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%
Equal

of US adults 20 y.o. have HTN (SBP 140)

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

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

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)

Lower LDL and triglycerides and small rise HDL.

b)

Used for initial therapy.

c)

Serious adverse effects Liver damage & myopathy (monitor

liver enzymes (ALT, AST) and complaints of muscle aches)

2.

Niacin Increases HDL Flushing, pruritus

3.

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
B-blockers and for Prinzmetals angina

Patient teaching for

Response to chest pain
Stop
activity
and rest.
and
sublingual
NTG

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

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

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

ARTERIAL OCCLUSIVE
DISEASE

VENOUS 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

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