Cardiovascular Management RET 301 Laboratory Education Program
CV Anatomy and Physiology
Prior to a discussion of hemodynamic monitoring. A brief review of CV A&P is helpful.
The purpose of the CV system is distribute oxygen and other nutrients to the body tissues and to assist in the removal of waste products. This is accomplished by the heart acting as a pump to circulate the blood throughout the cardiovascular tree.
The heart is a four chambered organ that can be divided into right and left sides. The right side receives the venous blood from the tissues. This blood is low in oxygen and higher in carbon dioxide than arterial blood. The right heart pumps the venous blood into the pulmonary circulation (via the pulmonary artery) to pick up oxygen and release carbon dioxide. This is the process of arterializing the blood.
Once the blood is oxygenated, it returns to the left side of the heart (via the pulmonary vein) and is pumped by the left ventricle to into the systemic circulation. The blood is distributed to the tissue via the arteries and arterioles.
Under normal conditions, the left side of the heart has to pump the blood a greater distance and through vascular beds with higher resistance than the right side of the heart. It is, therefore, larger and more capable of generating high pressures than the right heart.
Although the left ventricle is well supplied by coronary arterial perfusion, it is the chamber primarily involved when myocardial infarction occurs. The function of the left ventricle is of particular importance since it has the role of distributing the oxygenated blood to the various organs, thereby maintaining life.
The quantity of blood pumped per minute by the left ventricle is defined as the cardiac output. Normal values in the adult are 4 - 8 L/m
Because this is such a large range and varies significantly with the size of the individual, many clinicians prefer to look at cardiac index. This is defined as the volume of blood pumped by the left ventricle per minute in relation to body surface area. Cardiac index is reported in L/min/square meter. Normal values are 2.5 - 4.0 L/min/m 2
The myocardial cell is the basis of the ventricular myocardium. It is composed of multiple linearly arranged myocardial fibrils with cell nuclei. The myocardial fibril is made up of sarcomeres which are the basic functional unit of the heart muscle. The sarcomere shortens with contraction. The strength of the contraction is determined by the degree of stretch applied to the sarcomere prior to contraction.
Within physiological limits, the degree of tension created by contraction is directly related to the degree of myocardial stretching caused by ventricular filling. Overstretching of the sarcomeres will result in little or no tension during the subsequent contraction.
The heart is extensively innervated by the sympathetic and parasympathetic nervous systems. Sympathetic stimulation increases the rate and force of myocardial contraction. Parasympathetic stimulation does not directly influence contractility but does reduce the sinoatrial rate and inhibit AV conduction, thus slowing the heart rate.
1. The total blood flow out of the left ventricle per unit of time is defined as:
a. Stroke volume
b. Heart rate
c. Cardiac index
d. Cardiac output
STOP, answer the question and continue
2. Which part of the heart pumps the blood into the pulmonary circulation?
a. Right atrium
b. Right ventricle
c. Left atrium
d. Left ventricle
3. Which part of the heart pumps blood into the systemic circulation?
a. Right atrium
b. Right ventricle
c. Left atrium
d. Left ventricle
4. The quantity of blood pumped related to the person’s body size is defined as:
a. Stroke volume
b. Cardiac output
c. Cardiac index
d. Stroke index
5. Within certain physiological limits, the more the ventricle is filled with blood, the:
a. Greater the strength of contraction
b. Greater the stroke volume
c. Greater the cardiac output
d. All of the above
Determinants of Cardiac Outputs
There are two major factors determining cardiac output: 1) heart rate and 2) stroke volume. Stroke volume (SV) is the volume of blood ejected from the ventricle with each heart beat and is approximately the same for each ventricle. Since the normal HR is 60 - 100 bpm in the adult, the normal range for cardiac output is 4-6 lpm. This is determined by multiplying the HR by the SV. Each factor that influences cardiac output (Qt) is listed.
HR: Normally in the adult, HR does not play a major role in the determination of Qt unless it varies significantly from normal range. In most cases, bradycardia is compensated for through an increase in SV. In patients with heart disease however, the heart can not increase SV enough to compensate for bradycardia and subsequently Qt falls.
Tachycardia is the body’s compensatory mechanism for maintaining Qt when SV can not be increased. Tachycardia decreases diastolic time which reduces the filling time for the ventricles. At rest, most patients will experience a fall in SV when the HR exceeds 120-130 bpm. With heart disease, even at a HR of 100 bpm or less, the SV may decrease.
The 2 nd major factor determining Qt, SV, is influenced by 3 sub factors: preload, afterload, and contractility.
Preload is the stretch on the ventricular muscle fibers before contraction. Preload is created by end-diastolic volume. Remember that up to a critical limit the heart muscle fibers will contract with a force proportional to the degree of stretch on the fiber prior to contraction. Simply put, the greater the stretch on the resting ventricle, the greater the strength of contraction within physiological limits.
A rubber band can be used as an analogy. The tighter the rubber band is stretched, the further it flies on release.
It can be said that increasing volume increases output. When the pump is no longer able to eject all of its blood efficiently because it is over stretched, cardiac output begins to fall.
Traditionally, filling pressures have been used to reflect ventricular end-diastolic volume, since measuring the actual volume is very difficult. It is important to understand that this pressure is the result of the volume, space, and compliance of the chamber that the blood is entering. Many factors influence the compliance of the ventricles and will therefore effect the relationship between volume and pressure.
For example, myocardial ischemia makes the myocardium less compliant resulting in higher pressure readings for smaller end-diastolic volumes. In such cases the hemodynamic measurements must be interpreted in light of the patients clinical condition. Construction of ventricular function curves for specific patients will assist in identifying optimal filling pressures at a given point in time.
When ventricular compliance is reduced, a higher filling pressure is needed to optimize stroke volume.
The most important factor influencing preload is the amount of blood returned to the ventricles. This is often referred to as venous return. Venous return is affected by three factors:
1. Changes in the circulating blood volume
2. Changes in the distribution of blood volume
3. Atrial contraction
There are many things that may influence any one of these factors, however, venous return is most often reduced with hypovolemia, PEEP therapy, vasodilators, and atrial fibrillation.
Afterload is the resistance to ventricular ejection. The peripheral component of afterload is primarily determined by the radius of the peripheral vessels. The smaller the radius, the greater the resistance to flow out of the ventricle and the higher the afterload.
A certain degree of impedance to blood flow is needed to maintain normal hemodynamics, however, if afterload increases too much, the myocardium must work harder to pump blood. This will increase myocardial oxygen consumption (MVO 2 ) and often cause a fall in SV.
Although afterload is not directly measured, vascular resistance can be determined from hemodynamic measurement. Pulmonary vascular resistance (PVR) is used to assess right ventricular afterload. It often increases with hypoxemia, hypercapnea, and pulmonary emboli. Systemic vascular resistance (SVR) is used to evaluate left ventricular afterload. This will be elevated with vasoconstrictors, hypertension, cold extremities, and hypoperfusion. The SVR is reduced with vasodilators such as nitroprusside and morphine.
Contractility is the strength and speed of the shortening of the heart muscle and represents the ability of the heart to pump blood. Even with normal blood volume and vascular resistance, the heart must possess the ability to pump blood through the circulatory system. Contractility can not be measured directly but is inferred from certain hemodynamic measurements and calculations.
Contractility is reduced with hypoxemia, acidosis, poor coronary perfusion, and beta blockers. Cardiac output falls in proportion to the reduction in contractility.
Agents that affect contractility are called inotropes. Drugs with a positive inotropic affect increase the force of muscle shortening. These drugs should only be used when preload has been optimized and afterload has been reduced to a normal level. Use of positive inotropes will increase myocardial ischemia since myocardial workload is increased.
6. Normal stroke volume ranges from:
a. 30-60 cc’s
b. 40-80 cc’s
c. 60-130 cc’s
d. 80-200 cc’s
7. At best, the SV begins to drop when the HR exceeds:
a. 80 b/min
b. 100 b/min
c. 130 b/min
d. 150 b/min
e. 180 b/min
8. Which of the following can influence stroke volume?
e. all of the above
9. Which of the following is, by definition, created by end-diastolic pressure?
d. Heart rate
10. Ventricular function curves are helpful to assess:
b. Optimal filling pressures
d. Independent ventricular function
11. Myocardial infarction will result in:
a. Higher filling pressures for less volume
b. Lower filling pressures for less volume
c. Lower filling pressures for the same volume
d. No change in ventricular compliance
12. Which of the following should have little or no affect on venous return and preload?
a. PEEP therapy
d. Faster heart rates
13. Afterload is increased most with:
b. Peripheral vasoconstriction
14. Elevation of afterload above normal has what effect on hemodynamics?
a. Increased Qt
b. Decreased BP
c. Decreased SV
15. Which of the following is used to asses afterload for the right ventricle?
d. Arterial blood pressure (BP)
16. Contractility is reduced with each of the following EXCEPT:
d. Beta blockers
17. Positive inotropic agents increase:
b. Cardiac excitation
d. Left ventricular preload
Hemodynamic Pressure Measurements
Through the placement of central venous and/or pulmonary artery catheters several parameters are available for hemodynamic assessment. The assessment of preload and afterload for the right and left ventricle is possible. The values used include central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary capillary wedge pressure (PCWP).
This is the pressure of the blood in the vena cava or right atrium, where blood is returned to the heart form the venous system.
CVP is regulated by a balance between the ability of the heart to pump blood out of the right atrium and right ventricle and the amount of venous return. In general, increases in venous return elevate CVP and decreases in venous return decrease CVP.
In addition, decreases in right heart pumping function backs up blood flow into the right atrium and vena cava and elevate CVP. In contrast, improvements in right heart function usually decrease CVP unless venous return also increases.
Normal CVP is 0-6 mmHg. Elevation of CVP occurs with:
1. right heart failure
2. pulmonary valvular stenosis
3. pulmonary hypertension
4. Pulmonary embolism
5. Volume overload
6. Chronic or severe left heart failure
Decrease in CVP occurs with:
3. Spontaneous inspirations
Most often CVP is measured by placement of a catheter in the external or internal jugular veins with the tip of the catheter in the vena cava or right atrium. Once the catheter is in place, it can be used for the administration of fluids, blood, medications, and for aspiration of blood for laboratory studies. The CVP catheter should not be used for mixed venous blood samples.
True mixed venous samples can be obtained only when blood has passed the right ventricle which requires the use of a pulmonary artery catheter. This permits true mixing of the sample.
While CVP is an accurate reflection of the filling pressures for the right ventricle, it is a poor reflection of left side filling pressures. This fact has led to the development of balloon flotation catheters. These catheters allow direct measurement of pulmonary artery pressures.
In addition, by occluding the pulmonary capillary by inflating a small balloon, left heart filling pressures can be assessed. Pulmonary artery catheters are most often positioned in the patient by floating them into place, using intravascular pressure waveforms to indicate catheter position. The distal lumen of the catheter is connected to a transducer-monitor system. The tip of the catheter is initially placed in one of the central veins. In this position a CVP tracing appears on the monitor.
The balloon is inflated and the blood flow carries the catheter tip towards the right atrium and into the right ventricle. A rapid increase in the height of the pressure wave form is seen then. RV pressure waveforms are unique in that they have high peaks but the right side or down stroke goes straight down almost to zero. The normal RV pressure is 20-30 mmHg.
Entry into the pulmonary artery is recognized by a change in the diastolic portion of the waveform. Normal pulmonary artery systolic pressure is 20-30 mmHg and the diastolic pressure is less than 15 mmHg. A normal mean value is 10-20 mmHg.
Elevation of PAP’s occur with left heart failure and problems that elevate PVR such as hypoxemia, COPD, and pulmonary emboli.
When the catheter advances to a wedged position in a small branch of the pulmonary artery, the arterial blood flow is stopped and the wave form takes on the appearance of an atrial pressure waveform (like CVP). When the balloon is deflated, the pulmonary artery wave form should reappear. From this point the balloon is only inflated when PCWP measurements are required. It is important to make sure the balloon is not left inflated as a pulmonary infarct may occur.
PCWP is used to reflect left heart filling pressure (preload) since there are no barriers (valves) between the pulmonary capillaries and the left atrium. PCWP elevates when the left heart fails to pump blood adequately and the blood volume backs up into the pulmonary circulation. Other causes of an increased PCWP include aortic stenosis and systemic arterial constriction (increased SVR). In such cases preload is elevated above normal physiological limits and the stroke volume and subsequently Qt will drop off.
Treatment is usually aimed at lowering the filling pressure with diuretics and/or vasodilators.
Decrease in PCWP occurs with right heart failure and with pulmonary embolism. In this situation preload is often below optimal range. Ventricular filling is inadequate and the resulting drop in stroke volume causes Qt to fall. The treatment is to correct the underlying cause.
The application of PEEP to a patient may result in an erroneous PCWP reading. This primarily occurs when the tip of the PA catheter is positioned above the level of the left atrium. The pressure in the pulmonary capillaries is low and the application of PEEP causes the alveolar pressure to exceed the pulmonary capillary pressures. This causes a measurement of at least some component of alveolar pressures rather than left heart filling pressures alone.
This problem may occur with hypovolemia or when extremely high levels of PEEP are used. Proper placement of the PA catheter (checked via x-ray) and adequate circulating volumes will minimize this problem. An abrupt change in PCWP that occurs with increased PEEP should be noted. Removing PEEP for PCWP measurement is NOT recommended. Since PEEP therapy often causes a reduction in Qt by reducing preload of the left ventricle, it is important to assess PCWP accurately in patients being treated with PEEP.
In the ICU, arterial pressure is frequently measured by the placement of an intra-arterial catheter. This allows continuous monitoring of arterial pressures and sampling of arterial blood for blood gases. This catheter is a more accurate means of pressure monitoring than the use of a BP cuff. In the critically ill, this is the preferred technique.
Normally blood pressure is reported as 120/80 mmHg - systolic/diastolic. In the ICU, MAP or mean arterial pressure, is also recorded. Normal values for BP vary with age. Systolic pressure should be 110-150 mmHg, diastolic 60-90 mmHg, and MAP 80-100 mmHg.
Reduction in BP may occur with pump failure (decreased contractility), low blood volume, and profound vasodilation. Since a low BP indicates that perfusion is inadequate, rapid treatment must be initiated to avoid tissue hypoxia.
Elevated BP occurs with peripheral vasoconstriction or with an increase in the force of ventricular contraction. Clinicians must remember that normal or elevated BP does not guarantee adequate perfusion. Peripheral vasoconstriction can maintain blood pressure in the normal range even though Qt is well below normal. This mandates evaluation of other indicators of perfusion than blood pressure exclusively.
Placement of a pulmonary artery catheter allows assessment of Qt. This parameter is very important as it describes the ability of the left ventricle to pump arterial blood through the body. The two most popular techniques for measuring Qt are thermodilution and dye dilution. Both techniques are based on the principal that the rate of blood flow is directly related to
the rate in which a concentration of a substance (dye or cold water) is diluted down to baseline. The greater the Qt the faster the dye or water is diluted. Both methods require skill and elaborate equipment to be accurate and reliable.
Normal Qt is 4-8 l/min. Many ICU centers report CI (cardiac index) which is the Qt divided by the body surface area. Normal CI is 2.5-4.0 l/min/m 2 . A CI below normal indicates that the heart is not pumping an adequate volume of blood.
Other parameters should then be looked at but regardless of the cause, the patient’s tissue needs for oxygen are not being met and if this is not rapidly corrected tissue damage will occur. The combination of a low Qt and metabolic acidosis suggests the production of anaerobic lactic acid which can be an ominous sign.
18. Preload for the right ventricle is reflected by:
d. Arterial BP
19. Preload for the left ventricle is reflected by:
d. Arterial BP
20. Normal CVP is:
a. 2 mmHg
b. 20 mmHg
c. 6 mmHg
d. 12 mmHg
21. CVP would NOT be elevated with which of the following?
a. Right heart failure
b. Pulmonary embolism
c. Pulmonary hypertension
22. Balloon flotation pulmonary artery catheters provide the ability to:
a. Assess LV filling pressures
b. Evaluating right heart function
c. Evaluating RV afterload
d. All of the above
23. The CVP catheter should NOT be used for:
a. Administering fluids
b. Sampling mixed venous blood gases
c. Administration of drugs
d. Assessing blood volume
24. Normal PCWP is:
a. 4-12 mmHg
b. 8-18 mmHg
c. 5-10 mmHg
d. 15-24 mmHg
25. Pulmonary artery catheters placed with the tip above the left atrium:
a. Reflect elevated measurements
b. Should be repositioned
c. Accurately reflects LV preload
d. Are in good position for PEEP therapy
26. PCWP elevates with all the following except:
a. Left heart failure
b. Right heart failure
c. Mitral stenosis
d. Cardiac tamponade
27. Normal mean arterial pressure is:
a. 40-60 mmHg
b. 60-80 mmHg
c. 80-100 mmHg
d. 100-120 mmHg
28. A drop in arterial pressure occurs with which of the following?
b. Increased contractility
c. Increased afterload
d. Increased preload
29. Normal Qt is:
a. 1-3 l/min
b. 3-6 l/min
c. 4-8 l/min
d. 5-12 l/min
30. A low Qt combined with which of the following indicated that tissue oxygenation is NOT adequate?
b. Metabolic acidosis
d. Respiratory alkalosis
The systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) are two other measurements that can be made with a PA catheter. Vascular resistance is the amount of pressure that is required to cause blood flow across a system. Normal SVR is 800-1600 dynes/sec/cm 5 .
(MAP - CVP) x 80
An elevated SVR may imply the presence of vasoconstriction and require vasodilator therapy. A low SVR usually indicates vasodilation or hypovolemia.
The PVR normal is 20-200 dynes/sec/cm 5
PVR = ( MPAP - PCWP) x 80
A high PVR generally indicates pulmonary vasoconstriction, a common finding in pulmonary disease.
Applications of the Pulmonary Artery Catheter
The PA catheter is useful for the following general situations:
1. Fluid management
2. Evaluation if L and R ventricular performance
3. Measurement of mixed venous blood gases
4. Measurement of acute pulmonary edema
5. Measurement of cardiac output
Specifically, PA catheters may be helpful in the assessment and monitoring of the following conditions:
1. Complicated myocardial infarction
3. Pulmonary edema
4. High risk surgical patients
Noninvasive Assessment of Perfusion
Normally, the flow of blood to the body is controlled by the need for oxygen. When the need for O 2 increases (as with exercise) or the amount of O 2 delivered to the tissues is inadequate, the vessels dilate and bring an increased supply of blood and O 2 . When the heart and circulatory system cannot supply an adequate blood flow to meet the demand, the vasodilation causes a drop in arterial pressure.
This leads to a series of compensatory events that try to maintain blood flow to the vital organs. This manifests originally as the following clinical changes.
HR: Hypoxia and hypotension result in sympathetic nervous stimulation. Tachycardia ensues that may be the first clue to inadequate perfusion. Other causes of tachycardia must not be overlooked: pain, anxiety, medications, and fever.
Sensorium (LOC): When the brain is not adequately perfused and oxygenated, the patient will become less responsive. Orientation to time, place, and person may be abnormal. As deterioration continues, the patient will become comatose. A return of oxygenated perfusion may return consciousness if the period of hypoxia was not too severe or prolonged.
Extremity temperature: Peripheral vasoconstriction occurs in order to shunt blood to vital organs during periods of inadequate perfusion. This usually results in cold hands and feet. This is most often assessed through touch.
When perfusion to the extremities is decreased, a point of temperature change can be assessed by slowly moving the hand up the leg from the foot. This point can be marked and reassessed periodically to evaluate therapy. Along with extremity temperature, the capillary refill time can be assessed. A 5-second compression of the nail bed will blanch the underlying tissue. Upon release, a return of pink color should occur within 3 seconds if circulation is adequate.
A capillary refill time of greater than 3 seconds is definite indication of hypoperfusion, at least of that extremity.
Urine output: Urine output (UO) is a good indicator of arterial pressure and Qt. Normal UO is ~30-60 cc/h. UO of less than this may occur as compensatory efforts to conserve blood volume occur in the presence of hypotension. Renal disease and medications may bring the reliability of UO in to question as a predictor of circulation.
Arterial Blood Pressure: Arterial BP is the most frequently measured hemodynamic value but it must be remembered that falling BP is a late sign of decreased Qt. Peripheral vasoconstriction will maintain BP in the presence of poor perfusion. For this reason, other clinical measurements must be used in order for early detection of hypoperfusion states. Certainly, anytime hypotension is present it is safe to say that circulation is not adequate. A normal BP doesn’t always indicate adequate perfusion.
31. One of the initial clinical signs that indicates perfusion may NOT be adequate is:
32. Hypoperfusion usually causes each of the following EXCEPT:
a. Confusion or coma
b. Cold extremities
c. Rapid capillary refill
33. Capillary refill is assessed by a 5 second compression of the:
b. Nail beds
c. Ear lobe
d. Skin on the back of the hand
34. Urine output is normally:
a. 10-30 cc/h
b. 30-60 cc/h
c. 50-80 cc/h
d. 60-80 cc/h
35. A drop in urine output may indicate:
a. A decrease in perfusion
c. A need for oxygen
d. Elevation of afterload
36. Which of the following parameters may read normal when perfusion is inadequate?
b. Extremity temperature
c. Arterial blood pressure
d. Capillary refill time
The following is a discussion of some of the more common situations in which hemodynamic measurement will be useful. Typical clinical findings and a brief discussion on treatment will also be provided based on hemodynamic measurements.
This frequently occurs following hemorrhaging in post-operative patients and trauma patients. Overuse of diuretics in patients not carefully monitored or at home can also occur. Initially the CVP and PCWP are reduced indicating the L and R preload are inadequate. Stroke volume is reduced and compensatory tachycardia may keep Qt at a normal level.
Severe losses in blood volume cannot be compensated for with tachycardia and decreased Qt occurs. BP may remain within normal range initially but may drop below normal as Qt continues to fall. The combination of decreased CVP, PCWP, PAP, and BP offers a strong suggestion of hypovolemia.
Treatment would be directed at optimizing preload by replacing circulating volume with the appropriate fluid. This fluid challenge should be continued until CVP and/or PCWP are within normal range. If Qt remains low despite optimized preload then other causes of hypoperfusion must be investigated.
Left Heart Failure
This is a common occurrence following myocardial infarction and requires rapid recognition and treatment to ensure survival. As the left side fails to pump blood, BP falls causing a compensatory vasoconstriction in effort to restore BP. This peripheral vasoconstriction may cause a relative hypovolemia. PCWP elevates as blood flow backs up into the pulmonary circulation.
PCWP assists in identifying, quantifying severity , and guiding therapy of LHF. CVP are often initially normal but will elevate as the failure progresses. Clinical signs of hypoperfusion will also be present - cool extremities, long capillary refill times, tachycardia, altered LOC, and reduced UO.
Treatment is aimed at reducing preload to optimal levels through the use of diuretics. Contractility can be improved with positive inotropes and afterload can be reduced with vasodilators. These vasodilators must be used with caution as a reduction in venous return can result in decreased Qt.
This occurs as a result of chronic lung disease increasing PVR. Over a long period of time the RV will dilate and eventual begin to fail. PCWP will be normal but CVP will be markedly increased. Qt is usually with in normal range. PAP’s will be elevated significantly in response to the increase in PVR. End-stage disease can result in left heart failure causing elevated PCWP.
Treatment will be designed to reduce right ventricular afterload. This is accomplished by appropriate oxygen therapy that returns PaO 2 to a more normal level. This allows the pulmonary vascular bed to relax and reverse the the workload of the right heart.
In this disease, the circulatory is for the most part unaffected. The problem centers around “leaky” pulmonary capillary beds that cause pulmonary edema and hypoxia resistant to treatment. Chest x-ray and other clinical presentations will reveal pulmonary edema but hemodynamic monitoring will help determine the cause. With ARDS, LH failure is not common so PCWP, CVP, and Qt are frequently normal.
Non-cardiogenic pulmonary edema can be identified by these findings.
PCWP monitoring can help track the course of the disease process and should be responded to if elevated as more edema occurs at this time. A reduced PCWP in this patient population allows the patient to be more susceptible to reductions in Qt with the use of PEEP and mechanical ventilation.
37. Hypovolemia is characterized by all of the following EXCEPT:
a. Low CVP
b. Reduced stroke volume
c. Reduced PCWP
d. Reduced vascular resistance
38. Hemodynamic measurements consistent with left heart failure include:
a. Low CVP
b. Elevated PCWP
c. Elevated BP
d. Elevated stroke volume
39. Treatment of left heart failure is directed towards each of the following EXCEPT:
a. Elevating preload
b. Decreasing afterload
c. Increasing contractility
d. Increasing Qt
40. Treatment of hypovolemia is intended to:
a. Increase afterload
b. Decrease afterload
c. Decrease preload
d. Increase preload
41. Which of the following hemodynamic measurements is NOT consistent with Cor Pulmonale?
a. Normal PCWP
b. Normal Qt
c. Normal CVP
d. Elevated PAP
42. Treatment of Cor Pulmonale is directed towards:
a. Decreasing RV preload
b. Decreasing RV afterload
c. Increasing SV
d. Increasing contractility
43. Hemodynamic measurements typical for ARDS include:
a. Normal PCWP
b. Normal CVP
d. Adequate cardiac output
e. All of the above
44. An elevation of PCWP in an ARDS patient may:
a. Increase pulmonary edema
b. Decrease afterload
c. Decrease Qt
d. Improve arterial oxygenation
Case Study One
A 60 year old white male came to ER complaining of severe chest pain for the past 3 hours. The pain was crushing and radiated to the left shoulder and arm. He appeared diaphoretic and mildly short of breath. His vital signs include:
HR: 115 bpm
RR: 22 breaths/min
BP: 110/68 mmHg
Oral temp. 37.6 o C
O/A, fine inspiratory crackles in the lower lobes with a galloping heart rhythm was heard. There was no cyanosis or digital clubbing noted. He was alert and oriented. The chest pain was partially relieved with nitroglycerin and morphine. ABG’s revealed:
PaO 2 - 58 mmHg
PaCO 2 - 36 mmHg
pH - 7.45
Sat - 88%
PaO 2 improved to 85 mmHg with 3 lpm of oxygen via nasal cannula. A chest x-ray revealed a normal size heart with clear lung fields bilaterally. The ECG showed ST segment elevation in lead I and V1-4. Cardiac enzymes were drawn and the results are pending. Hematocrit and CBC were normal.
Over the next 12h, AMI was confirmed with enzyme studies and serial ECG’s. The patient gradually deteriorated and he became lethargic and disoriented.
UO fell to 10-15 cc/h and BP was palpable at 70 mmHg. He was cool to the touch in the extremities. His persistent signs of hypoperfusion lead to the placement of a PA catheter.
MAP - 55 mmHg
PAP - 38/16 mmHg
PCWP - 12 mmHg
CI - 1.3 l/min/m 2
CVP - 6 mmHg
45. Which of the following indicates that perfusion is inadequate?
a. CVP - 6 mmHg
b. PCWP - 12 mmHg
c. Altered LOC
d. HR - 115 bpm
e. All of the above
46. The PCWP measurement would be interpreted as:
47. Increasing the PCWP to what value may improve Qt?
a. 15 mmHg
b. 18 mmHg
c. 25 mmHg
d. 30 mmHg
48. Increasing the PCWP to a more optimal range would be accomplished by:
a. Positive inotropes
d. Volume loading
49. With an adequate MAP. A mildly elevated PCWP, a low Qt and elevated SVR, the appropriate therapy would be:
a. Decrease afterload
b. Increase preload
c. Increase contractility
d. Decrease preload
50. In this case, with hypotension and no improvement in Qt after volume loading (PCWP - 18 mmHg), the appropriate treatment would be a:
c. Positive inotrope
51. Which of the following has a vasodilating effect on the patient?
d. Chest pain
In the patient, volume loading did not improve Qt. One can then assume that contractility is the problem if preload has been optimized and blood pressure is low. Positive inotropic agents should be given in an effort to improve pump function coupled with continued hemodynamic monitoring.
Case Study Two
A 39 year old male was brought to ER after a motor vehicle accident. He arrived in a semiconscious state with vital signs of BP - 80/60 mmHg, HR - 115, and RR - 28. There were no obvious broken bones but his abdomen was tender and distended. Heart and breath sounds were normal. Because of strong evidence of abdominal bleeding he was transported to the OR. Volume replacement was started via peripheral IV’s.
In the OR, the spleen was removed and a lacerated liver was repaired. He was transferred to ICU and placed on a ventilator.
PaO 2 - 95 mmHg
PaCO 2 - 36 mmHg
pH - 7.42
On 50% oxygen
Admission vitals: BP 90/65 mmHg, HR - 110, RR 22, CVP - 2 mmHg, UO - 2 cc/h, and he was unresponsive.
52. At this point, the patient’s most immediate need is:
a. To reduce FiO 2
b. Increase the minute volume
c. Assure adequate perfusion
d. Control pain
53. After 12h in the ICU, which of the following findings in this patient suggests that perfusion is inadequate?
a. CVP - 2 mmHg
b. U/O - 2 cc/h
c. Patient is unresponsive
d. All of the above
At this point, oxygenation is more than adequate. A decrease in FiO 2 is suggested to minimize the risk of O 2 toxicity. Other parameters suggest hypoperfusion. It is important to maintain adequate perfusion without fluid overload. This patient may be prone to develop non-cardiogenic pulmonary edema (ARDS) especially if fluid overloaded. A PA catheter is recommended.
Over the next several days, the patients pulmonary status deteriorates. Adequate oxygenation now requires 70% oxygen. Hemodynamically he presents with:
CVP - 6 mmHg
MAP - 90 mmHg
PAP - 24/15 mmHg
PCWP - 11 mmHg
Qt - 5.8 lpm
HR - 124 beats/min
PEEP therapy at 12 cmH 2 O was started to improve oxygenation. At this PEEP, PaO 2 was 67 mmHg on FiO 2 of 0.45. Hemodynamics revealed:
CVP - 8 mmHg
MAP - 68 mmHg
PAP - 25/15 mmHg
PCWP - 16 mmHg
Qt - 4.7 lpm
HR - 137 beats/min
55. Regarding the patient’s pulmonary status, which of the following should be done?
a. Increase FiO 2
b. Increase PEEP
c. Increase minute volume
d. Maintain current settings
56. Which of the following may have deteriorated after the implementation of PEEP therapy?
a. Oxygen delivery to the tissues
b. Oxygen saturation
c. PaO 2
57. The appropriate therapy at this point would be:
a. Give diuretics
b. Reduce PEEP
c. Give a positive inotrope
d. Give a vasodilator
58. Which of the following most indicates fluid therapy may be helpful in improving Qt in this patient?
a. PaO 2 - 67 mmHg
b. PCWP - 11-16 mmHg
c. MAP 68 mmHg
d. HR 124-137 beats/min
Qt and oxygen delivery to the tissue often fall following the initiation of PEEP therapy. The temptation is to back off on PEEP but is usually better to maintain the PEEP level to achieve an adequate PaO 2 with the minimum amount of oxygen. Optimize hemodynamics with fluid challenges and positive inotropes as required.