1. THE CASE OF MR. STARLING
The treatment for Mr. Starling’s CHF condition
Presented by:
Ingvild Kummen
Yoav Litani
Daniela Levy
Khitam Hajuj
2. TREATMENT METHODS
USED:
Furosemide (diuretic, to treat edema and decrease
preload)
Captopril (ACE inhibitor, to decrease preload)
Intravenous fluids (to increase blood pressure)
Dobutamine (to increase contractility)
Cardiac transplantation
3. FUROSEMIDE
Diuretic
Venodilator
Mechanism:
Inhibits loop of Henle and proximal and distal convoluted tubule
sodium and chloride resorption. furosemide itself stimulates the
release of renin, thereby increasing levels of angiotensin 2 3 4 5 as
well as of prostaglandins from the kidney. The effects on these two
vasoactive hormonal systems have been associated with arterial
vasoconstriction and venous vasodilation observed after systemic
administration of the drug.
4. CAPTOPRIL
ACE inhibitor
Mechanism:
Inhibits the Angiotensin Converting Enzyme that is found in the
lung thus inhibits the conversion of Angiotensin I to Angiotensin II.
Angiotensin II has many mechanism to increase blood pressure. By
blocking the conversion to Angiotenstin II, Captopril decreases the
blood pressure.
6. EFFECTS ON MR.
STARLING’S VALUES
Blood pressure decreases from 102/85 to 80/60 mmHg
In addition Mr. Starling reports that is feeling is
somewhat improved:“though I don’t feel great, I feel so
much better that I now realize how sick I was.”
* the administered drugs did not solve the problem
since the cardiac output was not improved
7. INTRAVENOUS FLUIDS
Normal intravenous transfusion is giving a
liquid substance directly into the patient's vein.
In this case a "Normal Saline" solution was
given.
The normal saline is a solution of sodium
chloride at 0.9% concentration which is isotonic.
It was given in order to elevate the decreased
blood pressure. The intravenous route is the
fastest way to deliver fluids and medications
throughout the body.
8. DOBUTAMINE
Positive ionotropic agent
Mechanism:
Stimulates β¹ receptors of the sympathetic
nervous system. By increasing the contractility,
Dobutamine increases the cardiac output
while decreases the end systolic volume.
Dobutamine is used for congestive heart failure, but it is not useful in
case of cardiac ischemia because it increases the oxygen demand of
the myocardium.
Dobutamine decreases systemic vascular resistance while increasing
9. DOBUTAMINE
Dobutamine Dopamine
Dobutamine has many similarities with
Dopamine. Dobutamine has the extra ring
section which means it is too bulky to activate
dopamine receptors and cause norepinephrine
release i.e. it is a selective beta-1 receptor agonist.
10. EFFECTS ON MR.
STARLING’S VALUES
The right atrial pressure decreases from 12 to 20 mmHg
The decrease in right atrial pressure reflects the fact that more blood is ejected
from the heart with each beat as a result of increased contractility and increased
stroke volume.
The cardiac output increases from 2,2 to 4,2 L/min
The cardiac index increases from 1,2 (cardiogenic shock) to 2,4 L/min/m²
The heart rate decreases from 120 to 100 beats pr minute (indirect effect)
The brachial artery pressure goes from 100/90 to 120/70 mmHg
The Systemic vascular resistance decreases from 2600 to 1400 dyn*sec/cm5
12. CARDIAC TRANSPLANT
Heart transplantations are administered to patients with end stage heart
failure.
As Mr. sterling still suffered from reoccurring sessions of pulmonary edema
and hypotenstion despite the previous heart treatment, he became a
suitable candidate for a heart transplantation.
The most common procedure is to take a
working heart from a recently deceased organ
donor (allograft) and implant it into the
patient. The patient's own heart may either be
removed (orthotopic procedure) or, less
commonly, left in to support the donor heart
(heterotopic procedure).
The patient is also given immunosuppressant
medication so that their immune system will not
reject the new heart.
13. CARDIAC TRANSPLANT
The procedure begins with the surgeons performing a median sternotomy
to expose the mediastinum. The pericardium is opened, the great vessels are
dissected and the patient is attached to cardiopulmonary bypass. The failing
heart is removed by transecting the great vessels and a portion of the left
atrium. The pulmonary veins are not transected; rather a circular portion of
the left atrium containing the pulmonary veins is left in place. The donor
heart is trimmed to fit onto the patients remaining left atrium and the great
vessels are sutured in place. The new heart is restarted, the patient is
weaned from cardiopulmonary bypass and the chest cavity is closed.
