Cardiac functions

Automaticity – ability to initiate electrical stimulus independently

Excitability – ability to respond to electrical stimulation
Conductivity – ability to transmit electrical stimulus from the cell in the heart
Contractility – ability to stretch as a single unit and recoil
Rhythmicity – ability to repeat the cycle with regularity

Myocardial blood supply

• the LEFT CORONARY ARTERY branches out into the LEFT ANTERIOR
DESCENDING (LAD) ARTERY and the CIRCUMFLEX ARTERY
o LAD artery supplies the anterior wall of the ventricle, the anterior
ventricular septum, and the bundle branches
o The circumflex artery provides blood to the lateral and posterior portions
of the left ventricle

• The RIGHT CORONARY ARTERY (RCA) fills the groove between the atria
and ventricles and gives rise to the RIGHT MARGINAL ARTERY ending as
the POSTERIOR DESCENDING ARTERY
o The RCA sends blood to the sinus and atrioventricular nodes to the right
atrium
o The posterior descending artery supplies the posterior and inferior wall
of the left ventricle and the posterior portion of the right ventricle

• Coronary arteries receive blood primarily during ventricular relaxation

(diastole)
• Blood is pumped out to the systemic circulation during contraction of the
ventricles (systole)

Electrical Conduction

• the heart contains specialized muscle fibers that generate and conduct their
own electrical impulses spontaneously
• the SINOATRIAL (SA) NODE< INTERNODAL TRACTS,
ATRIVENTRICULAR (AV) NODE, BUNDLE OF HIS, RIGHT and LEFT
BUNDLE BRANCHES, and PURKINJE FIBERS make up the system that
conducts electrical impulses and coordinates chamber contractions
• impulses follow a RIGHT-TO-LEFT, TOP-TO-BOTTOM path
• a normal electrical impulse is initiated at the SA NOPDE, the heart’s intrinsic
pacemaker

Cardiac Function

CO – total amount of blood ejected per minute

SV – amount of blood ejected with each beat
Coronary artery disease
• narrowing / obstruction in the coronary circulation resulting to ↓↓ tissue
perfusion

atherosclerosis
• accumulation of lipid-containing plaque in the coronary arteries
• leads to ↓↓perfusion to myocardial tissue thus inadequate myocardial O2 supply
• can cause angina, dysrhythmias, myocardial infarction, heart failure and death

RISK FACTORS
• family Hx of coronary heart disease * high blood cholesterol
• increasing age * cigarette smoking/tobacco use
• gender * HPN
• race * diabetes mellitus
• high blood cholesterol * physical inactivity
* obesity

- symptoms occur when the coronary artery is occluded to the point that
inadequate blood supply to the muscle occurs, causing ischemia
- coronary artery narrowing is significant if the lumen diameter of the LCA is
reduced at least 50%, or if any major branch is reduced at least 75%
- the goal of the treatment is to alter the atherosclerotic progression

lipid/atheroma formation or accumulation in arterial wall

↓↓
immune system activation
↓↓
inflammatory response
↓↓
chemotaxis (macrophages, lymphocytes)
engulf fat deposits and then die
↓↓
proliferation of smooth muscle forming fibrous cap over dead fatty core
↓↓
atheroma / plaque formation
↓↓
narrowing of the artery
↓↓
obstruction
↓↓
(rupture of the atheroma)
↓↓
(thrombus formation)
↓↓
(Myocardial Infarction)
CLINICAL MANIFESTATION

a. chest pain
b. palpitation
c. dyspnea/ SOB
d. syncope
e. nausea
f. excessive fatigue
g. cough or hemoptysis

PREVENTION
A. controlling cholesterol abnormalities
LDL > 160mg/dl (with no risk)
>130 mg/dl (with 2 or more risk factors)
> 100mg/dl (with CAD)

HDL normal value > 40 mg/dl

Ideal value > 60mg/dl

TGA >200mg/dl (abnormally high)

B. diet modification
Soluble dietary fibers
Fresh fruits
Cereal gains
Vegetables
Legumes
C. physical activity
Regular, moderate activity = 30min, 3-4x per week
Activity adjusted to an intensity that does not preclude their ability to talk
Hot and humid weather, exercise is best early in the morning/ indoors
Stop activity when: +chest pain
Unusual SOB
+dizziness
Lightheadedness
Nausea
D. medications
Control cholesterol levels
1. HMG-CoA
Lovastatin, Atorvastatin, Pravastatin, Simvastatin
2. Nicotinic Acid
3. Fibrinic Acid/ fibrates
Clofibrate, Fenofibrate
4. Bile acid sequestrants/resins
Cholestyramine

E. manage/ prevention of other risk factors

Therapeutic Regimen
1. Percutaneous Transluminal Coronary Angioplasty (PTCA)
Coronary arteries are dilated with balloon-tipped catheter

2. Coronary stents
Insertion of meshwork in the narrowed artery

3. Coronary Artery Bypass Graft (CABG)

Occluded coronary arteries are bypassed with the client’s own blood
vessel

4. Heart transplant

Angina pectoris

• chest pain resulting from myocardial ischemia caused by inadequate myocardial

blood and oxygen supply
• caused by imbalance between O2 supply and demand
• goal of treatment:
to provide relief of an acute attack
correct the imbalance between myocardial oxygen supply and demand,
prevent the progression of the disease and further attacks to reduce the
risk of MI

• pathophysiology

obstruction of the coronary blood flow

risk factors –
atherosclerosis, coronary artery spasm, ↑↑ myocardial O2 demand

↓↓

↓↓ blood perfusion

↓↓ O2 supply/ ↑↑O2 demand

↓↓
Ischemia

↓↓
pain

**precipitating factors: physical exertion, exposure to cold, eating a heavy meal,

stress/emotion – provoking situation

Patterns of Angina
 1. stable angina/ exertional angina
- occurs with activities that involve exertional or emotional stress, and is relieved
with rest or nitroglycerin
- has stable pattern on onset, duration, severity, and relieving factors

2. unstable / preinfarction/ crescendo angina

- occurs with unpredictable degree of exertion or emotion and increases in
occurrence, duration and severity over time
- pain may not be relieved with nitroglycerine

3. variant / prinzmetal/ Vasospastic angina

- results from coronary artery spasm and may occur at rest
- attacks may be associated with ST segment elevation on ECG

4. intractable angina
- chronic, incapacitating that is unresponsive to interventions

5. silent ischemia
- objective evidence of ischemia ( ECG changes with stress test) but patient
reports no symptoms

ASSESSMENT
1. pain
a. can develop slowly or quietly
b. usually describes as mild or moderate pain
c. substernal, crushing, squeezing pain
d. may radiate to he shoulders, arms, jaw, neckm back
e. usually lasts less than 5 minutes but may last up to 15-21 minutes
f. relieved by nitroglycerine or rest
2. dyspnea
3. pallor
4. sweating
5. palpitations and tachycardia (apprehension; feeling of impending death)
6. dizziness and faintness
7. hypertension
8. digestive disturbances

DIAGNOSTIC STUDIES

1. ECG: ST depression or elevation/ T wave inversion

2. stress test: chest pain or changes in ECG
3. cardiac catherization: provides definitive diagnosis by providing information about
the patency of coronary arteries
pre-procedure: obtain consent
assess for allergies to seafoods, iodine and radiopaque dyes
withhold meals before the procedure
 document baseline VS
have the client void
administer sedatives as ordered
mark distal pulses
inform the client that a warm or flushing feeling sensation
may be felt as the contrast medium is injected; fluttery
feeling as the catheter passes through the heart
post-procedure
monitor VS and cardiac rhythm for dysrhythmias
assess for chest pain
monitor peripheral pulses, color, warmth and sensation distal
to the insertion sites
monitor for bleeding and hematoma
extremity is extended for 4-6 hours post procedure
strict bed rest for 6-12 hours
encourage fluids
monitor for signs of hypersensitivity

MEDICAL MANAGEMENT
Goal: decrease O2 demand and increase O2 supply

1. pharmacologic Therapy
a. Nitrates: Nitroglycerine
MOA: dilates coronary artery
Decrease preload and afterload
Routes: sublingual, topical (patch), IV
S/e: headache, hypotension

b. Beta-blockers: propranolol, metoprolol, atenolol

MOA: block B-adrenergic sympathetic stimulation
↓↓HR, BP , myocardial contractility = ↓↓↓ O2
demand
C/I : hypotension, bradycardia, AV block, HF
Asthma/ COPD

c. Ca- channel blockers: amlodipine, verapamil, diltiazem

MOA:
↓ conduction --- ↓↓ HR and muscle contraction = ↓↓↓ O2
demand
Relax blood vessels--↓↓BP, coronary vasodilation = ↓↓O2
demand

d. antiplatelet ad anticoagulant
MOA: Prevents platelet aggregation and formation of new blood clots
aspirin
 heparin (monitor for APTT: therapeutic level = 1.5 to 2x normal)
S/e: bleeding!!!!!!!!!!!
2. O2 therapy

NURSING INTERVENTION
A. treating angina
Stop all activities – rest in semi-fowler’s to decrease O2 requirement
Assess the pain
Measure VS, obtain 12-lead ECG
Administer NTG
O2 therapy at 2-3L/min

B. reduce anxiety
Provide information about illness, diagnostic procedures, treatment and
methods to prevent progression

C. Preventing pain
Identify level of activity and plan for rest periods

D. Provide Home and community based care

Lifestyle changes

Myocardial infarction

• occurs when myocardial tissue is abruptly and severely deprived of oxygen

• ischemia can lead to necrosis of myocardial tissue if blood flow is not restored
• infarction evolves over several hours
• obvious physical changes do not occur in the heart until 6 hours after the
infarction, when the infracted area appears blue and swollen

total blockage of coronary artery

↓↓
ischemia
↓↓
necrosis
↓↓
neutrophils invade the infracted area
↓↓
granulation of tissue,
scar development
↓↓
permanently changes due to scar formation
- changes in the size and shape of the entire myocardium

Location of MI

1. Left anterior descending (LAD) artery – anterior MI or septal MI or both

 2. circumflex artery – posterior wall MI or lateral wall MI
3. right coronary artery (RCA) – inferior wall MI
Risk Factors
1. atherosclerosis
2. CAD
3. smoking
4. hypertension
5. obesity
6. physical inactivity
7. impaired glucose tolerance
8. stress

Diagnostic studies

1. ECG
a. Ischemia = ST segment depression, T wave inversion
b. Infarction = ST segment elevation, followed by T wave inversion

Hypocalcemia – U wave, depressed ST segment, short T wave

Hyperkalemia – prolonged QRScomplex, elevated STsegment, peaked T wave
MI – ST segment elevation, inverted T wave, pathologic Q wave

2. Laboratory tests: Cardiac enzymes increase when myocardial cells die

Enzyme Onset Peak Return to normal

CPK-MB 3-6 h 12-18h 18h
Myoglobin 1-3h 4-12h 12h
Troponin I 3-4h 4-24h 1-3wk
LDH 12h 18h 10-14days

3. cardiac catheterization
- provides the most definitive source of diagnosis
- shows the presence of atherosclerotic lesions

R sided heart catheterization: medial cubital or brachial vein

L sided heart catheterization: brachial or femoral artery

Medical management
Goal: to minimize myocardial damage
To preserve myocardial function
To prevent complications

1. Emergent Percutaneous Transluminal Coronary Angoplasty

To open occluded coronary artery and promote reperfusion

2. Pharmacologic Therapy
a. Thrombolytics: dissolve and lyse thrombi
 Indications: chest pain > 20min unrelieved by NTG
ST segment elevation in at least 2 lead systems
< 24 hour from onset of pain

Nursing considerations:
Minimize skin puncture
Treat major bleeding by discontinuing thrombolytic therapy
and anticoagulants, apply pressure and notify
physician immediately
treat minor bleeding by applying direct pressure is accessible
and appropriate
Examples:
urokinase
streptokinase
tissue plasminogen activator

b. analgesics: Morphine sulfate

: decreases pain and anxiety
: promotes blood vessel dilatation, decreasing preload and heart
Workload
: relaxes bronchioles, increasing oxygenation
Nsg consideration:
Monitor BP, RR, and ECG

c. Angiotensin-Converting Enzyme (ACE) inhibitor

: prevent Heart failure
Nsg consideration:
WOF s/e of the medication (coughing)
Examples: captopril, enalapril, remipril, lisonopril

d. Nitrates : dilates arteries and veins, decreasing cardiac workload and thus
oxygen demand; increases coronary perfusion
: decreases vasospasm
Examples: NTG
S/E : headache, hypotension

e. Beta adrenergic blocking agents

: decrease myocardial oxygen consumption by blocking beta
adrenergic sympathetic response: ↓↓ HR, BP, contractility
C/I : patients with asthma and congestive heart failure
Examples: propranolol, metoprolol

f. Calcium Channel blockers :slows HR and relaxes blood vessel

: relieves vasospasm
: Diltiazem. Verapamil, Nifedipine, Amlodipine, Felodipine

g. Antiplatelets: Aspirin
 : prevents platelet aggregation

h. anticoagulant: Heparin
: prevents formations of new blood clots
: amount is based on APTT result

3. O2 administration
4. bed rest

Nursing Implementation

a. goal: reduce pain, discomfort

1. analgesic: Morphine SO4
2. humidified oxygen
3. position: semi-fowler

b. goal: maintain adequate circulation

1. monitor VS and UO, observe for signs of shock
2. monitor ECG for arrhythmia
3. give medications as ordered:
Antiarrhythmic drugs: lidocaine
Anticoagulants : heparin
Thrimbolytic: streptokinase
4. recognize HF: edema, cyanosis, dyspnea, cough, crackles
5. check lab data: serum enzymes, blood gases, electrolytes
6. check CVP: increases with HF

c. goal: decrease O2 demand and promote oxygenation

1. oxygen therapy
2. activity: bed rest and increase activity as ordered
3. position: semi-fowler
4. quite and comfortable environment

d. goal: maintain fluid and electrolyte, nutritional status

1. IV, CVP, VS, UO
2. lab data (esp electrolytes) within normal limits
3. monitor ECG changes
4. diet: progressive low calorie, low sodium, low fat diet

e. goal: health teaching

1. diagnosis and treatment regimen
2. medications: administration, importance, untoward effects
3. control risk factors
4. need for follow-up care for regulation of medications and evaluation of
risk factors

f. goal: provide emotional support

REVIEW

 Preload – degree of stretch of cardiac muscle fibers at the end of diastole:

Frank-Starling Law – the greater the stretch on the heart, the greater the
shortening
 Afterload – amount of resistance to ejection of blood from the ventricle

Nursing assessment for CARDIOVASCULAR DISORDERS

 Genetic disorders:
1. Familial hypercholesterolemia
2. Hypertrophic cardiomyopathy

 Chest pain or discomfort – angina pectoris, dysrhythmias, VHD

 Shortness of breath or dyspnea- cardiogenic shock, HF, VHD
 Peripheral Edema and weight gain – HF
 Palpitations
 Fatigue – early warning of HF, VHD
 Dizziness, syncope or changes in level of consciousness

 Chest pain should be taken seriously until cause is determined

 Substernal chest pain can result from a number of causes:
1. Pericarditis
2. Pulmonary disorder – pneumonia
3. Esophageal disorders – hiatal hernia, reflux esophagitis
4. Anxiety and panic disorders
5. Musculoskeletal disorders

 The severity or duration of chest pain or discomfort does not predict the
seriousness of its cause.
 Elderly people and patients with diabetes may not experience chest pain as a
typical symptom

Risk factors
Non-Modifiable risk factors
 Familial history of coronary artery disease (CAD)
 Increasing age
 Male gender
 Postmenopausal women – have 2-3x the CAD rates of premenopausal women
of same age
 Race – higher incidence in African American than Caucasians due to greater
risk of hypertension

Modifiable risk factors

LDL < 100 mg/dL; (CAD) < 70mg
 HDL > 40 mg/dL
TAG <150 mg/dL.
 Hyperlipidemia
 Hypertension
< 140/90; diabetic- < 130/80
 Cigarette smoking, exposure to tobacco smoke
 Diabetes mellitus
FBS < 110 mg/dL
HgA1C - <7%
 Obesity
BMI 18.5-24.9 kg/m2
waist circum male< 40 inches
female < 35 inches
 Physical inactivity – 30-60 min of moderate intensity activity

Physical assessment
 General appearance and cognition
 Inspection of the skin
 Blood pressure
 Pulse pressure- 30-40 mmHg
 Postural blood pressure changes
 Arterial pulses
 Jugular venous pulsations
 Heart inspection and palpation
 Chest percussion
 Cardiac auscultations S1- closure of mitral and tricuspid valve
S2- closure of aortic and pulmonic valves

 Inspection of the Extremities

1. Decreased capillary refill time ->3 secs
2. Vascular changes due to decreased arterial circulation
3. Hematoma – due to cardiac procedures
4. Peripheral edema
5. Clubbing of fingers
6. Lower extremity ulcers – arterial or venous insufficiency

 LUNGS:
1. Tachypnea- rapid, shallow breathing
2. Cheyne-Stokes respirations – rapid respiration alternating with apnea; seen in
severe left ventricular failure
3. Hemoptysis – pink frothy sputum indicates pulmonary edema
4. Cough – dry, hacking cough due to pulmonary congestion from HF
5. Crackles – HF and atelectasis
6. Wheezes – caused by interstitial pulmonary edema

 ABDOMEN:
1. Hepatojugular reflux – liver engorgement occurs bec of decreased venous
return due to RVF
 2. Bladder distention – urine output is an important indicator of cardiac function