Chapter 17 Heart Failure

four major pathological changes that can lead to the development of heart failure:

1. increased fluid volume or volume overload 2. impaired ventricular filling 3. degeneration of ventricular muscle 4. decreased ventricular contractile function. Any one of these can lead to a reduction in cardiac output and compensatory mechanisms associated with heart failure. Heart failure is initiated by a precipitating event, and the four pathological changes occur over time. *It is important to identify the most likely cause of heart failure, because it will guide treatment.

How changes in the afterload affect contractility and the heart's SV

As peripheral arterial resistance (afterload) increases, cardiac contractility and SV decrease. At a level of maximal afterload, the heart begins to weaken. In clinical settings, afterload is most commonly defined as the systemic arterial blood pressure or aortic pressure force exerted against the left ventricle.

RAAS in heart failure

In heart failure, the RAAS continuously cycles and increases weakening of the heart. The net effect of the RAAS is increased blood volume, increased resistance against the heart, increased workload on the heart, and ventricular remodeling that weakens the heart. The net effects of the RAAS are elevated blood pressure and blood volume, which increase workload for the left ventricle. In left ventricular failure (LVF), this extra blood volume and high blood pressure further weakens the heart pump. Because this can be a vicious cycle, it can be said that heart failure begets heart failure.

ascites

Increased hydrostatic pressure within all the gastrointestinal veins is transmitted to the capillary beds, which creates edema within the peritoneal cavity the patient develops a fluidfilled, distended abdomen. The abdominal distension of ascites can restrict full thoracic excursion during inspiration, impairing respiratory function.

SV varies ________ with preload and _________ with afterload

directly, inversely In the healthy heart, an increased volume of blood filling the ventricle stretches ventricular myocardial fibers and consequently increases cardiac contractility and SV. Cardiac output is enhanced by preload and can be reduced by afterload The strength of the heart's cardiac contractility has a major effect on SV. As the heart pump fails, cardiac contractile strength diminishes and the ventricle ejects a progressively decreased amount of SV from preload. Decreased SV, in turn, diminishes cardiac output. Cardiac contractile strength can be weakened by such conditions as direct injury of the myocardium, excessive afterload, or extremely low preload.

cardiac output is _________ by preload and __________ by afterload

enhanced, reduced

Dilated cardiomyopathy

enlargement and hypertrophy of the left or right ventricles in response to chronic injury. The distended ventricle loses contractile ability and exhibits poor systolic function. The enlarged ventricle becomes prone to dysrhythmias, stasis of blood, and consequent formation of emboli.

interstitial fluid

fluid between cells

extracellular fluid

fluid outside the cell, located inside the capillary

intracellular fluid

fluid within cells

inotropic function

force of contraction of the cardiac muscle The heart's contractility can be influenced by the amount of calcium available for interaction between the actin and myosin filaments of the cardiac muscle fibers impaired calcium activity within cardiac ventricular muscle can negatively affect contractility.

Chronotropic function

heart rate

Pulmonary hypertension

high pulmonary artery pressure In pulmonary HTN, the right ventricle, which must pump its contents into the pulmonary artery, is confronted with increased resistance. This increased workload on the right ventricle eventually causes right ventricular hypertrophy. As the right ventricle muscle wall enlarges, it requires increased coronary circulation. Demand for coronary blood flow eventually exceeds supply and the right ventricle sustains ischemia. Ischemic insults to the right ventricle consequently weaken the muscle, leading to RVF

forward effects of the weak left ventricle

inadequate ejection of blood into the aorta and diminished perfusion throughout the whole arterial circulatory system. The decreased perfusion of vital tissues activates a neurohormonal response that includes stimulation of the RAAS, ADH, and SNS. When the kidney senses decreased perfusion, it releases renin from the nephron juxtaglomerular apparatus and initiates cycling of the RAAS. Simultaneously, with decreased forward pumping of blood, the aorta and peripheral arteries experience diminished blood flow, which initiates other compensatory mechanisms. The baroreceptors within the artery walls sense a drop in blood pressure and this activates the SNS. The SNS stimulates adrenergic receptors in the heart and blood vessels to create further effects. Adrenergic stimulation of the heart increases HR and adrenergic stimulation of the vasculature causes vasoconstriction. Also, in response to diminished perfusion, the posterior pituitary gland releases ADH, which acts at the nephrons to increase water reabsorption into the bloodstream and, in turn, leads to increased blood volume.

an increase in preload will ________ cardiac output

increase The force of contraction of the healthy heart is directly related to the blood volume that fills the ventricle in diastole (preload). The maximum force of contraction of the ventricle occurs when an increase in preload stretches muscle fibers to 2½ times their resting length.

positive chronotropic effect

increase heart rate epinephrine, an adrenergic or sympathetic stimulant, has positive inotropic and positive chronotropic effects on the heart. Under the influence of epinephrine, the heart has a greater force of contraction and increased heart rate.

Dysrhythmias

irregular heart rhythms Tachydysrhythmias, rapid irregular rhythms of the ventricle, reduce the time available for ventricular filling, which can precipitate heart failure. Bradydysrhythmias, which are slow irregular rhythms of the ventricle, can slow the HR excessively, minimize cardiac output, and precipitate heart failure. Atrial dysrhythmias can diminish the atrial "kick" volume emptied into the ventricle, which in turn decreases SV. Decreased SV lessens the blood pumped out of the ventricle to meet the needs of the tissues.

Diminished perfusion of the kidney in LVF

it stimulates the secretion of renin from the juxtaglomerular apparatus of the nephron, which initiates cycling of the RAAS.

Chronic Hypertension

leading cause of LVF: • High systemic arterial blood pressure is reflected in the aorta as high aortic pressure. • High aortic pressure creates increased resistance against the left ventricle, which causes left ventricular hypertrophy. • The hypertrophied left ventricle requires increased coronary circulation, and demand eventually exceeds coronary artery supply. • The hypertrophied left ventricle becomes predisposed to ischemia (MI) and systolic dysfunction. • The hypertrophied left ventricle impedes optimal ventricular filling, causing restrictive cardiomyopathy and diastolic dysfunction type of heart failure.

high-output failure

less common cause of heart failure heart cannot pump sufficient amounts of blood to meet the high circulatory needs of the tissues. The heart is driven to high rates and contractile force to facilitate the delivery of blood to tissues demanding a greater amount of circulation. Under the strain of this effort, the heart can weaken and the ventricle can fail. High-output heart failure can be caused by systemic conditions that require increased arterial circulation caused by high metabolic demands, but this is a relatively uncommon occurrence. However, it is associated with thyrotoxicosis, AV shunting, severe anemia, Paget's disease of the bone, and thiamine deficiency.

Autonomic Nervous System Regulation.

The parasympathetic nervous system stimulates cholinergic receptors to slow the HR and decrease the force of contraction. Conversely, sympathetic stimulation of beta-1 adrenergic receptors results in an increase in HR and a strengthening of the force of contraction, which results in increased SV and cardiac output. However, sympathetic stimulation also leads to activation of alpha-adrenergic receptors within arterial vessel walls, which results in vasoconstriction.

ventricular end diastolic volume

The preload volume of blood that originates from the venous system and ultimately empties into the right ventricle Preload causes stretch and increased pressure within the ventricular chamber, which increases SV. With increased venous return, preload increases, and SV is enhanced. If venous return is diminished, preload decreases, and SV is reduced. However, excessive venous return can overload a weakened ventricle, resulting in decreased cardiac output leading to heart failure.

Frank-Starling law

The relationship between cardiac contractility, preload, afterload, SV, and cardiac output of the heart

left-sided cardiac catheterization

a catheter is inserted into a peripheral artery and then into the aorta. From the aorta, the catheter is threaded into the coronary arteries. At that point, an opaque dye is infused to outline the interior of the coronary arteries and visualize blood flow. A specialized x-ray called a coronary angiogram is then completed. Obstruction to blood flow, thrombi, arteriosclerotic plaque, aneurysm, or other malformations of the arteries can be visualized through this procedure

Pulmonary Capillary Wedge Pressure (PCWP)

continuous measure of pulmonary capillary pressure Upon inflation of the balloon on the tip of the SwanGanz catheter, when the catheter remains in place

angiotensin-converting enzyme (ACE)

converts angiotensin I to angiotensin II in the lungs

negative chronotropic effect

decrease HR digitalis decreases HR by slowing conduction of impulses through the atrioventricular (AV) node Betaadrenergic blocking agents antagonize the SNS effect on the heart by slowing impulses at the sinoatrial (SA) node

cardiomyopathy

describe a disease that targets the heart muscle itself. infers that the myocardium has been directly injured by an agent or damaged as a side effect of another disease process. Infections that cause myocarditis, endocarditis, autoimmune disorders such as sarcoidosis, neuromuscular diseases such as muscular dystrophy, and alcoholic toxicity are examples of conditions that can directly injure the myocardium.

diastolic dysfunction

diastolic heart failure, the ventricle has difficulty relaxing, is less elastic, and cannot expand fully. The stiff ventricle cannot fill with blood adequately and therefore pumps out insufficient blood volume. SV and cardiac output are diminished because there is low blood volume in the ventricle

Ischemic cardiomyopathy

diffuse myocardial fibrosis and scarring of the heart muscle caused by coronary artery insufficiency and MI.

low-output failure

less common mechanisms of heart failure the heart is unable to fill with adequate amounts of blood to pump out to the tissues. This is not a common cause of heart failure, but it can occur in conditions of impaired venous return to the heart. With less than adequate venous return, there is a lack of sufficient blood to recirculate through the heart and into the pulmonary and systemic arterial circulation. Consequently, in low output failure, insufficient blood volume is pumped into the circulation, causing a lack of delivery of adequate oxygen to the tissues. For example, low output failure can occur in traumatic injuries that block venous return from the legs up to the heart.

renin-angiotensin-aldosterone system

major mechanism in the regulation of arterial blood pressure. It is a compensatory mechanism that raises blood pressure and increases blood volume in response to decreased renal perfusion

Mitral regurgitation

mitral insufficiency, occurs when the mitral valve does not close completely during systole. As the left ventricle contracts, blood from the ventricle refluxes back into the left atrium. This increased blood volume in the left atrium increases backward pressure within the pulmonary veins. Pulmonary capillary hydrostatic pressure increases as a result, and fluid diffuses out of the capillaries into the pulmonary interstitium.

Progressive Ventricular Remodeling

molecular substances are secreted. TNF-alpha, insulinlike growth factor, growth hormone, and endothelin cause detrimental ventricular remodeling. The ventricular cells undergo apoptosis, fibrosis, and degeneration. BNP secreted by the ventricles causes water loss from the body (called natriuresis). ANP secreted by the atria enhances water loss from the body (called natriuresis). Impaired utilization of calcium by ventricular myocytes (reduced contractility) This cycle within the myocardium contributes to a continuous process of unfavorable progressive ventricular remodeling that worsens heart failure.

Cycling of the RAAS

neurohormonal effects of heart failure. renin circulates and reacts with angiotensinogen, a protein synthesized by the liver. Angiotensinogen is cleaved into a smaller protein; angiotensin I. Angiotensin I circulates, and in the lungs it is transformed into angiotensin II by angiotensin converting enzyme (ACE). angiotensin II stimulates the adrenal gland to release aldosterone.

Renin

nzyme that is released from the juxtaglomerular apparatus of the kidney in response to decreased renal perfusion. When blood pressure drops, renal perfusion diminishes, which, in turn, provokes renin release. After release, renin circulates and reacts with angiotensinogen, a protein synthesized by the liver.

restrictive cardiomyopathy

the ventricle is impeded from filling to full capacity A minority of cases of heart failure result from diastolic dysfunction, an inability of the ventricle to relax, expand, and fill sufficiently during diastole. Restrictive cardiomyopathy occurs when the ventricle is unable to attain an adequate volume of blood because of a constrictive structural problem. This ventricular filling deficiency can occur in left ventricular hypertrophy, myocardial fibrosis, or pericarditis. Each of these conditions create a smaller space within the ventricular chamber that cannot fill sufficiently with blood volume.

Preload

the volume of blood in the heart at the end of diastole or the volume of blood that enters the right atrium from the venous system

Left ventricular ejection fraction (LVEF)

the volume of blood pumped with each ventricular contraction, can be approximated from the systolic and diastolic pressure measurements. In healthy individuals, approximately 60% to 70% of blood volume in the left ventricle is pumped out with each contraction. A LVEF lower than 40% is indicative of heart failure. To directly measure left heart pressures, a catheter is inserted into the femoral or radial artery and advanced against the flow of blood into the aorta; it is then further advanced into the left ventricle. Measurements can be taken of aortic pressure and systolic and diastolic pressures of the left ventricle from the catheter tip.

Starling's capillary forces

two major opposing pressure forces at every capillary bed in the body: hydrostatic pressure and oncotic (osmotic) pressure Capillary membranes are semipermeable, which means they allow diffusion of fluid out of the blood through the capillary pores into the interstitial and intracellular spaces. Oncotic pressure forces and hydrostatic pressure forces oppose each other at every capillary membrane. Under normal conditions, these forces balance each other out, creating an equilibrium that exists at the capillary beds.

Backward Effects of Right Ventricular Failure

• Jugular vein distension: result of high SVC pressure • Elevated jugular venous pressure • Elevated central venous pressure: high SVC and IVC pressure • Ascites: backup of hydrostatic pressure in peritoneum • Hepatomegaly: venous congestion/swelling of liver (elevated enzymes, impaired drug metabolism, hepatojuglar reflex) • Splenomegaly: venous congestion/swelling of spleen (jaundice, coagulation problems) • Ankle or sacral edema

Effects of Angiotensin II in Heart Failure

• Peripheral arterial vasoconstriction • Increased blood pressure • Increased resistance against the LV (afterload) • Cardiac myocyte hypertrophy • Detrimental ventricular remodeling • Stimulation of adrenal aldosterone

Development of LVH and LVF caused by aortic stenosis.

calcification of the aortic valve with aging, a process called aortic sclerosis. This produces a narrowing of the aortic valve that impedes the ejection of blood flow from the left ventricle into the aorta during systole Step 1 shows aortic stenosis (narrowing of the aortic valve). Step 2 shows how the left ventricle hypertrophies because of the increased resistance. Step 3 shows how eventually the left ventricle fails when exhausted from excessive workload because of the narrowed aortic valve.

Digitalis

cardiac glycoside drug positive inotropic agent and a negative chronotropic agent because it increases force of ventricular contraction of the heart and decreases the heart rate.

right-sided cardiac catheterization

catheter is inserted via a peripheral vein, commonly the femoral vein. It is then threaded into the inferior vena cava, right atrium, right ventricle, and into the pulmonary artery. Finally it is wedged in a pulmonary capillary. The PCWP is used to assess the severity of left ventricular failure.

Aldosterone effects in heart failure

causes sodium and water retention and potassium excretion from the bloodstream. The sodium and water retention increases total blood volume and raises blood pressure. Therefore, the stimulation of aldosterone by angiotensin II further challenges the weakened left ventricle. The net effects of angiotensin II and aldosterone include an increased blood pressure and blood volume as well as increased resistance against the left ventricle. These conditions require the failing ventricle to pump out a greater volume of blood against high resistance within the arterial circulation. As a result, the effects of angiotensin II and aldosterone further strain the weakened left ventricle, resulting in diminished forward pumping of blood into the aorta, which further diminishes arterial circulation and organ perfusion

edema

collection of fluid, which traverses into the interstitial and intracellular spaces, Fluid accumulation in and around the cells, which causes swelling. When hydrostatic pressure increases within the capillary, the forces become unbalanced. A high hydrostatic pressure force can overcome the opposing balancing effect of the oncotic pressure. High capillary hydrostatic pressure causes fluid to diffuse out of the capillary pores into the interstitial and intracellular spaces.

Biventricular Heart Failure

combined left and right-sided heart failure Dysfunction of any one chamber causes compensatory changes within the other chambers. If dysfunction of one heart chamber persists, compensatory mechanisms become exhausted, begin to diminish, and decompensation of the whole organ occurs. Failure of one side of the heart ultimately results in detriment of the other side of the heart. Depending on the extent of the disease, the patient commonly presents with a combination of the signs and symptoms of left and right ventricular failure.

Cardiomegaly or left ventricular enlargement

shifted point of maximal impulse or apical pulse. When the left ventricle is enlarged, the apical pulse, normally located at the left fifth intercostal space midclavicular line, can be palpated further into the left axillary region.

Activation of the parasympathetic nervous system

stimulates the vagal or cholinergic receptors in the heart, which decreases the force of contraction

systolic dysfunction

systolic heart failure, the weakened ventricle has difficulty ejecting blood out of the chamber. The ventricle is a poor forward pump which, in turn, causes inadequate ventricular emptying. SV and cardiac output, both functions of forward heart pumping action, are diminished. Blood accumulates in the weakened ventricle, elevating pressure within the chamber; this causes a backup of hydrostatic pressure into the atrium above it.

cardiac afterload

the amount of resistance that the ventricle must overcome in order to pump blood out of the heart It is the tension or stress developed in the wall of the ventricle during ejection. In the clinical setting, afterload is most commonly measured as the aortic pressure against the left ventricle. Aortic pressure reflects the systemic arterial pressure. Therefore, if there is high systemic arterial pressure (also referred to as HTN), this is considered high afterload. Pulmonary HTN, which is high pressure within the pulmonary arteries, creates high afterload for the right ventricle.

hypertrophic cardiomyopathy

the left ventricular muscle is enlarged, usually on the side of the interventricular septum. The asymmetric hypertrophy of the left ventricle causes muscle wall stiffness and can obstruct the ejection of blood into the aorta during systole. Primary hypertrophic cardiomyopathy is commonly caused by a genetic predisposition for the muscular enlargement of the interventricular septal wall of the left ventricle. Chronic HTN is referred to as a secondary cause of hypertrophic cardiomyopathy. HTN usually causes more diffuse enlargement of the left ventricle, not limited to the interventricular septal wall region, than is seen in primary hypertrophic cardiomyopathy.

cardiac contractility

the myocardium's ability to stretch and contract in response to the filling of the heart with blood

hepatojugular reflux

the patient is supine and the clinician presses on the liver. Pressure on the liver increases portal venous pressure and in turn raises jugular venous pressure, producing visible JVD.

positive inotropic effect

Sympathetic stimulation can increase force of contraction, Epinephrine provides enhanced contractility because of stimulation of beta-1 adrenergic receptors in the heart

Risk factors for heart failure

1. Age: increases with age, older than 65 years 2. Ethnicity: African Americans more at risk 3. Family history and genetics: history of cardiomyopathies 4. Diabetes: >risk arteriosclerosis (CA-insufficiency, ischemia, MI) 5. Obesity: >risk HTN and DM (arteriosclerosis, development LVH) 6. Lifestyle: smoking, sedentary lifestyle (CAD, IHD) 7. Medications: anabolic steroids, Sporanox, Gleevec, radiation/chem 8. Sleep apnea: pulm HTN, rhythm disturbances (hypoxia) 9. Congenital heart defect: change pressures (present at birth) 10. Viruses: myocarditis 11. Alcohol abuse: cardiomyopathy (dilation), HTN (LVF) 12. Kidney conditions: >BV, edema, HTN, nitro. waste (toxic)

normal cardiac output

5L/min (amount of blood pumped out of left ventricle each minute) Cardiac output = SV × HRSV = milliliters of blood ejected per ventricular contractionHR = number of ventricular contractions per minute In a healthy heart, SV equals approximately 70 mL of blood ejected per ventricular contraction. The average HR is 70 beats per minute or 70 contractions/minute. Therefore, cardiac output equals 70 mL/contraction x 70 contractions/minute or a blood volume of 4,900 mL/ minute (approximately 5,000 mL or 5 liters/minute).

Antidiuretic Hormone

Another physiologic response to decreased tissue perfusion from the posterior pituitary gland. This hormone promotes water reabsorption into the bloodstream at the nephron in the kidneys and also has vasoconstrictor effects.

How changes in preload affect the contractility and SV of the healthy heart

As ventricular end diastolic volume (preload) increases, myocardial contractility and SV increase until a maximal level is reached. In the healthy heart, cardiac contractility and SV increase until the stretch of myocardial muscle fibers is 2 1/2 times their resting length. As blood fills the ventricle during diastole, tension in the heart muscle wall steadily increases, and stretching of the chamber occurs. Actin and myosin filaments of the myocardial muscle wall interact to create a force of contraction. The muscle filaments can change the force of contraction with varying amounts of stretch caused by blood volume or preload. SV is the amount of blood within the ventricle that is ejected with each contraction. Therefore as preload increases, SV increases and the actin-myosin filaments in the heart wall stretch to accommodate the increased volume. These conditions enhance contractility in a healthy heart

How increasing preload influences contractility and SV in the failing heart

As ventricular end-diastolic volume (preload) increases, a weakened heart muscle develops decreased cardiac contractility and SV. In the failing heart, an increase in preload causes high blood volume filling the ventricle; however, the weakened ventricular muscle may not have the strength to pump the excessive volume out. SV decreases when the weakened ventricle cannot optimally eject its blood. Also, the ventricular muscle's fibers can become overly taxed by the burden of the excessive filling of blood in the chamber and contractile force diminishes. Therefore, in a failing heart, with increased preload filling the weakened ventricle, contractility and SV can decrease

B-type natriuretic peptide (BNP)

BNP exerts the same effects as ANP, inducing the process of natural diuresis. when increased blood volume causes increased ventricular volume and stretch, the ventricular myocytes release B-type natriuretic peptide (BNP) In heart failure, both these natriuretic peptides are released because of the increased blood volume and edema, which allows water loss from the kidneys (decrease volume) An elevated level of BNP is commonly used as a diagnostic indicator in heart failure. Synthetic BNP is also administered as a therapeutic pharmacological agent in heart failure to induce diuresis.

cerebral and constitutional symptoms of L heart failure

Cerebral Symptoms. With diminished strength of the left ventricle to pump blood into the arterial circulation, perfusion of the brain decreases. The patient may manifest decreased cerebral perfusion as confusion, headache, memory loss, insomnia, anxiety, or disorientation. Constitutional Symptoms. Because of the diminished strength of the left ventricle, the organs receive less blood flow. Decreased gastrointestinal perfusion may cause anorexia, nausea, and abdominal discomfort. Reduced skeletal muscle perfusion can cause weakness and exercise intolerance. Poor urinary output and suboptimal filtration of blood can occur because of diminished renal perfusion. Diminished peripheral circulation results in decreased pulses bilaterally, as well as cold, pale extremities.

Cor pulmonale.

Cor pulmonale is right-sided heart failure that develops because of lung disease. The heart starts out healthy but, because of chronic lung disease, the right side of the heart weakens. The events occur as follows: Step 1: The lung is diseased and causes chronic hypoxia. Step 2: Chronic hypoxia causes pulmonary arterial vasoconstriction (pulmonary hypertension). Step 3: The pulmonary vasoconstriction causes high resistance against the right ventricle and eventually weakens the right ventricle.

hydrostatic pressure

Fluid within the blood exerts a force that attempts to push fluid out of the capillary pores into the interstitial and intracellular spaces.

heart rate is controlled by

HR is controlled by the sympathetic (adrenergic) and parasympathetic (cholinergic) nervous systems. Adrenergic stimulation raises HR and cholinergic stimulation slows heart rate

heart failure

Heart failure is a clinical condition commonly resulting from a weakened ventricular muscle that is unable to sufficiently pump blood into the arterial circulation to meet the needs of the tissues. Less commonly, heart failure can be caused by the ventricle's inability to expand and fill with sufficient blood volume. With an inability to fill, the ventricle cannot pump blood into the peripheral or pulmonary circulatory system. When it is accompanied by fluid retention, it is sometimes called congestive heart failure.

risks of heart failure

Hypertension (HTN) is the greatest risk factor for the development of heart failure, as more than 75% of patients with heart failure are treated for HTN before developing it. About 22% of men and 46% of women will develop heart failure within 6 months following an acute MI. Other causes of heart failure include coronary artery disease and metabolic syndrome; a history of diabetes mellitus also increases the risk of developing the disorder. Women are often diagnosed with heart failure at an older age than men because natural estrogen is cardioprotective. After menopause, the risk of cardiovascular disease for men and women are equal. Within the U.S. population, there is a greater prevalence of heart failure among African Americans compared with Caucasian Americans related to effectiveness of pharmacology.

Signs and Symptoms of Biventricular Heart Failure

LEFT VENTRICULAR FAILURE •Dyspnea • Cough, crackles lung bases • Orthopnea • PND • Weak peripheral pulses • Decreased cerebral perfusion; confusion, disorientation RIGHT VENTRICULAR FAILURE • JVD • Ascites • Gastrointestinal disturbances caused by venous congestion • Hepato-jugular reflux • Hepatomegaly • Splenomegaly • Peripheral edema; ankle or sacral edema; fingers, feet, decreased dorsalis pedis pulses

ischemic heart disease

Lack of sufficient coronary circulation causes repeated ischemia or infarction of the myocardium. The consequence of repeated MI is a scarred, fibrotic heart muscle with diminished contractile strength One of the most common areas of arteriosclerosis is in the left coronary artery, a major arterial supply of the left ventricle. The LV is the most common site of ischemia and MI. Infarcted heart muscle doesn't contract or conduct impulses. Repeated myocardial infarcts are extremely harmful to the strength of the ventricular muscle, which predisposes the individual to heart failure.

Cardiac Index (CI)

Normal range 2.5 to 4 L/min. around half of the cardiac output. < 2.1 inconsistent for weaning. varies by body size, a hemodynamic measurement termed cardiac index can be calculated to give a more accurate assessment of each individual's cardiac output. Cardiac output divided by an individual's body surface area yields the cardiac index.

Orthopnea

Orthopnea is the feeling of shortness of breath when in a flat, supine position. Orthopnea most often occurs in LVF when fluid builds in the lungs. In the flat, supine position, the patient's pulmonary fluid traverses throughout the lung tissue. The person has the most difficulty breathing in this position. As the head of the bed is raised, orthopnea can be relieved because the fluid in the lungs is pulled downward to the bases of the lungs. Semi-Fowler's position (head at a 45° angle) can ease breathing and the seated position can bring more relief because fluid is in the bases of the lungs. With fluid only in the bases of lungs, the patient can breathe easier. Clinically, orthopnea can be described in terms of how many pillows the patient needs to breathe comfortably. For example, "2 pillow orthopnea" may be described in the clinical assessment of a patient. This term indicates that to breathe comfortably, the patient requires a head elevation at a level of two pillows. Excess fluid caused by heart failure may be noticeable as pulmonary edema at night when the patient is supine. However, during the day when the patient is standing and fluid gravitates to the lung bases, there may be no respiratory difficulty.

Jugular venous distension (JVD)

Pressure in the jugular veins is a reflection of right atrial pressure and CVP, which are important clinical indicators of right ventricular function. As the right ventricle fails, right atrial pressure increases, which in turn increases CVP and JVP. Hence, RVF raises JVP. Under normal conditions, jugular veins are collapsed and not visible in the seated or standing patient. Neck veins may be slightly distended under normal conditions when the patient is supine. However, in RVF, jugular veins are distended even when the patient is upright

central venous pressure (CVP)

Pressure measurement within the IVC To directly measure right heart pressures, a SwanGanz catheter is threaded into the subclavian vein and advanced into the inferior vena cava (IVC) and right atrium. The catheter can measure CVP, which is the same as right atrial pressure at this location.

Anasarca

RVF is severe, peripheral edema can be massive and gradually affect most of the tissues in the body (generalized edema or total body swelling); periorbital edema, facial puffiness

paroxysmal nocturnal dyspnea (PND)

Refers to attacks of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep fluid extravasation into the pulmonary interstitial and intracellular spaces. The opening and closing of alveoli against this fluid is heard as crackles through a stethoscope and is exhibited as cough, dyspnea, orthopnea. backward effects of LVF Patients often describe PND as nightmares or night terrors that awaken them from sleep. Commonly, a patient is not able to accurately describe PND as shortness of breath because it occurs during sleep.

Adrenergic Stimulation

SNS activation occurs early in heart failure. Initially in LVF, there is a drop in arterial blood pressure caused by the inadequate forward pumping of blood into the aorta. The decline in blood pressure stimulates baroreceptors within arterial walls, which sense pressure changes. Baroreceptors, in turn, activate the SNS. Vasoconstriction of peripheral arteries occurs as a result of activation of the adrenergic (sympathetic) nervous system. This acts as a compensatory mechanism to raise blood pressure, but it also increases resistance within the arterial circulation. The increased resistance acts as increased afterload against the left ventricle, which further challenges the heart. Simultaneously, adrenergic stimulation increases HR by activating the SA node. The already failing heart is then stimulated to increase its rate, which further strains the ventricle

Right ventricular failure

The backward effects of RVF cause high hydrostatic failure in the right ventricle, which backs up into the right atrium and superior and inferior vena cava. From the vena cava, hydrostatic pressure builds throughout the body, causing widespread venous congestion (increase in CVP) Forward contractile force into the pulmonary artery is diminished. This decreases pulmonary arterial blood flow, which results in suboptimal alveolar-oxygen diffusion into the capillaries and, in turn, causes hypoxemia. The patient also may experience hypoxia and cyanosis. Compared with the backward failure effects of venous congestion and peripheral edema in RVF, forward failure effects are less dramatic.

transmural MI of the left ventricle

The infarction commonly injures the papillary muscles, which are muscular projections that extend from the internal left ventricular wall. These small muscular projections are attached to the chorda tendineae, which are membranous, stringlike cords that hold the heart valve leaflets in place. Chordae tendineae and papillary muscles assist in valve function. When rupture of a papillary muscle occurs because of MI of the left ventricle, the mitral valve becomes incompetent. The mitral valve leaflets become loose and do not come together to close off blood flow from the left atrium to the left ventricle. This dysfunction of the valve causes a classic, holosystolic murmur heard loudest at the heart's apex. As the left ventricle contracts during systole, blood refluxes upward into the left atrium through the incompletely closed mitral valve. Consequently, backward pressure builds into left atrium pulmonary veins and pulmonary interstitium.

auscultation of the heart, a third and fourth heart sound

The third heart sound (S3) is a low-pitched sound heard after S2, during rapid filling of the ventricle in the early part of diastole. In children and young adults, an S3 may be normal. In adults older than age 40 years, the presence of an S3 is abnormal and indicative of heart failure. High ventricular end diastolic volume and increased pressure within the chambers consequent to heart failure are responsible for a third heart sound. A fourth heart sound (S4) is heard when the atrium contracts against a noncompliant, stiff ventricle. Normally, when the atrium contracts, there is no sound. An S4 is a low-pitched sound heard at the end of diastole, before S1. An S4 commonly occurs in chronic HTN, caused by the structural changes that occur in the left ventricle as a result of high blood pressure. In HTN, high aortic pressure creates high resistance and hypertrophy of the left ventricle. The hypertrophic left ventricle is less elastic and distensible. Atrial contraction against this stiff left ventricle causes an audible S4 during diastole. Upon palpation of pulse, resting tachycardia is often present in moderate or severe heart failure.

Measuring Jugular Venous Pressure

To assess JVP, the supine patient should have the head of the bed raised to a 45° to 60° angle. The clinician should place a centimeter ruler on the sternal angle of the patient's chest, the bony ridge of the sternum adjacent to the second rib. The sternal angle is approximately 5 cm above the right atrium. Using a straight edge, the clinician should measure the distance in centimeters from the sternal angle to the horizontal level of the highest visible pulsations of the distended neck veins. Neck: + JVD: jugular veins 9 cm from right atrium at 45° alternatively + JVD: jugular veins 4 cm above sternal angle at 45° This assessment indicates that the clinician observed a level of jugular vein distension at 9 cm above the right atrium or 4 cm above the sternal angle, which is considered elevated JVP.

Peripheral Edema

Venous congestion within the lower body causes high hydrostatic pressure within all the capillary beds of the extremities and leads to edema. If the patient is supine or on bedrest, edema tends to accumulate around the sacral region. If the patient is in the supine position for prolonged periods, sacral edema increases the skin's fragility and can lead to skin breakdown. Erythema of the skin and edema in the sacral area is the first sign of pressure in this area. Sacral edema predisposes the patient to formation of sacral decubitus ulcers. Because of the gravitational forces, bilateral dependent ankle edema develops in the standing or ambulatory patient. The feet and lower legs may also develop edema in RVF.

Pulmonary Edema in heart failure

a fluid accumulation in the pulmonary in terstitial spaces that hinders oxygen diffusion from alveoli to capillary. The blood cannot become sufficiently oxygenated and hypoxemia develops. The patient suffers severe dyspnea (fluid hinders oxygen diffusion), cough (fluid accumulation between alveoli and capillary membranes), crackles (alveoli attempt to open against fluid), and pink frothy sputum as the forward ventricular pump is weakened, backward pressure builds within the left atrium, resulting in high hydrostatic pressure in the pulmonary veins. This high hydrostatic pressure is transmitted further backward into the pulmonary capillary bed. At the pulmonary capillaries, high hydrostatic pressure causes fluid extravasation into the interstitial spaces, leading to edema. Changes caused by pulmonary vascular congestion appear as vessel engorgement in the perihilar region on chest x-ray. High hydrostatic pressure within the pulmonary veins can also cause pleural effusion, which is edema accumulation in the pleural cavity. Pleural effusion can be identified on chest x-ray as a fluid level within the pleural cavity.

Oncotic (osmotic) pressure

a force that attempts to pull fluid from the interstitial and intracellular spaces into the capillary. Particles within the blood, such as albumin, sodium, and glucose, exert oncotic or osmotic pressure.

Aldosterone

a hormone that acts at the nephron to increase sodium and water reabsorption from the distal tubule into the bloodstream. It also increases secretion of potassium into the nephron tubule, resulting in potassium excretion. The sodium and water retention caused by aldosterone increases total blood volume and raises blood pressure.

Endothelin

a peptide that is secreted by the heart's endothelium and vasculature in heart failure. It is often elevated in heart failure following an acute MI. It stimulates vasoconstriction of the arterial blood vessels, which increases resistance against the left ventricle. Increased resistance causes high workload for the left ventricle. If resistance becomes excessive, the workload strains the heart. Endothelin also provokes fibrotic changes within the myocardium, which is part of the heart's ventricular remodeling, which occurs in heart failure.

Atrial natriuretic peptide (ANP)

a protein molecule that induces a process of natriuresis, which is increased excretion of sodium and water by the nephron. Release of ANP stimulates the glomerulus to increase filtration of the blood, inhibits reabsorption of sodium at the proximal tubule, blocks release of renin and aldosterone, and opposes the vasoconstrictive effects of angiotensin II. All these actions enhance the excretion of water from the body and decrease blood volume. Within the circulatory system, increased water and sodium retention raises blood volume. High blood volume entering the heart stretches the heart's atrial chambers, which activates the release of natriuretic peptides from the atrial myocytes.

hemodynamic monitor

accomplished by right heart cardiac catheterization or placement of a Swan-Ganz catheter. These are distinct invasive procedures that employ a specialized cardiac catheter device to diagnose heart disease and monitor treatment in heart failure. A cardiac catheter is capable of measuring pressure and flow within the heart chambers. It is connected to a transducer that converts the pressure waves into a digital read that can be seen on a monitor screen

pulmonary embolism causes what type of heart failure

acute RVF An embolus lodged in the pulmonary artery suddenly raises pressure within the pulmonary artery. This acute rise in pulmonary artery pressure places an overwhelming amount of resistance against the right ventricle. This can rapidly and severely weaken the right ventricular muscle

tumor necrosis factor-alpha (TNF-alpha)

an inflammatory cytokine that stimulates hypertrophy, fibrotic changes, and cell death, or apoptosis of the myocardium. It also negatively affects the heart's inotropic function. This leads to dilation of the ventricle with decreasing cardiac output. Myocardial apoptosis, degeneration of heart muscle, puts further strain on the functional myocytes. The net effect is diminished strength of ventricular contraction, worsening heart failure, and detrimental remodeling of the heart. In heart failure, elevated levels of tumor necrosis factor-alpha (TNF-alpha) are present in the bloodstream and cardiac muscle.

Left ventricular diastolic dysfunction

occurs from reduced relaxation or increased stiffness of the ventricular muscle. The increased afterload of HTN is commonly the cause for the development of these changes in the left ventricle. HTN causes increased resistance against the left ventricle, and the left ventricular muscle hypertrophies to compensate for the increased workload. LVH creates a noncompliant, enlarged, stiff-walled ventricular chamber. The thickened, muscular ventricular wall encroaches into the left ventricular chamber and diminishes the size of the left ventricle's interior. This leads to decreased left ventricular filling, as well as reduced SV and cardiac output. Because the ventricular filling or diastolic phase of heart function is most affected, this condition is often termed diastolic dysfunction.

cardiogenic shock

occurs when there is a significant loss of the ventricle's ability to pump blood adequately to maintain optimal blood pressure within the body. It often occurs because of extensive acute MI.

left ventricular systolic dysfunction

occurs when there is reduced forward pumping strength of the ventricular muscle. The left ventricle is weak and cannot eject its blood volume into the aorta, thereby decreasing SV and cardiac output. Systolic dysfunction of the left ventricle has two major consequences: backward effects and forward effects of failure. The backward effect of a failing left ventricle creates a buildup of hydrostatic pressure in the left atrium, pulmonary veins, and pulmonary capillaries. The forward failure effects cause decreased perfusion of the brain, kidneys, and other organs. The backward effects consist of a buildup of hydrostatic pressure backward up into the left atrium and pulmonary vasculature

COPD (chronic obstructive pulmonary disease)

one of the most common lung conditions that leads to cor pulmonale (RVF)

Angiotensin II

potent arterial vasoconstrictor that raises blood pressure within the systemic arterial system. It is also a trigger for myocardial changes referred to as ventricular remodeling. Frequent stimulation of angiotensin II will activate genetic changes in the cardiac myocyte that lead to hypertrophy, apoptosis, and myocardial fibrosis. As some cardiac myocytes hypertrophy, the ventricular muscle enlarges. Other cardiac myocytes degenerate, causing ventricular muscle weakness. As the myocardium degenerates it becomes infiltrated with collagenous fibrous tissue, which is noncontractile and nonconductive. In addition, angiotensin II stimulates the adrenal gland to release aldosterone.

Nitric oxide (NO)

potent vasodilator produced by vascular endothelial cells. Through its vasodilator action, it is a local regulator of blood flow to the tissues.

stroke volume is influenced by

preload, afterload, and cardiac contractility.

Activation of the sympathetic nervous system (SNS)

provides enhanced contractility because of stimulation of beta-1 adrenergic receptors in the heart

acute heart failure

rapid, sudden development of heart failure that is often caused by substantial ventricular muscle injury as in massive MI

major sensors within the cardiovascular system that respond to decreased blood pressure and blood volume

renin-angiotensin-aldosterone system (RAAS) autonomic nervous system senses low circulation via baroreceptors that are embedded within the arteries posterior pituitary releases antidiuretic hormone (ADH) in response to decreased blood volume or blood pressure endothelin, nitric oxide, natriuretic peptides and TNF: regulate circulation to the tissues and cardiovascular changes