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Heart & Neck Vessels. ** Position & Surface Landmarks:. precordium : area overlying heart & great vessles. Which are the major arteries & veins connected to heart. heart extend from 2 nd to 5 th ICS & from Rt boarder of sternum to Lt MCL.

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position surface landmarks
** Position & Surface Landmarks:
  • precordium: area overlying heart & great vessles. Which are the major arteries & veins connected to heart.
  • heart extend from 2nd to 5th ICS & from Rt boarder of sternum to Lt MCL.
  • -top of the heart is the base, bottom is the apex, during contraction the apex beats against chest wall, producing an apical impulse, which palpable at 5th ICS MCL. Heart rotated so Rt side is anterior &Lt is posterior.
- Great vessels are SVC{superior vena cava}-IVC{inferior vena cava}- PA {pulmonary artery}-PV{pulmonary veins}- Aorta.
heart wall chambers valves
** Heart Wall, Chambers,&Valves:
  • heart wall has layers: 1- pericardium ;atough double walled sac surround heart contain pericardial fluid to friction-free movement of heart. 2- myocardium; the musclar wall of heart, 3- endocardium; a thin layer of endothelial tissue lines inner surface of chambers& valves.
  • heart is 2 pump;Rt side pumps blood into lung,& Lt side pumps blood into body, separated by septum.
chambers are
Chambers are:
  • RA(Rt Atrium)- LA(Lt atrium)- RV(Rt ventricle)-LV(Lt ventricle).
  • chambers separated by valves, which prevent backflow of blood, its unidirectional, open passively according to pressure, the 4 valves are; 2 atrioventricular (AV) separate atria & ventricles
chambers cont
Chambers: cont
  • Rt AV valve is tricuspid& Lt Av valve is bicuspid or mitral valve, valves leaflets connected by collagenous fibers(chordae tendineae) to papillary muscles. 2 semilunar valves(SL) set between ventricles & arteries, each has 3 cusps look as half moon, they are pulmonic valve(Rt)& aortic valve(Lt).
no valves between vena cava & RA, nor between pulmonic veins & LA,so abnormally high pressure in Lt side of heart cause pulmonary edema, high pressure in Rt side cause peripheral edema( distended neck& abdomen veins).
direction of blood flow
** Direction Of Blood Flow:
  • liver (IVC) RA →RV→ PA→ lung

head & upper limbs(SVC)

  • lung → PV → LA →LV →aorta →body
  • ** Cardiac Cycle: it’s the rhythmic movement of blood through the heart, has 2 phases; Diastole& systole.
- Diastole :
  • ventricles relaxed & AV valves open, pressure in atria is higher than in ventricles, so blood pours rapidly into ventricles, this 1st passive filling phase is called early or protodiastolic filling., at the end of diastole atria contract push blood into ventricles, this active filling phase called presystole or atria systole or atia kick.
- Systole:
  • so much blood in ventricles so ventricular pressure is higher than in atria, so AV valvea swing shut(S1) to prevent regurgitation of blood to atria,for a moment 4 valves closed, ventricular walls contract against closed system so pressure in ventricles increased(isometric contraction) till presssure exceed pressure in aortic valve open & blood ejected.after ejection blood pressure decreased some blood back to ventricle causing aortic valve closure(S2) signal end of systole.
diastole again
- Diastole Again:
  • all 4 valves closed & ventricles relax,(isometric relaxation), meanwhile atria have been filling with blood delivered from lungs, atrial pressure now higher than ventricular pressure, mitral valve open & diastolic filling begin again.
events in rt lt side
- events in Rt & Lt side:
  • same in both sides, but pressures in Rt side is lower than those in Lt,& events is slightly later. Mitral closes before tricuspid in S1 & in S2 aortic closure before pulmonary .
heart sounds
** Heart sounds:
  • events in cardiac cycles generate sounds heard by stethoscope.- in 1st heart sound S1 occurs with closure of AV valves thus signals beginning of systole, heard over all precarium but loudest at the apex.
  • - in 2nd heart sound S2 occurs with closure of SL valves& signals end of systole, S2 heard loudest at base
effect of respiration
- Effect of respiration:
  • volume of Rt & Lt ventricle systole equal but affected by respiration, during inspiration intrathoracic pressure decreased, pushes more blood into vena cava, increasing venous return to Rt side prolonging Rv systole & delay PV closure, { MoRe to the right heart- Less to the Left} .meanwhile on Lt side, a greater amount of blood in lung during inspiration decreasing LV stroke volume so shorten LV systole allows Aortic valve to close a bit earlier than pulmonary valve so we hear the two separatly this is a split S2.
extra heart sounds
** Extra Heart Sounds:
  • S3: ventricular fillings creates vibrations that can be heard over chest, these vibrations are S3 ;occurs when ventricles are resistant to filling during early rapid filling phaseafter S2. S4:occurs at the end of diastole , atria contract & push blood into a noncompliant ventricles, create vibrations heard as S4(occur before S1).
  • ** Murmurs: it’s a gentle blowing sound heard on chest wall.
** Conduction:
  • heart has ability of automaticity; can contract by itself in response to electrical current by a conduction system begin in SA node near SVC (pace maker), across atria to AV node low in atria septum, delayed so atria contract before ventricles stimulated, then impulse travel to bundle of His& bundle branch then through ventricles, impulse stimulates heart to contract small amount spread to body recorded by ECG labeled PQRST stands for:
P wave __ atria depolarization
  • PR interval __ from beginning of P wave to beginning of QRS( time necessary for atrial depolarization plus time for impulse to travel through AV node to ventricles)
  • QRS complex__ depolarization of ventricles
  • T wave __ repolarization of ventricles.

electrical events precede mechanical events.

pumping ability
** Pumping Ability:
  • pumps between 4-6 L of blood/ min, this COP (cardiac out put) equal volume of blood in each systole (stroke volume) times the number of beats / min. CO = SV X HR, preload & after load affect heart ability to increase COP.
- preload: is the venous return that builds during diastole, length to which ventricle stretched at the end of diastole before contraction. Frank-Starling law the greater the stretch the stronger is the heart’s contraction.
  • - After load: is the opposing pressure the ventricle must generate to open aortic valve against the higher aortic pressure.
the neck vessels

** The Neck Vessels:

reflect the efficiency of cardiac function

carotid artery pulse
·        Carotid Artery Pulse:
  • pulse is a pressure wave generated by each systole pumping blood into the aorta, carotid located between the trachea & sternomastoid muscle, a smooth rapid upstroke, rounded & downstroke that is more gradual & dicrotic notch caused by closure of aortic valve.
jugular venous pulse pressure
· Jugular Venous Pulse & Pressure:
  • jugular vein empty unoxygenated blood directly into SVC, since no valves there jugular gives information about Rt side of heart, specifically reflect filling pressure & volume changesvolume& pressure increase when Rt side fails to pump effeciantly the jugular veins expose this. 2 jugular veins the larger internal jugular lies deep & medial to sternomastoid muscle .
not visible but pulse can be seen in sternal notch, external jugular superficial lateral to sternomastoid muscle, pulse result from a backwash, a waveform moving backward. Waves are:
A wave: atrial contraction
  • C wave: ventricular contraction
  • X descent: atrial relaxation
  • V wave: passive atrial filling
  • Y descent: passive ventricular filling.