Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain
First lecture Summary
Right and left side of the heart are separated from each other by fibrous tissue .There are two opening in the heart in the fetal life and should be closed after birth : 1-foramin ovali. 2-ductus arteriosus.
The impulse transmit in the heart by the conductive system not direct between the atrium &ventricle ,except in rare situation called muscular bridge.The location of the heart: in the mediastinum between the 2nd -5th intercostal space.PMI= point of maximum impulse "where you can feel the impulse".Cardiomegaly :enlargement of the heart "the PMI will increase ".Papillary muscle: it's the muscle attached to the atrioventricular valves via the chordae tendinae.Arteriole: control blood pressure.Vein: blood reservoir .The heart is self-excited .The heart work not under the direct control of the Brian ,but it's affected by the sympathetic and parasympathetic system.
For your information
ductus arteriosus ,what is it??
In the developing fetus, the ductus arteriosus (DA), is a blood vessel connecting the pulmonary artery to the aortic arch. Upon closure at birth, it becomes the ligamentum arteriosum.
Atrium innervated mainly by parasympathetic system & ventricle mainly by sympathetic system. The heart is affected by hormones mainly adrenaline and noradrenaline which is secreted by adrenal gland, they cause central vasodilation and peripheral vasoconstriction.
Alpha 1 :blood vessel vasoconstriction
Alpha 2 : heart vasodilatation
Beta 1 : increase heart rate & contractility
Beta 2 : bronchi dilatation
The vein affected by the sympathetic system more than any other blood vessels because they are blood reservoir .
Done by: Hadeel sumrain.
Hypertension lec. summary
Hypertension : It is sustained blood pressure beyond the normal average .- The normal blood pressure :
- systolic : 120-139 mm- diastolic : 80-89 mm
- BP = diastolic + 1/3(systolic – diastolic )
Regulation of blood pressure :
A. Short term regulation : moment to moment regulation controlled by barrow receptors .
B. Long term regulation: the mechanism to maintain blood volume “there is compensated blood loss” !
Signs & symptoms of hypertension :
“ silent killer “ usually no symptoms but rarely it shows :
- Headache - Blurry vision - Chest pain - Frequent urination at night
1. Primary hyper tension: which is 90 -95 % of the cases that the cause of it is unknown.
2. Secondary hypertension , it’s only 5-10% that the cause might be cardiac , renal or endocrine ( these systems involved in the maintenance of blood pressure )
We can classify the factors which cause hypertension into two categories:
a) Controllable factors : increased salt intake , obesity , alcohol , stress, lack of exercise and smoking .
b) Uncontrollable factors : heredity , race and age ( men 35-50 , women after menopause ).
Hypertension may lead to Ischemic heart disease Myocardial infraction
Stroke Congestive heart failure Kidney failure Heart attack Heart rhythm problems Aneurysm (localized, blood-filled balloon-like bulge . in the wall of a blood vessel).
Medications :1. Diuretics – get rid of excess fluids 2. Beta blockers –reduce HR3. Calcium antagonist – reduce HR & relax BV4. Angiotensin II receptors blockers 5. Vasodilators
- malignant hypertension if it’s not treated it will be fatal - resistant doesn’t respond to treatment of three
Done by: Abeer dirawi.
Heart Failure lec. summary
The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body.
An abnormal accumulation of fluid in the lungs.
Causes of Heart Failure
1-Ischemic Heart Disease
Valvular Heart Disease Congenital Heart DiseaseAlcohol and Drugs. Arrhythmias
Ventricular Dilatation. Myocyte Hypertrophy.Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction.
When we need more Blood due to the body demand but at that time we were suffering from HF and low Cardiac Output then the Heart will do the Following
1-Sympathetic stimulation ( lead to #2) 2-Increase in heart rate , contractility ,cardiac output .3-Release/formation of Angiotensin II to increase of the volume.4-Vasoconstriction (Increase in the after load ) 5-Increase in the heart size (cardiomegaly )
How can we discover that we have HFSigns:
Cardiomegaly Elevated Jugular Venous Pressure Tachycardia Hypotension Bi-basal crackles – in the lungs Pleural effusion Ankle Edema Ascites Tender hepatomegaly
Classification of heart failure" Symptoms of HF occur at rest and are exacerbated by any
Kussmaul’s sign Not Seen in1- acute cardiac tamponade
What is PMI and Where ?is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt.
PMI is at left 5th intercostals space, at the point of intersection
with the left midclavicular line.
PMI Abnormalities! 1- Dextrocardia, the apex beat may be felt on the right side. 2-Cardiomegaly , enlargement of the heart (at the 6th or 7th intercostals space).
Heart Sound NameTime
S1Close of AV valveS2Close of Semilunar valve
S3 "Pathological after 40"Start of DiastoleS4 "always Pathological "After Aerial Contraction
Note that! an increase in jugular venous pressure and it is a sign of Right side heart
To do Compensatory mechanism
Dilation-Frank Starling -Contractility
Neurohormonal Redistribution of
Blood to the Brain
NOTE THAT !Vicious cycle will
-Decrease in cardiac output
-The body demand for more
Increase in the afterlaod TPR + Increase in the preload COP
lead to more and more deteriorated of the heart!
People who developed acute pulmonary edema , should have endotracheal, To get rid of excessive fluid
Treatment of HF !
1. Diuretics . 2. Beta blockers . (Decrease CO)
3. ACE inhibitors (both preload and afterload will decrease .)
Digoxin- increase the force of contraction by increase the Ca concentration in the myocytes and decrease the HR. - Digoxin isn’t a safe drug the therapeutic index of it is narrow
- Digoxin toxicity: High amount of the Drug
Leads to 1. Dizziness.2. Confusion3. Discoloration, the patient will have yellowish discoloration4. Loose of consciousness
Treatment: -Digoxin immune fab -antidote for Digoxin
What is Cyanosis!It is the Blue discoloration of skin and mucus membranes, we can see it in the patient who has heart failure.
We Can't treat the acute pulmonary edema by chest tube there is no air or fluid in the pleural cavity(cover the lung)
excessive fluid usually are absorbed.
Done By Prince
Note About Viagra -general vasodilator
-Cause Tachycardia -Fatal for Old people
arrhythmia lec. Summary
Arrhythmia :abnormality in the conductive system of the heart.The SA node is the pacemaker of the heart where the impulse should be initiated ,but some time the impulse could be initiated elsewhere in the heart this is called "ectopic beat ". Refractory period : the period of time come after each AP and the heart muscle can't be excited through it because of the inactivation of fast Na channel. Herat block :
o 1-Block at the level of AV node : a- first degree heart block (PR > 0.22 sec.) b- second degree heart block(some P wave conduct ). C-third degree heart block(complete heart block).
o 2- block below the AV node: a- block at bundle of his. b- block at the branches.
Causes :acute MI, calcify aortic stenosis ,cardiomyopathy, drug,ischemia.Tachycardia : the HR more than 100/min (in ECG short PR interval)Bradycardia : the HR is less than 60/min( in ECG prolonged PR interval).The main cause of fibrillation are:
o Strong electrical shock.o Sever ischemic heart disease.
The main cause of AP re-entry :o Long pathway around the circle.o Decrees velocity of conduction .o Shortened refractory period of the muscle .
Premature beat:o Premature atrial contraction:- the P wave occur too soono Premature ventricular contraction:- the QRS complex prolonged .
Ventricular tachy-arrhymia :Decrees in the COP , the ECG is odd shape. Anti-arrhythmic drug:B blockers & Ca or Na channels blockers & digoxin.