3- Heart Failure (modified)

8/6/2019 3- Heart Failure (modified)

1/17

Shock:

1.It is circulatory collapse with resultant hypo-

perfusion and decrease oxygenation of tissues.


2/17

Causes of shock:

Decreased cardiac output: asoccurs in hemorrhage or sever left

ventricular failure.

Widespread peripheralvasodilatation: as occurs in sepsis

or sever trauma, with hypotension

often prominent feature.


3/17

Types of shock:1-Hypovolemic shock: it is circulatory collapse

resulting from the acute reduction in circulating blood

volume caused by:

1.Sever hemorrhage (loss of blood) or massive loss offluid from skin (loss of plasma) as in burn.

2.Loss of fluid from the GIT (loss of ECF) as in sever

vomiting or diarrhea.

2-Cardiogenic shock: It circulatory collapse resulting from pump failure of the left ventricle, most often caused by

massive myocardial infarction.


4/17

3. Anaphylactic shock: anaphylaxis is clinical

syndromes that represent the most sever systemic

allergic reaction. It results from animmunologically mediated reaction in which

vasodilator substances such as histamine are

released into blood. These substances causevasodilatation of arteriols and venules along with

marked increase in capillary permeability. The

vascular response in anaphylaxis is often

accompanied by life-threatening laryngeal edema

and broncho-spasm, circulatory collapse,

contraction of GIT and uterine smooth muscles,

and urticaria or angioedema.


5/17

4. Septic shock: it is mostly caused by

gram-negative endotoxemia. Initially,vasodilatation may result in an overall

decrease in blood flow. But significant

peripheral pooling of blood from peripheral

vasodilatation results in relative hypo-

volemia and impaired perfusion.


6/17

Heart Failure:

a.It is an imprecise term used to describe thestate that develops when the heart cannot

maintain an adequate cardiac output or can

do so only at expense of an elevated filling

pressure. b.In the mildest forms of heart failure,

cardiac output is adequate at rest and

becomes inadequate only when the metabolicdemand increase during exercise.


7/17

Compesatory changes in heart

failure:1. Local changes:

Chamber enlargements

Myocardial hypertrophy

Increase heart rate.


8/17

HEAR FAILURE

Simply it is define as reduce in Ejection fration

EF=SV/EDV=>50% (stroke volume/end Diastol

Vol.) Mild HF EF=40-49%

Mod HF EF=30-39%

Severe HF EF>30%


9/17

2. Systemic changes:

Sympathetic nervous system stimulation: both cardiac sympathetic

tone and catecholamine levels are elevated during the late stage of

most forms of heart failure. By direct stimulation of heart rate and

cardiac contractility and by regulating of vascular form, the

sympathetic nervous system helps to maintain perfusion of various

organs, particularly brain and heart. Both mechanisms will increase

after-load, pre-load and contractility.Renin-angiotensin-aldosterone system stimulation: increase

angiotensin II will has the following functions:

vasoconstriction will increase after-load and pre-load

Stimulation of the release of ADH (anti-diuretic hormone) will

increase pre-load

Stimulation of the release of aldosterone will increase pre-load.

Release of natriuretic peptide (atrial and brain natriuretic peptide:

ANP and BNP).


10/17


11/17

At first these changes may help to optimize cardiac

function by altering the after-load or pre-load and by

increasing myocardial contractility. However,ultimately they become counter-productive and often

reduce cardiac output by causing an in-appropriate

and excessive increase in peripheral vascular

resistance. A vicious circle may be establishedbecause a fall in cardiac output will cause further

neuro-humeral activation and increasing peripheral

vascular resistance. The onset of pulmonary and/or

peripheral edema is due to high atrial pressurecompound by salt and water retention by impaired

renal perfusion and secondary aldosteronism.


12/17

The types of heart failure are:

1. Acute and chronic failure: Acute when occurs suddenly as in

myocardial infarctionchronic occurs gradually as in progressive

valvular heart failure.2. Left, right and bi-ventricular failure: Left ventricular failure:

there is reduction in left ventricular output or an increase in left atrial

or pulmonary venous pressure. An acute increase in left atrial

pressure may cause pulmonary congestion or edemaright ventricular

failure: there is reduction in right ventricular output at any given right

atrial pressure. Causes of isolated right ventricular failure includes

chronic lung disease (cor-pulmonal) as chronic bronchitis or asthma,

multiple pulmonary embolism, and pulmonary valvular stenosisBi-

ventricular failure: it occurs because the disease process (e.g. dilatedcardiomyopathy, ischemic heart disease) affects both ventricles, or

because disease of the left heart leads to chronic elevation of left

atrial pressure, pulmonary hypertension and subsequently right heart

failure.


13/17

4. Diastolic and systolic failure: Heart failure

may develops a result of impaired myocardial

contraction ( systolic dysfunction) but can also

due to poor ventricular filling and high filling

pressures caused by abnormal ventricular

relaxation (diastolic dysfunction). The latter iscommonly found in patients with left ventricular

hypertrophy and ischemic heart disease. Systolic

and diastolic dysfunction often coexists,

particularly in patients with coronary artery

disease.


14/17

5. High output failure: conditions that

are associated with a very high cardiacoutput (e.g. a large AV shunt, beri-beri,

sever anemia or thyrotoxicosis) can

occasionally cause heart failure. In suchcase additional causes of heart failure

are often present.


15/17

Investigation

ECG- may be used to identify arrhythmia, ischemicheart disease, Rt. Lft vent. Hypertrophy & presence

of conduction delay or abnormality e.g.lft bundle

branch block although, abnormal ECG excludes L.V.systolic dysfunction

CHES X RAY- aid in diagnosis of CHS, may show

cardiomegaly ECHOCARDIOGRAPHY- to support a clinical

diagnosis of H.F.


16/17

Blood tests

Routinely preformed include

electrolytes(sodium/potassium), measure of

renal function, liver function tests, thyroid

function tests, a complete blood count, and

often C-reactive protein if infection is

suspected

An elevated B-type natriuretic peptide (BNP)isa specific test in deactivate of heart failure.


17/17

Treatment of heart failure:

Diuretics: water and Na excretiondecrease plasma

volumedecrease venous returndecrease pre-load.

Vasodilators: blood stay at venous side decrease venous

returndecrease pre-load in addition vasodilatation

decrease after-loadACE inhibiters: it works in two ways

first because it causes vasodilatation so it has the same effect

as vasodilators and second prevents the release of

aldosterone so it prevents water and Na excretiondecrease

plasma volumedecrease venous returndecrease pre-load.

Angiotensin II receptor antagonists: it has similar effect as

ACE inhibitor but it will block the effect of angiotensin

IIBeta-adreno-ceptor antagonist (-blockers): it will block

the sympathetic effect on the heartDigoxin: increase

contractility of the heart.

3- Heart Failure (modified)

Documents

Transcript of 3- Heart Failure (modified)