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Heart failure.pdf
- 1. Heart failure Heart failsto accomplish his normal function => Provide enough cardiac output In normal or above normal filling pressures heart is unable to maintain enough output to meet the minimum metabolic need of body tissues Factors determining cardiac output CO = HR * S.V which depends on – intrinsic health of myocardium – preload – afterload Preload: the amount of blood present in the LV at the end of diastole = EDV End Diastolic Volume on which the LV has to work on systole to push it out, to push out a part of it not all = 50% ejection fraction Ejection fraction : the part of EDV which is ejected per contraction Preload = EDV the amount of blood on which the ventricle has to work EDV => preload Ex : Venous return, diastole duration Then the left heart has to eject this blood against total systemic resistance generated by arteriols (muscular) and precapillary sphincters The right heart works against the pulmonary resistance Afterload is the resistance which the ventricle has to generate cardiac output Heart is like a donkey Heart failure Intrinsically unhealthy myocardium preload afterload Severe bradycardia Severe tachycardia => empty cycles oxygen demand 5 million people in usa alone HF Every year ½ million is added As age chances of HF
- 2. Old age Terms 1- Highoutput heart failure 2- Low output heart failure 3- LV HF 4- RV HF 5- Biventriculaire or congestive 6- Systolic F 7- Diastolic F 8- Forward F 9- Backward F 10- Acute HF 11- Chronic HF 1- Output Output HOF LOF Heart is relatively healthy It can generate CO Pathological increased demand on CO Inspite of CO it s unable to meet tissues demand so it s a failure Heart can’t maintain normal CO Peripheral demand is normal Thyrotoxicosis Very very sever anemia Myocardial Contractility failure intrinsic prblms :
- 3. Pregnancy more than1 baby Paget disease of bones : bone turnover become so fast it requires more blood flow Beri beri deficiency of thiamine AV fistula - IHD - infiltrative extrinsic prblms - Negative inotropic agents (anti tachyarrithmic) –acidosis Preload EDV volume overload => preload => stretch myocytes more than physiological limits Starling Laplace : P = T/R if Preload => R so P => CO - valvular diseases of heart MR, AR, Afterload : P = T/R Afterload => P that must be generated => heart must generate T if it can’t it fails - systemic hypertension - A S - HOCM Rate rhythm problems : sever - bradycardia - tachycardia : diastole duration HR is so fast => total cardiac cycle duration is especially diastole time => ventricle doesn t relax for enough time to fill properly (Starling again ) Thiamine deficiency => glucose partial degradation => lactate => vasodilatation => blood moves from arterial to venous side rapidly => no enough oxygen extraction can be done Frank Starling low : more EDV => more stretch => more contraction - in physiological limits Laplace’s low : P = T/R P overload V overload Thickness Length normal no elongation Hypertrophy then eventually dilatation Thick and Elongated Hypertrophy and dilatation in the same time 2- RVF LVF biventricular LVF RVF - Secondary to LV F - Core pulmonale : RV hypertrophy, dilatation and eventual failure due to pulmonary hypertension which is not due to LVF Isolated are less common -Myocardial unhealthy : MI -Preload MR AR -Afterload HTA coarctation of aorta AS EF is reduced LV receives more + pumps less => dilatation
- 4. - PS, TR, RVP RA can t fill it so RA : P => P in systemic veins P in liver micro circulation because it can t drain in IVC anymore but it still receives blood from Overfield LV receives more blood in diastole => S3 LV : P LA can t fill it so LA : P P in pulmonary veins => interstitial edema => pulmonary edema features => bronchial edema Pulmonary reaction : - fibrosis - reactive arteriole vasoconstriction HTAP => pressure overload to RV JVP Hepatomegaly painful if rapid constitution Liver pulstale liver : TR Portal hypertension - SPMG - edematous GIT - Ascitis Congestion of systemic circulation Leackage of fluid from every where Anasarca generalized edema - epanchements pleuraux pericardique Dyspnea : less compliant lungs => respiration muscles are tired extra effort Orthopnea: dyspnea worsened by lying down PND: paroxysmal nocturnal dyspnea Lying down => venous return to RA=> RV => edemated lung => Frotty pink sputum bronchial edema - cough - severe => narrowed especially during expiration => cardiac wizzing Crepitations : alveoli open and close with sound Systemic congestion and edema Edema and congestion in the pulmonary system Rate and rhythm => both ventricles simultaneousely Biventricular HF : CHF Dyspnea : heavy and buggy lung reperatory muscles diaphragm and intercostals become tired => excessive effort for breathing => unpleasant Systolic F Diastolic F D is normal S is disturbed EDV is normal but V can’t produce enough ejection fraction no matter what it receives it can’t eject it => dilatation Ventricles do not relax properly they are not as compliant as they should be Ischemic heart disease HTA later (early is diastolic failure) Toxicity of inotropic negative drugs Anti arrythmics hypertrophy : - cavity becomes smaller and => ability to receive EDV is reduced - hypertrophied can’t relax properly enough => don’t accommodate enough => they can’t maintain enough C.O LVH or RVH because of pressure overload amyloidosis
- 5. Rapid feeling ofoverfilled V => S3 S1+S2+S3+0 early phase of HOCM Galop S4 : atrial contraction against stiffened ventricle => S4 S1+ S2 + 0 + S4 EDV EDP EDV EDP => congestion More common Better diagnosis Heart has 2 fonctions : Ventricle is supposed to - relax enough to fill enough - contract enough to maintain proper co EDV depends on : - filling pressure - filling time : duration of diastole - how easily ventricle relaxes When a ventricle fails => there are 2 problms LV RV Backward f Pulmonary congestion Peripheral edema JVP Forward f Systemic underperfusion Poor blood oxygenation Acute/ Chronic CF A- Acute CF -LV: acute pulmonary edema du to cardiac failure (of cardiac origin) (dyspnea, orthopnea, PND, crepitations) - both V : cardiogenic shock Cardiac cacchexia To see later : second part of part3 Causes of acute cardiac failure 1- Massive MI 2- Sudden failure of valve, - MI of papillary muscle or of the myocardium to which it is inserted => rupture => mitral - infective endocarditis => aortic valve 3- MI involving interventricular septum => inter ventricular communication ventricular septum defect 4- Massive pulmonary embolism => RV sudden failure acute RVF
- 6. LV doesn’t receiveenough blood 5- Cardiac tamponnade JVP and BP distant heart sounds Cardiac cachexia CHF : => anorexia => oedematous GIT => malabsorption => loss of nutrients from GIT => weight loss => loss from urinary system => anabolic rate is down and metabolism is up Pathophysiology 1- Initial insult to cardiac function 2- Onset and triggering of compensatory mechanisms 3- Advantages of compensatory mechanisms 4- Disadvantages of // // 5- Progressive irreversible CCF 5 year mortalité => 50 % 1- Initial insult to cardiac function MI Massive loss of myocardium which is replaced by scar tissue => hypokinetic ou dyskinetic 2- Onset and triggering of compensatory mechanisms A- Sympathetic adrenergic stimulation mechanism CHF => + carotid sinus => sympathetic outflow Initially advantageous : HR tachycardia => => CO Inotropic + => contractility => SV stroke volume Adrenaline release from medulla => HR and SV => CO + smooth muscles in blood vessels : - veinoC => venous return => EDV (pre load) => SV => CO - arterioloC => redistribution of blood in the body to vital organs (heart, brain) preferential perfusion initially advantageous B- RAAS CO => renal hypo perfusion Sympathetic activity => constrict renal vessels
- 7. ==> hypoperfusion => GFR => Na+ retention ==> + RAA => renine activity => AT II which is - sympathetic nerves ending stimulation - venoC - arterioloC - action on adrenal medulla => zona glomerulosa => release of Aldosterone C-ADH water retention vasopressine (veino and arterioloconstriction) D- enotheline released by endothelial cells 1) => strong vasoC => generalized vasoC 2) Sympathetic overflow 3) + RAAS 4) LV hypertrophy D- ANP and BNP (Brain Natriuretic peptide it is ventricular) => beneficial trying to face the deleterious effects of other compensatory mechanisms They face Na retension, water retensio, vasoC, +RAAS with el 3aks 3- Advantages of compensatory mechanisms Short term advantages, all together they are producing : + inotropisme, veinoC, selective arterioloC 4- Disadvantages of prolonged compensatory mechanisms Neuro hormonal activations Heart is exposed to chronic High volume (retension) => high pre load vasoC => chronic elevation of after load 1) Chronic excessive preload 2) Chronic excessive afterload myocardial damage ===> remodeling process Loss of lyocardial cells, fibrosis, LVH Altered genomic expression => abnormal unsusual => abnormal handling proteins are abnormal => myocardial function is decreased => further cardiac failure due to prolonged neuro humoral activations => remodling => dilatation Laplace’s law P = T/R Because of myocardial remodeling : T => generated pressure => more blood is trapped in the ventricle => progressevily EDV => D is increasing
- 8. As time passesby, capanility pf pressure generation is reduced => CO is decreasing as time passes by => compensatory mechanisms become maladaptive => more neuroH activation => further reduction of CO CO => + neuriH activation Cercle vicieux Dangerous vicious cercle 5- Progressive irreversibale CCF 5 year mortalité => 50 % Frank starling : Within physiological limits if you increase LV filling, LV increases ejection More you stretch a fiber more it contracts (within physiological limits ) MI at the same EDV less CO => compensatory mechanisms => more venous return => more CO