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CORONARY HEART

DISEASE

HNI 455

Impact of CVD in the US


2012 Update
Cardiovascular disease (CVD) caused 811,940
deaths in 2008 (more than one in three) and is the
single leading cause of death in America today
(more than cancer, trauma and chronic respiratory
disease combined).
More than 2200 Americans die from CVD each
day
1 death every 39 seconds
Coronary Heart Disease responsible for 405,309
of these deaths
CHD=coronary heart disease.
American Heart Association. Heart Disease and Stroke Statistics2012 Update .

Impact of CVD in the US


2012 Update
Hypertension (HTN)
33.5% of US adults 20 y.o. have HTN (SBP 140)
Equal in men and women
African Americans make up 44%
Smoking
21.2% men, 17.5% women smoke
19.5% students in grades 9-12 report smoking
Cholesterol
15% of Americans 20 y.o. have total cholesterol
240 mg/dL
CHD=coronary heart disease.
American Heart Association. Heart Disease and Stroke Statistics2012 Update .

Impact of CVD in the US


2012 Update
Obesity
33.7% of US Adults are obese (BMI 30 kg/m 2)
33% adults report no physical activity
31.7% children aged 2-19 are overweight or
obese
29.9% girls and 17% boys in grades 9-12
report not engaging in 60 mins of moderate
physical activity once a week

CHD=coronary heart disease.


American Heart Association. Heart Disease and Stroke Statistics2012 Update .

Impact of CVD in the US


2012 Update
Angina pectoris (chest pain or discomfort caused by
reduced blood supply to the heart
muscle) 9,000,000
Myocardial infarction
610,000 new
325,000 recurrent
Every 34 seconds
about one fourth of these will die in an emergency
department or before reaching a hospital.
*From 1998 to 2008 the death rate from coronary
heart disease decreased 30.6 percent
CHD=coronary heart disease.
American Heart Association. Heart Disease and Stroke Statistics2012 Update .

Cardiac Output
The amount of blood ejected from the
heart in one minute. (4-8 L/min)
CO=SV X HR
Stroke volume is the amount of blood
pumped with each contraction

Factors Affecting Cardiac


Output
Preload volume of blood in the LV at the
end of diastole. Starlings Law
Afterload The resistance against which
the LV must pump.
Contractility Refers to the intensity with
which the cardiac fibers contract.

Hemodynamic
monitoring
Special indwelling catheters that
provide information about blood volume
and perfusion, fluid status and how well
the heart is pumping.
Central

venous pressure (CVP)


Pulmonary artery catheters (PA)
Intra-arterial pressure (a-line)

Atherosclerotic
Progression

3 stages of atherosclerotic
plaque development
Fatty streaks earliest lesions age 15.
LDL lowering agents may reverse.
Fibrous plaque phase endothelial
damage cholesterol deposition in intima
Complicated lesion stage continuation of
inflammation leads to an unstable plaque
lesion. Rupture platelets thrombus!

Hemodynamic effects of
CAD
Disturbance in the delicate balance between
myocardial oxygen supply and demand
Vessels become stiff and lose ability to dilate
Decreased O2 is supplied to myocardium;
resulting in tissue hypoxia or ischemia

Review - Risk factors for


CAD
Age, gender, ethnicity
Family history and genetic
*Elevated serum lipids Mayo clinic- most people should
aim for an LDL below 130mg/dl
*Hypertension Normal is <120/80
*Tobacco
Physical inactivity 30 min on most days
Obesity
DM
Psychologic state Type A

Treatment of CAD
HEALTH PROMOTION** IDENTIFY
PEOPLE AT RISK EDUCATE!
HEALTHY PEOPLE BOX ON P. 766 AND
PT GUIDE ON P. 767
ASSESS WHEN READY TO LEARN!
GIVE CONTINUED SUPPORT TO
ENCOURAGE LIFE-LONG BEHAVIORS
NUTRITIONAL THERAPY BOX ON
PAGE 768

Drug therapy usually lifetime


1.
Statins (Lipitor - atorvastatin) block cholesterol
synthesis by blocking HMG-CoA reductase.
a)
b)
c)

2.
3.

Lower LDL and triglycerides and small rise HDL.


Used for initial therapy.
Serious adverse effects Liver damage & myopathy (monitor
liver enzymes (ALT, AST) and complaints of muscle aches)

Niacin Increases HDL Flushing, pruritus


Fibric acid derivatives (lopid Gemfibrozil)
accelerate elimination of VLDLs and increases
production of apoproteins A-I and A-II.
a)

Effect is increasing HDL and lowering triglycerides.

4.

5.

6.

Bile acid sequestering agents (cholestyramine


-Questran) bind cholesterol in intestine.
Cholesterol absorption inhibitor (ezetimibe
Zetia)
Aspirin low dose 81mg

3 Manifestations of CAD
Angina - symptoms when 70% occluded
Stable Angina
Unstable angina Acute coronary syndrome, preinfarction
angina
Silent ischemia

M.I.
Sudden cardiac death

Angina Pectoris pain in


the chest
Symptom of CAD; indicates myocardial ischemia
Oxygen demand exceeds supply
Precipitating factors:
Physical exertion
Temperature Extremes
Strong emotions
Eating heavy meal

Types of Angina
Stable angina (exertional angina) Lack of O2 is temporary
and reversible. Predictable, usually occurs with exertion.
Unstable angina Acute coronary syndrome or ACS more prolonged lack of O2, unpredictable and represents
an emergency, occurs during rest, sleep and increasing
frequency.
Variant Prinzmetalss angina coronary spasm
Atypical Women Fatigue, SOB, indigestion and anxiety.

Care of patient with


Chronic Stable Angina
Goal is to decrease O2 demand or increase O2
supply
Nitrates use short acting (sublingual) for treatment of
angina. Long acting (isosorbide mononitrate) to reduce
incidence. SE headache, complication orthostatic
hypotension.
B-blockers decrease contractility, HR, SVR and BP.
SE bradycardia, hypotension, wheezing, sexual
dysfunction, depression
Calcium channel blockers Used if pt cant tolerate Bblockers and for Prinzmetals angina

Patient teaching for


Response to chest pain
andand
sublingual
NTG
Stop activity
rest.
Place NTG under tongue and let dissolve. Should
feel tingling under tongue. Spray on tongue.
Can take up to 3 NTG tablets 5 min apart; then go
to ER/call 911.
Replace NTG after 6 months
Protect from light and heat sources.
Caution against quickly rising to a standing
position orthostatic hypotension
Side Effect pounding headache, flushing
May be taken prophylactically before activity

Acute Coronary
Syndrome
Because unstable angina and acute MI
are considered to be the same process
but different points along a continuum
The term Acute coronary syndrome
(ACS) is used.
Pain unrelieved by rest or nitroglycerin
and lasting for more than 15 min
differentiates MI from angina.

Manifestations of ACS
Chest pain that is new in onset, occurs at rest
or has a worsening pattern is called unstable
angina.
As the cells are deprived of O2, ischemia
develops, cellular injury occurs, and the lack
of O2 results in infarction or the death of cells.
Myocardial infarction (MI).
MI is associated with nausea, epigastric
distress, dyspnea, anxiety, diaphoresis

SLIDTA Assessment of
Angina
S 1-10 scale
L Where is the pain and where does it go? Substernal
radiating to neck and jaw, left shoulder and down both
arms, epigastric radiating to neck, jaw and arms.
I What initiated and relieved? Argument, exercise, resting
and what relieved? Sitting down, NTG
D How long? Have you had pain like this before?
T What does it feel like? Pressure, dull, aching, tight,
squeezing, heaviness
A Other symptoms? diaphoresis, nausea, vomiting,
anxiety, feeling of doom. Women?

Pathophysiology
Ischemia occurs within 20 minutes;
necrosis occurs within 6 hours.
Time is muscle!!
1.

2.
3.

Zone of ischemia inverted T waves; ST


depression
Zone of injury (ST elevations)
Zone of infarction Q waves

Myocardial Infarction
Chest pain unrelieved by rest and NTG
Deficiency of coronary artery blood supply
resulting in NECROSIS of myocardial tissue
25 % die before reaching hospital
Eighty to 90% of all acute MIs are secondary to
thrombus formation Interventions (emergent
PCIs or fibrinolytic therapy) have greatly reduced
mortality rates.

Anatomical Location of
MI
Inferior wall RCA; also perfuses SA node
and conduction system look for
conduction disturbances
Lateral wall left circumflex -LCX
Anterior wall - LAD; large portion of LV;
look for problems with mechanical pumping
ability of heart

Assessment and
Diagnostic Findings of MI
History
Presenting symptoms:
Pain unrelieved by rest and NTG (described as
severe and immobilizing, heaviness, pressure,
tightness, burning, constriction or crushing.)
Associated symptoms - diaphoresis, nausea,
vomiting
12 lead EKG changes (Q waves, ST elevation or
depression)

Assessment and
Diagnostic Findings of MI
Serum cardiac markers: These tests are based on the
release of cellular contents in the circulation when
myocardial cells die.
Troponin I (marker of choice) norm <0.1mg/ml (rises
4-6 hr, peak 10-24, normalizes 10-14 days)
CK MB (rises 6 hr, peak 18 hr, normalizes 24-36)
Physical Exam can be normal

ED-CCU or telemetry unit


nursing care- ACS
Assess subjective complaints, pain scale
Establish IV
12 lead ECG and continuous ECG monitoring
O2 2 to 4 L/min
IV Nitroglycerin (Tridil), Morphine Sulfate, beta blockers,
aspirin, ACE are first line.
Frequent VS and pulse oximetry - q1-2hrs
Maintain patent venous access and monitor I & O
Stool softeners
Initially bedrest for 12-24 hours then activity progression
Initially the pt is NPO

Collaborative care- ACS


Goals:

limit infarct size


Prevent and manage complications
Preserve myocardial function

Gold standard Evaluate for indications for reperfusion


therapy - Percutaneous coronary intervention (PCI stents and angioplasty) and Fibrinolytic therapy.
PCI should be performed less than 90 minutes from
the arrival time in the ED. Door-to balloon time

Care of the patient with


acute coronary syndrome
Anxiety related to perceived or actual threat of death,
pain and possible lifestyle changes.
Nursing interventions
Observe for verbal and nonverbal signs of anxiety.
Use a calm reassuring approach so as not to increase a
patients anxiety.
Assess need for further emotional support (relaxation
techniques, individualized visiting, spiritual support)
Encourage verbalization of feelings and concerns
Provide factual information concerning diagnosis so as to
decrease fear of the unknown.

Complications of MI
Arrhythmias
Acute LV failure (HF)
Cardiogenic shock

Cardiac Rehabilitation for


the patient after an MI
Goal restoration of person to an optimal state of
function: physiologic/psychologic/spiritual/economic and
vocational.
Topics S&S of angina/MI, and reasons they occur.
Anxiety, use of SL NTG (and other meds), lifestyle
changes, includes diet (low in sodium and sat fats),
sexual matters, exercise program.
1.
2.
3.
4.

CCU
Stepdown unit
Home rehab most patients in our area
Community rehab program

Geriatric considerations
Older adults often do not feel the intense
crushing pain.
Arteries are less elastic, less distensible. Systolic
HTN
CO decreases by 1% per year after age 70
Antianginal agents that cause postural
hypotension and decrease preload may not be
tolerated.
More complications. After MI > afib.
However, they do have well established
collaterals

ANEURYSMS and
VASCULAR DISEASE
HNI 455
Professor Patricia Voelpel
Revised 2014

THORACIC ANEURYSM
Secondary to atherosclerosis
Men ages 40-70
Most common site for dissection
Pain is prominent symptom
Dyspnea, cough, hoarseness, and
dysphagia
Surgically repaired

ABDOMINAL AORTIC
ANEURYSM (A.K.A. AAA)
Secondary to atherosclerosis
More common in Caucasians
Men >60 yoa
Complain they can feel their heart
beating in their abdomen
80 % are palpable with bruit over mass
Surgically repaired

ARTERIAL OCCLUSIVE
DISEASE

Arterial vs Venous
Disease
Arterial

Venous

Pulses

Weak, thready

Bounding

Color

Pale, mottled

Red

Temperature

Cool

Warm

Optimal Positioning

Dependent

Elevated

DIAGNOSTICS
Doppler studies
Angiography
Thrombolytics
Exercise testing

DEEP VEIN
THROMBOSIS
Symptoms are edema, swelling of the
extremity because outflow of blood is
obstructed, can be warm and tender
Management