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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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Control of Coronary Blood Flow
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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Control of Coronary Blood Flow
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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D ecompensated Heart Failure
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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D ecompensated Heart Failure
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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High- Output Cardiac Failure
Most often caused by a circulatoryabnormality that total peripheral resistancesuch as: Arteriovenous fistulas
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High- Output Cardiac Failure
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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