Cardiovascular PBL

Patient Presentation

You are working an overnight shift in the

Emergency Department and Mary Smith, a 66
year old, is brought by EMS reporting severe
shortness of breath and swelling of her belly. Ms.
Smith reports that over the last several months,
she has been experiencing progressively worsening
dyspnea (shortness of breath) especially when she
exerts herself.
 History

 Hypertension, diagnosed 25 years ago – started on an

anti-hypertensive agent at that time. Does not recall
the name or dosage of the medication. She has not
taken the medication in “over 20 years.”
 Diabetes, diagnosed “in my 30’s” – advised to watch
her diet at that time, which she denies doing. Has not
had this condition evaluated in “many years.”
 Smoker – half a pack of cigarettes/day x 35 years
 Overweight
 The patient states that she has not seen a physician
“since the late 1990’s.”
 Physical Examination

 Appearance: Anxious, overweight, middle-aged

female who has moderate dyspnea. HR = 95
BPM, RR = 28/min; BP = 178/118; Temp –
37.1
 Mental Status: alert, awake, oriented to person,
place, and time
 HEENT: Grossly normal
 Neck: Click for Examination Results
 Extremities: Click for Examination Results
Please click here once you finish reviewing all of the
physical examination
 Clinical Reasoning

 Write one to two sentences that summarizes the

patient’s condition based on the history and PE
 Based on the patient’s problems, what would you
consider in the differential diagnosis?
 What additional diagnostic studies would you
order?
Diagnostic Tests
 Diagnostic Tests

EKG: Click here to see EKG

Chest X-Ray: Click to see Chest X-Ray
Echocardiogram: Click to see Echocardiogram
B-type natriuretic peptide (BNP): 870 pg/ml
(normal <100 pg/ml)
What is your diagnosis?
Describe the likely progression of
heart failure in our patient and
the physiological compensatory
mechanisms that are activated
during this progression.
 Disease Progression

 The patient has chronic hypertension (increased afterload), which if

left untreated leads to ventricular remodeling (hypertrophy).
 At first the heart compensates for the increased afterload via the
Frank-Starling Mechanism (i.e., preload increases).
 Over time, to help reduce wall stress, (recall that wall stress =
p x r/2*t, where t = wall thickness) left ventricle remodeling leads to
increased left ventricular thickness and wall mass.
 As the myocardium hypertrophies, however, fibrosis occurs, in part due to
high angiotensin II and SNS activity, which ultimately impairs contractility.
 As contractility declines, stroke volume is reduced and end-diastolic
pressure rises, resulting in high left atrial pressures that eventually
result in pulmonary hypertension.
 The latter increases the afterload for the right ventricle, which may
fail, leading to increased right atrial pressures, as seen in this patient.
 Endogenous neurohumoral responses also play an important role as
seen on the next slide.
Please draw a cardiac output curve and explain the Frank-
Starling Mechanism and how it relates to our patient.
 The Frank-Starling Mechanism (from the perspective
of the left ventricle) describes the effects of increasing
the preload/LVEDV on cardiac contraction. As
preload increases, the stretch on the myocardial
fibers increases.
 Increased stretch causes a greater ejection of blood
from the heart, thus, stroke volume/cardiac output
increases.
At this time, please draw a normal pressure-volume loop and
explain each phase. Be sure to label the axes correctly.
 Why does the patient have fluid in her
lungs(pulmonary edema) and peripheral edema?
Increased left atrial
pressure
increased pulmonary
venous pressure 
increased capillary
hydrostatic pressure.

When RA pressure is
increased, lymphatic
drainage is impaired.

Capillary filtration  K
* (hydrostatic pressure
gradient – oncotic
pressure gradient.)
 Pharmacologic Management
of Heart Failure

Vasodilators are used in the management of heart

failure. How does this help a patient with heart
failure?
Afterload & Ventricular Function
 Pharmacologic Management
of Heart Failure: Digoxin

Digoxin (Digitalis) is an inotropic agent that is

sometimes given to patient’s with systolic heart failure.
How does this medication exert its positive inotropic
effects?
 Digoxin (Digitalis) is a positive inotropic agent that will cause
an increase in cardiac contractility.
 It will inhibit the Na+/K+-ATPase on cardiac myocytes.
 This will result in an increased intracellular [Na+], which will
reverse the direction of the Na+/Ca2+ exchanger.
 As a result, the cytosolic [Ca2+] in cardiac myocytes will
increase.
 This will increase the contractility of the heart and will result
in greater cardiac output/stroke volume.
 Pharmacological Approaches to
Management of Heart Failure

 Agents shown to reduce mortality:

 ACE inhibitors/ARB
 -adrenergic blockers (carvedilol, metoprolol ER,
bisoprolol)
 Aldosterone antagonists (spironolactone,
eplerenone)
 Angiotensin-neprilysin inhibition (sacubitril-
valsartan)
 Digoxin – reduces hospitalization in patients with EF
<45%
Thank You!
Return to Physical Exam
Return to Physical Exam
 Click to Listen to
Respiratory Examination

Please turn up the volume on your monitor

Return to Physical Exam

I

II

III

Normal shown
For comparison

What is this patient’s mean electrical axis? Answer

Do you observe any signs of ventricular hypertrophy? Answer

Return to Diagnostic Tests
 Return to Diagnostic Tests

Normal Chest X-ray Patient’s Chest X-Ray

 Echocardiogram

Normal Echocardiogram Patient’s Echocardiogram

Return to Diagnostic Tests

 This EKG shows a Left Axis Deviation. This can be
calculated rather quickly, as the QRS complex in Lead I is
positive and the QRS complex in aVF is mainly negative.

Please click here to return the EKG.

 Yes.

Please click here to return the EKG.