Nursing Management for Patients with Cardiovascular Disorders

 Anatomy and physiology

The cardiovascular system delivers oxygenated blood to tissues and removes waste products.
Heart
 The heart is a hollow, muscular organ about the size of a closed fist, Located between the lungs in
the mediastinum, it’s about (12.5 cm) long and (9 cm) in diameter at its widest point. It weighs
between (250 to 285 g)
 The heart, controlled by the autonomic nervous system.
 The heart has four chambers, two atria and two ventricles separated by a cardiac septum, also the
heart has four valves.
The heart has two sets of valves:
 Atrioventricular (between atria and ventricles) — tricuspid valve on the heart’s right side and
mitral (bicuspid) valve on its left
 Semilunar — pulmonary valve (between the right ventricle and pulmonary artery) and aortic valve
(between the left ventricle and aorta).
• Coronary arteries originate from the aorta just above the aortic valve leaflets
• The coronary artery perfused during diastole.
Myocardial perfusion
With a normal heart rate of 60 to 80 bpm there is ample time during diastole for myocardial
perfusion. However, as heart rate increases, diastolic time is shortened, which may not allow adequate time
for myocardial perfusion. As a result, patients are at risk for myocardial ischemia (inadequate oxygen
supply)

Blood pathways
Blood moves to and from the heart through specific pathways.
Deoxygenated venous blood returns to the right atrium through three vessels:
Superior vena cava — returning blood from the upper body
Inferior vena cava — returning blood from the lower body
Coronary sinus — returning blood from the heart muscle
Blood in the right atrium empties into the right ventricle (diastole) and is then ejected through the
pulmonic valve into the pulmonary artery when the ventricle contracts (systole).
The blood then travels to the lungs to be oxygenated.
From the lungs, blood travels to the left atrium through the pulmonary veins. The left atrium empties the
blood into the left ventricle, which then pumps the blood through the aortic valve into the aorta and
throughout the body with each contraction.
Because the left ventricle pumps blood against a much higher pressure than the right ventricle, its wall is
three times thicker.
Normal Heart Sound
S1: the first heart sound produced by closure of the atrioventricular (mitral and tricuspid) valves
S2: the second heart sound produced by closure of the semilunar (aortic and pulmonic) valves
Abnormal Heart Sound
S3: an abnormal heart sound detected early in diastole as resistance is met to blood entering either
ventricle; most often due to volume overload associated with heart failure
S4: an abnormal heart sound detected late in diastole as resistance is met to blood entering either ventricle
during atrial contraction; most often caused by hypertrophy of the ventricle
Key terms
Contractility: ability of the cardiac muscle to shorten in response to an electrical impulse.
Depolarization: electrical activation of a cell caused by the influx of sodium into the cell while potassium
exits the cell.
Repolarization: return of the cell to resting state, caused by reentry of potassium into the cell while
sodium exits the cell.
Diastole: period of ventricular relaxation resulting in ventricular filling.
Systole: period of ventricular contraction resulting in ejection of blood from the ventricles into the
pulmonary artery and aorta.
Sinoatrial (SA) node: primary pacemaker of the heart, located in the right atrium.
Atrioventricular (AV) node: secondary pacemaker of the heart, located in the right atrial wall near the
tricuspid valve
Cardiac conduction system.
 The SA node has the highest inherent rate (60 to 100 impulses per minute), the AV node has the
second- highest inherent rate (40 to 60 impulses per minute), and the ventricular pacemaker sites
have the lowest inherent rate (30 to 40 impulses per minute).
 If the SA node malfunctions, the AV node generally takes over the pacemaker function of the heart
at its inherently lower rate.
 Impulses from the autonomic nervous system affect the SA node and alter its firing rate to meet the
body’s needs.
Sign & symptoms related to cardiovascular disorders
 Chest pain or discomfort
 Shortness of breath or dyspnea
 Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver or ascites
(HF)
 Palpitations (tachycardia)
 Vital fatigue, sometimes referred to as vital exhaustion (characterized by feeling unusually tired or
fatigued, irritable, and dejected)
 Dizziness, syncope, or changes in level of consciousness
 Change in vital signs (Blood Pressure, Pulse rate, Body temperature, Respiratory rate)
 Diagnostic Evaluation
 Cardiac Biomarker Analysis
Myocardial cells that become necrotic from prolonged ischemia or trauma release specific enzymes
(creatine kinase [CK]), CK isoenzymes (CK-MB), and proteins (myoglobin, and troponin) *
*myocardial protein; measurement is used to assess heart muscle injury.
Brain (B-Type) Natriuretic Peptide Brain (B-type) natriuretic peptide (BNP) is a neurohormone that
helps regulate BP and fluid volume. It is primarily secreted from the ventricles in response to increased
preload with resulting elevated ventricular pressure.
**Diagnostic, monitoring, and prognostic tool in the setting of HF
Lipid Profile
Cholesterol, triglycerides, and lipoproteins are measured to evaluate a person’s risk of developing
atherosclerotic disease, especially if there is a family history of premature heart disease, or to diagnose a
specific lipoprotein abnormality.
Cholesterol Levels
Cholesterol (normal level is less than 200 mg/dL) is a lipid required for hormone synthesis and cell
membrane formation.
Triglycerides
Triglycerides (normal range is 100 to 200 mg/dL), composed of free fatty acids and glycerol, are stored in
the adipose tissue and are a source of energy
** HDLs (normal range in men is 35 to 70 mg/dL; in women, 35 to 85 mg/dL) have a protective action.
** They transport cholesterol away from the tissue and cells of the arterial wall to the liver for excretion.
** The risk of CAD increases as the LDL more than HDL:
** LDLs (normal level is less than 160 mg/dL) are the primary transporters of cholesterol and triglycerides
into the cell.
** One harmful effect of LDL is the deposition of these substances in the walls of arterial vessels.
The lipoproteins are referred to as low-density lipoproteins (LDLs) and high-density lipoproteins (HDLs).
Chest X-Ray and Fluoroscopy
A chest x-ray is obtained to determine the size, contour, and position of the heart.
Echocardiography
• Is used routinely to diagnose valvular disease. Thickened valve leaflets, vegetations or growths on valve
leaflets, myocardial function, and chamber size can be determined, and pulmonary artery pressures can be
estimated.
Electrocardiography records the electrical impulses generated from the heart muscle and provides a
graphic illustration of the summation of these impulses and their sequence and magnitude.
 Exercise ECG (stress test)
Exercise ECG is a noninvasive test that helps the practitioner assess cardiovascular response to an
increased workload.
Cardiac catheterization:
 Invasive diagnostic procedure in which radiopaque arterial and venous catheters are introduced
into selected blood vessels of the right and left sides of the heart?
 Right Heart Catheterization
It involves the passage of a catheter from an antecubital or femoral vein into the right atrium, right
ventricle, pulmonary artery, and pulmonary arterioles.
 Left Heart Catheterization
Left heart catheterization is performed to evaluate the patency of the coronary arteries and the function of
the left ventricle and the mitral and aortic valves.

IHD (Ischemic heart disease)

Angina Pectoris
Myocardial Infraction (MI)
Angina Pectoris: Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of
pain or pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in a
decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical
exertion or emotional stress.
Type of angina
Clinical manifestation (angina)
 The pain is often felt deep in the chest behind the sternum (retrosternal area).
 Weakness or numbness in the arms, wrists, and hands.
 Shortness of breath.
 Pallor.
 Dizziness.
 Nausea and vomiting.
 Anxiety.

Myocardial Ischemia
Anaerobic metabolism: - Lactic acid irritates cardiac nerves
 Ischemia more than 20 minutes lead to acute myocardial infarction
Modifiable Risk Factors
 Nicotine use (ie, tobacco smoking or chewing)
 Diet (contributing to hyperlipidemia)
 Hypertension
 Diabetes mellitus
 Obesity
 Stress
Sedentary lifestyle (Physical inactivity)
 Hyperhomocysteinemia
Nonmodifiable Risk Factors
 Age
 Gender
 Familial predisposition/genetics
Acute Coronary Syndrome and Myocardial Infarction ACS is an emergent situation characterized by
an acute onset of myocardial ischemia that results in myocardial death (ie, MI) if definitive interventions
do not occur promptly. (Although the terms coronary occlusion, heart attack, and MI are used, the
preferred term is MI.)
Etiology:
• In unstable angina, there is reduced blood flow in a coronary artery, often due to rupture of an
atherosclerotic plaque, but the artery is not completely occluded.
• In an MI, an area of the myocardium is permanently destroyed, typically because plaque rupture and
subsequent thrombus formation result in complete occlusion of the artery.
Clinical Manifestations
• Chest pain that occurs suddenly and continues despite rest & medication
• Shortness of breath.
• Indigestion and nausea.
Anxiety.
Cool, pale, and moist skin.
Heart rate and respiratory rate may be faster than normal.
Heart failure
Heart failure is a syndrome that occurs when the heart can’t pump enough blood to meet the body’s
metabolic needs, resulting in intravascular and interstitial volume overload and poor tissue perfusion. HF
was often referred to as congestive heart failure (CHF) because many patients experience pulmonary or
peripheral congestion.
Etiology
 Cardiomyopathy.
 Hypertension.
 Valvular disorders.
 Diabetes mellitus.
  Coronary artery disease (Ischemia causes myocardial dysfunction)
 Several systemic conditions, including progressive renal failure.
Heart failure may be:
 Left ventricular (sided) or right ventricular (sided) failure • Acute or chronic failure
 Left-sided Heart Failure (Left Ventricular Failure):
 The left ventricle cannot effectively pump blood out of the ventricle into the aorta and the systemic
circulation to meet the needs of the body tissues for oxygen and nutrients.
 The increased left ventricular blood volume and pressure, which decreases blood flow from the left
atrium into the left ventricle during diastole.
 The left atrium blood volume and pressure increases that lead to the pulmonary congestion, forcing
fluid from the pulmonary capillaries into the pulmonary tissues and alveoli.

Manifestations of left-sided heart failure.

 Fatigue and activity intolerance.
 Dizziness and syncope also may result from decreased cardiac output.
 Pulmonary congestion causes dyspnea, shortness of breath, and a cough.
 Orthopnea (difficulty breathing while lying down).
 Cyanosis from impaired gas exchange.
 Inspiratory crackles and wheezes, on auscultation of the lungs.
 Right-sided Heart Failure (Right Ventricular Failure):
 Inability of the right ventricle to fill or pump (empty) sufficient blood to the pulmonary circulation
 Increased pressures in the pulmonary vasculature, or right ventricular muscle damage impair the right
ventricle’s ability to pump blood into the pulmonary circulation.
 The right ventricle and atrium become distended, and blood accumulates in the systemic venous system.
 Increased venous pressures cause abdominal organs to become congested and peripheral tissue edema to
develop.
 Because of the effects of gravity; edema develops in the feet and legs.
 Congestion of gastrointestinal tract vessels causes anorexia and nausea.
 Right upper quadrant pain may result from liver engorgement.
 Neck veins distend and become visible even when the patient is upright due to increased venous
pressure.

Acute Versus Chronic Failure

• Acute failure is the abrupt onset of a myocardial injury (such as a massive MI) resulting in suddenly
decreased cardiac function and signs of decreased cardiac output.
• Chronic failure is a progressive deterioration of the heart muscle due to cardiomyopathies, valvular
disease, or coronary heart disease (CHD).

Endocarditis
The heart’s wall is composed of three layers:
Epicardium includes the outer layer of the heart wall and the visceral layer of the serous pericardium.
Myocardium is the middle and largest portion of the heart wall. This layer of muscle tissue contracts with
each heartbeat.
Endocardium is the innermost layer of the heart wall. It contains endothelial tissue made up of small blood
vessels and bundles of smooth muscle.
Endocarditis: - inflammation of the endocardium, heart valves, or cardiac prosthesis, results from
bacterial or fungal invasion.
◊ It usually develops in people with prosthetic heart valves or structural cardiac defect (eg, valve
disorders), invasive catheters (e.g., a central venous catheter, or an indwelling urinary catheter), dental
procedures or, it is more common in older people.
Clinical Manifestations
1. Chills and Fever
2. Heart murmur
3. Cardiomegaly, heart failure, tachycardia.
4. Headache
5. Weakness
6. Valvular stenosis or regurgitation, myocardial damage
7. Embolic phenomena
8. Cough, dyspnea

 Hypertension
• Blood pressure is the force exerted by the blood against the walls of the blood vessels.
• How great the pressure is depending on the work being done by the heart and the resistance of the blood
vessels.
• Blood pressure of less than 120/80 mm Hg as normal, 120 to 129/80 to 89 mm Hg as prehypertension,
and 140/90 mm Hg or higher as hypertension
Potential Complications of hypertension
• Long-standing elevated blood pressure may result in increased stiffness of the vessel walls,
• Leading to vessel injury and a resulting inflammatory response within the intima.
• Inflammatory mediators then lead to the release of growth-promoting factors that cause vessel
hypertrophy and hyperresponsiveness.
• These changes result in acceleration and aggravation of atherosclerosis.
• Hypertension also increases the work of the left ventricle, which must pump harder to eject blood into the
arteries. Over time, the increased workload causes the heart to enlarge and thicken (ie, hypertrophy) and
may eventually lead to heart failure.

Many factors have been implicated as causes of hypertension:

• Increased sympathetic nervous system activity.
• Increased renal reabsorption of sodium, chloride, and water.
• Increased activity of the renin–angiotensin–aldosterone system.
• Decreased vasodilation of the arterioles related to dysfunction of the vascular endothelium
• Resistance to insulin action, which may be a common factor linking hypertension, type 2 diabetes
mellitus, obesity, and glucose intolerance
Nursing management of cardiovascular disease
Nursing Diagnoses:
•Activity intolerance and fatigue related to decreased cardiac output.
•Excess fluid volume related to the HF syndrome
•Anxiety related to breathlessness from inadequate oxygenation
•Ineffective Breathing Pattern related to heart failure
•Ineffective therapeutic regimen management related to lack of knowledge

Planning and Goals

•Major goals for the patient may include:
•Promoting activity and reducing fatigue,
•Relieving fluid overload symptoms and improve respiration,
•Decreasing anxiety or increasing the patient’s ability to manage anxiety,
•Teaching the patient about the self-care program.