PPT CARDIAC FAILURE BY DR QAZI IMTIAZ RASOOL

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DR QAZI IMTIAZ RASOOL H.O.D DEPARTMENT OF PHYSIOLOGY BLA KASHMIR INDIA

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CARDIAC FAILURE:

CARDIAC FAILURE DR. QAZI IMTIAZ RASOOL

Learning Objectives:

Learning Objectives After the session the Students will be able to;- Define cardiac failure Classify the various types of cardiac failure Compare the pathophysiology of systolic and diastolic cardiac failure. Describe compensatory mechanisms associated with cardiac failure Clinical manifestation of Heart Failure REF;-  1. Guyton & Hall Textbook of Physiology - 12 th ed. Ch 21-24 2 . Harrison's Principles of Internal Medicine, 18th ed pg.3899

Definition:

Definition -is the pathological process in which the systolic or/and diastolic function of the heart is impaired, and CO is unable to meet metabolic demands of the body . - C linical syndrome result ing from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood . Congestive heart failure – refers to the state in which abnormal circulatory congestion exists a result of heart failure

Clinical classification:

Clinical classification According to the course of disease - - Acute HF - Chronic HF According to the cardiac output (CO) - Low-output HF - High-output HF According to the location of heart failure - L eft -side heart failure (Pulmonary edema ) - Right-side heart failure ( Peripheral edema ) - Biventricular failure (whole heart failure ) According to the function impaired - Systolic failure - Diastolic failure According to the direction impaired -Forward failure - Backward failure

Law of LaPlace:

Law  of  LaPlace

Systolic Dysfunction Diastolic Dysfunction (Common) EF =NAD :

Systolic D y sfun c tion Diastolic D y s f un c tion ( Common ) EF =NAD V ent : ca n ' t pump effectively V ent ; ca n' t relax , fill during diastole EXAMPLE 1. 2.

Etiology:

Etiology Ca r dia c per f or m an c e dep ends 4 components: 1. Preload 2. . . … After load 3. Contractility of the muscle 4. Heart rate Donkey Analogy

Preload (Rubber band):

Preload ( Rubber band) Volume of blood in ventricles at the end of diastole - Due to CO Blood volume remains after systole Stretch of myocardial fibers . ( F.S.LAW) But in failed heart Did not response As heart failure worsens Preload contributes to symptoms - Dyspnoea - Hepatic enlargement 8

Afterload: The pressure against which the left ventricle ejects.:

Afterload : The pressure against which the left ventricle ejects. S y s t e m ic re s i s ta n ce CO Afterload is the tension or stress developed in the wall of the left Ventricle during ejection . - Hypertension , - Aortic stenosis; - Pulmonary hypertension 9

Contractility of the muscle::

Contractility of the muscle: It is the force of contraction generated by myocardium under loading conditions . - myocardial infarction; - Cardiomyopathy -Myocarditis - Restriction of cardiac dilation Pericardial effusio n Heart Rate: it is the major determinant of the cardiac failure As the function of heart in failure, in heart rate is the first compensatory mechanism.

PRESSURE AND VOLUME LOOP:

PRESSURE AND VOLUME LOOP VOL/ml EDV Pressure/mm 120 120 ESV 50 SV MO A O MC AC ------- Vent; elastance EDVPR -------- Contractility ESVPR --------- - Afterload

PRESSURE AND VOLUME LOOP:

PRESSURE AND VOLUME LOOP

PRESSURE AND VOLUME LOOP INCREASED PRELOAD:

PRESSURE AND VOLUME LOOP INCREASED PRELOAD

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PRESSURE AND VOLUME LOOP Increased Afterload

PRESSURE AND VOLUME LOOP Increased Contractilty:

PRESSURE AND VOLUME LOOP Increased Contractilty

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Disturbance in the electrolyte :

Disturbance in the electrolyte 1 . Excessive plasma K + - concentration decreases the resting membrane potential of myocardial cells, and low blood Ca ++ -reduces excitation- contraction coupling. and low blood Ca ++ can thus cause heart to stop in diastole . 2. Low blood K + and high blood Ca ++ can arrest the heart in systole.

Compensatory Mechanisms:

Compensatory Mechanisms A . Neurohumoral or extrinsic compensation 2 major mechanisms: 1. The sympathetic nervous system 2. Renin-angiotensin aldosterone B. M ost important intrinsic compensatory mechanism is ;- 1. Myocardial Hypertrophy 2. HR 3. Ventricular Remodel l ing .

A. Neurohormonal changes:

A. Neurohormonal changes N/H changes Favorable effect Unfavor. effect  Sympathetic activity  HR ,  contractility, vasoconst.   V return,  filling Arteriolar constriction  After load  workload  O 2 consumption  Renin-Angiotensin – Salt & water retention  VR Vasoconstriction   after load Aldosterone  Vasopressin Same effect Same effect  interleukins &TNF  May have roles in myocyte hypertrophy Apoptosis  Endothelin Vasoconstriction  VR  After load

Cellular changes:

Cellular changes Changes in Ca +2 handling. Changes in adrenergic receptors: Slight increase in α 1 receptors up regulation β 1 receptors desensitization followed by down regulation Changes in contractile proteins Program cell death (Apoptosis) Increase amount of fibrous tissue

Acute Effects of Moderate Cardiac Failure and with compensated :

Acute Effects of Moderate Cardiac Failure and with compensated   2 effects: - Cardiac output - Damming of blood increased venous pressure. Compensation;-(SNS) 1.Baroreceptor reflex ,. 2.Chemoreceptor reflex,  3.CNS ischemic response , 4.Reflexes that originate in the damaged hear t  

Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS):

Vasoconstriction Oxidative Stress Cell Growth Proteinuria LV remodeling Vascular remodeling Angiotensin II AT I receptor A ng i o t en s i nogen Renin Angiotensin I A ng i o t en s i n Converting Enzyme Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS )

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 MAP = (  S V x  HR) x  TPR Salt-water retention Thirst Sympathetic augmentat i on Vasoconstriction Renin-Angiotensin-Aldosterone (  renal perfusion)

Compensatory Neurohormonal Stimulation: Summary:

Compensatory Neurohormonal Stimulation: Summary Decreased Cardiac Output Sympathetic nervous system R en i n - ang i oten si n system Antidiuretic hormone (vasopressin) H ea r t rate Contractility Circulating volume M a i n t a in blood p r e ss u r e C a r d i a c output + SV - + Vasoconstriction Ante r i o l ar V enous Venous return to heart ( preload) Peripheral edema and pulmonary congestion

Neurohumoral compensation (short-term compensatory; long-term contributes to failure):

Neurohumoral compensation ( short-term compensatory; long-term contributes to failure ) Peripheral Va s o c o n s t r i c t i on  Afterload  Cardiac Output Heart Failure  Preload  Cardiac Workload  Plasma Volume Salt & Water Retention E d ema Aldosterone Secretion Renin-angiotensin system Renin + Angiotensinogen Angiotensin I Angiotensin II

Ventricular Remodeling:

Ventricular Remodeling 1.PHYSIOLOGICAL (exercise) 2.PATHOLOGICAL Most important intrinsic compensatory mechanism ---P rocess by which - mechanical, - neurohormonal , - possibly genetic factors alter ventricular size, shape, and function . ----i.e, Remodeling in MI, hypertension and cardiomyopathy . H allmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis.

Ventricular remodeling in diastolic and systolic heart failure :

Ventricular remodeling in diastolic and systolic heart failure

Decompensated Heart Failure:

Decompensated Heart Failure CO cannot rise high enough to make the kidneys excrete normal quantities of fluid. more edema, decompensated heart failure . Treatment;- 3 D”s -   strengthening the heart  cardiotonic drug ,  digitalis,  diuretic drugs salt intake,

Compensatory changes in heart failure:

Compensatory changes in heart failure Activation of SNS Activation of R A AS Increased HR Release of ADH Release of atrial natriuretic peptide (BNP) Chamber enlargement Myocardial hypertrophy

What Are The Symptoms of Heart Failure?:

What Are The Symptoms of Heart Failure ? Think FACES ... F atigue A ctivities limited C hest congestion E dema or ankle swelling S hortness of breath

CLINICAL FEATURES:

CLINICAL FEATURES LV failure Cardiac sign Enlargement of LV gallop rhythm Systolic murmur in apex Pulmonary sign Dry rales Moist rales RV failure Symptom of gastro- intestinal Symptom of Renal Pain in hepatic area Dyspnea Sign Hepatojugular reflux Hepatomegaly Edema pleural fluid and ascites

New York Heart Association (NYHA) Classification of cardiac failure:

New York Heart Association (NYHA ) Classification of cardiac failure Class- 1 No limitation. Normal physical exercise does not cause fatigue,dyspnoea or palpitations Class- 2 Mild limitation. Comfortable at rest but norma l p h y sical a c t i vity p r odu c es fatigue, d y s p no e a or palpitations Class- 3 Marked limitation. comfortable at rest but gentle physical activity produces marked symptoms of cardiac failure Class- 4 Symptoms of heart failure occur at rest and are exacerbated by any physical activity.

DIAGNOSIS:

DIAGNOSIS Electrocardiogram (ECG, “EKG”) Chest x-ray Echocardiography (“Echo”) Heart catheterization Stress test Blood tests

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DIET Approach With Heart Failure D iagnose – Etiology I nitiate Diuretic/ACE inhibitor - blocker Spirololactone Digoxin E ducate – Diet – Severity (LV dysfunction) – Exercise Lifestyle CV Risk T itrate Optimize ACE inhibitor Optimize b locker

Diuretics, ACE Inhibitors and ARB’s Reduce tmber of sacks on the wago:

Diuretics, ACE Inhibitors and ARB’s Reduce t mber of sacks on the wago Reduce the number of sacks on the wagon

SUMMARY:

SUMMARY

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