Circulatory Failure PDF

CIRCULATORY FAILURE Main functions of the circulatory system • Supplying tissues with nutrients/building materials (oxygen, substrates) and removing metabolic products (CO2, H+ ions) • Transport of substances between tissues, mediation in hormonal regulation - signaling between the body's componen...

CIRCULATORY FAILURE Main functions of the circulatory system • Supplying tissues with nutrients/building materials (oxygen, substrates) and removing metabolic products (CO2, H+ ions) • Transport of substances between tissues, mediation in hormonal regulation - signaling between the body's components • Participation in the body's immune response → cells and mediators of the immune system circulate in the blood • Removing the waste products of metabolism to the excretory organs for disposal • Thermoregulatory function • The cardiovascular system is composed of two circulatory paths: →pulmonary circulation → systemic circulation • Pulmonary c.: movement of blood from the heart to the lungs for oxygenation, then back to the heart again • At the lungs, the blood travels through capillary beds on the alveoli where gas exchange occurs, removing carbon dioxide and adding oxygen to the blood • Systemic c.: movement of blood from the heart through the body to provide oxygen and nutrients to the tissues of the body while bringing deoxygenated blood back to the heart Vascular Network • The left ventricle pumps blood into the aorta, which then distributes the blood flow throughout the body using a network of blood vessels • → the major distributing arteries that arise from the aorta branch into successively smaller arterial vessels until they become capillaries (the smallest vessels) • HERE gas and nutrient exchange with the tissues occurs • → capillaries join to form veins, which then continue to join with other veins until they enter either the superior or inferior vena cava that brings the blood back into the right atrium of the heart Ventricles • The left ventricle (pumps the oxygen-rich blood to the whole body) is thick-walled and pumps blood into the aorta under pressure, up to 120 mm Hg during systole and 80 mm Hg during diastole. • The right ventricle (pumps the oxygen-poor blood to the lungs) is thin-walled and works under falling pressure, and the systolic pressure for the pulmonary artery is only 25 mm Hg • → anatomical differences between the left and right ventricles From arteries to veins • the aorta and arteries have the highest blood pressure → mean aortic pressure is about 90 mmHg in a resting individual with normal arterial pressures • the mean blood pressure drops significantly as the blood flows down the small arteries and arterioles • by the time blood reaches the capillaries, the mean pressure may be 25-30 mmHg (depending on the organ) → the pressure falls further as blood travels into the veins and back to the heart → pressure within the vena cava near the right atrium is very close to 0 and fluctuates from a few mmHg negative to positive with respiration Characteristics of blood vessels • ARTERIES: • high – pressure system • have a thick layer of smooth muscle → arteries are low compliance vessels and require a high pressure to expand them even by a small amount • also called resistance vessels due to their ability to increase vascular resistance, which is a significant determinant of blood pressure • VEINS: • low – pressure system • have a thin layer of smooth muscle → have a high compliance • contain valves to keep blood flowing • veins as blood reservoirs → systemic veins contain approximately 64 % of the blood volume • CAPILLARIES: • the smallest type of blood vessel • have a very thin wall (only 1 layer of endothelial cells) • carry both oxygenated and deoxygenated blood Blood flow • Like all fluids, blood flows from a high pressure area to a region with lower pressure → arteries to capillaries to veins • Blood flow can either be laminar or turbulent • LAMINAR • occurs when the flow is slowest near the vessel wall (where there is more friction) and fastest in the center of the blood vessel (where there is less friction) • occurs in most blood vessels • TURBULENT • describes a situation in which blood flows in all directions → incoherent • occurs at branch points, during vessel obstruction (thrombus) The Laws of Flow • Blood flow is described by: Starling’s law, Lavoisier-Laplace law, Hagen-Poiseuille law, etc. • BEFORE – Stroke Volume (SV) • is the volume of blood in millilitres ejected from the each ventricle due to the contraction of the heart muscle • SV is the difference between end diastolic volume (EDV) and end systolic volume (ESV) • 3 primary factors that regulate SV are preload, afterload and contractility • also HR has an impact (heart rate = no of beats/min) • BEFORE – Cardiac Output (CO) • is how many liters of blood heart pumps in one minute CO = SV * HR • to calculate → multiply stroke volume by heart rate The Laws of Flow • Blood flow is described by: Starling’s law, Lavoisier-Laplace law, Hagen-Poiseuille law, etc. • Poiseuille law • explains blood flow rate, decribes relationship between vessel diameter, lenght of the vessel, viscisity of the fluid and pressure gradient along vessel • which of these factor has the greatest impact on the blood flow rate? • Starling’s law • states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) • the increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more strongly (the so-called FrankStarling mechanisms) The Laws of Flow • Laplace law • describes the force with which blood stretches the walls of the heart chambers • wall tension is directly proportional to the pressure in the chamber and its radius, and inversely proportional to the chamber thickness • this law is important in the heart because it explains how multiple pathological conditions affect heart function, e.g.: When a ventricle is dilated the radius of it increases, which increases the tension When a ventricle is thickened the wall thickness increases, which decreases tension CIRCULATORY SYSTEM Aim: to supply the tissues with enough oxygenated blood to meet their metabolic demands → to maintain the perfusion CIRCULATORY FAILURE: INABILITY OF THE CARDIOVASCULAR SYSTEM TO SUPPLY THE ORGANS (CELLS, TISSUES) OF THE BODY WITH ENOUGH OXYGENATED BLOOD TO MEET THEIR METABOLIC DEMANDS = INABILITY TO MAINTAIN THE PERFUSION CIRCULATORY FAILURE INABILITY OF THE CARDIOVASCULAR SYSTEM TO SUPPLY THE ORGANS (CELLS, TISSUES) OF THE BODY WITH ENOUGH OXYGENATED BLOOD TO MEET THEIR METABOLIC DEMANDS PATHOLOGICAL DECREASE OF BLOOD FLOW Cardiac = central circulatory failure Vascular = peripheral circulatory failure ➢ Cause ➢ Adaptation mechanisms ➢ Consequences → clinical appearance CIRCULATORY FAILURE Cardiac = central circulatory failure Vascular = peripheral circulatory failure CAUSES: • increased preload (increased venous return) → e.g. impaired kidney function, water retention in the body • increased afterload (e.g. hypertension, aortic stenosis) → the afterload can be decreased by any process that lowers blood pressure Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. Afterload is the force or load against which the left ventricle has to contract to eject the blood. Afterload is proportional to the average arterial pressure CARDIAC CIRCULATORY FAILURE HEART FAILURE IS DEFINED AS THE INABILITY OF THE HEART TO GENERATE CARDIAC OUTPUT ADEQUATE TO MAINTAIN THE METABOLIC DEMANDS OF THE TISSUES AT REST OR DURING EXERCISE WHILE OPERATING AT A NORMAL OR ENHANCED LEFT VENTRICULAR FILLING PRESSURE (BRAUNWALD, 2001) RESULTS FROM DECREASED CARDIAC OUTPUT Cardiac output is the volume of blood being pumped by the heart in the time interval of one minute. Depends on: myocardial contractility, blood volume, heart rate heart rhythm https://www.youtube.com/watch?v=hpQFToprlH8 CARDIAC CIRCULATORY FAILURE (HF) HEART FAILURE IS DEFINED AS THE INABILITY OF THE HEART TO GENERATE CARDIAC OUTPUT ADEQUATE TO MAINTAIN THE METABOLIC DEMANDS OF THE TISSUES AT REST OR DURING EXERCISE WHILE OPERATING AT A NORMAL OR ENHANCED LEFT VENTRICULAR FILLING PRESSURE (BRAUNWALD, 2001) DECREASED CARDIAC OUTPUT → decreased blood flow through tissues and organs → this means heart can’t supply the cells with enough blood with nutrents and OXYGEN → can say that heart doesn't pump blood as well as it should HF is a chronic, progressive condition Heart Failure • THREE-STAGE MECHANISM OF HF FORMATION:. • The immediate adaptation phase • Chronic adaptation phase and ventricular hypertrophy • Phase of cardiac remodeling ADAPTATION Problem: the circulatory system fails to supply the organs with enough blood to meet their metabolic demands (decreased cardiac output) Aims: ✓to maintain the proper blood flow and perfusion Solution: increase cardiac output ✓By increasing myocardial contractility ✓By increasing cardiac rhythm ✓Maintain the proper blood presure • Sympathetic system stimulation • Activation of RAA system SYMPATHETIC STIMULATION • • activates body “fight-or-flight” response releases the hormones (catecholamines epinephrine and norepinephrine) • peripheral vessels have α-adrenergic receptors coronary vessels have β-adrenergic receptor • Heart: coronary vessels vasodilation Blood vessels:contraction of the peripheral vessels (renal, skin, visceral arteries and veins) SYMPATHETIC STIMULATION cardiac sympathetic nerve fibers are located at subepicardium and travel along the major coronary arteries • releases the hormones (catecholamines - epinephrine and norepinephrine) Heart: positive chronotropy, positive inotropy SYMPATHETIC STIMULATION As the effect of sympathetic stimulation there will be IMPROVEMENT for heart function → increased heart rate/contraction force lead to increased stroke volume, which in turn results in the restoration of cardiac output ACTIVATION OF RAA SYSTEM 2nd mechanism of adaptation in HF is activation of RAA system • The RAA system is critical for fluid-electrolyte homeostasis and long-term blood pressure regulation (crucial in HF) • Regulates blood pressure by increasing: • sodium (salt) reabsorption, • water reabsorption (retention) • vascular tone Finally leads to: vasocontriction → increased arterial blood pressure ACTIVATION OF RAA SYSTEM STEP BY STEP 1. When blood pressure falls, kidneys release the enzyme renin into the bloodstream 2. Renin splits angiotensinogen (a protein that liver makes and releases) into pieces → one piece is the hormone angiotensin I 3. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) (produced in lungs) 4. Angiotensin II causes the release of aldosterone from adrenal glands ACTIVATION OF RAA SYSTEM EFFECTS OF ANGIOTENSIN II 1. Stimulates the release of aldosterone from adrenal glands. 2. Increases blood pressure by constricting blood vessels. 3. Triggers the sensation of thirst through hypothalamus. 4. Triggers the desire for salt (sodium) through hypothalamus. 5. Stimulates the release of antidiuretic hormone (ADH, or vasopressin) from pituitary gland, which causes kidneys to reabsorb water. ACTIVATION OF RAA SYSTEM EFFECT OF ALDOSTERONE Regulates the salt and water balance of the body by increasing the retention of sodium and water and the excretion of potassium by the kidneys ADAPTATION Activation of symphatetic and RAA systems lead to → TEMPORARY IMPROVEMENT → increased cardiac output +increased blood pressure = better perfusion BUT chronic activation of these responses result in haemodynamic stress and exert negative effects on the heart and the circulation → WORSE CLINICAL CONDITION OF THE PATIENT Drugs used in cardiac failure ACE inhibitors Neurohormonal activation is now known to be one of the most important mechanisms underlying the progression of heart failure Diuretics VENTRICULAR HYPERTROPHY Becouse of the chronic adaptation (chronic activation of neurohormonal systems) the ventricular hypertrophy occurs → usually occurs within left ventricle (is the heart's main pumping chamber) → cardiac hypertrophy is usually characterized by an increase in cardiomyocyte size and thickening of ventricular walls → uncontrolled high blood pressure (activation of RAA) is the most common cause of left ventricular hypertrophy (compensated)→ response of the heart to increased workload VENTRICULAR HYPERTROPHY Becouse of the chronic adaptation (chronic activation of neurohormonal systems) the ventricular hypertrophy occurs → initially, such growth (compensated hypertrophy) is an adaptive response to maintain cardiac function → BUT in prolonged increased workload (prolonged activation od RAA + symphatetic NS) these changes become maladaptive and the heart ultimately fails → this cardiac enlargement is typically referred to as pathological cardiac hypertrophy → if HF progresses these changes will turn into further heart remodelling (decompensated HF) CARDIAC REMODELLING Phase of decompensated HF Decompensated heart failure (DHF) is defined as a clinical syndrome in which a structural or functional change in the heart leads to its inability to eject and/or accommodate blood within physiological pressure levels, thus causing a functional limitation and requiring immediate therapeutic intervention → pathological myocardial hypertrophy and stimulation of apoptosis → necrosis may also appear in advanced HF → the effect of apoptosis and necrosis is cardiac fibrosis, which is replacement of cardiomiocytes with connective tissue → as HF develops, there is a net loss of cardiomyocytes → impaired contractility of myocardium → conduction disturbances (problems with the electrical system that controls heart's rate fibrosis is associated with and rhythm) arrhythmias CARDIAC REMODELLING leads to: →cellular changes → genetic changes → molecular changes → biochemical changes → structural changes Altered energy metabolism has been reported in cardiac remodeling → results in low energy availability for myocardial proteins with ATPase activity, and generation of reactive oxygen species, oxidative stress and its consequences Strong evidence supports an association between cardiac remodeling and oxidative stress resulting from increased reactive species production and decreased antioxidant defense CARDIAC REMODELLING Calcium handling → Contraction of the heart is regulated by cyclic changes in calcium (Ca2+) within cardiomyocytes. →Relaxation of cardiomiocytes occurs when Ca2+ is pumped back into the SR by sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) or out of the cell by the Na+/Ca2+ exchanger (NCX) • in the HF, calcium-handling abnormalities contribute to contractile dysfunction, e.g.: • impaired function of this protein (SERCA2a) leads to accumulation of Ca2+ in the cytosol, which prevents relaxation and reduces the pool of Ca2+ available for release from the SR during heart contraction • ALSO there is a leaking out the Ca2+ ions from SR due to dysfunctional release channel (RyR2) → this may contribute to contractile dysfunction increasing the incidence of arrhythmias and increasing the cell’s energy requirements CARDIAC REMODELLING Heart remodeling is characterized by alterations in the main contractile protein myosin changes cause a decrease in the power and/or kinetics of contractions and their desynchronization https://www.youtube.com/watch?v= x8aBKMYqGPY CARDIAC CIRCULATORY FAILURE ➢ Cause ➢ Adaptation mechanisms ➢ Consequences, clinical appearance CARDIAC CIRCULATORY FAILURE - CAUSES Hypertension and increased blood volume (e.g. kidney issues) • Morphological changes in myocardium (CADIOMYOPATHY) • Changes in heart rhythm • Valves insufficiency (mechanical restriction of blood flow) • Metabolic diseases • Neural and endocrine diseases (diabetes, hypo/hyperthyroidism, Cushing's syndrome, etc.) CARDIAC CIRCULATORY FAILURE CHRONIC ACUTE HEART FAILURE Right-sided Left-sided often, failure of one ventricle leads to failure of the other, SO may also affect BOTH ventricles means that the power of the left heart chamber, which pumps blood throughout the body, is reduced →it most often →may occurs due to coronary heart disease, heart attacks, or long-term high blood pressure →causes blood to build up in pulmonary veins, so common symptoms: →trouble breathing →shortness of breath →coughing, especially during exertion → most often develops from left-sided heart failure due to a backup of blood around lungs that puts more stress on the right side of heart → leads to blood buildup in veins, which in turn may lead to fluid retention and swelling → legs are the most common area to develop swelling → typical symptoms: fluid retention CARDIAC CIRCULATORY FAILURE HEART FAILURE Left-sided • • • The left ventricle cannot pump blood as it should. This causes blood to build up in the veins of the lungs. This can promote pulmonary congestion → pulmonary edema As the pressure in pulmonary blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs → this fluid reduces normal oxygen movement through the lungs CARDIAC CIRCULATORY FAILURE HEART FAILURE Right-sided • • • • The damaged right side of the heart stops pumping efficiently, and blood builds up in the veins As pressure increases in the veins, it pushes fluid into surrounding tissues The fluid buildup causes swelling and congestion throughout body → peripheral edema → ascites Ascites is the abdominal accumulation of fluid Ascites causes enlargement of the abdominal cavity, enlargement of the liver and fluid accumulation in the peritoneal cavity VALVE INSUFFICIENCY • results from degeneration of valves – thickening and deformation due to accumulation of mucopolysaccharides • characterised by the failure of the cardiac valves to close properly, resulting in blood flowing in the opposite direction; thereby, causing regurgitation or leakage VALVE INSUFFICIENCY • • may lead to regurgitation at the example of mitral insufficiency - the most common form of valvular heart disease Valve insufficiency in dogs • 75% of all cardiovascular diseases in dogs • most often mitral valve - mitral valve disease (MVD), no more than 30% cases related to tricuspid insufficiency VALVE INSUFFICIENCY IN DOGS • Often occurs with other conncective tissue changes – predisposing factor • Other factors (inflammatory): bacterial infections (teeth, gums), autoimmune diseases, viral infections, endocrine diseases • Usually mitral valve insufficiency (tricuspid valve insufficiency – up to 30% only) • Most prevalent in: KING CHARLES CAVALIER SPANIELS, Poodles, Dachshunds, Spaniels, Chihuahua, Pekingeses, Yorkshire Terriers • Clinical problem usually in older dogs VALVE INSUFFICIENCY IN HORSES AORTIC REGURGITATION • Common in OLDER horses, degeneration processes lead to valve fibrosis • blood flows back into the aorta and ventricle, which may lead to dilatation over time (dilated cariomyopathy) • Mild to moderate AR usually without clinical signs • Horses with worse prognosis: ✓ AR in horses under 16 years of age ✓ horses with moderate to severe AR and evidence of left sided volume overload, ✓ in horses with AR secondary to bacterial endocarditis Can cause ventricular premature beats (leading to changes in blood pressure and fainting) and atrial fibrillation VALVE INSUFFICIENCY IN HORSES MITRAL REGURGITATION • May result in sudden death due to pulmonary vessel rupture • Good prognosis in horses with mitral prolapse without left sided volume overload • Worse prognosis in horses with ruptured chordae tendineae and MR secondary to bacterial endocarditis VALVE INSUFFICIENCY IN HORSES TRICUSPID VALVE REGURGITATION • Usually physiological change, without significant hemodynamic disorders • Proper structure of the valve, only prolapse • Mild and moderate TR with unchanged atrial volume – NOT a clinical problem, the horse can be ridden safely • Severe regurgitation results in increased cardiac workload and congestive right heart failure (very rare) CARDIAC FAILURE/ INSUFFICIENCY • Degeneration of cardiomyocytes – cardiomyopathy – changes in ventricular volume and contactility CARDIOMYOPATHY The main types of cardiomyopathy include dilated, hypertrophic and restrictive cardiomyopathy CARDIOMYOPATHY IN DOGS • Dilated cardiomyopathy – changes in ventricular volume and contactility, then also electric activity of the heart • enlargement and widening of one/both chambers of the heart • often leads to arrhythmias (impared electric activity of the heart) and decreased heart contractility → which leads to pooling of blood in the left lower heart chamber → which can lead to blood clots, but ALSO to further dilation CARDIOMYOPATHY IN DOGS • Dilated cardiomyopathy • genetic background, • often leads to congestive heart disease → then to ascites • most often in purebred dogs (the most common canine CARDIOMYOPATHY), large, middle-aged, males: Doberman Pinschers, Boxers, Great Danes, Saint Bernards, Newfoundlands, Scottish Greyhounds, Irish Wolfhounds, Afghan Hounds, Old English Sheepdogs, Airedale Terriers, Royal Poodles, Labradors, golden retrievers occurs in up to 50% of male Doberman, 33% of female Doberman and 25% of Irish Wolfhounds CARDIOMYOPATHY IN CATS • Hypertrophic cardiomyopathy • characterized by cardiac hypertrophy with characteristic, small cavities in the absence of hemodynamic load • hypertrophy usually asymmetric→ usually of the interventricular septum and/or LV wall • leads to impaired diastolic function of the thickened ventricle and further to symptoms of heart failure, CARDIOMYOPATHY IN CATS • Hypertrophic cardiomyopathy • the most common heart disease in cats • disease progresses with time • typical symptoms: shortness of breath, exercise intolerance, pulmonary edema • genetic background most common in breeds: Maine Coon (9.5-26.3%), Ragdoll, British Shorthair, Sphynx and Persian cats, more often in male cats CARDIOMYOPATHY IN CATS • Dilated cardiomyopathy • less frequent (comparing to hypertrophic) • usually becouse of taurine deficiency – in cats fed vegetarian diets – more secondary nutritional cardiomyopathy exogenous amino acid for cats (their own synthesis does not cover their needs) → regulates the release of Ca2+ ions from the sarcoplasmic reticulum, is also responsible for maintaining the sensitivity of the contractile elements of the muscle fiber to the presence of Ca2+ ions CARDIAC FAILURE IN ANIMALS • RARE: congenital malformations: e.g. patent ductus arteriosus, ventricular or atrial septal defects, aortic or pulmonic stenosis • MOST COMMON occurs becouse of : Valve insufficiency Cardiomyopathy CARDIAC FAILURE • RIGHT HEART FAILURE • LEFT HEART FAILURE • Acute • Chronic CARDIAC FAILURE • Left heart failure –left ventricle cannot pump blood as it should. This causes blood to build up in the veins of the lungs → this can promote pulmonary congestion → pulmonary edema • Right heart failure - • damaged right side stops pumping efficiently, and blood builds up in the veins → as pressure increases in the veins, it pushes fluid into surrounding tissues → peripheral edema → ascites X X CARDIAC FAILURE CONSEQUENCES RESULTING FROM CONGESTION: • Microhaemorrhages • Fluid (transudate) accumulation in the interstitial tissue spaces and body cavities • Secondary lesions in organs RESULTING FROM DECREASED PERFUSION • HYPOXIA • CYANOSIS Fluid (transudate) accumulation Transudate develops from an imbalance of hydrostatic or oncotic pressure → results from increased hydrostatic or reduced oncotic pressure Congestive heart failure is one of the most common causes of transudates. Transudate is an ultrafiltrate of plasma that contains few, if any, cells and does not contain large plasma proteins, such as fibrinogen. • Transudate – low protein content <2,5%, total nucleated cell count < 1.5 X 109/L Exudate, on the other hand, is a sign of inflammation and is typically a consequence of increased vascular permeability. Exudate – protein rich (4-5%), total nucleated cell count > 7.0 X 109/L, results from increased vascular permability during inflammation, it is not a direct effect of passive hyperemia TRANSUDATE AND OEDEMA Edema (oedema) – an abnormal accumulation of fluid in interstitial tissue Types of accumulation of fluid in body cavities: ascites, hydrothorax (pleural effusion), hydropericardium Causes of fluid accumulation: 1. Increased hydrostatic pressure 2. Reduced plasma colloid osmotic pressure 3. Sodium retention 4. Lymphatic obstruction 5. Inflammation ASCITES http://pathophysiology.uams.edu Healthy dog, 5 ½ years http://pathophysiology.uams.edu Ascites in the same dog (about 5 l of fluid in abdominal cavity) ACUTE LEFT HEART FAILURE • Lung oedema (OEDEMA PULMONUM) • Results from rapid accumulation of the blood in pulmonary circulation → congestion and pulmonary hypertension → rapid transudate accumulation in alveoli and bronchioli CHRONIC LEFT HEART FAILURE Congestion and pulmonary hypertension results in cough and shortness of breath. Risk of lung oedema Brown induration of the lung (INDURATIO FUSCA) CHRONIC RIGHT HEART FAILURE Most right-sided heart failure occurs because of left-sided heart failure. The entire heart gradually weakens. • Sometimes, rightsided heart failure can be caused by: • • • High blood pressure in the lungs Pulmonary embolism Lung diseases such as chronic obstructive pulmonary disease 1. The left ventricle pumps less blood out to the body. 2. The reduced blood flow causes blood to back up behind the left ventricle, into the left atrium, lungs and eventually the right ventricle. 3. The backup causes higher blood pressure, which damages the right side of the heart. The damaged right side stops pumping efficiently, and blood builds up in the veins. 4. As pressure increases in the veins, it pushes fluid into surrounding tissues. 5. The fluid buildup causes swelling and congestion throughout body. CHRONIC RIGHT HEART FAILURE • Consequences: secondary lesions in the organs due to congestion (hypoxia→degenerative lesions→replacement by connective tissue) – Liver – swelling and degenerative lesions in the cells (nutmed liver – HEPAR MOSCHATUM), then cirrhosis (CIRRHOSIS HEPATIS CARDIACA) CARDIAC INSUFFICIENCY IN DOGS STAGE CRITERIA GROUPS A Patients at high risk for developing heart disease, but with no current identifiable lesions none B patients with structural heart disease, who have never had clinical signs of heart failure B1: patients without radiographic or echocardiographic evidence of cardiac remodeling in response to chronic valvular disease B2: patients with radiographic and/or echocardiographic evidence of left-sided heart enlargement C D Patients with past or current clinical signs of congestive heart failure. Acute stage – requires hospital treatment Patients with end-stage disease and clinical signs of congestive heart failure that are refractory to standard therapy Acute stage – requires hospital treatment Chronic stage – outpatient treatment Chronic stage – outpatient treatment PERIPHERAL CIRCULATORY FAILURE Causes: Decreased blood volume Relative decrease in blood volume – vasodilation due to neuronal or humoral disregulation CIRCULATORY SHOCK Shock is a medical emergency in which the organs and tissues of the body are not receiving an adequate flow of blood. • • • • • Hypovolemic – rapid loss of 1/3 blood volume Septic Anaphilactic Cardiogenic Neurogenic • Circulatory collapse – disproportion between circulating blood volume and vascular space CIRCULATORY SHOCK Loss of blood or massive vasodilation → decrease of blood pressure Aim: to maintain perfusion of CNS and the heart → redistribution of blood due to adrenergic stimulation Restore the blood flow? → tachycardia, tachypnoe, pale skin, decreased temperature of the skin, oliguria, anuria, loss of conscious Clinical appaerance depends on shock organs and released mediators CIRCULATORY SHOCK I phase – initial II phase – compensatory III phase – metabolic: • Tissue ischemia • Metabolic acidosis • Decreased coronary flow • Release of kinins and enzymes from damaged pancreas IV phase • Critical decrease of blood pressure • Vasodilation due to metabolic acidosis, DIC • Damage of intestinal mucosa and release toxins to the circulation • Necrosis of renal tubular epithelium, left after recovery