Heart Failure Lecture Notes PDF

Heart failure By : dr haider abd alridha baqer Definition: - inability of the cardiac muscle to pump enough blood supplies that meet with peripheral tissue requirement (despite of good venous return to heart). Clinically defined: - it’s a syndrome in which patient having symptoms & signs of heart f...

Heart failure By : dr haider abd alridha baqer Definition: - inability of the cardiac muscle to pump enough blood supplies that meet with peripheral tissue requirement (despite of good venous return to heart). Clinically defined: - it’s a syndrome in which patient having symptoms & signs of heart failure on presence of cardiac abnormality. Epidemiology : - affect 2% of adult population, Affect 10% of those above 75 years old. ‫ھو ﻛﻣﯾﺔ اﻟدم اﻟطﺎﻟﻌﺔ ﻣﺎل اﻟﻘﻠب ﺑﺎﻟﻧﺑﺿﺔ اﻟواﺣدة ‪Stroke volume:‬‬ ‫ﻛﻣﯾﺔ اﻟدم اﻟطﺎﻟﻌﺔ ﻣن اﻟﻘﻠب ﺑﺎﻟدﻗﯾﻘﺔ‪Cardiac output:‬‬ ‫ﯾﻌﻧﻲ ﺑﮭﺎﻟﺣﺎﻟﺔ اذا ﺗﺿرب ‪ SV*HR‬راح ﯾطﻠﻊ ‪CO‬‬ ‫ﻛﻣﯾﺔ اﻟدم ﺑﻧﮭﺎﯾﺔ ال ‪ diastole‬ﯾﺳﻣوھﺎ ‪end diastolic volume‬‬ ‫ﻛﻣﯾﺔ اﻟدم اﻟﻣﺗﺑﻘﯾﺔ ﺑﻧﮭﺎﯾﺔ ال ‪ systolic‬ھﻲ ‪end systolic volume‬‬ ‫ف ‪ SV‬ﺑﮭﺎﻟﺣﺎﻟﺔ ﯾﺳﺎوي ‪EDV-ESV‬‬ ‫اﻟدم اﻟراﺟﻊ ‪ ventricle‬ھو ﻧﻔﺳﮫ‬ ‫‪Venous return =preload = volume load =EDV‬‬ ‫ﻛﻣﯾﺔ اﻟدم اﻟراﺟﻌﺔ ﻟل ‪ heart‬اﻟﻲ ھﻲ ‪ preload‬ﺑﺎﻟﺿروف اﻟطﺑﯾﻌﯾﺔ ﻣن‬ ‫ﺗزﯾد رح ﯾﺻﯾر ‪ stretching‬اﻛﺛر ﻟل ‪ ventricle‬ﻓﯾﺻﯾر‬ ‫‪ contraction‬اﻗوة اﻛﺛر ﺣﺳب ﻗﺎﻧون ‪ frank starling law‬ﻓﺑﺎﻟﺗﺎﻟﻲ‬ ‫ﻛﻠﻣﺎ ﯾزﯾد ال ‪ preload‬رح ﯾزﯾد ‪SV‬‬ ‫ال ‪ afterload‬ھﻲ اﻟﻣﻘﺎوﻣﺔ اﻟﻲ ﺗﻘﺎﺑل ال ‪ ventricle‬اﺛﻧﺎء ﺿﺧﮫ ﻟﻠدم‬ ‫اﻟﻣوﺟودة ب ‪ aorta ,pulmonary artery‬ﻛﻠﻣﺎ ﺗزﯾد ﻣﻌﻧﺎھﮫ ال‬ ‫‪ ventricle‬ﯾﺣﺗﺎج ‪ contraction‬اﻛﺑر ﯾﻼ ﯾﺿﺦ اﻟدم ﻓﺑﺎﻟﺗﺎﻟﻲ ﻛﻠﻣﺎ ﯾزﯾد‬ ‫ال ‪ after load‬ﯾﻘل ‪SV‬‬ Factors affecting (S.V):- Pre load (volume load) if increase (S.V ) but with limit. After load (pressure load) IF increase (S.V ). Myocardial contractility IF increase (S.V ) with limit. Note: - the cardiac disease will decrease (C.O.P) but patient in mild cases there is no symptoms at rest because there are multiple compensation that act to maintain C.O.P Pathophysiology: - ( C.O.P = SV H.R). (C.O.P) less than tissue requirement, due to decrease of (S.V). Compensation its mechanisms occur in case of underlying heart disease to maintain (C.O.P), By increase (S.V) OR (H.R), to prevent manifestation of heart failure to appear under basal condition (ordinary daily activity). If patient is Asymptomatic under basal condition called (compensated heart failure). If patient become symptomatic under basal condition called (uncompensated heart failure). NOTE :- all compensation mechanisms work but within limit if exceeds it will aggravate heart failure. The failed of compensation occurs when there is factors as over stress (over- load) or further damage in cardiac muscle , known as (precipitating factors of heart failure). {Precipitating factors change from compensated (Asymptomatic) heart failure to uncompensated (symptomatic) heart failure} 1 - Ventricular dilitation : occur in case of volume over load ( preload) this change will lead to increase muscle stretching which lead to more strong contraction increase (S.V). But over stretching will decrease contractility performance (frank-starling low).Causes of volume over load (renal failure, over fluid replacement, A.R , M.R , T.R , P.R ). NOTE: - ventricular dilatation lead to change site of ventricles (displacement) but hypertrophy not. 2 - Ventricular hypertrophy : occur in pressure over load ( after load ) by time lead to increase muscle mass and increase contractility and then increase (S.V). But hypertrophy not associated with increase blood supply so increase risk of ischemia of hypertrophied muscle, sever ischemia will cause fibrosis in muscle lead to decrease contractility and decrease C.O.P. S.HTN , A.S , pulmonary HTN , P. S ). The Frank-Starling law explains that the heart pumps more forcefully when filled with more blood. In conditions like heart failure, this mechanism weakens, meaning the heart can't effectively increase its output, leading to reduced cardiac function and symptoms like fatigue and shortness of breath. 3 - tachycardia increase heart rate by different mechanisms :- Marry low :- heart rate is inversely proportional with blood pressure ( H.F have hypotension). Bainbridge reflex :- increase right atrial pressure will increase heart rate by stimulate (SAN). Increasing heart rate will increase the C.O.P but within limit, because marked and sever tachycardia will decrease the diastolic time (ventricular filling) so decrease of C.O.P. NOTE:- ventricular remodeling:- it’s the change of ventricular muscle size and configuration (Hypertrophy or dilatation) caused by (catecholamine & AgII) BUT this hormones by time will lead to apoptosis of cardiac muscle which lead to aggravation of symptoms and increase mortality rate. So :- if given to patent with heart failure drugs as (ACEI or b-blockers) will decrease mortality rate and improve prognosis 4 - redistribution of blood flow activation of sympathetic system due to decrease in C.O.P will lead to diversion of blood flow from less vital organ (skin) to more vital organs ( brain , heart). 5 - Hypervolemia :- the reduction in C.O.P lead to decrease in renal blood flow especially at day time (time of work) this lead to decrease (GFR) gromular filtration rate (oliguria) and kidneys in response to decrease blood flow will activate ( renin- angiotensin – aldosterone system) which responsible of salt and water retention and vasoconstriction,Also ADH (antidiuretic hormone) secretion from posterior pituitary gland leads to more salt and water retention from the kidneys (this hormone secreted in late and severs heart failure). Note: - All this will increase the blood volume and then the venous return and preload increase so the C.O.P will increase but within limit as noted before. ANP secreted in late and sever cases ( if very hight carry poor prognosis ) It’s secreted from heart to blood in response to cardiac muscle stretching there is two type, 1. Atrium called (ANP atrial natriuretic peptide). 2. Ventricles called (BNP brain natriuretic peptide). Their action: - 1 - antagonize the aldosterone (increase urinary Na exertion, diuretic effect). 2- Vasodilators effect (decrease after load) BNP is used in diagnosis , prognosis and monitoring 6 - neurohormonal mechanism ( very important ) : Decrease of C.O.P will stimulate both (neuronal & hormonal pathway), Neuronal : carotid sinus firing decrease increase sympathetic discharge, Sympathetic activation lead to ( rate, contractility, preload, afterload, remodeling). Hormonal : decrease renal flow will activation of renin release from kidney and then renin convert the circulating angiotensinogen to (AgI) then angiotensin converting enzyme in lung convert the (AgI) TO (AgII) the AgII lead to vasoconstriction and increase (afterload), and stimulate adrenal cortex to secret (aldosterone) which lead to salt and water retention and cause increase in (preload) by increasing volume, also AgII lead to remodeling.So ACEI will decrease both ( preload & afterload ). Sympathetic activation leads to: Increased heart rate (chronotropy). Increased contractility (inotropy). Increased preload, as venoconstriction drives more blood back to the heart. Increased afterload, due to vasoconstriction, which raises vascular resistance. Cardiac remodeling, which over time can lead to structural changes in the heart, often associated with conditions like hypertension or heart failure  Etiology of heart failure (all cardiac disease can cause heart failure) Most common cause of left side heart failure (LVF) is (IHD) ischemic heart Most common cause of right side heart failure (RVF) is left side failure. NOTE: - left side heart failure can cause right side heart failure , but right side failure cannot cause left side failure.. Corepulmonal: - Any chronic lung parenchyma or chest wall diseases lead to isolated right ventricular hypertrophy with or without failure.  Clinical manifestations of heart fealiure its divided in two groups :- Forward symptoms & signs: - occur due to decrease C.O.P from left side of heart. Backward symptoms & signs: - occur due to congestion of blood in venous system, Pulmonary venous congestion (P.V.C) in left side heart failure. Systemic venous congestion (S.V.C) in right side heart failure. symptoms of low C.O.P in left sided failure (forward symptoms) 1. brain: Dizziness, confusion, headache, syncope, insomnia. 2. cardiac :- palpitation, Ischemic heart disease ( chest pain in sever decline in C.O.P). 3. Skeletal muscle: fatigue, weakness & intermittent claudication. 4. Cheyne stoke breathing :- periodic breathing occur in advanced sever H.F 5. Kidney:- day time Oliguria & Nocturia ( bed rest act as diuretic in patient with heart failure) because at time of daily activity limited cardiac output shifted from kidney to skeletal muscle lead to decrease blood flow to kidney ( oliguria < 30ml/hr.) and at bed rest blood flow shifted from relaxed skeletal muscle to kidney (Nocturia). Symptoms of pulmonary venous congestion in left sided failure (backward symptoms) 1-Dyspnea:- exertional, orthopnea, paroxysmal nocturnal dyspnea (PND):- The increase of hydrostatic pressure in pulmonary veins lead to escape of fluid in interstitial space of lung (interstitial edema),that decrease lung compliance lead to breathlessness(dyspnea),if there further and more congestion lead to disruption of tight junction between alveoli this lead to fluid escape inside alveolar space (pulmonary edema). 2- Exertional Cough:- dry cough in interstitial edema , but wet (frothy binky sputum) in pulmonary edema. 3-Recurrent chest infections :- congestion of vessels simulate excessive & thick secretion of mucous inside airway increase risk of infection. 4-Hemoptysis :- if rupture of congested blood vessels. Note :- in chronic and gradual onset of heart failure, the pulmonary venous congestion start gradually so there is enough time to make the thickness in basement membrane in lung and no pulmonary edema at this point but in acute heart failure or acute in top of chronic there is rapid pulmonary venous congestion (rapid elevation in pulmonary hydrostatic pressure), so no time to change of basement membrane then pulmonary edema develops rapidly hear. Orthopnea:- dyspnea on lying flat improve in setting or semi setting position. Occur due to increase venous return from lower extremity to right side of heart and this will increase blood congestion in lung. Paroxysmal nocturnal dyspnea (cardiac asthma):- attacks of sudden breathlessness after period of sleep , may associated with (cough & wheeze) but not well respond to bronchodilator as bronchial asthma. Systemic venous congestion in right side heart failure (backward symptoms) 1. Insomnia: - due to cerebral congestion. 2. dyspnea due to Pleural effusion. 3. Bilateral lower limb edema, later on ascites (lower limb edema start at ankle then ascending in proximal according to severity, its painless and respond to diuretics & elevation of legs at rest). Note :- generalized edema (anasarca) may develops in severe cases, and edema start usually at depending area (if patient standing in lower limbs or in bedridden patient around sacrum). 4. Liver: congestion leads to dull aching right hypochondrial or epigastric pain (due to stretching capsule of liver). 5. GIT: dyspepsia (anorexia, nausea, vomiting), abdominal distension due to ascites or organomegally, malabsorption may lead to cardiac cachexia (sever weight loss) the Wight is elevated due to edema but true Wight is decreased. So :- weight measurement using in monitor the response to treatment. NOTE: - Right heart failure cannot be diagnosed from symptoms and signs alone. Objective evidence of cardiac dysfunction, for example from echocardiography, is needed  Manifestations of advanced sever heart failure 1. Bradycardia without effect of digitalis or b blockers. 2. Hypotension. 3. Pulses alternans. 4. Cheyne stock breathing. 5. Hyponatremia (delusional hyponatremia due to increase ADH secretion).  Precipitating factors of heart failure H- Hypertension (common). E- Endocarditis / environment (heat wave). A- Anemia. R- Rheumatic heart disease. T- Thyrotoxicosis. F- Failure to take medication. A- Arrhythmia (common). I- infection (special chest), ischemia (common). L- Lung problems. E- Endocrine (phaeochromocytoma, DM). D- Drinking alcohol (common), especially when lead to dilated cardiomyopathy. note :- this factors responsible to change state of patent with heart failure from compensated to uncompensated , so must be ask about it in history and screening in examination and investigation to treat it.  Complications of heart failure 1. Renal failure :- Caused by poor renal perfusion due to a low cardiac output. 2. Hypokalemia:-may be the result of treatment with potassium-losing diuretics or hyperaldosteronism. 3. Hyperkalemia :- may be due to the effects of treatment, particularly the combination of (ACEI) and spironolactone. 4. Hyponatremia:- is a (feature of severe heart failure) and may be caused by diuretic, OR inappropriate water retention due to high ADH secretion, It is a poor prognostic sign., 5. Impaired liver function& GIT:- is caused by hepatic venous congestion. And poor arterial perfusion, malabsorption. 6. Thromboembolism:- Deep vein thrombosis and pulmonary embolism may occur due to the (a low cardiac output and enforced immobility).Whereas systemic emboli may be related to arrhythmias, atrial flutter or fibrillation, or intracardiac thrombus 7. Atrial and ventricular arrhythmias very common and may be related to electrolyte changes (e.g. hypokalemia, hypomagnesaemia), the underlying structural heart disease, OR Drugs (dioxins).. 5. Impaired liver function& GIT:- is caused by hepatic venous congestion. And poor arterial perfusion, malabsorption. 6. Thromboembolism:- Deep vein thrombosis and pulmonary embolism may occur due to the (a low cardiac output and enforced immobility).Whereas systemic emboli may be related to arrhythmias, atrial flutter or fibrillation, or intracardiac thrombus 7. Atrial and ventricular arrhythmias very common and may be related to electrolyte changes (e.g. hypokalemia, hypomagnesaemia), the underlying structural heart disease, OR Drugs (dioxins).. Note : Most common cause of death from HF is sudden death from ventricular arrhythmias. Ischemia provokes ventricular arrhythmias.  Investigations Management of CHF must focus on the cause of the heart failure, not simply on The reliving of symptoms, because Heart failure is not a diagnosis but it's the common end result of many pathological processes. Divided into investigations for Diagnosis Others (to determined, underline cause, precipitating factors, complication and severity of the case)  ECG:- may show the cause Chamber enlargement. Abnormal rhythms (arrhythmias). Ischemia / infarction. Note :- radionuclide ventriculography is used to measure right and left ventricular ejection fraction. (Better than echocardiography measuring ejection fraction)  TREATMENT 1. Systolic dysfunction a. General lifestyle modification Sodium restriction (less than 4 g/day) Fluid restriction (1.5 to 2.0 L daily) Weight loss Smoking cessation Restrict alcohol use Exercise program All patients should monitor weight daily to detect fluid accumulation Annual influenza vaccine and pneumococcal vaccine recommended b. Diuretics Most effective means of providing symptomatic relief to patients with moderate to severe CHF Recommended for patients with systolic failure and volume overload Have not been shown to reduce mortality or improve prognosis, just for symptom control. Goal is relief of signs and symptoms of volume overload (dyspnea, peripheral edema) Loop diuretics: Furosemide (Lasix)—usually used. Other options include bumetanide (Bumex) and torsemide Thiazide-like diuretics: Metolazone and chlorothiazide. Used to augment diuresis with loop diuretics. The RALES trial showed that spironolactone reduces morbidity and mortality in patients with class III or IV heart failure with EF 2). c. Therapies to improve outcomes: Standard therapy includes the following (medications in parentheses have been shown to improve mortality in HFrEF): ACE inhibitor (enalapril, lisinopril, captopril) or ARB (valsartan, losartan,candesartan) β-Blockers (metoprolol succinate, carvedilol, bisoprolol) Aldosterone antagonists (spironolactone, eplerenone), if EF