THE CASE OF MR. STARLINGThe treatment for Mr. Starling’s CHF condition

Presented by:Ingvild Kummen

Yoav LitaniDaniela LevyKhitam Hajuj

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

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.

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.

RENIN ANGIOTENSIN SYSTEM

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

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.

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

DOBUTAMINE

DopamineDobutamineDobutamine 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.

EFFECTS ON MR. STARLING’S VALUES

The right atrial pressure decreases from 12 to 20 mmHgThe 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/m²The 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

EFFECTS ON MR. STARLING’S VALUES

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.

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.