Shock:

1.It is circulatory collapse with resultant hypo-

perfusion and decrease oxygenation of tissues.
Causes of shock:
Decreased cardiac output: as
occurs in hemorrhage or sever left
ventricular failure.
Widespread peripheral
vasodilatation: as occurs in sepsis
or sever trauma, with hypotension
often prominent feature.
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 of
fluid 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.
3. Anaphylactic shock: anaphylaxis is clinical
syndromes that represent the most sever
systemic allergic reaction. It results from an
immunologically mediated reaction in which
vasodilator substances such as histamine are
released into blood. These substances cause
vasodilatation 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.
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.
Heart Failure:
a.It is an imprecise term used to describe the
state 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 metabolic demand
increase during exercise.
Compesatory changes in heart
failure:
1. Local changes:
Chamber enlargements
Myocardial hypertrophy
Increase heart rate.
 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%
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).
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 established
because 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 pressure
compound by salt and water retention by impaired
renal perfusion and secondary aldosteronism.
The types of heart failure are:
1. Acute and chronic failure: Acute when occurs suddenly as in
myocardial infarctionchronic 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 edemaright
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 stenosisBi-ventricular failure: it occurs because the
disease process (e.g. dilated cardiomyopathy, 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.
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 is
commonly found in patients with left ventricular
hypertrophy and ischemic heart disease. Systolic
and diastolic dysfunction often coexists,
particularly in patients with coronary artery
disease.
5. High output failure: conditions that
are associated with a very high cardiac
output (e.g. a large AV shunt, beri-beri,
sever anemia or thyrotoxicosis) can
occasionally cause heart failure. In such
case additional causes of heart failure
are often present.
 Investigation
• ECG- may be used to identify arrhythmia, ischemic
heart 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.
 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)is
a specific test in deactivate of heart failure.
Treatment of heart failure:
Diuretics: water and Na excretiondecrease plasma
volumedecrease venous returndecrease pre-load.
Vasodilators: blood stay at venous side decrease venous
returndecrease pre-load in addition vasodilatation
decrease after-loadACE 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 excretiondecrease
plasma volumedecrease venous returndecrease pre-load.
 Angiotensin II receptor antagonists: it has similar effect as
ACE inhibitor but it will block the effect of angiotensin
IIBeta-adreno-ceptor antagonist (β-blockers): it will block
the sympathetic effect on the heartDigoxin: increase
contractility of the heart.