CHAPTER 6 DR. CARLOS ORTIZ BIO-208 PULMONARY BLOOD FLOW CHAPTER 6 DR. CARLOS ORTIZ BIO-208

PULMONARY VASCULATURE THE BODY’S VASCULAR SYSTEM HAS SEPARATE PULMONARY AND SYSTEMIC CIRCULATIONS OPERATING IN SERIES. THE RIGHT VENTRICLE RECEIVES MIXED VENOUS BLOOD, AND PUMPS IT THROUGH THE PULMONARY VALVE INTO THE PULMONARY CIRCULATION. THIS DEOXYGENATED BLOOD FLOWS THROUGH PULMONARY ARTERIES AND ARTERIOLES TO AN IMMENSE ALVEOLAR CAPILLARY BED WHERE IT IS OXYGENATED. THE NEWLY OXYGENATED BLOOD FLOWS THROUGH FOUR MAJOR PULMONARY VEINS INTO THE LEFT ATRIUM, THE RESERVOIR FOR THE LEFT VENTRICLE.THE LEFT VENTRICLE PUMPS OXYGENATED BLOOD TO THE SYSTEMIC CIRCULATION. SYSTEMIC VENULES AND VEINS CONVERGE TO RETURN THE DEOXYGENATED BLOOD FROM THE TISSUES TO THE RIGHT ATRIUM VIA THE VENA CAVAE.

PULMONARY VASCULATURE THUS THE TOTAL CARDIAC OUTPUT (Qt) IS PUMPED THROUGH BOTH CIRCULATIONS EACH MINUTE. RIGHT AND LEFT VENTRICULAR OUTPUTS MUST BE EQUAL OVER TIME; OTHERVISE, BLOOD ACCUMULATES IN ONE OF THE CIRCULATIONS. PULMONARY ARTERIOLES CAN NOT CONSTRICT AS EFFECTIVELY AS SYSTEMIC ARTERIOLES. PULMONARY VEINS AND VENULES ALSO CONTAIN LITTLE SMOOTH MUSCLE. PULMONARY CAPILLARIES ALSO DIFFER SIGNIFICANTLY FROM SYSTEMIC CAPILLARIES. BRONCHIAL VASCULATURE THE TRACHEOBRONCHIAL TREE IS SUPPLIED WITH OXYGENATED BLOOD THROUGH THE SYSTEMIC BRONCHIAL ARTERIES. ABOUT HALF OF THE BRONCHIAL VENOUS BLOOD ENTERS THE PULMONARY VEINS. (ANATOMICAL SHUNT).

PULMONARY AND SYSTEMIC PRESSURES THE PULMONARY CIRCULATION IS A LOW PRESSURE, LOW RESISTANCE SYTEM COMPARED WITH THE SYSTEMIC CIRCULATION. BECAUSE THE PULMONARY CIRCULATION’S PULSE PRESSURE (SYSTOLIC-DIASTOLIC) IS LARGE RELATIVE TO ITS MEAN PRESSURE, ITS FLOW IS HIGHLY PULSATILE. IN CONTRAST TO THIS, SYSTEMIC PULSE PRESSURE IS SMALLER WITH RESPECT TO MEAN PRESSURE, AND FLOW IS RELATIVELY MORE CONTINUOUS. THE TOTAL BLOOD VOLUME OF THE PULMONARY CIRCULATION (PULMONARY ARTERY TO LEFT ATRIUM) IS ABOUT 500ml, ONLY 10% OF THE TOTAL CIRCULATING BLOOD VOLUME.

PULMONARY AND SYSTEMIC PRESSURES THE RIGHT VENTRICULAR STROKE VOLUME (CAPILLARY BLOOD VOLUME) IS APPROXIMATELY 75-100 cc. THE CAPILLARY BLOOD THUS IS ALMOST COMPLETELY REPLACED WITH EACH HEART BEAT, ALLOWING A RED BLOOD CELL TO REMAIN IN THE CAPILLARIES FOR ABOUT 0.75 sec. THIS IS MORE THAT ENOUGH TIME FOR 02 AND CO2 PRESSURES TO EQUALIZE. THE PULMONARY VASCULAR VOLUME SERVES AS A BACKUP RESERVOIR THAT SHIELDS THE LEFT ATRIUM FROM SUDDEN CHANGES IN RIGHT VENTRICULAR OUTPUT. IF VENOUS RETURN TO THE RIGHT VENTRICLE INCREASES SUDDENLY, LEFT VENTRICULAR FILLING DOES NOT CHANGE GREATLY FOR TWO TO THREE CARDIAC CYCLES.

CLINICAL MEASUREMENT OF PULMONARY PRESSURES AND FLOWS SYSTEMIC BLOOD PRESSURE IS EASILY MEASURED BY SIMPLE NONINVASIVE MEANS. IN CONTRAST, PRESSURES IN THE PULMONARY CIRCULATION ARE DIFFICULT TO MEASURE, REQUIRING AN INVASIVE PROCEDURE. THIS PROCEDURE IS CALLED PULMONARY ARTERY CATHETERIZATION. PULMONARY VENOUS PRESSURE IS ABOUT EQUAL TO LEFT ATRIAL PRESSURE(LAP). AT THE END OF DIASTOLE, WHEN THE MITRAL VALVE IS OPEN, LAP IS ABOUT EQUAL TO LEFT VENTRICULAR PRESSURE. LEFT VENTRICULAR END-DIASTOLIC PRESSURE (LVEDP) IS THE PRESSURE IN THE VENTRICLE AFTER IT FILLS WITH BLOOD. FOR THIS REASON, THE LVEDP IS OFTEN CALLED THE LEFT VENTRICULAR FILLING PRESSURE. THE PRESSURE OBTAINED FROM THE DISTAL TIP OF THE SWAN-GANZ CATHETER IS THE WEDGED(BALLON-INFLATED) POSITION IS THE PULMONARY CAPILLARY WEDGE PRESSURE(PCWP). THE PCWP THUS REFLECTS LEFT VENTRICULAR FILLING PRESSURE, ALSO KNOWN AS LEFT VENTRICULAR PRELOAD.

CLINICAL MEASUREMENT OF PULMONARY PRESSURES AND FLOWS ASSESSING PCWP HELPS ASSESS THE PUMPING FUNCTION OF THE LEFT VENTRICLE. WHEN THE BALLOON IS DEFLATED, FLOW RESUMES AND THE CATHETER TIP MEASURES PULMONARY ARTERY PRESSURE (PAP). THE SWAN-GANZ CATHETER CAN ALSO ASSESS RIGHT VENTRICULAR PRELOAD AND PUMPING FUNCTION BECAUSE IT MEASURES THE PRESSURE IN THE RIGHT ATRIUM, ALSO KNOWN AS THE CVP. A MIXED VENOUS BLOOD SAMPLE REFLECTING A TRUE AVERAGE OF TOTAL BODY VENOUS BLOOD CONTENTS IS OBTAINED FROM THE PULMONARY ARFTERY THROUGH THE CATHETER’S DISTAL CHANNEL. BY COMPARING THE OXYGEN CONTENT OF MIXED VENOUS BLOOD WITH THAT OF SYSTEMIC ARTERIAL BLOOD, TISSUE OXYGEN CONSUMPTION CAN BE ASSESSED.

CLINICAL MEASUREMENT OF PULMONARY PRESSURES AND FLOWS BY MEASURING AND COMPARING PRESSURES OBTAINED FROM THE SWAN-GANZ CATHETHER (CVP, PAP, AND PCWP) THE CLINICIAN CAN EVALUATE RIGHT AND LEFT VENTRICULAR FUNCTION, DIFFERENTIATE THE CAUSE OF HIGH PAP, AND ASSESS THE RISK OF PULMONARY EDEMA. FOR EXAMPLE, ALL PULMONARY PRESSURES MAY BE HIGH BECAUSE OF EXCESSIVE INTRAVENOUS FLUID INFUSION (HYPERVOLEMIA) OR LEFT VENTRICULAR PUMPING FAILURE. HIGH PRESSURES IN EITHER VENTRICLE AT THE END OF DIASTOLE,COUPLED WITH A LOW CARDIAC OUTPUT, SIGNAL OF LOSS OF VENTRICULAR CONTRACTILITY. HIGH PCWP, REGARDLESS OF THE CAUSE, ENGORGES PULMONARY CAPILLARIES, INCREASING THE LIKELIHOOD THAT FLUID WILL BE FORCED INTO INTERSTITIAL LUNG SPACES AND CAUSE PULMONARY EDEMA.

PULMONARY VASCULAR RESISTANCE PVR IS THE PRESSURE REQUIRED TO PRODUCE BLOOD FLOW THROUGH THE PULMONARY VESSELS OR THE RESISTANCE AGAINST WHICH THE RIGHT VENTRICLE PUMPS. THUS THE HIGH PVR INCREASES RIGHT VENTRICULAR WORK. CALCULATION OF PVR PVR IS CALCULATED BY DIVIDING THE PRESSURE DIFFERENCE BETWEEN BEGINNING AND ENDING POINTS OF THE PULMONARY CIRCULATION BY THE BLOOD FLOW. PVR= MEAN PAP - PCWP PVR= 14mmHg- 8 mmHg= 1.2 mmHg QT 5 L/min L/min THIS MEAN A PRESSURE OF 1.2 mmHg IS NEEDED TO PRODUCE A FLOW OF 1 L/min THROUGH THE PULMONARY CIRCULATION.

SYSTEMIC VASCULAR RESISTANCE CALCULATION OF SVR SVR IS THE PRESSURE DIFFERENCE BETWEEN BEGINNING AND ENDING POINTS OF THE SYSTEMIC CIRCULATION. THE DIFFERENCE BETWEEN MEAN ARTERIAL PRESSURE(MAP) AND CVP DIVIDED BY BLOOD FLOW IS THE SYSTEMIC VASCULAR RESISTANCE. SVR= MAP - CVP PVR= 93mmHg- 2 mmHg = 18.2 mmHg QT 5 L/min L/min THIS MEAN A PRESSURE OF 18.2 mmHg IS NEEDED TO PRODUCE A FLOW OF 1 L/min THROUGH THE SYSTEMIC CIRCULATION COMPARED WITH 1.2 mmHg IN THE PULMONARY CIRCULATION.

LIQUID MOVEMENT ACROSS THE ALVEOLAR CAPILLARY MEMBRANE THE PULMONARY CAPILLARY ACTS A A SEMIPERMEABLE MEMBRANE, FREELY PERMEABLE TO WATER BUT MUCH LESS PERMEABLE TO LARGE MOLECULES. LARGE PROTEINS MOLECULES ON EITHER SIDE OF THE CAPILLARY MEMBRANE IMPART OSMOTIC PRESSURE TO THEIR FLUIDS. THE INFLUENCE OF PROTEINS ON BLOOD PLASMA’S OSMOTIC ACTIVITY IS CALLED ONCOTIC PRESSURE. THE GREATER THE PROTEIN CONCENTRATION, THE GREATER THE ONCOTIC PRESSURE. ONCOTIC PRESSURE WORKS TO PULL WATER MOLECULES FROM AREAS OF LOW ONCOTIC PRESSURE INTO AREAS OF HIGH ONCOTIC PRESSURE. HYDROSTATIC PRESSURE PUSHES FLUID FROM HIGH TO LOW PRESSURES.

PULMONARY EDEMA PULMONARY EDEMA IS THE ACCUMULATION OF FLUID IN THE INTERSTITIAL SPACES. CAUSES OF PULMONARY EDEMA INCLUDE 1- INCREASE HYDROSTATIC PRESSURE. IF HYDROSTATIC PRESSURE IN THE PULMONARY CAPILLARY INCREASES ENOUGH, FLUID FILTRATION INTO THE INTERSTITIAL SPACE MAY EXCEED LYMPHATIC DRAINAGE. A COMMON CAUSE OF HYDROSTATIC PULMONARY EDEMA IS LEFT VENTRICULAR FAILURE.THIS TYPE OF EDEMA IS ASSOCIATED WITH HIGH PCWP. 2- INCREASED CAPILLARY PERMEABILITY ACUTE LUNG INJURIES THAT DAMAGE THE A-C MEMBRANE MAY INCREASE ITS PERMEABILITY TO FLUIDS AND PRECIPITATE PULMONARY EDEMA. TYPICALLY, PEOPLE WITH THIS KIND OF PULMONARY EDEMA HAVE NORMAL PCWP. 3- DECREASED PLASMA ONCOTIC PRESSURE 4- INSUFFICIENT LYMPHATIC DRAINAGE