Cardiac Dysfunction

>Coronary Insufficiency and myocardial infarction

-Most common

-due narrowing of coronary arteries the results to reduction/absence of blood flow to the any
are of myocardium.

Most common cause of coronary artery narrowing is the atherosclerotic cleft of the hardening of the
lining of the coronary arteries and the most common cause of this cause is atherosclerotic coronary
thrombosis.

Mycardial Infarction

>If there is a reduction in the blood, this will result to myocardial ischemia or infarction.

>The symptom of mycardial ischemia is anginal pain, a pain in the sternal area or in the precordial
area. The main maybe related to excersion of emotional stress. The pain maybe precordial or it may
radiate to the left shoulder or arm or even to the jaw. The pain is described as a tight bond or a heavy
weight on the chest.

>Results in a struggling sensation.

>Angina pectoris.

>The pain in coronary insuffiency lasts for 10 mins relieved by rest.

>Resting ecg is within normal image.

>May require, attachment of monitor to a patient, 24 hour ecg monitor/ halter monitor provided
images of ischemic changes during angina attacks. Stress test/ exercise test for ischemic episodes for
diagnostic purposes. ECG changes ST segment changes, current flow from a normal region to a
ischemic area, current of injury, results in st segment elevation, st segment depression on the
opposite side of the heart.

>Ischemia alters the path of repolarization, results in t wave inversion, ttt, major aim, reduce work of
heart with vasodilator.

>commonly used nitroglycerine, beta blockers, like propanolol this will reduce the heart rate.

>MI occurs when blood flow ceases or reduces to a critical level.

>Left ventricale almost always the site in MI, symptoms are similar with coronary insufficiency, except
pain is more intense lasts for 15 to 20 mins.

>not related to excersion or exercise, not relieved by nitrate.

>dx is based in hx.

>ecg will provide supportive evidence

>ask for the measurement of serum cardiac enzymes like creatinine phosphokinase, SGOT, LDH. If
these enzymes are elevated they may aid in dx, however, no specific enzyme in myocardium.

>ECG pattern in MI undergoes a series of changes following the infacarct. These changes should be
recorded daily for dx purposes. A transmural infarct will result in a deep q wave in chest leads
overlying in the infarcted area since this lead essential record infrapavitary potentialoverlying area.
These same leads demonstrate st segment elevation, in early hours after infarct there is an inversion
of the t wave. The tx for the relief of pain, support circulation if cardiogenic shock develops,
continuous ecg should be done in ICU, so you can detect easily the presence of arrythmia, paroxysmal
ventricular arrythmias which may trigger ventricular tach or ventricular fibrillation. If there is
fibrillation there may be a need for cardioversion, or give drug therapy drugs that may action as
membrane stabilizer to prevent arrthymias.

Ventricular hypertrphy

> happens if the work of ventricles increase sufficiently .

>VH increase diameter but not the number of individual myocardial cell.

>diffusion distance increases for oxygen and other metabolites.

>Increase in the diffusion distance may lead to ischemic conditions like coronary insuffiency or
infacrct

>dx

-r wave

-thickness of ventricle and height of r wave, increase in height increased magnitude in

depolarization, ST elevation,slightly sec to increase in muscle mass.

-QRS duration is increased slightly because of the increased muscle mass that is present.

-Qrs less than 0.12sec occasionally, but may exceed this value,

-st segment and t wave alteration, st segment depression, inversion of the t wave in chest leads.

-altered repolarization process, endocardial fibrosis or ischemia.

-if st segment changes are the only manifestation then the condition i referred to as a venticular
strain pattern not ventriculare hypertropjhy, yet.

-specific criteria for dx of lvh,

-mean electrical axis of the heart is shifted towards the left, superior

-transision zone is shifted to the left

-lvh is said to be present if R wave in V5 or V6 + S wave in V1 is greater than 35mm

-r wave in V5 or V6 is greater than 25 mm.

-R wave in AVL is greater than 13 mm

-R wave in AVF id graetaer than 25 mm

-there are also ST segments and T wave changes may may or may not be present.

-dx RVL

-main electrical axis is vertical or greater than +110* in frontal plane

-QRS R precordial leads show tall R waves rather than Normal S waves

-QRS is usually prolonged but less than 0.12sec, st segments is depressed and the T wave is
inverted in the right precordial lead.
 -Right venticular strain/ acute cor pulmonale

-appearance of ST segment and T wave changes are present,

-no abnormal r wave in precordial lead,

-occurs with acute exacerbation of lung disease

-important for dx of pulmonary embolism.

ECG

>Standard ecg consists of records from 12 different leads

>a lead is a recording from electrodes placed at specific area in the body.

>The torso is considered to be equilateral triangle with the right and left shoulders and the left leg as
the three apices, we call this the einthoven triangle.

>Unipolar limb leads, there are three (3) of this and they are formed by measuring the potential
differences b/n any two of limb electrodes, these leads can be selected by switch on the ecg machine.

>Lead 1 measure voltage in difference voltage potential in left arm and r arm (l arm- r arm).

>L2: potential diff of l leg- r arm

> lead 3: l leg-l arm.

>Unipolar/ chest/ v leads (V1-V6).

V1: placed on the 4th ics R of sternum

V2: 4th ics left of sternum

V3: left midclavicular line 5th ics

V4: halfway b/n v3 and v4

V5: left ant axillary line, same level as v4

V6: midaxillary same level as v4 and v5.

>Augmeted leads (avr, avl, avf)

-AVR is the potential diff b/n the R arm and sum of voltage from L arm and L leg,

-AVL is the potential diff b/n the L arm and sum of the R arm and L leg.

-AVF is the potentila diff b/n the L leg and sum of R arm and L leg.

>Normal ecg is a sinus rhythm,

-Pwave- atrial depolarization , normally postive, wave is upright.

-PR interval- measured form the onset of P wave and qrs complex varies from 0.12 to 0.21 sec.

>n rate 60-100 bpm

pq interval 120 to 200 msec.

>qrs width should be 60-100msec

>Qt interval shoiuld be 390-460msec

>heart axis: -30-+90

>p wave morphology: maximum height, 2.5 mm in leads 2 and lead 3; p wave is positive in lead 2
and avf; biphasic in lead 1; p wave ,duration, .08-1 sec/ 80-100ms; atrial rate determine time
interval b/n p waves,

>qrs complex: duration should be 0.06-1 sec; no pathologic q waves and microvoltage in qrs
complex, normal p wave propagation, p wave increase in amplitude from v1 to v5

>st morphology: no st elevation or depression, t wave should be concordant with qrs complex, pr
interval .12-.20 sec, equivalent to abt 3-5 small squares, qt intrval normally .42 sec can range
from .2-,4 sec, always upright, inversion= abn, u wave, small positive waves ff the t waves.

Ecg interprtation.

If n ecg pattern in absent then abn,

Hr lower than 60 bradycardia, more than 100 gtachycardia

Abn p waves, r/l atrial hypertrophy, premature beats, hypercalemia

Abn pr interval, shorter than n: wolf parkinson white syndrome, glycogen storage disease

Long PR interval: 1st degree heart block, trifasicular block,

Qrs wide: r/l bbb, present in l/r vent hyperthrophy

Long qt interval: MI, myocarditis, hypocalcemia, hypothyroidism, intracerebral hemorrhage, or due

to hereditary conditions ( Romano worth syndrome)

Abn st segment, elevation: acute MI. LBBB

depressedST segment: MI, vent hypertrophy, acute Myocardial infarction in post part of the heart,
LBBB

T waves are tall: hypokalemia

Twave are small flattenedinverted: ischemia, anxiety, pericarditis, conduction delay, electrolyte
imbalance

Normal heart axis: -30-90 degrees

> left axis deviation -30 to -90 deg

>right axis deviation +90-+/-180 degrees

>variation: intermediate axis deviation.

>Lead 1 and avf are perpendicular to each other, you can use these 2 leads in order to quickly
determine the axis of the heart.

>There are certain leads in the ecg that determine certain areas in the left ventricle, you can localize
where the infarct is. The prognosis often varies depending which are of the left ventricle is involved.
Example anterior wall infarct has the worse prognosis compared to an inferior wall infarct.

>If v1 and v2 represent the antero septal wall of the heart

 >v3 and v4 cathces the elctrical signal on the anterior wall of the heart

>v5 and v6 catches the electrical signal on anterolateral wall.

>Leads 2, 3 and avf catch the elec signal from the inferior wall of the heart

>leads 1,(may isa pa di maintindihan si doc >:/). and avl catch the lateral wall signals

>V1 and V2catch the signal in posterior wall of the heart, reciprocal of anteroseptal wall

>if there is ischemia

-there is a symetrical t wave inversion specifically in lead 1, 2 and v2to v6

>acute damage to the heart look for elevated st segment like iof there is pericarditis, or cardia
anneuryhsm can cause st elevation in the leads overlying the injury

>for infarct look for pathologic q wave, in order to be significant a q wave must be atleast 1 box wide
or 1/3 or qrs wide. Twave, initial deflection must be down even a tiny initial upward deflection makes
the apparent q wave may appear r wave so that a q wave even from the start should be
downward/negative deflection.

Refractory period of the heart

>the heart cannot generate a tetanic contraction since it has a low refracatory period: period ff an
action potential during which an excitable membrane cannot be reexcited, because of the long
plateau the absolute refractory period of the cardiac muscle will last as long as the contraction, about
250msec, the cardiac muscle cannot be reexcited in time to produce summation

>when an ectopic focus, the one that initiate an action potential just after the completion of a normal
contraction but before the next SA nodal impulse there will be a premature excitation wave and
contraction can occur, as a result the next normal nodal impulse fires during the refractory period and
the premature beat is not propagated because the myocardial cells are still refractory but the SA node
will still fire because it has a shorter refractory period.

>the second sa nodal impulse after the premature contraction will be propagated normally and so the
net result for all these is there will be unsually delay between the heartbeats. The contraction after
delay will usually be felt as a strong contractions and the person is aware of the skip beat of the
hearty. This entire phenomenon is usually benign, px usually describes this as Palpitation.

Cardiac cycle, divided in two major phases, named after the events that happened in the ventricle,

>period of ventricular contraction and blood ejection is called the systole

>period of ventricular relaxation diastole, where vents are filled with blood.

> average heart rate: hr of 75 bpm, each cardiac cycle will last abt 0.8 sec, with 0.3 sec for sytole and
0.5 sec for diastole

> both systole and diastole can be subdivided into several phases. During the very first part of the
systole, the ventricles are contracting but all the valves in the heart are closed, there is no blood that
is ejected, isovolumetric ventricular contraction, vent volume is constant, no increase or decrease
>ventricular wall continously develop to increase tension, it squeezes on blood because of the vol of
blood remains constant and blood in incomprensible like water,the ventricular muscle fiber cannot
shorten durting this 1st phase,but once the rising pressure in the vent becomes great enough to open
the aoritic and pulmonarty valves then the second phase starts, vent ejection period, blood will be
forced into the aorta or pulmonary trunk as the contracting vent fibers will shorten

>the vol of blood ejected from the vent during systole is called stroke volume

>during 1st part of diastole vent will relax, no blood enters or leaves vents since all valves are closed,
vent volume is not changing called as isovolumetric vent relaxation

>After it, the av valves open, vent are filled with blood and is called vent filling phase. Occurs when a
blood flows from atria to vents

>Atria contracts at very end of diastole and it adds to vent filling, almost all vent filling has already
taken place, from the mid diastole to the late diastole, the L atrium and vent are both relaxed, atrial
pressure is higher than vent pressure.

>Because of the pressure difference, av valves open and the blood entering the atrium from
pulmonary veins continue on into ventricles,

>During diastole, aortic valves are closed,because the aortic pressure is higher the the vent pressure.
Througout the diastole, the aortic pressure slowly falls because the blood is moving out of the artery,
in contrast the vent pressure rises bec blood is entering the vent, thereby expanding vent volume

>At the end of diastole, thesa node will discharge, the atrium will depolarize and it will contract, small
vol of blood is added to vents

>Amount of blood that is present in vents prior to systole is called the end diastolic volume.

>For the systole, from the av node the wave of the depolarization passes into the ventricle as it
signifies by QRS complex in the ECG, and this trigger ventricular contraction

>since the aortic pressure still exists, the ventricular and aortic valves remain closed and the vent
cannot empty despite each contraction.

>During systole vents have to empty blood it contains but vents do not empty completely, this is call
end systolic volume

>stroke volume= end systolic volume- end diastolic volume

>during the early diastole(begins when the ventricles contract and ejection stops, then vetricular
muscles relax).

> the fact that vent filling is almost complete during early part of diastole, this is very important bec to
ensure that filling is not seriously impaired during periods where heart is not beating rapidly, despite
reduction in the reduction in the diastole.

>Some px with atrial fibrillation can still live normally. :(

NOTE: pulmonary circulation pressure is very much lower than systemic arterial pressure, normally
120/70 or 120/80 mmHG.

Heart sounds

>Normal heart sounds are described as, a lub-dub sound

>the lub is due to the closure of the atrioventricular valve at the beginning of systole
>the second heart sound (dub) is due to the closure of the semilunar valves the aortic and pulmonary
valves and it happens at the end of systole

>normal heart cycle starts when the av valve closes at the start of systole

> the cause of these heart sound is due to the vibration of heart valves immediately after closure
together with the vibration of the adjacent walls of the heart and the main blood vessels around the
heart.

>the first heart sound or s1

-slow slightly prolonged sound

-duration: about 0.14 sec

-caused by the vibration that is set by the sudden closure of the mitral and tricuspid valves at the
start of the ventricular systole. During ventricular contraction this will cause a back flow of blood
against the AV valves causing these valves to close and bulge towards the atria

-because of the elasticity of the AV valves and Chorda tendinae there will be a back surge of
blood that bounces forward again into then ventricle, the blood, vent wall and valves will vibrate
causing the first heart sound

>the second heart sound

- shorter high pitched sound dub,

-duration: 0.11 sec

-caused by vibrations associated with closure of the aortic and oulmonary valves just after the
end of ventricular systole. During the period the valves will bulge backwards toward the ventricles.
-The elastic stretch recoil will cause the blood to flow back toward the arteries which causes the
reverberation blood and forth b/n the arterial wall and semilunar valves as well as the ventricular
walls.

-The vibrations in the arteries come in contact with the chest wall and creates the second heart
sound.

-This sound is slightly slower than the 1st sound because the semilunar valves are tougher

-has a higher frequency because the semilunar valves are thicker/tougher

>the 3rd heart sound of s3

-soft, low, low pitched sound

-heard about 1/3 of the way through the diastole

-can be heard in normal young individuals but not in all subjects

-coincides with period of rapid vent filling

-due to the vibration set by in rush of blood

-low frequency sound, usually not audible

-due to ossilations of blood back and forth between the walls of the ventricle because of the
rushing of blood from atria.

The fourth heart sound (s4)

-low frequency sound

 -usually about only 20cylce/sec or less

-not normally audible through a stethoscope but can be record via phonocardiogram

-due to vent filling and occurs when the atria contracts, caused by rushing of blood to vents

-usually referred as atrial heart sound

-rarely heard in normal adults, sometimes can be heard immediatly before s1, when atrial
pressure is high or vents are stiff, seen in vent hypertrophy.

-The interval b/n the aortic and pulmonary valve closure during inspiration is frequently low
enough for the second heart sound to be reduplicated.

-if 2 second heart sound are heard, it is called physiologic splitting of the 2nd sound.

>Auscultation areas:

-Areas of chest where you can hear best the heart sound coming from the different parts of the
heart

mitral valve: Left 5th ics, midclavicular line

Tricuspid valve: Right, lower part of body of sternum

Aortic valve: Right, 2nd ics

Pulmonary valve: Left, 2nd ics.

>Abnormal in heart valves, abnormal sounds can be heard and is termed clinically as murmurs

>valves of the heart can suffer from either stenosis or insuffiency

>Stenosis: is when they are tight enough where less amount of blood can pass through it.

>Insufficiency: valves do not close entirely so that systole or diastole, there are certian amount can
flow back and forth through these valves

>In aortic/pulmonary valve abn if there is stenosis the murmur will be a systolic murmur

>If there is insufficiency in aortic/pulmonary valve the murmur will be a diastolic murmur

> If mitral/ tricuspid valve are stenosic: diastolic murmur; insufficiency: systolic murmur

>Low frequency sound can be detected through a microphone that is specially designed and is called
Phonocardiogram. Heart sounds can be recorded by a high speed recording apparatus coming from
the machine and it is placed on the chest

>the volume of blood that is pumped by each vent per minute is called the cardiac output

-it is usually stressed in liters per minute,

-also the vol of blood flowing from systyemic or pulmonary circulation per minute.

- CO= HR x stroke volume

-if Vent rate is 72 bpm, eject 70 ml of blood each beat.

CO is 72x.07L/beat= 50 L per min.

This value is approx normal in a resting adult since the total blood volume is about 5L,
essentially all the blood in your body is pumped around the circuit every minute.