Coronary Circulation and Cardiac Failures

8/8/2019 Coronary Circulation and Cardiac Failures

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Coronary Circulation andCardiac Failures

Reported by Monica Caballes

4dvmB


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Th e Coronary Circulation

Is the circulation of blood in the bloodvessels of the heart muscle. The vessels that

deliver oxygen-rich blood to the myocardiumare known as coronary arteries. The vesselsthat remove the deoxygenated blood fromthe heart muscle are known as coronary

veins.


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W h y does t h e Heart need Coronary

Circulation?Although much blood passes through theheart when it is being pumped, The muscleof the heart is very thick and only the inner75-100 micrometers of the endocardialsurface can obtain significant amounts of nutrition from the blood in the cardiac

chambers.


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W h at are t h e parts of t h e Coronary

circulation?Coronary Arteries Left Coronary Artery- supplies the anterior and lateral

portions of the left ventricle

Right CoronaryA

rtery- supplies most of the rightventricle and the posterior part of the left ventricleCoronary Veins Coronary Sinus- where the venous blood flow from the

left ventricle is emptied in

Anterior Cardiac Veins- empties the venous blood fromthe right ventricle directly into the right atrium

Thebesian Veins- empties a small amount of coronaryblood directly into all chambers of the heart


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Coronary Arteries


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Coronary Veins


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How does t h e Blood Flow in t h e

Coronary Circulation?

YouTube - Heart Animation with Coronary Arteries.flv

YouTube - The Heart's Blood Supply.mp4


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N ormal Coronary Blood Flow

Resting coronary blood flow 225 ml/min 0.7- 0.8 ml/gm of heart muscle 4- 5% of total cardiac output

The increase of Coronary Blood Flow is directlyproportional to the increase of the workload of

the heart. However, this does not mean that theamount of Blood flow in the Coronarycirculation is equal to the Cardiac output


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D uring Systole

The Blood Flow falls to a low value, which isopposite to the flow of other vascular bedsin the body

Due to the strong compression of the LeftVentricular muscle around intramuscular

vessels during systole


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Schematics of coronary circulation during cardiac systole of the left

ventricle.In systole, the heart muscle contracts, the aortic valve opens, andabout 60-70% of its contained blood is ejected into the aorta. The smallarteries that supply the heart muscle are squeezed in that contractileprocess, thereby markedly reducing the coronary blood flow in cardiacsystole.AO -aorta. RC A- right coronary artery. LC A-left circumflex artery.


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D uring D iastole

The Cardiac Muscle relaxes and no longerobstructs the blood flow through the leftventricular capillaries and blood flowsrapidly


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Schematics of coronary circulation in cardiac diastole (the filling phaseof the left ventricle). The aortic valve is now closed. The mitral valve (notshown in the schematics) opens into the left ventricle. The cardiacmuscle relaxes. The intramyocardial pressure is now relieved. The smallcoronary vessels dilated creating a relatively negative intramyocardialpressure. The combination of these factors helps the coronary arteriesto suck up more blood from the aortic root, markedly boosting thecoronary blood flow in diastole. In fact, the coronary blood flow indiastole improves by 400-500% when compared to systole.


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Coronary vessels at different

depth

s in th

eh

eartE picardial Coronary Arteries supply the heart; found at the surface of the

heart

Smaller Intramuscular Arteries penetrate the muscle supplying nutrients en

route to the endocardium

Subendocardial arterial plexus Lying immediately beneath the endocardium


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Coronary Flow

During Systole- Blood flow through thesubendocardial plexus of the left ventricle(where the contractile force of the heart isgreat) falls almost to zeroDuring Diastole- Blood flow in thesubendocardial arteries is considerablygreater than the blood flow in the outermostarteries (to compensate for the lack of flowduring systole)


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Control of Coronary Blood Flow

Local Metabolism Primary controller of Coronary Blood Flow

Local arterial vasodilation in response to cardiacmuscle need for nutrition Decreased activity is accompanied by decreased

coronary flow

O xygen demand Blood flow increases in proportion to the

metabolic consumption of oxygen by the heart


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O xygen demand Blood flow increases in proportion to the

metabolic consumption of oxygen by the heart

Decrease in oxygen concentration in the heartcauses vasodilator substances to be releasedfrom the muscle cells

Adenosine- from

ATP


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N ervous Control Indirect effects

Sympathetic nerves release N orepinephrine which

increases heart rate and contractility and the rate of metabolism, resulting in the dilation of coronaryvessels to meet the demands of the Heart.

Direct effectsPresence of Constrictor receptors(alpha receptors)and Dilator receptors(beta receptors)Depends on the absence or presence of N orepinephrine/ E pinephrine


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Special Features of Cardiac MuscleMetabolism

Cardiac Muscle normally mainly uses FattyAcids for energy rather than carbohydrates

Under anaerobic/ischemic conditions,undergoes anaerobic glycolysis supplying littleenergy and leaving large amounts of lactic acidIn severe Coronary ischemia, adenosine will

cause dilation of the vessels but the loss of adenosine for a prolonged period will causecardiac cellular death


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Collateral Circulation in t h e

HeartW hen one of the Large Coronary Vessels getssuddenly occluded, the small anastomoses dilatewithin seconds, and do not increase in the next 8-

24 hrs Blood flow is half of whats needed to keep the heart alive

But the Colateral flow will increase anddouble by the 2 nd or 3 rd day and may reachnormal coronary blood flow


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BUT

E ventually the sclerotic process developsbeyond the limits of even the collateral bloodsupply to provide the needed blood flow, and

sometimes the Collaterals developatherosclerosis.W hen this occurs the heart muscle becomesseverely limited in its work output, and may not

be able to pump the normal required amount of blood flowCommon Cause of Cardiac Failure


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Myocardial Infarctioninterruption of blood supply topart of the heart, causing heartcells to die. This is mostcommonly due to occlusion of acoronary artery following the

rupture of a vulnerableatherosclerotic plaque, which isan unstable collection of lipids(fatty acids) and white bloodcells in the wall of an artery. Theresulting ischemia and oxygen

shortage, if left untreated for asufficient period of time, cancause damage or death of heartmuscle tissue.


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Myocardial Infarction


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Myocardial Infarction

Subendocardial Infarction- thesubendocardial muscle frequency becomesinfarcted even without evidence of infarctionin the outer surface.


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Causes of D eat h after AcuteCoronary Occlusion

Decreased Cardiac O utput

Damming of Blood in the Pulmonary or

Systemic VeinsFibrilation of the Heart

Rupture of the Heart


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D ecreased Cardiac Output(Cardiac S h ock)

Too weak to contract with great force

Pumping ability of the affected ventricle isproportionately depressed

Systolic stretch- normal portions of the musclecontract while the ischemic portion is forcedoutward by the pressure inside


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D amming of Blood in t h ePulmonary or Systemic Veins

with death resulting from pulmonary edemaDamming of blood in the blood vessels in thelungsIncreased atrial pressures leads to increasedcapillary pressure in the lungsSymptoms develop a few days later, when thecardiac output results to diminished blood flowto the kidneys, which fail to excrete urine,adding to the blood volume leading tocongestive symptoms


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Fibrilation of t h e Heart

Two periods after coronary infarction: First 10 minutes right after Infarction Period of cardiac irritability beginning 1hr or so

later and lasting for another few hours


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Fibrilation of t h e Heart

Four Factors Rapid depletion of Potassium

E levated potassium ions in the E CF causes increasedcardiac irritability

Injury CurrentIschemic musculature cannot repolarize so the externalsurface remains negative

Powerful Sympathetic ReflexesBecause the heart does not pump the adequate volume of blood, sympathetic stimulation increases the cardiacirritability

E xcessive Dilation of the VentricleIncreasing the pathway length and causing abnormalconduction pathways around the infarcted area


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R ecovery

W hen the area of ischemia is small Little or no death of muscle cells may occur but

part of it becomes non functional

W hen the area of ischemia is large The muscle fibers in the center area die rapidly

and around that is a nonfunctional area and

around that is a weakly contracting area due tomild ischemia


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R eplacement of dead muscle byscar tissue

After a few days to 3 wks the nonfunctionalarea either dies or becomes functional again

Meanwhile, fibrous tissue develop among deadfibers because ischemia stimulates growth of fibroblasts and fibrous tissue

Dead fibers gradually gets replaced by fibrous

tissueW hile the normal areas of the heart hypertrophyto compensate for the lost cardiac musculature


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Value of R estDegree of cellular death is determined by the degreeof ischemia X degree of metabolism of the heartmuscleIf the metabolism of the heart is greatly increased(exercise, emotional strain, fatigue, etc) the need foroxygen and nutrients also increasesW hen the heart becomes excessively active thevessels of normal musculature becomes greatlydilated and so blood flows to the normal musculatureleaving little blood for the ischemic areasAfter Recovery, The person can still perform activityof a quiet, restful type but not strenuous exercisethat would overload the heart


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Pain in Coronary D isease

Angina Pectoris- progressive constrictionof their coronary arteries. Cardiac pain feltbeneath the upper sternum

Treatment using vasodilator drugs N itroglycerin and other nitrate drugs


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Surgical T reatment of CoronaryD isease

Coronary Angioplasty- a small balloon-tippedcatheter is pushed through the partiallyoccluded artery and is inflated to stretch theartery.


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Compensation for acute cardiacfailure by sympat h etic reflexes

W hen Cardiac output falls low, circulatoryreflexes are activatedBaroreceptor reflex- activated by diminished

arterial pressureChemoreceptor reflex, C N S ischemic responseand reflexes that originate in the damagedheart- contribute to the nervous responseSympathetics become stimulated within a fewseconds and Parasympathetics becomeinhibited


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Ch ronic R esponses to HeartFailure..

Involve Renal sodium and water retentionand recovery of the damaged Heart Depressed cardiac output reduces arterial

pressure and urinary output. Sodium and water retention increases blood

volume Hypervolemia increases the mean systemic

filling pressure and the pressure gradient forvenous returns, it also distends veins adding tothe increase in venous return


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Compensated Failure

Diagnostic Features: Right Atrial Pressure Distended N eck Veins

Causes Blood backs up into the Right Atrium Venous Return due to Sympathetic stimulation Retention of Renal sodium and water increases

blood volume


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R enal Sodium and W ater R etention

Retention of Renal sodium and water occurbecause of the sympathetic reflexes,decreased arterial pressure and stimulationof Renin- Angiotensin- Aldosterone System


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R enal Sodium and W ater R etention

Causes of Retention: Decreased arterial Pressure Sympathetic Constriction of the Afferent

Arterioles

Increased Angiotensin II formation Increased Aldosterone release

Increased Antidiuretic hormone release


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D ecompensated Heart Failure

W ith Decompensated Heart Failure,Compensatory Responses cannot maintainan adequate cardiac output


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The heart becomes to weak to restorenormal cardiac output needed by the bodyand the kidneys continue to retain fluid, TheHeart muscle continues to be stretched untilthe interdigitation of the actin and myosinfilaments is past optimum levels then the

cardiac contractility decreases further


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Causes: Longitudinal Tubules of SR fail to accumulate

sufficient calcium

Myocardial weakness causes excess fluidretention

Fluid retention causes edema, causing stiffening ventricular wall

N orepinephrine content of Sympathetic nerveendings decreases which decreases cardiaccontractility


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Unilateral Left Heart Failure

Blood backs up into the Lungs, increasing pulmonary capillary pressure and tendencyfor pulmonary edema to develop

Features: Left atrial Pressue Pulmonary Congestion Pulmonary E dema (when pulmonary capillary

pressure exceeds 28 mm Hg)


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High- Output Cardiac Failure

Can occur even in a normal heart that isoverloaded

Pumping ability of the heart is notdiminished but is overloaded by excessvenous return


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Most often caused by a circulatoryabnormality that total peripheral resistancesuch as: Arteriovenous fistulas


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Beriberi Thyrotoxicosis orHyperthyroidism


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Low -Output Cardiac Failure

Cardiogenic Shock can occur in conditionsassociated with depressed myocardialfunction

Most common occurrence is after myocardialinfarction


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Low -Output Cardiac Failure

Treatments: Digitalis (to increase cardiac strength) Vasopressor drug (to increase arterial pressure) Blood/Plasma (to increase arterial pressure and

coronary flow)

Tissue plasminogen activator (to dissolve the

coronary thrombosis)


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Acute Progressive pulmonaryedema

sometimes occur in patients with long-standing heart failure

Treatment: Applying torniquets to both arms and legs

(reduces pulmonary blood volume)

Bleeding the patient

Administering a rapidly acting diuretic(furosemide)


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Administering oxygen for patient to breathe Administering digitalis to increase heart

strength

Volume expanding agents are given forCardiogenic Shock to increase arterialpressure but Volume reducing measures areused to decrease edema fluid in the lungs


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Cardiac Reserve decreases with alltypes of Heart failure

Cardiac Reserve is the percentage increaseof cardiac output that can be achievedduring maximum exertion

Formula:[(Maximum Cardiac O utput N ormal Cadiac O utput) X 100]

Cardiac Reserve = ___________________________________________________

N ormal Cardiac O utput


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Coronary Circulation and Cardiac Failures

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