cardiac tips

First you have to know the function of the heart as a
vital organ.Make sure you know the circulation of
blood.from inf and superior vena cava to aorta.The
heart sound will be produced on CLOSURE of valves,that
S1 correspond to closure of Mitral and tricuspid valve
and not Aortic and pulmonic valve which is ur S2.They
both occur during systole or ventricular contraction.

S1 marks the begining of rapid ejection of blood so ur
aorta should be open!It make sense right?S3 sound is
associated with CHF(3 letter) and S4 for MI and
hypertension also known as atrial kick associated with
hypertropied ventricle,both occur on diastole,with S3
produced after S2 and S4 before S1.S1 starts while
blood is pump out so to prevent back flow mitral valve
shld be close,once blood is ejected and volume
decreases mitral valve should open to refill(inc.
PRELOAD) and to create an increase pressure inside the
heart for contraction to be effective (frank starling
law)aorta should be closed(S2).just remember its the
closures of the valves that creates the sound( as in
closing door when ur mad (BANG!!),hard to produce
sound when you open)).Should be remembered coz when
you panic or get nervous you might forget.

Nothing much to know about coronary circulation except
for (R) coronary artery that supplies most(80%) of ur
SAnode(pace maker of the heart) and AV node as injury
can cause a fatal arrhytmia.Coronary arteries fills
during DIASTOLE contrary to other organs that fills
during Systole.Most posterior part of heart is left
atrium and enlargement can cause dysphagia.The apex
beat is located at 5th ICSLMCL,its the most reliable
way to assess heart rate when peripheral pulses are
absent,too weak or unaccesible. Make it a practice to
appreciate abnormal heart sound and for accuracy for
patient with very weak pulses or having
atrial/ventricular fib may present with normal
palpable pulses.Elderly have collapsable artery
(pulse) not good to assess if with heart
condition.Brachial pulse is best for assessment in
kids.

You should know the formula for blood pressure to
understand the diseases esp CHF and effects of meds on
management of hypertension.Remember that BP is the
amount of pressure that the heart should have to pump
the blood and distribute it to circulation.

BP=Cardiac output(CO) x total peripheral
resistances(TPR)
your CO=stroke volume x HR.Your Stroke volume is the
amt of blood inside the heart being pump per
contraction,Your TPR represents the resistance to
blood flow primarilly due to arteries/arterioles which
is your resistance vessels(remember how
atherosclerosis or hardening of ur arteries lead to
hypertension!).Stroke volume is primarirly dependent
on the amount of blood that goes in ur heart ,the
veins which is ur capacitance vessels,and the fluid
both plasma and serum component of blood.It is also
dependent on how strong ur heart contracts(contractile
property of heart loss in CHF).
Now, what are the common meds and how they work?
initial management or meds will include your diuretics
(what makes you pee)this should decrease the preload
or fluid that goes in as CO(same amt with what goes
in)a little of afterload(the load similar to
TPR).Should watch out for fainting or dizziness with
sudden drop of BP.Strong diuretics like
LASIX(furosemide) can even include deafness bec. of
loss of fluid in your circular canal,or loss of
potassium leading to arrythmia and weakness.

2nd line is Beta blockers(those with
OLOL,propranolol(inderal)metoprolol,atenolol,..) will
decrease BP by decreasing HR and force of
contraction(dec. INOTROPIC property).And since its a
beta blocker it should be used with caution in patient
with asthma(treatment for asthma is beta agonist like
albuterol)Should know that Beta 1 is for the heart(u
only have 1 heart) and beta 2 for Lungs(2 lobes)
particularly on ur bronchus.In DM, beta blockers can
masked the effect of TACHYCARDIA as sign of
hypoglycemia,you might think that ur patient have
normal HR but his HR without beta blockers might be
already more than 100.It can also increase blood
glucose level.Use RPE on exercise assessment instead
of HR which is use on most cases.Other relative or
absolute CI is PVD, since it has an effect on smooth
ms lining ur peripheral vessels leading to compromise
blood flow.

So, 3 things to remember:Asthma,DM and PVD.Learn the
rationale so you wont forget!

May include CHF as CI but remember that it can be use
once STABLE not on ACUTE cases (previous and recent
studies shows that like ACEI it can decrease mortality
and morbidity in post MI and CHF including HTN)
Consistent effects of beta blockers is dec. in BP and
HR but for those with sudden drop in BP a compensatory
tachycardia may appear.FYI there are betablockers that
are selective and affect only B1 receptors,relatively
safe for those with previous condition that are CI.

Popular drug like ACE inhibitors(CAPTOPRIL) which
prevent conversion of Angiotensin I to angiotensin II
which is a potent vasoconstrictors(inc. TPR)and
decrease preload like diuretics due to decrease
production of aldosterone(salt production
Na(sodium))Most common side effect is dry COUGH due to
persistent bradykinin production,may be present for
several weeks ,may or may not persist.Replace with
ARB(angiotensin receptor blocker)those with SARTAN ,no
SE of cough.Directly block receptor of Angiotensin
II.Both are not safe for pregnant,teratogenic effect
bec. the fetus need AII for renal development.Renal
protective and prolong life in DM and MI.May increase
level of potassium in combination with
SPIRINOLACTONE(Aldactone)a potassium sparing diuretics
different from other diuretics that dec.level of
potasium, can also lead to arrhytmia.(brady
arrhytmia)remember potassium equals repolarization!

Other not so important meds : vasodilators/calcium
channel blockers-blocks calcium and relaxes arteries
leading to vasodilation,(calcium equals
contraction)some have effect on veins decreasing
preload,more blood remains on the capacitance vessels
not on the heart(nifedipine,hydralazine-can cause drug
induced SLE,verapamil-constipation).

Alpha 1 blockers/antagonist-prevent release of
NE(norepinephrine)-Prazosin(MINIPRESS) known for the
SE of FIRST DOSE EFFECT or sudden drop of BP leading
to syncope.

Alpha II AGONIST(the only adrenergic agonist)Clonidine
(CATAPRESS) facillitates/stimulates reuptake of NE not
to be release in presynaptic terminals.Decrease TPR.SE
includes sudden withdrawal lead to rebound
hypertension.

Remember that common cough and cold preparation that
contains phenylephrine,phenylpropanolamine(PPA) can
cause hypertension due to their vasoconstrictive
effect in preventing congestion.TCA
(tricyclicantidepressant)Amitryptylin(ELAVIL),imipramine
(DOFRANIL)- can increase NE,serotonin and dopamine
which is dec. in patient with depression but they also
block alpha adrenergic receptors(leading to
HYPOTENSION) and histamine leading to SEDATION.More
reasons to get depress if you fail to monitor
vitals...

Remember that you have Baroreceptors and
chemoreceptors that regulate your HR and BP.your
Baroreceptors includes ur carotid SINUS and aortic
arch.

Carotid sinus transmits via GLOSSOPHARYNGEAL nerve to
medulla.Your AORTIC arch transmits via VAGUS to
medulla(respond only to increase in BP)vagus as
parasympathetic will dec.HR and BP.Carotid massage
thru increase pressure in carotid will stimulate vagus
leading to dec.HR then BP.Simply stated when you have
increse BP your parasympathetic response will be
activated(dec.BP,contraction and HR) and reverse with
dec.BP as you activate ur symphatetic or as you
decrease stimulation of parasympathetic signals coming
from afferent receptors (CN 9 and 10)take note that 10
or vagus has also an efferent signals coming from
medulla.

REMEMBER that when you examine patency of carotids do
it one at a time not simultaneouslly or patient will
faint.wearing a turtle neck thats to tight may do the
same thing.other reason why stranguation lead to loss
of conciousness.
Remember that your medulla oblongata has
CARDIOINHIBITORY(parasymphatetic via vagus nerve)as
well as CARDIOACCELARATORY center(symphatetic or
adrenergic via T1-T4 releasing NE and Epinephrine).
Chemoreceptors from carotid and aortic BODIES which
responds to dec. in PO2,inc. CO2 and dec.
ph.(acidosis).

In response to cerebral ischemia( more of inc. in CO2
than dec. in O2) ur body will inc. ICP and inc. BP and
HR as sympathetic response but with dec. in HR as O2
level increases.

Some terms to remember:Chronotropic describes property
on inc.
HR(chrono=time)Inotropic(contractility)Dromotropic(pressure).

source: from PTforum