Ch - 20 Heart Failure and Circulatory Shock Flashcards
What is heart failure? Pathophysiology of Heart Failure?
Heart failure is a complex syndrome resulting from functional or structural impairment of ventricular filling or ejection of blood into the circulation. Common causes are CAD, hypertension, dilated cardiomyopathy and valvular heart disease. Can affect any age group but usually the elderly. It is associated with either a reduced or preserved left ventricular ejection fraction.
Pathophysiology - In heart failure the heart doesn’t adequately pump and or fill with blood, which results in the inability to meet the metabolic needs of the body. They may used their cardiac reserve for just daily movement.
cardiac performance and output - Cardiac cycle consists of diastole and systole. During diastole, normal filling of the ventricles increases the volume of each to about 110 to 120 mL. Then as the ventricles contract during systole, blood is ejected from the heart and the volume decreases by about 70 mL, which is called the stroke volume. Cardia output is the determinant of cardiac performance, reflects how often the heart beats each minute HR and how much blood it ejects with each beat. CO = HR x SV. Sympathetic nervous system inc HR and parasympathetic slows it down.
Preload and afterload - reflects the volume of blood that stretches the ventricle and the end of diastole. Afterload represents the force that the contracting heart muscle must generate to eject blood from the filled ventricles.
Myocardial contractility? Compensatory Mechanisms? Frank-starling mechanism? Sympathetic Nervous System?
Also known as inotropy refers to the contractile performance of the heart, or the ability of the contractile elements of the heart muscle to interact and shorten against a load. The contractility uses the interaction between actin and myosin filaments during cardiac muscle contraction requires ATP and Calcium ions. The L type calcium channel also contains several other types of receptors. Blockade of L type calcium channels by drugs that bind to these receptors results in a selective reduction in cardiac contractility Another mechanism is the increased activity of the Na/Ca exchange pump and the ATPase-dependent Ca pump in the myocardial cell membrane
Cardiac reserve is largely maintained through compensatory mechanisms such as the Frank-Starling mechanism, activation of neurohumoral influences such as sympathetic nervous system reflexes, the renin-angiotensin-aldosterone mechanism, natriuretic peptides, locally produced vasoactive substances and myocardial hypertrophy and remodeling.
Frank-starling mechanism describes the process whereby the heart increases its stroke volume through an increase in end-diastolic volume or preload.
Stimulation of the SNS plays an important role in the compensatory response to dec cardiac output and in the pathogenesis of heart failure. Both cardiac sympathetic tone and catecholamine levels are elevated during the late stages of most forms of heart failure. Although is meant to maintain BP and Cardiac output it quickly becomes maladaptive and contributes to the deterioration of heart function.
Renin-angiotensin-aldosterone mechanism? Natriuretic peptides?
One of the most important effects of lowered cardiac output in heart failure is a reduction in renal blood flow and glomerular filtration rate, which leads to sodium and water retention by way of aldosterone production. With dec renal blood flow, there is a progressive inc in renin secretion by the kidneys with parallel inc in circulating levels of angiotensin II. The increased concentration of angiotensin II contributes directly to generalized and excessive vasoconstriction, as well as facilitating norepinephrine release and inhibiting reuptake of norepinephrine by the sympathetic nervous system. Angiotensin II also provides a powerful stimulus for aldosterone production by the adrenal cortex.
Natriuretic peptides -the heart muscle produces and secretes a family of related peptide hormones, called the natriuretic peptides, which have potent diuretic, natriuretic, vascular smooth muscle, and other neurohumoral actions that affect cardiovascular function. Two of the 4 are atrial natriuretic peptide and Btype natriuretic peptide. ANP is released from atrial cells in response to atrial stretch, pressure or fluid overload. BNP is primarily secreted by the ventricle as a response to increased ventricular pressure of fluid overload. they promote rapid and transient natriuresis and diuresis through an increase in the glomerular filtration rate and inhibition of tubular sodium and water reabsorption.
Endothelins? Myocardial Hypertrophy and remodeling?
Endothelins released from the endothelial cells throughout the circulation, are potent vasoconstrictors. Can also be synthesized and released by a variety of cell types, such as cardiac myocytes. They can induce vascular smooth muscle cell proliferation and cardiac myocyte hypertrophy and fibrosis, increase the release of ANP, aldosterone, and catecholamines and exert antinatriuretic effects on the kidneys.
Myocardial hypertrophy constitutes one of the principal mechanisms by which the heart compensates for an increase in workload. Inappropriate hypertrophy and remodeling can result in changes in structure and cardiac function that often lead to further pump dysfunction and hemodynamic overload.
Types of Heart failure? Reduced versus preserved ejection fraction?
Heart failure is commonly classified by the ejection fraction or as left sided or right sided failure. To be diagnosed they must also exhibit signs SOB, dec exercise tolerance, and orthopnea.
Reduced - Heart failure with reduced ejection fraction or systolic heart failure is defined as an EF < 40%. May result from conditions that impair the contractile performance of the heart, produce a volume overload or generate a pressure overload on the heart. Cardinal symptoms are dyspnea, fatigue, and peripheral edema. other include orthopnea, paroxysmal nocturnal dyspnea signs of jugular venous distention and cardiac enlargement.
Preserved - In half of the cases systolic function is preserved EF>50% and heart failure results from an inability of the left ventricle to fill sufficiently during diastole. Hypertension is the leading cause. With diastolic dysfunction, ventricular relaxation and distensibility are impaired leading to an increase in intraventricular pressure at any given volume. It is influenced by the HR so increase in HR can be aggravating and improved by a reduction in HR.
Left sided versus right sided heart dysfunction? Left ventricular dysfunction? Right ventricular dysfunction?
The ventricles must maintain equal outputs, so if it starts in one side it will progress overtime to include both sides.
Left - Clinical features result from a diminished cardiac output with a resultant dec in peripheral blood flow and a progressive accumulation of blood in the pulmonary circulation. With left there is decrease in the ejection of blood into the systemic circulation, an inc in left ventricular and left atrial end diastolic pressures, and congestion of the pulmonary circulation. Common causes are hypertension and acute myocardial infarction.
Right - Is often the consequence of disease of the left ventricle; an inc in pulmonary blood volume eventually produces an inc burden of the right side of the heart. It is less common and occurs in pt with intrinsic lung disease or pulmonary hypertension. It impairs the ability to move the blood from the systemic venous circulation into the pulmonary circulation. A major consequence is peripheral edema. It also causes congestion of the viscera.
Manifestation of Heart Failure?
Depend on the extent and type of cardiac dysfunction that is present and the rapidity with which it develops.
A pt with previously stable compensated heart failure may develop signs of heart failure for the first time when the condition has advanced to a critical point.
1. Fluid retention and edema - from increased capillary pressure. Nocturia and oliguria can occur.
2. Respiratory manifestations - dyspnea due to congestion of the pulmonary circulation in a major manifestation. Sleep apnea may play a part.
3. fatigue, weakness and cognitive impairment - Is not apparent in the morning but progresses through out the day.
4. Cachexia and malnutrition - is a condition of malnutrition and tissue wasting that occurs in person with end stage heart failure.
5. Cyanosis -
6. Arrhythmias and sudden cardiac death.
Acute Heart Failure Syndromes?
Are defined as gradual or rapid change in heart failure signs and symptoms resulting in a need for urgent therapy. Are primarily the result of severe pulmonary edema due to elevated left ventricular filling pressures, with or without a low cardiac output. To encompass 3 different types 1. worsening of chronic systolic or diastolic dysfunction that appears to respond to treatment; 2 new onset acute heart failure that occurs secondary to a precipitating event such as a large myocardial infarction or a sudden increase in blood pressure superimposed on a noncompliant left ventricle 3. worsening of end stage/advanced heart failure that is refractory to treatment, with predominantly left ventricular systolic dysfunction associated with a low output state. Acute pulmonary edema is the most acute sign. Resulting in SOB and cyanosis. Pt is usually sitting and gasping for air. HR is rapid, skin is moist and cool, cyanotic. As oxygen supply drops confusion and stupor appear. Dyspnea and air hunger are accompanied by a productive cough with frothy blood tinged sputum. Air produces a fine crepitant called crackles.
Diagnosis - usually based on signs, labs, ECG, xray, echocardiography. BNP to confirm heart failure. Intra arterial blood pressure monitoring.
Treatment - depends on the rapidity on onset and severity of the heart failure.
Nondrugs - exercise training is important starting slowly. Na and fluid restriction and weight management.
Drugs - polypharmacy becomes a management standard. B adrenergic inhibitors, angiotensin converting enzyme ACE/ angiotensin receptor inhibitors and diuretics. might need if these don’t work aldosterone antagonists or digoxin. Diuretics are the most prescribed. IV loop diuretics furosemide.
Oxygen therapy including CPAP
Advanced - implantation of cardioverter defibrillator or ventricular assist devices to transplantation
Circulatory Failure (shock)?
Circulatory shock can be described as an acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia.
Pathophysiology of shock - circulatory failure results in hypoperfusion of organs and tissues, which in turn results in an insufficient supply of oxygen and nutrients for cellular function and the accumulation of waste products.
Cellular responses - shock ultimately exerts its effect at the celllular level, with failure of the circulation to supply body cells with the oxygen and nutrients needed for production of ATP. Because cell move to anaerobic metabolism because of lack of oxygen. This builds up an excess of lactic acid
Compensatory mechanisms - the sympathetic nervous system and the renin-angiotensin mechanism, blood is shunted from the kidneys to other vital organs. SNS reflexes increase HR and stimulate constriction of blood vessels throughout the body. There alpha a receptors cause an increase in HR and force of myocardial contraction and B2 receptors vasodilation of the skeletal muscle beds and relaxation of the bronchioles. It can’t be sustained for long.
Types of shock? Hypovolemic shock? Cardiogenic shock?
Occurs when there is an acute loss of 15% or more of the circulating blood volume. May be whole blood plasma, extracellular fluid or excessive dehydration. Can be from hemorrhage or from third space losses.
Manifestations - depend on severity - are closely related to low peripheral blood flow and excessive sympathetic stimulation. Thirst, inc HR, cool and clammy skin, dec arterial BP, oliguria and changes in mentation.
Treatment - Ongoing blood loss must be stopped such as in surgery. IV fluids, blood and blood products. Oxygen to inc delivery to the tissues. Vasoactive meds are capable of constricting or dilating blood vessels
Cardiogenic - occurs when the heart fails to pump blood sufficiently to meet the body’s demands. Is usually from acute MI, but may be from non ischemic including myocardial contusion, acute mitral valve regurgitation due to papillary muscle rupture, sus
tained arrhythmias, severe dilated cardiomyopathy and cardiac surgery. There is a failure to eject blood from the heart, hypotension and inadequate cardiac output
Mani - Signs are consistent with those of end stage heart failure, Cyanosis, mean arterial and systolic BP dec due to poor stroke volume. Urine output dec because of lower renal perfusion
Treatment - requires striking a precarious balance between improving cardiac output, reducing the workload and oxygen needs of the myocardium and inc coronary perfusion. Drugs - dopamine, dobutamine and norepinephrine are the most commonly used inotropic and vasopressor agents. Mechanical using an intra aortic balloon pump or extracorporeal membrane oxygenation can help to inc systemic blood flow and stabilize the pt
Obstructive shock? Distributive Shock?
Obstructive shock describes circulatory shock that results from mechanical obstruction of the flow of blood through the central circulation. Maybe caused by dissecting aortic aneurysm, cardiac tamponade, pneumothorax, atrial myxoma and evisceration of abd contents into the thoracic cavity because of ruptured hemidiaphragm. most frequent is pulmonary embolism. Primary physiologic result of obstructive shock is elevated right heart pressure due to right ventricular dysfunction. Signs are elevation of CVP and jugular distention. Treatment - correct obstruction, surgery pulmonary embolectomy, pericardiocentesis, chest tube. Severe PE fibrinolytic drugs may be used.
Distributive shock - is characterized by loss of blood vessel tone, enlargement of the peripheral vascular compartment, and displacement of the vascular volume away from the heart and central circulation. Two main causes; a dec in the sympathetic control of vasomotor tone or the release of excessive vasodilator substances.
Three shock states? Neurogenic shock? Anaphylactic shock? Sepsis and septic shock?
Neurogenic shock is caused by dec sympathetic control of blood vessel tone due to a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels. Can be interrupted by brain injury, the depressant action of drugs, general or spinal anesthesia, hypoxia, lack of glucose. HR is ofter slower than normal, the skin is dry and warm. Is rare and usually transitory.
Anaphylactic shock - is a clinical syndrome that represents the most severe systemic allergic reaction. Results from an immunologically mediated reaction in which vasodilator substances such as histamine are released into the blood. They cause vasodilation of arterioles and venules along with a marked inc in capillary permeability. Is accompanied by life threatening laryngeal edema and bronchospasm, circulatory collapse, contraction of GI and uterine smooth muscle and urticaria or angioedema. Most frequent are penicillin, foods, nuts and shellfish, insect venoms. Latex allergy. Treatment - immediate discontinuation of inciting agent or action to dec its absorption. Epinephrine is given but oxygen and antihistamine drugs, corticosteroids, and bronchodilators.
Sepsis and septic shock - is the most common. immune response to severe infection. Defined as a suspected or proven infection plus the clinical mani of what has been termed the systemic inflammatory response. Septic shoc k - is defined as severe sepsis with hypotension, despite fluid resuscitation. Signs are hypotension and warm, flushed skin. Usually with dec systemic vascular resistance. Abrupt changes in cognition and behavior. Fever and inc leukocytes. Elevated serum lactate or metabolic acidosis. All the way to multiple organ dysfunction.
Treatment - early recognition can lead to better outcomes. Administration of antibiotics that are specific to the infectious agent is essential. Swift and aggressive fluid administration is needed and aggressive use of norepinephrine or epinephrine. With >180 mg glucose should receive insulin therapy
What are the complications of shock? Acute lung injury/ acute respiratory distress syndrome? Acute Kidney Injury/ Gastointestinal complications? Disseminated Intravascular coagulation DIC? Multiple Organ dysfunction syndrome?
Shock not only stops the machine is wrecks the machinery.
ALI/ARDS is a potentially lethal form of pulmonary injury that may be either the cause or result of shock. ARDS is the more severe form. After injury or infection the respiratory rate and effort of breathing increase. Arterial blood gas analysis establishes the presence of profound hypoxemia that is refractory to supplemental oxygen.
Acute kidney injury - often occurs in the context of sepsis and multiple organ failure. Acute tubular necrosis is usually reversible but can take weeks to months, Watching urine output and serum creatinine and blood urea nitrogen levels.
Gastrointestinal - is particularly vulnerable to ischemia because of changes in distribution of blood flow to its mucosal surface. Proton pump inhibitors and histamine 2 receptor antagonists may be given prophylactically to prevent GI ulcerations and bleeding in pt.
DIC - by widespread activation of the coagulation system with resultant formation of fibrin clots and thrombotic occlusion of small and mid sized vessels. 30-50% pt with gram negative. Treatment is to fix the underlying disorder and measures to interrupt the coagulation process. But mortality rates jump when DIC is involved. Can use anticoagulation therapy and administration of platelets and plasma.
Multiple organ dysfunction syndrome - MODS is the presence of altered organ function in an acutely ill pt such that homeostasis can’t be maintained without intervention. Is particularly life-threatening complication of shock. Management is primarily supportive.
