Cardiovascular System Assessments

 

The ECG

You should be familiar with how the electrical activity of the heart is recorded, and be able to recognize some basic rhythms. Actual analysis of the EKG will be covered in later courses.

The four key properties of myocardial tissues (the heart muscle) are

Excitability - sensitive to electric-chemical stimulation

Automaticity - able to self-depolarize and generate an electrical current, can transport ions across cell membrane and change electrical balance with in the cell

Conductivity - able to conduct a current

Contractility - able to shorten in length in response to stimulation

Heart muscle also has a refractory ability - prevents depolarization from occurring before the cell is ready.

The pacemaker dictates the rate at which the heart cycles through its pumping action - the cells that depolarize first act as the pacemaker for the heart. The normal pacemaker of the heart is the Sino-atrial node (responsible for sinus rhythms). However, other cells can take over if the SA node is damaged. The cells that depolarize the quickest will set the rate for the heart. The intrinsic rates in descending order are:

 

SA Node

60 - 100 BPM

Atrial Cells

50 - 60 BPM

AV Node

45 - 50 BPM

Bundle of His

40 - 45 BPM

Bundle Branch (R or L)

40 - 45 BPM

Purkinje Cells

30 - 40 BPM

Myocardial Cells

30 - 35 BPM

 

Pacing of the heart by non-atrial sites is usually inadequate for tissue and organ perfusion.

 

 

 

CPAP4.JPG

The normal sinus rhythm EKG consists of the following depolarization/repolarization wave forms:

EKG.jpg

 

EKG_heart-Activ.jpg

In the strip below you should be able to see that the time between the first two QRS complexes is shorter than the time between the second and third QRS complex - this is a variation in response to respiratory effort and is not considered pathological, unless blood pressure is adversely affected.

SinusAR.jpg

The next strip is still a sinus rhythm - a sinus tachycardia. This is not necessary pathologic - but should be evaluated if it persists, or becomes extreme as it may compromise cardiac perfusion and cause ischemia (perfusion of the heart occurs during diastole).

Using the formula 300 / number of large boxes between QRS complexes, you could calculate the rate. (300/3 = 100 BPM)

 

SinusT.jpg

The following strips are considered pathologic. You should recognize the one below from your book as being sinus bradycardia. Using the formula 300 / number of large boxes between QRS complexes, you could calculate the rate. (300/8 = 37 BPM)

SinusB.jpg

 

This atrial arrhythmia (flutter) indicates the atria are depolarizing and contracting much faster (300 times per minute) then the ventricles (60 times per minute). Cardiac output may be a little compromised but generally will try to treat the cause and not the arrhythmia.

 

Atril_flut.jpg

Atrial fibrillation below however does effect ventricular filling enough to reduce cardiac output. This arrhythmia will be treated by electric shock called cardioversion - usually done with conscious sedation. Cardioversion is the delivery of an electrical shock to the heart that depolarizes the whole heart at the same time - essentially putting it in standstill, with the hope that the normal SA node will regain control of the rate first.

ATRfib.jpg

An isolated premature ventricular contraction (PVC) or sometimes called VPC (ventricular premature contraction), is not really unusual - we all have them occasionally. When they happen frequently is when we get concerned as it indicates some ventricular irritability or abnormal reentry of electrical stimulus. The more frequently they occur the more concern there is: a pattern of two regular complexes followed by PVC is called trigeminy; a pattern of one regular complex followed by a PVC is called bigeminy and may lead to the next tracing!

 

PVC.jpg

The following arrhythmias would be aggressively addressed with cardiac medications, patient at this point is most likely not responsive:

Ventricular Tachycardia is where the ventricle takes over the pacing of the heart at a rapid rate. Decreases cardiac output and BP

vtach.jpg

Ventricular flutter: no pulse discernable, inadequate filling of ventricles, also means no perfusion to cardiac muscle, may see defibrillation used with this.

vflutter.jpg

Lastly this shows ventricular fibrillation leading to asystole (flat line). Defibrillation is most effective during fibrillation - less effective when heart has gone into standstill as that is a sign at this point of muscle death. You will see this in code situations and in the emergency department.

vfib_asys.jpg

 

 Noninvasive Hemodynamic Monitoring Assessments

Noninvasive parameters are those that can be measured with simple devices without inserting anything into the patient. Pulse oximeters will give you heart rate, however you should always correlate the reading on the pulse ox with a manual palpation of the pulse.

Heart rate (pulse)

Blood pressure

Tissue perfusion state - nail bed capillary refill indicates adequacy of peripheral tissue perfusion -you squeeze the nail bed and cause it to blanche (whiten) then release it quickly and count the seconds it takes to return to normal color. Normal refill is less than 5 seconds.

Invasive Hemodynamic Monitoring Assessments

 Invasive hemodynamic monitoring is done in the intensive care unit and requires the placement of catheters at various points in the systemic and pulmonary circulation. This enables more precise monitoring of the patient's cardiac and blood volume status and helps in regulating treatment. At this point in the program I want you to be able to define the abbreviations and know what they refer to. The normal values in Table 6.1 are important for you to know. I do not expect you to know how to calculate the values in Table 6.2 or to know the normals for those parameters - but I do expect you to be able to define the abbreviations for those measurements.

 

Pulmonary artery catheter - is inserted into a major vein - usually the subclavian or the external jugular, and the balloon at the tip carries it through the chambers of the right heart out into the pulmonary artery. The physician can identify where the tip of the catheter is based on the pressure wave form and readings on the monitors. This catheter is used on hemodynamically unstable patients, and there is some controversy as to its risk versus benefit.

 

 

 SWGanz.jpg

 

Figure 6-11. A, Position of pulmonary arterial catheter in heart. B, As monitored by pressure tracings.

RA, Pressure tracing from right atrium; RV, pressure tracing from right ventricle; PA, pressure tracing

from pulmonary artery; PAWP, pulmonary artery wedge pressure. (From Wilkins RL, Stoller JK, canlan CL: Egan's fundamentals of respiratory care, ed 8, St. Louis, 2003, Mosby.)

The measurements on Table 6-1 are taken from the pulmonary catheter. Current technology provides for monitoring as well. (Mixed venous saturation)

Tbl6_1.jpg

Tble6_2.jpg

Arterial catheters, or lines, are usually inserted into the radial or femoral arteries. They continuously monitor arterial pressure, and can be used to obtain arterial blood for blood gas analysis. Blood pressure is used to evaluate SVR (systemic vascular resistance).

Another catheter that can be inserted is the central venous catheter. The tip of this catheter lies in the superior vena cava. This assists in determining preload, and is used for medication administration and managing volume replacement. CVP lines and pulmonary artery catheters are not used simultaneously.

Think about the anatomical changes in the lungs as the result of the disease listed below. As those diseases effect pulmonary capillary perfusion (increase resistance to flow through the pulmonary capillaries) they have the most compromising effect on the upstream side (Right heart). The systemic indices are most effected by left heart pathology.

Tble6_3.jpg Tble6_3c.jpg  

 

 

Determinants of Cardiac Output

 Cardiac output must be adequate to meet tissue and organ oxygen and nutrient needs. It indicates the total amount of blood pumped by the heart over one minute and is calculated by multiplying the heart rate by the stroke volume. (Sounds a lot like minute ventilation doesn't it?)

Factors that effect stroke volume include:

Preload - the ventricular end diastolic pressure

Afterload - the force against which the heart pumps (systemic vascular resistance) which is determined by

  1. the volume and viscosity of the blood ejected
  2. peripheral vascular resistance
  3. total cross sectional area of vascular space into which the blood is ejected.

End systolic volume (kind of like residual volume in the lungs) - the amount of blood left in the ventricle after systole. An indicator of how efficient the heart is, reflected in the ejection fraction (the % of volume that is ejected per beat - the lower the number the more end systolic volume is left over and the less efficient the heart is).

Cardiac overheads.jpg

Ventricular preload - reflected by CVP and pulmonary capillary wedge pressure

Ventricular afterload - arterial end-diastolic BP reflects left ventricular afterload

Myocardial contractility - the strength of the contraction impacts the ejection fraction - a poorly contracting heart muscle cannot eject as much volume and is not a good sign.