliative treatment for CAD – not a cure
Postoperative care: Care of cardiac patient with chest
tubes / sternotomy; pain management; short
ventilator support; early ambulation; 4-5 day hospital
stay
Coronary Artery Bypass
Coronary Artery Bypass
Complications of MI
Arrhythmias – lethal PVC’s within 4 hours of onset of
chest pain
Congestive Heart Failure
Cardiogenic Shock – severe left ventricular failure –
intra-aortic balloon pump & vasoactive medications
Papillary Muscle Dysfunction – Mitral valve
regurgitation – treat dyspnea, pulmonary edema &
decreased CO
Ventricular Aneurysm Pericarditis – 1-3 days post MI;
pleural friction rub & fever
Dressler Syndrome – pericarditis with effusion & fever
1- 4 wks post MI; elevated WBC & Sed Rate. Tx-Steroids
Pulmonary Embolism
Acute Coronary Syndrome
Pair Share
Discomfort or a heavy feeling in the chest can signal a heart attack.
A. True
B. False
Women do not frequently experience heart attacks.
A. True
B. False
African-American women die of heart attacks at the same rate as white women.
A. True
B. False
Some people who are experiencing the symptoms of a heart attack may wait
hours or even days before seeking needed medical care.
A. True
B. False
Being treated within about an hour of the first symptoms can make a significant
difference.
A. True
B. False
Acute Coronary Syndrome
Pair Share
Many heart attack victims say their heart attack wasn’t what they’d expected.
A. True
B. False
A family member, such as a spouse, can persuade a loved one having a heart
attack to seek help immediately.
A. True
B. False
Calling 9-1-1 for chest pain alone would probably turn out to be a waste of the
emergency medical personnel’s time.
A. True
B. False
Most heart attacks occur in people over 65.
A. True
B. False
The major issue in delay is how long it takes for emergency medical personnel to
find the address and deliver the patient to the hospital.
A. True
B. False
Nursing Diagnoses
TOP 4
?????
Nursing Process
Nsg Dx: Acute Pain related to
Cardiac Ischemia
Assess: Chest pain—intensity, location,
duration, precipitating, alleviating factors;
Monitor cardiac rate & rhythm; effect of pain
medication; peripheral pulses; VS; Pulse
Oximetry
Nsg Action: Administer O2 NC; IV access;
position of comfort
Patient Education: Rationale for all
procedures; pain scale; instruct to report pain
Nsg Dx: Ineffective Tissue
Perfusion related to Myocardial
Injury
Assess: VS & Pulse Oximetry qh; continuous
cardiac monitoring; respiratory status if
Morphine IV is used; fluid balance – strict I&O
peripheral edema; heart & breath sounds
Nsg Action: Rest periods; Administer meds &
oxygen as ordered
Patient Education: Rationale for rest; energy
conservation
Nsg Dx: Anxiety related to
perceived or actual threat of death
Assess:
verbal & nonverbal queues
Nsg
Action: Calm, reassuring approach;
encourage verbalization of feelings, fears,
perceptions; family involvement;
Patient
Education: Relaxation
techniques; simple instructions
Nsg Dx: Ineffective therapeutic
regimen management related to
lack of knowledge
Assess: Current knowledge level & readiness to
learn; family dynamics
Nsg Action: Assist pt in identifying small
successes; Assist pt is identifying lifestyle that
needs to be changed; Community referrals—
smoking cessation, cardiac rehab, support
groups,
Patient Education: Lifestyle changes,
Medications—desired effect/side effects;
comprehensive discharge plan—continuity with
community cardiac rehabilitation
Nsg Dx: Activity Intolerance
related to fatigue & chest pain
Assess: Monitor patient’s response to
medications, activity tolerance as increased;
Cardiac rate, rhythm, respiratory effort
Nsg Action: Include family; advance activity as
tolerated; supplement oxygen as needed
Patient Education: Teach patient energy
conservation – activity/rest – activities that will
promote independence and decrease oxygen
consumption; Cardiac Rehab: exercise & sexual
activity
Patient Education: Exercise
Guidelines post MI
Type of Exercise – regular, rhythmic & repetitive –
using large muscle groups
Intensity – determined by patient’s HR – should not
exceed 20 beats per min > resting HR
Duration – Build to 20 -30 mins
Frequency -- 3-4x/week
Warm-up/Cool-down – 5 mins before and after
aerobic exercise. Exercise should not be stopped
abruptly
Cardiac Rehab – Metabolic
Equivalents of Energy Expenditure
Patient Education:
Sexual Activity post MI
Plan of resumption of sexual activity should correspond to activity prior to MI
Physical training improves physical response to coitus
Food & alcohol < prior to sexual activity
Familiar & relaxed surroundings; positions of comfort
Avoid hot or cold showers
Foreplay is desirable – gradual increase in heart rate prior to orgasm
Prophylactic use of nitrates decreases angina
Orogenital sex places no undue strain on the heart
Anal intercourse may cause undue cardiac stress – vasovagal response
Emotional & Behavioral Response
to Acute MI
Denial – Ignores symptoms; minimizes severity; ignores activity
restrictions
Anger – “Why did this happen to me?”
Anxiety & Fear – Fear of death & disability –apprehension,
tachycardia, restlessness, hypochondria, projection of feelings
Dependency – reliant on staff; hesitant to leave ICU or hospital
Depression – Mourning period; realizes seriousness of situation
Realistic Acceptance – Focuses on optimum rehabilitation; plans
changes compatible with cardiac function