The Cardiovascular System

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 07/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3153 times


The Cardiovascular System


Physiologic Anatomy

1. Heart (Figures 3-1 and 3-2)

2. Cardiac wall structure

a. Pericardium: Fibrous sac surrounding the heart and containing small amounts (15 to 50 ml) of pericardial fluid. This lubricated space protects the heart from friction, allowing it to easily change volume and size during contractions. The pericardium also keeps heart muscle anchored within the mediastinum.

b. Epicardium: Outer surface of the heart (includes epicardial coronary arteries, autonomic nerves, adipose tissue, lymphatics)

c. Myocardium: Muscular, contractile portion of the heart. Muscle fibers wrap around the heart in multiple, interlacing layers.

d. Endocardium: Inner surface of the heart

e. Papillary muscles: Myocardial structures extending into the ventricular chambers and attaching to the chordae tendineae

f. Chordae tendineae: Strong tendinous attachments from the papillary muscles to the tricuspid and mitral valves; prevent prolapse of the valves into the atria during systole

3. Chambers of the heart

a. Atria: Thin-walled, low-pressure chambers

b. Ventricles: Major “pumps” of the heart

4. Cardiac valves

a. Atrioventricular (AV) valves

i. Location and structure: Situated between the atria and the ventricles (tricuspid valve on the right, mitral valve on the left)

ii. Function: These are one-way “check” valves that permit unidirectional blood flow from the atria to the ventricles during ventricular diastole and prevent retrograde flow during ventricular systole

b. Semilunar valves

i. Location and structure

ii. Function: Permit unidirectional blood flow from the outflow tract during ventricular systole and prevent retrograde blood flow during ventricular diastole

5. Coronary vasculature (Figure 3-3)

a. Arteries

i. Two main arteries branch off at the base of the aorta, supplying blood to the heart

ii. Right coronary artery (RCA)

iii. Left coronary artery (LCA)

(a) Left main coronary artery (LMCA): Branches into the left anterior descending and circumflex arteries

(b) Left anterior descending (LAD) artery

(c) Left circumflex (LCX) artery also branches from the LMCA

iv. Coronary collaterals: Potential vascular connections between the RCA and LCA exist

b. Cardiac veins

c. Coronary blood flow

6. Neurologic control of the heart

a. Autonomic nervous system: Influences contractility, depolarization-repolarization, and rate of conductivity

i. Sympathetic stimulation: Norepinephrine release is the main impetus of stimulation to the heart; its two effects include the following:

ii. Parasympathetic stimulation: Occurs via the tenth cranial (vagus) nerve. Acetylcholine release is the main parasympathetic impetus to cardiac effects.

iii. Ventricles have mainly sympathetic innervation and only sparse vagal innervation

iv. Parasympathetic influences normally predominate in the conducting system (SA node, AV node)

b. Chemoreceptors: Afferent receptors located in the carotid and aortic bodies. Sensitive to changes in partial pressure of oxygen, partial pressure of carbon dioxide, and pH, causing changes in heart rate and respiratory rate via stimulation of vasomotor center in the medulla.

c. Baroreceptors: Stretch receptors in the heart and blood vessels that respond to pressure and volume changes

7. Cardiac muscle microanatomy and contractile properties: See Box 3-1 for key elements

8. Anatomy of the cardiac conduction system (Figure 3-4)

a. SA node

b. Internodal atrial conduction

c. AV node

d. Bundle of His: Arises from the AV node and conducts the impulse to the bundle branch system. The bundle of His is close to the annulus of the tricuspid valve.

e. Bundle branch system: Pathways that arise from the bundle of His and branch at the top of the interventricular septum

f. Purkinje system

9. Electrophysiology

a. Electrophysiologic properties of cardiac muscle cells

b. Resting membrane potential (RMP): Electrical charge of cardiac muscle cell at rest. Cell ions consist primarily of sodium, potassium, and calcium.

c. Depolarization: Change in the electrical charge of a stimulated cell from negative to positive by the flow of ions across the cell membrane. Sodium moves into the cell, potassium moves out.

d. Repolarization: Recovery or recharging of a cell’s normal polarity. Sodium moves back out of the cell, potassium moves into the cell. The cell recovers its negative charge.

e. Threshold potential: The electric voltage level at which cardiac cells become activated and produce an action potential, which leads to muscular contraction

f. Stimulation of myocardial cells

g. Action potential: As cardiac cells reverse polarity, the electrical impulse generated during that event creates an energy stimulus that travels across the cell membrane—a high-speed, short-lived, self-reproducing current (heart only). This is represented on an action potential curve (Figure 3-5).

h. Cardiac pacemaker cells (SA and AV nodes) action potential

i. Refractoriness of heart muscle

10. Events in the cardiac cycle (Figure 3-6)

a. Ventricular systole: Contraction and emptying of the ventricles

i. QRS complex: Represents ventricular depolarization (an electrical event)

ii. First phase of ventricular contraction (systole) is called isovolumetric contraction. Pressure increases, but no blood is ejected until LV pressure exceeds aortic pressure (and opens the aortic valve).

iii. As pressure rises in the ventricles, the AV valves close, producing the first heart sound (S1, composed of mitral [M1] and tricuspid [T1] components)

iv. The “c” wave of the atrial pressure curve is produced when the AV valves are pushed backward toward the atria as ventricular pressure builds

v. When LV pressure exceeds the pressure in the aorta, the aortic valve opens (comparable events in the RV occur with the pulmonic valve)

vi. Blood is rapidly ejected into the aorta (systolic ejection)

vii. LV pressures decrease, falling below the pressure in the aorta, ventricular ejection stops, and the aortic valve closes. (Comparable events occur in the pulmonary artery, closing the pulmonic valve.)

viii. Closing of the aortic and pulmonic valves produces the second heart sound (S2, composed of aortic [A2] and pulmonic [P2] components)

ix. Aortic valve closure is represented by the dicrotic notch in the aortic pressure waveform

x. Repolarization of the ventricles occurs at this time and produces the T wave on the electrocardiogram (ECG)

xi. After the aortic valve closes, pressure in the LV falls rapidly (isovolumetric relaxation phase); no blood enters the ventricle

xii. LA “v” wave is produced by rapid filling of the atria during ventricular systole, against closed AV valves. This marks the end of systole.

b. Ventricular diastole: Filling phase of the ventricles

11. Variables affecting LV function and cardiac output (CO)

a. CO: Amount of blood ejected by the LV in 1 minute

b. Preload: The degree to which muscle fibers are lengthened (stretched) prior to contraction

c. Afterload: Initial resistance that must be overcome by the ventricles to develop force and contract, opening the semilunar valves and propelling blood into the systemic and pulmonary circulatory systems (systolic contraction)

i. Factors affecting afterload include arterial resistance (wall stress and thickness), aortic impedance, and blood viscosity

ii. Systemic vascular resistance (SVR) is used as a rough estimate of afterload

iii. To calculate SVR: Mean arterial pressure (MAP) minus central venous pressure (CVP); this number is divided by CO; the resulting value then is multiplied by 80 and converts into dynes/sec/cm−5 (1 dyne is the force that gives a mass of 1 g an acceleration of 1 cm/sec2):


iv. Normal SVR = 900 to 1400 dynes/sec/cm−5

v. Excessive afterload: Increases LV stroke work, decreases SV, increases myocardial oxygen demands, and may result in LV failure

vi. Increased afterload is seen in

vii. Decreased afterload is seen in

d. Contractility (inotropic state): Heart’s contractile strength

e. Heart rate

f. Cardiac index (CI)

g. Ejection fraction (EF)

h. Ventricular function curve: Shows how to relate the contributions of preload, afterload, and contractility (but not heart rate) to ventricular function (Figure 3-7)

12. Systemic vasculature

a. Major functions: Provides tissues with blood, nutrients, and hormones and removes metabolic wastes

b. Resistance to flow: Depends on diameter of vessels (especially arterioles), viscosity of blood, and elastic recoil in vessel walls

c. Circulating blood volume: There is approximately 5 L of total circulating blood volume in the adult body

d. Major components of the vascular system

i. Arteries

ii. Arterioles

iii. Capillary system

(a) Tissue bed exchange of oxygen and carbon dioxide and solutes between blood and tissues; site of fluid volume transfer between plasma and interstitium

(b) Gas exchange caused by diffusion. Diffusion of a substance is from an area of high concentration to an area of low concentration until equilibrium is established.

(c) Fluid homeostasis

(d) Capillaries lack smooth muscle

iv. Venous system

13. Control of peripheral blood flow

a. Autoregulation: Ability of the tissues to control their own blood flow (vasodilatation, vasoconstriction)

b. Autonomic regulation of vessels

c. Stretch receptors: Baroreceptors (pressoreceptors) keep MAP constant

14. Arterial pressure

a. Neurohumoral regulation

i. Renin-angiotensin-aldosterone system also helps control arterial pressure (see Chapter 5)

ii. Renin is a protease secreted by the kidneys; converts angiotensinogen to angiotensin I

iii. Renin release from the kidneys is affected as follows:

iv. Angiotensin I is converted to angiotensin II. (These effects are blocked by angiotensin-converting enzyme [ACE] inhibitors.)

v. Angiotensin II, the most potent vasoconstrictor known, is produced when increased renin secretion stimulates its formation

b. Pulse pressure: Difference between systolic and diastolic pressures

c. MAP: Average arterial pressure during the cardiac cycle; dependent on mean arterial blood volume and elasticity of the arterial wall

Patient Assessment

1. Nursing history

a. Main complaint: Patient’s explanation for seeking medical assistance

b. History of present illness: Ascertain the following:

i. Description of complaint

ii. Onset: Date, time of day, duration, course, precipitating factors

iii. Signs and symptoms: Exacerbations, remissions

c. Medical history: Identify all previous illnesses, injuries, and surgical procedures

d. Family history: Identify

e. Social history: Identify

f. Medication history: Identify all prescribed or over-the-counter medications. Determine why and how often the patient is taking drug(s), dosages, any side effects, compliance issues.

g. Allergies: Medications, foods (i.e., shellfish), environmental substances, iodine (potential reaction to contrast medium used during cardiac catheterization procedures)

2. Nursing examination of patient