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Ventricular tachycardia Case Study

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Case Study
Ventricular Tachycardia
Ms. Betty W. Johnson Case: Wald D, Heckman J, Cripe J, Basic Science- Clinical Correlation Exercise Using a High Fidelity
Simulator: A case of Ventricular Tachycardia. MedEdPortal
Case History:
Ms. Johnson is a 73-year-old female who presents to the emergency
department with a complaint of chest pain and dizziness after passing
out. These complaints started about 30 minutes before arrival while she was
waiting in line at the bank. She recalls feeling warm and flushed and was
noted by a bystander at the bank to have a brief fainting episode.
Upon arrival at the hospital, the patient is awake, answering questions, but
complains of feeling weak, chest heaviness and shortness of breath.
Vital signs – HR 184 bpm, RR 26,
BP 82/40 mmHg, SaO2 92%
(increase to 97% with supplemental oxygen)
General Appearance
She is awake, alert and able to answer your questions.
Lungs – Rales (crackles)
Abdomen – Soft, non-tender
Extremities – no edema
Skin – Cool and clammy
Discuss the following questions:
What is the definition of tachycardia?
What are the determinants of cardiac output?
What is the definition of stroke volume?
What is the definition of tachycardia?
HR >100 bpm
What are the determinants of cardiac output?
The determinants of CO are HR and SV, (CO = HR x
SV). The CO represents the amount of blood that is
pumped by the heart (ventricles) in one minute.
What is the definition of stroke volume?
SV represents the volume of blood that is pumped
from the heart with each heart beat (from the
ventricles). This is calculated by subtracting endsystolic volume (ESV~50 ml) from the end-diastolic
volume (EDV~120 ml) (SV = EDV – ESV).
In a typical 70 kg adult the SV is ~70 ml of blood. In a
patient with a HR of 70 bpm, the CO approximates
4.9 liters/minute.
• What factors affect stroke volume?
• A number of factors can affect the SV including
•
•
•
•
•
heart size
aerobic conditioning
cardiac contractility
preload (EDV)
afterload
Discuss the answers to the following:
How will this patient’s heart rate affect her stroke
volume?
What effect does this patient’s heart rate have on her
cardiac output?
How will this patient’s heart rate affect her stroke
volume?
Because the ventricular rate is very fast, the SV will
decrease. This occurs because of the decrease in
the diastolic filling time that can occur with marked
tachycardia. This leads to a decrease in the EDV.
Remember, during the cardiac cycle, the heart is in
systole for approximately 1/3 of the time and
diastole for 2/3 of the time. The heart fills during
diastole.
What effect does this patient’s heart rate have on her
cardiac output?
The CO is reduced due to the very fast ventricular rate
and lack of a properly timed or coordinated atrial
and ventricular contraction. Hemodynamic
compromise is more likely when underlying left
ventricular dysfunction is present or with very fast
ventricular rates. A significant decrease in CO may
lead to a cascade of complications including;
diminished myocardial perfusion, worsening
inotropic response (decreased cardiac contractility),
and subsequent pulmonary edema. The rapid HR
can not compensate for the marked decrease in SV.
Overview of Volume Changes
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 Right ventricular
output exceeds left
ventricular output.
2 Pressure backs up.
3 Fluid accumulates in
pulmonary tissue.
1
2
3
(a) Pulmonary edema
19-11
Figure 19.21a
• If the left ventricle
pumps less blood
than the right, the
blood pressure
backs up into the
lungs and causes
pulmonary edema
Q: Why did this patient pass out?
1/19/15
The patient developed VT which resulted in a marked increase in ventricular rate
which lead to a decrease in CO (CO = HR X stroke volume - SV) which in turn lead to a
precipitous drop in MAP (MAP = CO X systemic vascular resistance - SVR). The
above series of events resulted in a decrease in cerebral perfusion.
She fainted because of orthostatic hypotension. This is a relatively common scenario
and is encountered in some patients, particularly the elderly or those
dehydrated. When a patient stands, there is a redistribution of approximately 750
mL of blood volume into the lower extremity venous circulation (capacitance
vessels). The baroceceptor reflex, in an otherwise normal patient, helps to
compensate for the decreased MAP associated with this redistribution of blood
volume by increasing the SVR.
1/19/15
The mean arterial pressure is defined as the average
pressure in the arteries during the cardiac
cycle. MAP = [(2 x diastolic pressure) + systolic
pressure] / 3, or MAP = Diastolic pressure + 1/3
pulse pressure.
What are the determinants of the mean arterial
blood pressure?
1/19/15
The determinants of MAP are CO and SVR,
(MAP = CO X SVR). At the bedside, it is difficult
to monitor CO and SVR, as these values are
typically unable to be measured in real
time. These values however can be obtained
with the use of a pulmonary artery catheter.
1/19/15
Discuss: How do each of the four factors increase
SVR
1) an increase in sympathetic nerve activity to
selected systemic arterioles (e.g. enteric,
cutaneous)
2) increased release of norepinephrine
3) increased tone of the vascular smooth muscle in
the arterioles
4) the reduction in the radii (r).
1/19/15
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