Cardio Vascular Physiology 2 Part2

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rakesh1959@gmail.com

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Cardio Vascular Physiology: 

Cardio Vascular Physiology PART 2

Part - II: 

Dr.Rakesh Chintalapudi, M.D., D.A ., Asst.Professor – King George Hospital, Visakhapatnam –Andhra Pradesh-INDIA mail id : rakesh1959@gmail.com Part - II

CARDIAC MECHANICS: 

CARDIAC MECHANICS THE HEART AS A PUMP VENTRICULAR STRUCTURE FUNCTION CARDIAC CYCLE CARDIAC OUTPUT

VENTRICULAR STRUCTURE: 

VENTRICULAR STRUCTURE CARDIAC MUSCLE

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VARIABLE THICKNESS OUTER INNER MIDDLE

CARDIAC CYCLE: 

CARDIAC CYCLE CARDIAC CYCLE

CARDIAC CYCLE : 

CARDIAC CYCLE Cardiac events that occur from the beginning of one heart beat to the beginning of the next is called C Cycle. TIME OF ONE CYCLE : O.8 SECONDS So, 75 beats x 0.8 = 60 seconds or 1 mnt . MECHANICAL & ELECTRICAL EVENTS DIASTOLE SYSTOLE

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1.ATRIAL SYSTOLE 2.ISOVOLUMETRIC V CONTRACTION. 3.VENTRICULAR EJECTION 4.ISOVOLUMETRIC V RELAXATION. 5.VENTRICULAR FILLING 1 2 3 4 5 O 0.2 O.4 0.6 0.8 ATRIAL SYSTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE

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ATRIAL SYSTOLE 1 Function of Atria as primer pumps : 80 % of Blood directly flows in 20 % of blood by Atrial Contraction ATRIAL PRESSURE ELEVATION WAVES a – wave c – wave v – wave a – wave = atrial contraction and the Pressure from 4 -6 goes up to 7-8 mmHg c- wave = ventricular contraction bulging of AV Valves. v – wave = end of ventricular contraction flow blood from veins to atria.

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2 ISOVOLUMETRIC VENTRICULAR CONTRACTION ISOVOLUMIC + ISOMETRIC = ISOVOLUMETRIC Ventricular pressure rises abruptly causing AV VALVES closes. Then additional 0.02 -0.03 seconds Required for the ventricle to build Sufficient pressure to push aortic , pulmo . Valves. Therefore this period is called Iso Vol. contraction meaning –tension is building up with no shortening of muscle

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3 Ventricular pressure raises above to 8 and 80 mm Hg in RV & LV . PERIOD OF RAPID EJECTION PERIOD OF SLOW EJECTION VENTRICULAR EJECTION FIRST -- RAPID 1/3 - 70 % SECOND – SLOW 2/3 - 30 %

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4 ISOVOLUMETRIC VENTRICULAR RELAXATION DIASTOLE Intra ventricular pressure drops at the end Of the ventricular systole. Aorta, Pulm . Artery snaps back blood and Aortic, pulmonary valves closes . For about 0.03 to 0.06 seconds ventricular muscle relaxes even though ventricular volume does not change giving rise to Isovolumetric relaxation.

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During this period intra ventricular pressure decreases rapidly back to their low diastolic levels. Then the AV Valves open to begin a new cycle of Ventricular pumping.

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5 VENTRICULAR FILLING DIASTOLE 1 / 3 1 / 3 1 / 3 PERIOD OF RAPID FILLING VENOUS COMPONENT ATRIAL COMPONENT 25 %

ASSESSMENT OF VENTRICULAR FUNCTION: 

ASSESSMENT OF VENTRICULAR FUNCTION VENTRICULAR FUNCTION CURVES ASSESSMENT OF SYSTOLIC FUNCTION ASSESSMENT OF DIASTOLIC FUNCTION

VENTRICULAR FUNCTION CURVES: 

VENTRICULAR FUNCTION CURVES

SYSTOLIC DYSFUNCTION ASSESSMENT : 

SYSTOLIC DYSFUNCTION ASSESSMENT

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Clinically commonly used Non Invasive INDEX of Contractile FUNCTION is ‘’EJECTION FRACTION”. Which is measured by 2 D ECHO Angiography Radio nuclide ventriculography.

EJECTION FRACTION: 

EJECTION FRACTION EJECTION FRACTON L V E D V – L V E S V L V E D V E D V - E S V E D V

DIASTOLIC FUNCTION: 

DIASTOLIC FUNCTION

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Diastole is ventricular relaxation, and it occurs in TWO distinct phases: 1.ISOVOLUMETRIC RELAXATION 2.AUXONTOMIC RELAXATION or (1) isovolemic relaxation; (2) the rapid filling phase (i.e., LV chamber filling at variable LV pressure (3) slow filling, or diastasis; (4) final filling during atrial systole.

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The isovolemic relaxation phase is energy dependent. During the auxotonic relaxation phases (phases 2 through 4), ventricular filling occurs against pressure. It encompasses a period during which the myocardium is unable to generate force and filling of the ventricular chambers takes place.

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The isovolemic relaxation phase does not contribute to ventricular filling. The greatest amount of ventricular filling occurs in the second phase, whereas the third phase adds only about 5% of total diastolic volume and the final phase provides 15% of ventricular volume from atrial systole.

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ASSESSMENT OF DIASTOLIC DYSFUNCTION

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Left ventricular diastolic function can be assessed clinically by Doppler echocardiography on a transthoracic or transesophageal examination.

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Three patterns of diastolic dysfunction are generally recognized based on 1. Isovolumetric relaxation time, The ratio of peak early diastolic flow (E) to peak atrial systolic flow (A), The deceleration time (DT) of E (DT E )

DIASTOLIC DYSFUNCTION: 

DIASTOLIC DYSFUNCTION E > A Doppler echocardiography of diastolic flow across the mitral valve. A

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E < A B

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A & B represents diastolic dysfunction. E: early diastolic flow; A: peak atrial systolic flow; IVRT = isovolumic relaxation time; DT E , deceleration time of E.

CARDIAC WORK : 

CARDIAC WORK INTERNAL WORK : Ventricle to change shape of the heart, and prepare it for ejection of blood Wall Stress EXTERNAL WORK : For Contraction of Ventricle and to eject blood

EXTERNAL WORK : 

EXTERNAL WORK External work or Stroke Work = Stroke volume x p (pressure developed during the ejection of stroke volume. Both external and internal work consume oxygen. During Cardiac Bypass Surgery, even though heart does not work, it consumes oxygen because of internal work.

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CARDIAC OUTPUT: 

CARDIAC OUTPUT

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Amount of blood pumped out per unit of time Heart rate X Stroke volume Preload After load Contractility

HEART RATE: 

HEART RATE CO is generally directly proportional to heart rate. But is modified by many factors like 1.autonomic 2.humoral 3.local factors HR in normal young adults is 90-100 beats /min., but decrease with age with following formula 118beats /min. – (0.57 x age )

STROKE VOLUME : 

STROKE VOLUME It is the Volume pumped out by each ventricle per contraction (each Stroke) Usually 70ml x 72 beats = 5000 ml That is CARDIAC OUTPUT

MAJOR FACTORS STROKE VOLUME: 

MAJOR FACTORS STROKE VOLUME PRELOAD AFTERLOAD CONTRACTILITY WALL MOTION ABNORMALITIES VALVULAR DYSFUNCTION

PRE LOAD: 

PRE LOAD

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Ventricular preload is end-diastolic volume, which is generally dependent on ventricular filling. The relationship between cardiac output and left ventricular end-diastolic volume is known as Starling's law of the heart . Note that when the heart rate is constant, cardiac output is directly proportional to preload, until excessive end-diastolic volumes are reached.

Preload In Vitro: 

Preload In Vitro Preload In Vivo Preload is muscle length prior to contraction, while afterload is the tension against which the muscle must contract . Ventricular preload is end-diastolic volume, which is generally dependent on ventricular filling.

FRANK- STARLING’S LAW: 

FRANK- STARLING’S LAW

FRANK STARLING’S LAW: 

FRANK STARLING’S LAW VENOUS RETURN INCREASED MUSCLE STRETCH CONTRACTS WITH INCREASED FORCE EXTRA BLOOD PUMPED OUT WITHOUT ANY DELAY

Otto Frank – E.H.STARLING: 

Otto Frank – E.H.STARLING

Frank Starling Law of the Heart: 

Frank Starling Law of the Heart Increased blood volume = increased stretch of myocardium = Increased force to pump blood out.

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FRANK – STARLING’S RELATIONSHIP = FORCE vs MUSCLE LENGTH = PRESSURE -- VOLUME Stretching of myocardial Sarcomere results in enhanced myocardial performance, for subsequent contractions.

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Pressure – volume loop Of Left Ventricle During diastole, the Ventricle fills and pressure increases from d to a Pressure then rises sharply from a to b during ivolumetric contraction and from b to c during ventricular ejection. At c, the aortic valves close and pressure falls during isovolumetric relaxation from c back to d.

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Pressure-volume loops, albeit requiring catheterization of the left side of the heart, are currently the best way to determine contractility in an intact heart .The pressure-volume loop represents an indirect measure of the Starling relationship between force (pressure) and muscle length (volume).

PRESSURE - VOLUME LOOPS: 

PRESSURE - VOLUME LOOPS

PRESSURE - VOLUME LOOPS: 

PRESSURE - VOLUME LOOPS

PRELOAD: 

PRELOAD DEPENDS ON 1.DETERMINANTS OF VENTRICULAR FILLING. 2.DIASTOLIC FUNCTION & VENTRICULAR COMPLIANCE.

1. DETERMINANTS OF VENTRICULAR FILLING: 

1. DETERMINANTS OF VENTRICULAR FILLING

Factors affecting Ventricular Preload: 

Factors affecting Ventricular Preload Venous return Blood volume Posture Intrathoracic pressure Venous tone Rhythm (atrial contraction) Heart rate

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The most important of all factors is venous return. i.e., the amount of venous blood reaching into the RA per minute. For Right Ventricle important factor for preload is ---venous return. For Left Ventricle important factor for preload is --- venous return provided, there is no pulmonary or RV dysfunction. Normally the End Diastolic Volumes of both ventricles are similar.

Venous Return –Stroke Volume role of Heart Rate: 

Venous Return –Stroke Volume role of Heart Rate Significantly impaired – high heart rates > 120 /mt. Absent – Atrial Fibrillation Ineffective – Atrial Flutter

2. DIASTOLLIC DYSFUNCTION & VENTRICULAR COMPLIANCE: 

2. DIASTOLLIC DYSFUNCTION & VENTRICULAR COMPLIANCE

2. DIASTOLLIC DYSFUNCTION & VENTRICULAR COMPLIANCE: 

(A) Intrinsic Factors like Hypertrophy – Ischemia - fibrosis (B) Extrinsic Factors like pericardial diseases – over distension of contralateral ventricle, increased airway pressures, pleural pressures tumours , surgical compression -- 2. DIASTOLLIC DYSFUNCTION & VENTRICULAR COMPLIANCE

AFTER LOAD: 

AFTER LOAD

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Cardiac output is inversely related to after load. Because of its thinner wall, the right ventricle is more sensitive to changes in after load than the left ventricle. Cardiac output in patients with marked right or left ventricular impairment is very sensitive to acute increases in after load. The latter is particularly true in the presence of myocardial depression (as often occurs during anesthesia).

CONTRACTILITY: 

CONTRACTILITY

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Cardiac contractility (inotropism) is the intrinsic ability of the myocardium to pump in the absence of changes in preload or after load. Contractility is related to the rate of myocardial muscle shortening, which is in turn dependent on the intracellular calcium concentration during systole. Increases in heart rate can also enhance contractility under some conditions, perhaps because of the increased availability of intracellular calcium.

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Contractility can be altered by neural, Humoral, or pharmacological influences. Sympathetic nervous system activity normally has the most important effect on contractility. Sympathetic fibers innervate atrial and ventricular muscle as well as nodal tissues. In addition to its positive chronotropic effect, norepinephrine release also enhances contractility via 1 -receptor activation.

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IONOTROPIC DROMOTROPIC CHROMOTROPIC LUSITROPIC

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-Adrenergic receptors are also present in the myocardium but appear to have only minor positive inotropic and chronotropic effects. Sympathomimetic drugs and secretion of epinephrine from the adrenal glands similarly increase contractility via 1 -receptor activation.

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Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within the heart, and loss of functioning muscle mass as a result of ischemia or infarction. Most anesthetics and antiarrhythmic agents are negative inotropes (i.e., they decrease contractility).

MEASUREMENT OF CARDIAC OUTPUT: 

MEASUREMENT OF CARDIAC OUTPUT The Fick principle states that the amount of a substance taken up by an organ (or by the whole body) per unit of time is equal to the arterial level of the substance minus the venous level (A-V difference) times the blood flow. This principle can be applied, of course, only in situations in which the arterial blood is the sole source of the substance taken up.

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O 2 concentration of the pulmonary artery (Cpa o 2 ), the O 2 concentration of the pulmonary vein (Cpv o 2 ), and O 2 consumption.

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O 2 = 160 ml/L O 2 = 200 ml/L Right heart Left heart CARDIAC OUTPUT = 5000 ml/ mt Lungs Oxygen used 200 ml/ mt

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Output of Left Ventricle = 02 Consumption (ml/min) ( A o2 ) - ( V o2 ) 250 ml /min = 190ml/ L arterial blood - 140ml/L venous blood in pulmo . art = 250ml / min 50 ml/L = 5 L / min CARDIAC OUTPUT

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q 1 = OXYGEN DELIVERED FROM PULMONARY CAPILLARIES THROUGH PULMONARY ARTERY q 2 = OXYGEN DELIVERED FROM LUNG ALVEOLI q 3 = OXYGEN DELIVERED FROM PULMONARY VENOUS BLOOD

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The Fick ‘s principle is based on the concept of conservation of mass such that the O 2 delivered from pulmonary venous blood (q 3 ) is equal to the total O 2 delivered to pulmonary capillaries through the pulmonary artery (q 1 ) and the alveoli (q 2 ). q 3 = q1 + q2

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The amount of O 2 delivered to the pulmonary capillaries by way of the pulmonary arteries (q 1 ) equals total pulmonary arterial blood flow    times the O 2 concentration in pulmonary arterial blood (Cpa o 2 ): q1 = X Cpao2

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The amount of O 2 carried away from pulmonary venous blood (q 3 ) is equal to total pulmonary venous blood flow    times the O 2 concentration in pulmonary venous blood (Cpv o 2 ): q 3 = X Cpvo2

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The pulmonary arterial O 2 concentration is the mixed systemic venous O 2 , and the pulmonary venous O 2 concentration is the peripheral arterial O 2 . O 2 consumption is the amount of O 2 delivered to the pulmonary capillaries from the alveoli (q 2 ). Because q 1 + q 2 = q 3 ,

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(CpaO2) + q2 = (CpvO2) q 2 = (CpvO2) - (CpaO2) q2 = (CpvO2) – (CpaO2) = = q2 / (CpvO2 - CpaO2)

MEASUREMENT OF CARDIAC OUTPUT: 

MEASUREMENT OF CARDIAC OUTPUT INDICATOR DILUTION METHODS : Dye dilution method Thermo dilution method

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DYE DILUTION METHOD

CARDIAC INDEX: 

CARDIAC INDEX CARDIAC OUTPUT SQUARE METER OF BODY SURFACE 70 kg 1.7 sq mtrs 3 L/min/m2

CARDIAC RESERVE: 

The maximum percentage that the cardiac output can increase above the normal level is called the Cardiac Reserve. In healthy young adult it is around 500 to 600 percent, where as in Heart Failure there is no Cardiac Reserve. In exercise, cardiac output increases around 5 times ie . 400 percent. CARDIAC RESERVE

CARDIAC RESERVE: 

CARDIAC RESERVE 600 500 400 300 200 100 0 NORMAL ATHLETE DIPHTHERIA MODERATE VALVULAR DISEASE SEVERE VALVULAR DISEASE SEVERE CORONARY THROMBOSIS MODERATE CORONARY DISEASE

Wall Motion Abnormalities RWMA : 

Wall Motion Abnormalities RWMA The abnormalities may be due to ischemia, scarring, hypertrophy, or altered conduction. When the ventricular cavity does not collapse symmetrically or fully, emptying becomes impaired. Hypokinesis (decreased contraction), Akinesis (failure to contract), and Dyskinesis (paradoxic bulging) during systole

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reflect increasing degrees of contraction abnormalities. Although contractility may be normal or even enhanced in some areas, abnormalities in other areas of the ventricle can impair emptying and reduce stroke volume. The severity of the impairment depends on the size and number of abnormally contracting areas.

Valvular Dysfunction : 

Valvular Dysfunction Valvular dysfunction can involve any one of the four valves in the heart and can lead to stenosis, regurgitation (incompetence), or both. Stenosis of an AV (tricuspid or mitral) valve reduces stroke volume primarily by decreasing ventricular preload, whereas stenosis of a semilunar (pulmonary or aortic) valve reduces stroke volume primarily by increasing ventricular afterload.

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Reduced Stroke Volume—decreasing ventricular pre load. Reduced Stroke Volume—increasing ventricular after load. STENOSIS STENOSIS

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Reduced Stroke Volume—decreasing ventricular pre load. Reduced Stroke Volume—increasing ventricular after load. X X REGURGITATION REGURGITATION

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In contrast, valvular regurgitation can reduce stroke volume without changes in preload, afterload, or contractility and without wall motion abnormalities. The effective stroke volume is reduced by the regurgitant volume with every contraction. When an AV valve is incompetent, a significant part of the ventricular end-diastolic volume can flow backward into the atrium during systole

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the stroke volume is reduced by the regurgitant volume. Similarly, when a Semilunar valve is incompetent, a fraction of end-diastolic volume returns backward into the ventricle during diastole.

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HEART FULL THANKS TO YOU