Você está na página 1de 43

Methods to measure C.

O:
Direct Fick Method Thermal dilution method Echocardiography Ballisto-cardiography

DIRECT FICK METHOD:


OXYGEN FICK METHOD is based on FICK PRINCIPLE:

The amount (Q) of a substance removed by an organ from the blood per unit time is equal to the difference in the concentration of substance in the arterial blood and venous blood ,

Let us use O2 as the substance removed:


F= Amount of O2 consumed / min O2 in art. blood O2 in venous blood, in ml/L of blood

Q can be found with the help of respirometer.

For measuring O2 conc. in venous blood, mixed venous blood is used from the beginning of pulmonary artery with the cardiac catheter. Every tissue has different O2 utilization & if sample is taken from superficial vein, it will have less O2, so mixed venous blood is taken.

DISADVANTAGES of DIRECT FICK METHOD:


1) Only C.O at rest can be determined but not during exercise. 2) Hazards of catheterization may precipitate arrhythmias.

3) Patient becomes anxious, so C.O value will not be accurate.

DYE DILUTION METHOD:


Dye = Evans blue = T1824 Or dye = cardio-green

Dye used should have these properties: 1) Should not be toxic 2) Should be non-diffusible 3) Should not be metabolized in the body

We inject a measured amount of dye superficial vein (basilic vein). Note the time of injection of dye. Arterial blood samples are taken at 1-2 sec interval & these are put in a series of tubes. Analysed for dye conc. with photo electric colorimeter. Plot a curve called conc. Duration curve. When dye appears in arterial blood, the curve rises. When it disappears from arterial blood and appears in venous blood, the curve falls, and rises again with next cycle, when dye reappears in arterial blood.

Downfall of dye conc. if extended to touch the baseline, this is the time of one circulation of dye. Measure the area under the curve to find mean conc. of dye. Use the formula for C.O: C.O (ml / min) = A x 60 CXt A = amount of dye injected (mg) C = Mean dye conc. (mg/ml) t = time in sec (time of 1 circulation of dye) 60 to convert sec min

Dye large syst. Vein or in Rt. Atrium rt. Heart pulm. Vessels lt. heart systemic arteries. Dye conc is recorded when dye reaches one of the peripheral syst. artery & curve is obtained. 5mg of cardiogreen dye injected at 0 time.

Top recording
No dye passed into arterial tree till 3sec after the injection. After 3sec of injec, arterial conc of dye rose to max. in 6-7 sec. Then the conc. fell rapidly. But before the conc reached 0, some of the dye had already circulated all the way through some of the periph syst vessels & returned through the heart for a second time. So dye conc in the artery began to rise again.

For calculation we extrapolate the early down-slope of the curve to 0 point. (dashed portion).
So we obtain the extrapolated time-conc curve of the dye in the systemic artery, without recirculation (time of one circulation of the dye). Mean conc. of dye in the arterial blood for the duration of the curve is determined.

In the top example: Area under the entire initial and extrapolated curve was measured. Conc of dye for the duration of the curve was averaged from the shaded rectangle. It was 0.25 mg / dl of blood for 12 sec duration.

Average dye conc in 12 sec = 0.25 mg/dl for total injected dye = 5mg

For blood carrying only 0.25 mg of dye in each dl to carry the entire 5mg of dye through the heart and lungs in 12 sec, a total of 20 1-dl portions of blood would have passed through the heart during the 12 sec, which would be the same as a C.O of 2L/12sec.

0.25 mg --------------1 dl 5 mg---------------? 5 x 1 = 20 1-dl portions/12sec = C.O 0.25 20 1-dl / 12 sec = C.O so ? L / 12sec = C.O Now 10dl = 1 L 20dl = ?L / 12sec 20 x 1 = 2L / 12sec 10 2L ----------12sec ?L----------60sec or 1 min 2X 60 = 10 L / min 12

C.O (ml/min) = mg of dye inj x 60


(average conc of dye in each ml of blood x for the duration of the curve) (duration of curve in sec)

C.O (ml / min ) = 5 mg x 60 0.0025 mg / ml x 12 sec

= 10000 ml / min = 10 L / min


(10 dl = 1000 ml) or (1dl = 100 ml) 0.25 mg / dl = 0.0025 mg / ml HOME WORK: CALCULATE C.O FROM BOTTOM CURVE. (Fig. 20.19, Guyton 11th edition).

ADVANTAGES: 1) More accurate. 2) no hazard of cardiac catheterization. 3) can be used in exercise. 4) can be used in investigation of various acquired & congenital heart diseases, e.g, in cardiac failure dye appears in arterial system late & slow rise in dye conc in arterial blood that achieves a lower peak. 5) we can also use radio-isotopes instead of dye ( 131I = Radioactive iodine) 6) in VSD, dye appears in arterial circulation earlier & reaches greater peak.

THERMAL DILUTION METHOD


We introduce 2 catheters with thermisters (device which can record temp.) near their tips. 1 catheter is introduced in a superficial vein & 2nd in a superficial artery & then pushed till reaches beginning of aorta. A measured amount of cold saline is introduced into 1st catheter (in superficial vein). The thermister in 2nd catheter determines temp. of blood, before the injec of cold saline. Then serial change in blood temp. after the inj of cold saline.

We take changes in blood temp on vertical axis & time in sec on horizontal axis & plot a curve b/w blood temp & time. From this curve we find out C.O: C.O = V1 (TB T1) TB X t V1 = vol. of cold saline injected TB = blood temp before inj of cold saline T1 = Temp of cold saline TB = mean change in blood temp after the inj of cold saline t = Time of circulation of cold saline

INDICATION: It is used in small children because blood samples are not required.

ECHOCARDIOGRAPHY
Non-invasive. Principles: Sound / ultrasonic waves are emitted from a transducer & strike different parts of heart & then reflected back. These are received by a receiver. From the pattern of reflected waves, different cardiac parameters including stroke vol. are determined.

TRANSD

BALLISTOCARDIOGRAPHY
Historical importance. It is an apparatus which records fine movements of body produced due to blood ejection from the heart & other events in cardiac cycle. It functions on 3rd law of Neuton.

STROKE VOL IS DETERMINED FROM THIS RECORD (H-O waves)

CARDIAC OUTPUT CURVES:


HEART HAS LIMITS FOR C.O THAT IT CAN ACHIEVE, EXPRESSED QUANTITATIVELY AS C.O CURVES. Normal C.O / min at each Rt.atr.pr is shown. (plateau level = 13L / min = 2.5 x normal C.O of 5L / min), so normal heart without any stimulation can pump out venous return upto 2.5 x normal V.R. HYPEREFFECTIVE & HYPOEFFECTIVE hearts pump better than normal and below normal respectively. C.O curves relate pumping of blood by the heart to right atrial pressure.

FACTORS CAUSING
HYPER EFFECTIVE : Nervous stimulation. Hypertrophy of muscle. HYPO EFFECTIVE : Coronary block attack. Inhibition of nervous stimulation. Pathology abnormal h.rate / rhythm. Vascular disease. Hypertension. Cong. disease. Myocarditis & hypoxia.

Normal venous return curve


V.R curve relates V.R to Rt.At.Pr.,i-e, venous flow of blood into the heart from systemic circulation at different levels of R.A.P. Curve shows that when heart pumping capability decreases and causes the R.A.P to rise. back pr on veins decreased V.R (blood pool in systemic circulation, which serves as a distensible bag). V.R will become 0, when R.A.P rises to +7mmHg, if all nervous reflexes are prevented. At V.R = 0 , pumping by heart also becomes 0 arterial pr is in equilibrium with venour pr at pr of 7mmHg, so called MEAN SYSTEMIC FILLING PRESSURE (Psf).

Plateau in V.R Curve at negative atrial pressures- caused by collapse of large veins
When R.A.P falls below 0 (below atmospheric pr), there is no further increase in V.R. When R.A.P falls to -2mmHg, V.R reaches a plateau even if R.A.P falls further even to 50mmHg or below. Plateau is due to collapse of veins entering the chest.(sucking effect on walls of veins) prevents any further flow of blood from peripheral veins. So no increase in V.R at R.A.P below 0, which is normal R.A.P.

EFFECT OF INCREASED B.Vol ON C.O:


Sudden increase in B.Vol of 20% increase in C.O to 2.5-3 x normal. On infusion, Psf increases from 7 to 16 mm Hg. V.R curve is now shifted to right. Increased B.Vol distends the blood vessels decreased resistance to V.R. Curve rotates upward. Thus new V.R curve shifted to right equates with C.O curve at point B, showing that C.O & V.R increases 2.5-3 x, & R.A.P rises to +8mmHg.

Q1. In sinus arrhythmia, heart rate increases on inspiration & decreases on expiration. Why?
INSPIRATION decrease in I.Th.p increase in lung vol & increase in V.R. stretch receptors in lungs & right atrial stretch receptors (Bain Bridge reflex) stimulated vagal efferents inhibition of V.D area increased Heart rate. EXPIRATION increase in I.Th.p decrease in lung vol & decrease in V.R. No stimulation of stretch receptors in lungs & no Bain Bridge reflex no vagal efferent impulses no inhibition of V.D area. decrease in heart rate. REFERENCE: JAYPEE, 3RD ED, pg 459.

Q2. In cushing reflex, there is tachycaria followed by bradycardia. Why?


When I. C.Pr increases B.Vs compress in brain decreased blood supply to vaso motor area hypoxia & hypercapnia stimulation of VMC TACHYCARDIA + increased B.P (to restore). But if I.C.Pr keeps on increasing it becomes so great that VMC fails reflex decrease in heart rate (BRADYCARDIA) + decreased B.P. Reference: pg 609, GANONG.

Q3. In left ventricular reflex there is decrease in heart rate, unlike in right atrial & right vent. reflex. Why?
Left vent. Stimulation maintains the vagal tone. When stretch receptors in lt. vent are stimulated vagal tone is stimulated decrease in heart rate + decreased systemic arterial pressure. Scientists have proved that left vent stretch receptors are different from other low pressure stretch receptors. Reference: pg 608, GANONG.

Você também pode gostar