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Short-Term Accomodation by Increased Heart Rate INCREASE of the HEART RATE and ITS LIMITS

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Short-Term Accomodation by Increased Heart Rate INCREASE of the HEART RATE and ITS LIMITS Short-term accomodation by increased heart rate INCREASE OF THE HEART RATE AND ITS LIMITS A2 Pathological ratio: heart 170 syst:diast = 60:40 rate/min 160 Limits: - decrease of diastolic 150 filling time 140 - A2 starts during the ventricular systole 130 120 110 A1 and A2 : beginning of the atrial systole 100 90 80 70 60 A1 50 Physiological ratio: 40 syst:diast = 40:60 0 20 40 60 80 100 120 140 time in 1/100 sec 2 Ventricular sy stole Ventricular diastole COMPENSATION OF HEART FAILURE IN ORDER TO MAINTAIN SUFFICIENT ARTERIAL BLOOD PRESSURE 1. Heart failure (i.e. ↓ pump function, stroke volume and cardiac output) limited elevation of heart rate overlimited elevation of can compensate heart rate can worsen the ↓ situation restored pump function renal blood pressure decreases ↓ ↑ renin ↓ 3 COMPENSATION OF HEART FAILURE IN ORDER TO MAINTAIN SUFFICIENT ARTERIAL BLOOD PRESSURE 2. ↑ renin ↓ atrial natriuretic peptide (ANP): angiotensin I, II (III) a tissue hormone vasoconstriction aldosterone ↓ ↓ ↑ ↑ Na + and water retention peripherial resistance ↓ of blood vessels increased blood volume ↓ ↓ ↑ afterload ↑ preload ↑ arterial blood pressure, ↑ stroke volume, cardiac output (pump function restored ) Overcompensation can easily cause fatal consequences 4 HYPERTENSION Important syndrome in humans (hypertension/hypertonia disease) Causes • Vascular: arterial or capillary stenosis, compression (ie. atherosclerosis) • ! Renal : loss of renal parenchyma, increase of fibrous tissue (chronic renal failure, sclerosis, fibrosis) Important in vet. med.! • Endocrine: - increased function of adrenal medulla and cortex (iatrogen effects included) - hyperthyreosis Local consequence on the heart : hypertrophy ↓ cardiac muscle damage 5 HYPOTENSION There is little importance of primary hypotension/hypotonia in veterinary practice. Well known (secondary) forms of hypotension: • associated with shock syndromes • or with increased vagotony/parasympathicotony 6 SHOCK Definition: an acute , life-threatening disturbance of the peripherial circulation (circulatory collapse ) and that of the tissue perfusion as a result of the incongruency between the capacity of blood vessels and circulatory blood volume . - Widespread arteriolar dilation Cardiogenic shock =acute heart failure Shock is always secondary to some initiating event. Blood volume Blood vessel volume Shock Shock 7 SHOCK Collapse (acute brain hypoxia) – shock A condition of extreme prostration, associated with sudden loss of consciousness due to faulty circulation such as might occur from a defective heart, shock, or haemorrhage. Although the collapse of an athlete following strenuous activity may be physiological (for example, a marathon runner who stops suddenly at the end of a race may collapse because of the pooling of blood in the legs), any collapse should be investigated completely to eliminate sinister causes. 8 Reminder: three factors of circulation 1. Effective „motor/pump” (the heart) 2. Proper pipes (blood vessels ie. capillary bed)) 3. Proper volume of circulating fluid (blood volume) Alteration in any of them causes changes in the remaining two 9 CHARACTERISTICS OF SHOCK Facts: • Shock is a microcirculatory disorder (tissue perfusion is inadequate) • "Overfunctioning" during compensation (a pathological mechanism) often occurs. The question of the primary causes: 1. Is shock a primary disorder of vasoregulation? 2. Is shock a state caused by the decrease of cardiac output? This problem is similar to the "chicken or the egg" question: which came first? The etiology and pathomechanism of shock syndromes are different, the consequences are the same. 10 CLASSIFICATION OF SHOCK SYNDROMES According to causes : blood/plasma loss, water loss, trauma, burns, anaphylactic, septic/endotoxin, endocrine, cardiogenic shock According to pathophysiological principles: absolute or relative shock Shock syndromes to be studied: 1. Hypovolemic: blood or fluid loss → absolute 2. Blood maldistribution : neurogenic (i.e. central); → relative anaphylactic, septic (vasculogenic/angiogenic i.e. peripherial) 3. Cardiogenic → relative 4. Mixed form → abs.-rel. 11 Hypovolaemic shock ⊗ 12 PATHOGENESIS OF HYPOVOLAEMIC SHOCK Starting point: vasomotor centre, heart function and capillaries are normal Cause: whole blood or water (fluid, plasma) loss (P Blood : 35-45% - Cardiac output fails) (maintained : heart, brain, kidneys) ↓↓↓ Consequences: - general vasoconstriction and emptying of blood stores i.e. contraction of the spleen → compensated, absolute hypovolaemia develops Increased - further vasoconstriction occurs ! peripheral → vascular (differences among organs) oliguria, decreased resistance intestinal secretion → - organ function disorders develop due to hypoxia - vasodilation, decompensated hypovolaemia ↓↓↓ 13 PATHOGENESIS OF HYPOVOLAEMIC SHOCK - con’t decompensated hypovolaemia ↓ cardiac output decreases (cardiogenic factor) ↓ (hypoxaemia, hypoxia) decreased blood pressure failure of vasomotor centre (neurogenic factor ) Decreased peripheral vascular circulatory failure further decreased blood pressure resistance ↓ IRREVERSIBLE SHOCK 14 Vasculogenic shock (Blood maldistribution ) ⊗ 15 PATHOGENESIS OF VASCULOGENIC SHOCK (Blood maldistribution ) Starting point: normovolaemia, normal cardiac function Causes: anaphylactic reaction, posttraumatic pain, toxins (LPS), local hypoxy or state ie. release of compressed blood trauma of the CNS (these are vessels (angiogenic factors) neurogenic factors) ↓ ↓ primary vasodilation, increased damage of vasomotor centre permeability relative hypovolaemia, ↓preload ↓ ↓ cardiac output (cardiogenic factor) (hypoxaemia, hypoxia) ↓ The same further consequences as above ↓ IRREVERSIBLE SHOCK 16 CARDIOGENIC SHOCK ⊗ Former name: acute heart failure 17 PATHOGENESIS OF CARDIOGENIC SHOCK Starting point: heart failure. Normovolaemia, vasomotor centre is intact, no vasodilation Causes : ↓ Cardiac output and tissue ↑ CVP perfusion (forward effect) stasis, edema (backward effect) Relative hypovolaemia, tissue hypoxy ↑ compensatory ↓ vasomotor activity Vasoconstriction, afterload ↑ relative hypovolaemia, sudden P blood ↓ ↓ further cardiac damage, output decreases, tissue hypoxy ↓ The same further consequences as above ↓ 18 IRREVERSIBLE SHOCK CONSEQUENCES OF SHOCK Stages: 1. Nonprogressive 2. Progressive 3. Irreversible 19 CONSEQUENCES OF SHOCK Oxygen and energy stores are depleted anaerobic glycolysis instead of oxydative phosphorilation metabolic acidosis Membrane transport mechanisms are impaired Lysosomal enzymes are released Structural integrity is lost Tissue necrosis develops Dramatic accumulation of meidators – histamine, kinins, PAF, complements, cytokines Systemic inflammation Systemic activation of complement system, coagulation, fibrinolysis and kinin pathways 20 CONSEQUENCES OF SHOCK 1. 1. Haemodynamic consequences – the primary factors Shock factor ↑ permeability, ↓ cardiac output, ↓ perfusion ↓ constriction of arterioles, closing of precapillary sphincters, splenic contraction "overfunction": ↓ further vasoconstriction often occurs ↓ ↑ arterial (hydrodynamic) blood pressure ↓ tissue hypoxy, acidosis, accumulation of toxic metabolites, DIC (disseminated ↓ capillary (hydrostatic) blood pressure intravascular coagulation) ↓ ↓ interstitial fluid can re-enter the capillaries vasodilation ↓ ↓ ↓ PCV, ↑ blood volume IRREVERSIBLE SHOCK ↓ RECOVERY BAD NEWS! GOOD NEWS! 21 CONSEQUENCES OF SHOCK 2. 2. Disturbances in cellular metabolism Carbohydrate, lipid, protein metabolism is involved Shock factor → haemodynamic failure → metabolic disorder Hypoxia/hypoxy - the most important ↓ → pCO 2, piruvate and lactate production increases acidosis ↓ ATP, ADP, AMP (energy deficiency) → ↓Na/K & other „pumps” Increased glycogenolysis, lipolysis, proteolysis ↓↓↓ Changes in blood composition Further consequences: Increased ketogenesis Decreased heat production 2+ Accumulation of other intracellular metabolites (i.e. Ca ) 22 CONSEQUENCES OF SHOCK 3. 3. Changes in organ functions Shock factor → altered tissue perfusion → ↓ organ functions • Intestines: ↓ secretion (except for hypovolaemic shock as a result of diarrhoea, enteritis), then ↑ secretion, bacteraemia, endotoxaemia ↓ • Liver: deamination and NH 3-detoxifying • Kidney: ↓ GFR → "shock kidney” → extrarenal uraemia, reduce urine output • Pancreas: enzymes released into the blood stream; release of MDF (myocardial depressant factor) • Heart: ↑ heart rate, ↓ preload and cardiac output, myocardial damage → "shock heart„ , weak pulse • Lungs: tacyhpnea, DIC, hyperaemia, edema → "shock lung", RDS (respiratory distress syndrome) • RES/MPS: ↓ phagocytosis • Liver, myocardium, kidney tubules, adr. cort., muscle, brain cell (cerebral edema) damage • Hypothermia, edema, haemorrhage, thrombosis (esp. septic shock) 23.
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