ANATOMY of the
HEARTYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
The left main coronary artery (LMCA) arises from the left aortic sinus,
It quickly divides into the anterior interventricular branch also known as the left anterior
descending (LAD) artery and the circumflex artery.
The LAD runs along the anterior interventricular sulcus, (groove in the anterior surface of the heart
that separates the left and right ventricle) down towards the apex.
LAD runs around to the posterior surface of the heart in another groove called the posterior
interventicular sulcus.
The LAD artery supplies blood to the walls of both the left and right ventricles.
The circumflex, follows a different course to the LAD. It runs along the atrioventricular groove, which
seperates the atria from the ventricles, giving rise to the left marginal branch in the process.
The circumflex then continues around the heart, terminating on its posteroinferior aspect, to supply blood
to both the left and right atrium.
RIGHT CORONARY ARTERY
The right coronary artery (RCA) arises from the right aortic sinus, and along the right
atrioventricular groove.
From here, it curls around towards the inferior surface of the heart, forming the posterior
interventricular branch, more commonly known as the posterior descending artery (PDA).
The PDA runs along the posterior interventiculas sulcus, to supply blood to the walls of both the left
and right ventricle.
However, before turning towards the diaphragmatic surface of the heart the RCA gives rise to the right
marginal branch, that runs along the right margin, to supply the wall of the right ventricle.
Important branches from the RCA include, the conus branch and the sino-atrial node artery.
As an aside, compared to the left ventricle the right ventricle has a greater ratio of muscle fibres to
capillaries: it is more likely to suffer toxic damage but less likely to suffer ischaemic damage.
CORONARY BLOOD FLOW
Small arteries and arterioles are key players in altering vascular resistance and thus regulating
myocardial blood flow.
Myocardial blood flow is closely linked with oxygen demand, with an increase in cardiac activity resulting
in an increase in demand for oxygen.
This is achieved by an increase in myocardial blood flow, involving autoregulation.
Whenever there is a change in coronary perfusion pressure, through changes in aortic pressure, the
process of autoregulation ensures that myocardial blood flow is always maintained.
Adenosine and nitric oxide (NO) are important mediators in the regulation of coronary blood flow as
well as the involvement of the sympathetic and parasympathetic nervous system.
QUICK RELATION TO EGC
ISCHEMIA: ST depression and T-wave inversion
INJURY: ST elevation
INFARCTION: ST elevation
PREV INFARCTION: Q waves
SEPTAL: V!, V2
ANTERIOR: V3, V4
LATERAL: V5, V6, V1,
aVL
INFERIOR: II, III, aVF
THE CARDIAC CYCLE- VENTRICLE AP
YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
What is an action potential? It is when a cell transiently depolarizes, due to ion channels.
CARDAC ACTION POTENTIAL is a lot longer than those in nerves or skeletal muscle.
Because of a PLATEAU PHASE in cardiac muscle, lasting 200-300ms.
I V1 V4
HYPERKALAEMIA (K+)
o Plasma K+ can be increased in
RENAL FAILURE
TISSUE DAMAGE
o Can cause dangerous arrhythmias eg. VF, as the membrane depolarizes (positive) and
becomes closer to threshold potential.
o MORE K+ outside cell, so less wants to move out, so resting potential is more positive.
o Also slows and weakens the upstroke of the action potential, as it partially inactivates the
Na+ channels, and slows conduction.
o Above 8, this leads to complete cessation of conduction- and heart block.
HYPOKALAEMIA
o Hyperpolarises the membrane, making it difficult to reach threshold.
THE CARDIAC CYCLE SA NODE Action
PotentialYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
Phase 4
o The spontaneous depolarization (pacemaker potential) that triggers the action potential once
the membrane potential reaches threshold between -40 and -30 mV).
o (K+ out slower and slower, Na+ in) slow decline in the outward movement of K + as the K+
channels close- that were open in phase 3.
o At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion
channels open that conduct slow, inward (depolarizing) Na + currents.
o As the membrane potential reaches about -50 mV, another type of channel opens (transient or
T-type Ca++ channel)
o As Ca++ enters the cell through these channels down its electrochemical gradient, the inward
directed Ca++ currents further depolarize the cell.
o When the membrane depolarizes to -40 mV, a second type of Ca ++ channel opens (long-lasting
L-type Ca++ channels)
o Opening of these channels causes more Ca ++ to enter the cell and to further depolarize the cell
until an action potential threshold is reached (usually between -40 and -30 mV).
Phase 0 is the depolarization phase of the action potential. Action potential threshold has been reached!
CONTRACTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
Between the ends of adjacent cardiac muscle cells are specialised intercellular junctions called
INTERCALATED DISCS.
These are irregular transverse thickenings of the sarcolemma that contain structures called
DESMOSOMES.
Desmosomes are like spot-rivets, that hold adjacent cardiac muscle fibres together.
The intercalated discs act as points of anchorage for the contractile proteins, and they contain channels
called GAP JUNCTIONS.
These connect the cytoplasm of adjacent cardiac muscle fibres and permit the extremely rapid low-
resistance spread of action potentials from one cell to another.
o 1. AUTORHYTHMIC CELLS: Cells found at the junction of the great veins and the right atrium
have the fastest intrinsic rhythm (this is the sinoatrial (SA) node or 'pacemaker' of the heart).
o Nervous and hormonal input can alter the rate of this automatic discharge so that the normal
heart rate is about 70 beats per minute.
o 2. PURKINJE FIBRES (conduction fibres) allow fast conduction of action potentials around the
heart.
CYCLEYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
o Pulmonary and Aortic (semilunar valves) are closed- as the arterial pressure- both pulmonary
and aortic pressure is greater than the relaxed ventricular.
o AV valves open
o Ventricles are already partially filled from when the whole heart was relaxed.
o Ventricles receive the last 30% blood- final vol of approx. 130ml.
3. VENTRICULAR EJECTION
o Pressure in ventricles now higher than in pulmonary arteries and aorta, so semilunar (arterial)
valves open.
o Pressure in aorta is 80mmHg, and pulmonary artery 10mmHg- ventricular pressure is above
this.
CONDUCTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
o Lub
o In L or R bundle of HIS.
o Splits in young people due to inspiration of exercise- longer ejection period in right
ventricle.
o Lungs are lower pressure, want to keep blood, less returns to Left ventricle
o Increase in blood into Right ventricle from vena cava, as sucked into Right Atrium, and
wants to go into the lungs.
o Takes longer to empty Right ventricle as more blood, pulmonary valve stays open a bit
longer than aortic.
o S3: Rapid refilling, S4: atrial systole (S3 and S4 togther produce a gallop rhythem)- HF.
CARDIAC MUSCLE
o On the intercalated disc connections are GAP JUNCTIONS, where membranes of cells are very
close, consist of low resistance proteins: CONNEXONS
o If Action Potential is initiated in one cell, local currents via gap junctions will cause adjacent
cells to depolarize, initiating their own action potential.
o (Rate of conduction is related to gap junction resistance and size of depolarizing current-
related to upstroke of action potential).
HEART BLOCK
o Complete heart block (third degree) occurs when conduction between atria and ventricles
abolished.
o Abnormally slow conduction through AV Node- causes incomplete (1 st degree) Heart Block- delay
is greater than normal- extended P-R interval on ECG.
o 2nd degree heart block when only a fraction of impulses from atria are conducted- eg. Ventricular
contraction only initiated every 2nd or 3rd atrial contraction (2:1 or 3:1 block)
o Wencheback (Mobitz2) is another type of 2nd degree block- P-R interval progressively lengthens,
until no transmission from atria to ventricles, and a QRS is missed.
o The part of the ventricle it serves will still be stimulated by conduction through the myocardium
from unaffected areas.
o Conduction is slower, activation is delayed and QRS broadened (ventricular systole takes longer)
ARRYTHMIAS
o AV NODE normal, but a separate extra congenital conduction pathway (bundle of Kent) between
atrium and ventricle.
o Bundle of Kent faster, so part of ventricle stimulated before the rest- wide QRS COMPLEX. (pre-
excitation).
o A premature impulse can set up a re-entry circuit and bad and fast arrhythmia.
HAEMODYNAMICS
DARCYS LAW:
Pump Pressure
Flow =
resistance
BLOOD VISCOSITY
o ANAEMIA: haematocrit (cell concentration) is low, viscosity and vascular resistance decrease,
Cardiac Output rises.
LAMINAR FLOW
o As liquid flows through a tube, frictional forces are exerted by the tube wall.
o These, and viscous forces in the tube, set up a velocity gradient across the tube.
o Erythrocytes move away from vessel wall, and sit in the middle flow, aligned.
o Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (Fahraeus-
Lindqvist effect)
o The wall has a pressure exerted on it: Pressure inside the vessel, minus the interstitial pressure.
o This distends the blood vessel wall (ie, the pressure of the blood pushes it out)
o In the aorta, where the transmural pressure (blood pushing wall out) is high, atherosclerosis may
cause thinning of the blood vessel wall, and the development of a bulge/anyeurysm.
o This increases the vassel radius, and decreases wall thickness, which sets up a viscious cycle of
increasing wall tension, which if not treated may lead to rupture.
o Starlings law means that even if the afterload (blood pressure) increases, the stroke volume can
be maintained.
o The resistance to outflow increases, the left ventricle has to pump against a higher resistance,
and the amount of blood ejected is reduced.
o This means the EJECTION FRACTION has decreased, and the proportion of the END DIASTOLIC
VOLUME pumped out falls.
o So when the ventricle is being filled again in diastole, there is already more blood than usual in
the ventricle.
o The end diastolic volume is now larger! Ventricle wall is stretched more, so STROKE VOLUME
INCREASES.
o When BP increases, the ENP and EDV increase too, so CO can remain the same, despite pushing
against greater force.
AUTONOMIC NS
o Externally regulates CO
o Acidity
Heart
Rate Stroke Vol
END DIASTOLIC VOLUME
- Compliance
Positive Chronotropes, eg. SYMPATHETIC NS
- CVP (pessure pushing it) and so EDP (how much fills with
blood before contracts)
END SYSTOLIC VOLUME
- Arterial pressure
Negative Chronotropes, e.g. PARASYMPATHETIC NS - Contractility
(both of which affected by symp stimulation and tissue
health - o2, pH etc
CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
REFLEXES
o Fluctuations in MABP (Mean arterial BP) and volume need to be minimized, to maintain
adequate cerebral and cardiac perfusion.
Baroreceptor
Cardiopulmonary
Chemoreceptor
o Afferent (sensory) nerve endings in CAROTID SINUS (dilations at the origin of the carotid
arteries and aortic arch).
o Change the frequency they send action potentials- more pressure, more frequent.
o Also causes the CUSHING REFLEX: Brainstem hypoxia due to a tumor which is causing
increased CSF pressure: vasoconstriction and hypertension develop.
EXTRINSIC REFLEXES
o Cardiovascular autonomic control arises when areas of the brainstem, hypothalamus, cortex and
cerebellum interact.
o Afferent nerves carrying the stimulus from the receptors terminate in the NTS (NUCLEUS
TRACTUS SOLITARIUS) of the medulla.
o Neurones from here (NTS) project to areas of the brainstem which control parasympathetic and
sympathetic outflow.
o The nucleus ambiguous and dorsal motor nucleus contain the cell bodies of the pre-ganglionic
vagal parasympathetic neurons- slow the heart when NTS says theres an increased BP.
o Neurons from NTS project to areas of ventro-lateral medulla.. blah blah its complicated.
o Higher centres eg. Limbic system in cortex modify the action of the brainstem centres, integrated
and appropriate responses are generated.
o Brain can selectively override /modify the CV reflexes, behavioral responses and CV adjustments
CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
o Long term, body needs constant blood volume, to sustain constant BP.
o Changes in CO lead to adaptive effects of the vasculature that : Increase peripheral resistance
and therefore BP.
o Water
o Na
o Activate thist
o ADH acts on DISTAL NEPHRON- to increase its reabsorption of water: reducing loss water in
urine.
o Opposite happens if less osmolarity- more water excreted and less ADH.
o 95% of the osmotic solute in the ECF is Na+ with Cl- and HCO-
o After eg. Eating a salty meal, the plasma osmolarity is changed and the body will adjust the water
content (plasma vol)
INCREASING GFR
Reducing Na+ reabsorption throughout nephron- loose Na+ and therefore water.
Dilates arterioles
CARDIAC MONITORING
- Non invasive techniques better (less risks eg. Pneumothorax/ line infection)
- BLOOD PRESSURE
o BP doesnt reflect CO.. BP can be high, but CO low if peripheral vasoconstriction raises
peripheral vascular resistance (SVR)
o Vasodilated septic patients, with low SVR may have a high CO, but still be hypotensive.
o Useful means of assessing circulating blood volume- determine rate to administer fluid.
o Increased venous tone can act to maintain CVP, and mask volume depletion during
hypovoluemia/heamorrhage.
Fluid overload
BASIC CHEST PAIN HISTORYiix
CENTRAL
ASSOCIATED SYMPTOMS
IHD
o smoking, family, hypercholesterol,
hypertension, diabetes.
o (SF C HD Sausage Fest Causes HD!)
PE
LOOK FOR?
abnormal lipids:
o xantholasma
o tendon xanthoma
CHEST
Tar PAIN
stained INVESTIGATIONS
fingers (IHD) ix CHEST PAIN INVESTIGATIONSix
Hot, oedematous calf: DVT
GP,Hypertension
(non-acute chest (IHD)
pain) ECG (ACS)
Marfans syndrome
Diabetes (IHD)
FBC (to exclude anaemia). o New onset LBBB
o R. Axis deviation
Additional tests if a non-cardiac cause is
suspected - eg,
o RBBB
o CXR,
o S1Q3T3 (deep S wave in 1, Q
wave in 3, T-wave inversion in
o LFTs and amylase, 3)
Palpitation
s
PALPITATIONS HISTORY kkkkkmmmmm
REGULAR CAUSES ooo
REGULAR IRREGULAR
IRREGULAR
Non- Cardiac causes TACYCARDIA:
What the patient means by palpitations.
It should mean an awareness SLOW
SLOW
of the heart beating.
FAST
FAST
It may really be a pulsatile tinnitus or a carotid bruit. FAST PACE!!!!
Ask the patient
o how often it happens, PERSISTANT
PERSISTANT OCCASIONAL
how long it lasts and
o VT OCCASIONAL
VT SINUS
SINUS BRADY
BRADY Fever
o any precipitating or relieving factors.
Sometimes people are only aware of it whilst lying down
at night. AF
AF ECTOPIC
ECTOPIC
AF- Anaemia
Determine whether the rate is regular AF- degree
degree of block
of block
or irregular.
TACHYCARDIA
TACHYCARDIA
Ask the patient to tap out the beat.
This may be regular or irregular. It may be a normal rate ECTOPIC AF
COMPLETE HEART ECTOPIC
Sympathomimetic
S drugs AF
(paroxysmal)
or fast.
AF COMPLETE HEART S (paroxysmal)
Try toAFestimate the rate. BLOCK
BLOCK
Establish whether there are any symptoms that ATRIAL
ATRIAL
Thyrotoxicosis
accompany the palpitations, such as sweating or FLUTTER (with
FLUTTER (with
SVT
breathlessness.
SVT block)
These may be organic or psychosomatic in origin.
block)
Associated chest pain?.sinister significance! Pregnancy
Enquire about consumption of caffeine. Palpitations may
be related in time to consumption but assess daily intake
too Anxiety (pain) Arteriovenous
Ask about alcohol consumption. fistulae
Ask about smoking. The level of nicotine in cigars tends to
be rather higher than in cigarettes.
In young people ask about use of illicit substances, Cigrettes, alcohol, caffeine
especially cocaine, 'ecstasy' -
methylenedioxymethamfetamine (MDMA) - and
amfetamines. Exercise
OTC and prescribed meds!
High levels of anxiety can also result from withdrawal of
sedatives such as benzodiazepines. Causes of Bradycardia
Ask about general health and well-being. There may be
great anxiety in the individual's life at present.
There may be shortness of breath on exertion, loss of Athletes
weight or gain in weight, with ankle oedema.
Symptoms of thyrotoxicosis- can cause sinus tachycardia,
AF / Atrial flutter.
Hypothyroidism
History of:
PALPITATIONS- EXAMINATIONx
If the patient currently has the palpitations then it is easy to assess the rate and regularity of the
pulse and to get an ECG to confirm the diagnosis.
The gold standard is a full 12-lead ECG taken at the time of palpitations. It should, however, be
performed even if the palpitations have resolved. Shows
o irregular rate and it is easy to deduce the type.
o abnormalities suggestive of ischaemia, hypertrophy or cardiomyopathy.
o occasional ectopics that are not currently causing symptoms.
o incomplete heart block.
o short PR interval in WPW syndrome.
Basic blood
HEART MURMURS tests x HEART MURMURS Hx x
o FBC,
o U&Es
EJECTION oSYSTOLIC
TFTs. (A and P area) No real symptoms- so need to find out
A 24-hour ECG should be arranged (many GPs now have direct cause/ consequences.
access to this).
- Originate
o Thein either is
patient ventricle
given a outflow
device totract-
wear (a Rheumatic
sofor 24 hours feverwhich
Holter monitor) (mitral
is valve)
returned to the
either hospital
around the for pulmonary
analysis thearteries or the
following day. IHD (mitral regurg)
aorta
o The time that palpitations start and finish shouldbe noted so this
Congenital can disease
heart be correlated with the
- TheyreECGeither before the valves (in the
recording. Hypertension (flow murmus)
heart),Asin athe valves, oran
refinement, in the arteries.
event recorder can be used for
o patients
IVDU whose palpitation frequency is
- Reach less
a crescendo
than daily.mid-systole, die down
before second heart sound (semilunar Family Hx hypertrophic cardiomyopathy-
o For added convenience, leadless monitors have beenautosomal
developed. dominant.
shutting)
If the problem is related to exercise then a treadmill ECG is AORTIC
required. Sometimes there is with)
an
- irregularity
Causes in AORTIC AREA.. either valvular / REGURG (associated
at rest that is suppressed on exercise. These tend to be o ofRheumatoid
rather less sinister significance
arthritis
supravalvular / subvalvular
o Coactation of aorta o Seronegative arthropathies
HEARToMURMURS Supra-aortic stenosis x (ankloysing spondylitis, reiters
o Aortic sclerosis syndrome, psoriatitic arthritis
o Hypertrophic obstructive o Coarctation of aorta
Murmurs are vibrations due t turbulent blood flow in heart.
cardiomyopathy (subvalvular) MiTRAL REGURG
Non valvular causes o Lupus
o Hyperkinetic Cardiac Output states
o Innocent flow murmurs in children o Rheumatoid arthritis
- Causes in PULMONARY AREA
o High CO: fever, thyrotoxicosis, pregnancy. o Ankylosing spondylitis
o Pulmonary arterial stenosis
o Congenital heart diseases: ASD, VSD, PDA, Coarctation ofoaorta. Marfans
o Pulmonary valve stenosis
CLASSIFICATION o Ehlers-Danlos
o Flow murmurs, hyperkinetic states,
left-Right shunts (ASD)- left side o Osteogenesis imperfect.
EJECTIONbigger-SYSTOLIC
remember Consequences
PANSYSTOLIC o Aortic valve disease and mitral
PANSYSTOLIC DIASTOLIC
MURMURS (T and M area) regurg may be asymptomatic.
CONTINUOUS o LOW CO- fatigue and weakness
- Same intensity o Paliptations- AF
- Heard throughout the whole of systole and o Angina (aortic stenosis)
merge with the 2nd heart sound (semilunar o Symptoms of RV failure
valves shutting) Anorexia
- Causes at APEX (mitral) Ankle and leg oedema
o Mitral Regurg Hepatic pain
o Mitral valve prolapse Intestinal mucosal
- Causes at TRICUSPID area congestion
o Tricuspid regurg o Symptoms of LV failure
o VSDs- left side bigger/louder- Breathlessness exertion
remember Cough
Haemoptysis (mitral
DIASTOLIC MURMURS *always pathological, stenosis)
always hard to hear. Orthopnoea
Paroxysmal nocturnal
- When blood ejected from the ventricles dyspnoea
and the heart relaxes, Atria are filling. o Syncope (poor CO)- eg, severe
- Causes at PULMONARY area aortic stenosis.
o Aortic regurg (early diastolic) o Emboli- TIA/Stroke- mitral stenosis
o Pulmonary regurg (early diastolic) o Infective endocarditis
- Causes at APEX (MITRAL) area o Symptoms of enlarged LA,
o Mitral stenosis- think in pressing on other structures,
isovolumentic relaxation- ventricles especially in mitral stenosis
are filling through here. Recurrant laryngeal nerve-
o Carey Combs murmus (acute horseness- Ortners
rheumatic fever, mitral valves syndrome
MITRAL STENOSIS x
MITRAL REGURGITATION
x
-
Narrowing of the mitral valve (when LA-
LV)
Backpressure builds up behind the
narrowed valve
Reduced amount of blood ejected from LV.
Backpressure into lungs.
Most caused by past Rheumatic fever-
Mitral valve doesnt close properly follows a bacterial infection with
Blood leaks back into LA when LV streptococcus- body makes autoantibodies
contracts, instead of going into the to clear infection, but also attack mitral
body. valve- inflammation, damage and
Due to infective endocarditis, Ehlers thickening.
Danlos, Marfans, SLE, scleroderma, Can also be calcification, congenital,
acute rheumatic fever endocarditis.
SYMPTOMS More effort form LA to pump into LV- get a
o If acute, you get rapid hypertrophy of the LA.
backpressure into lungs and SYMPTOMS
acute pulmonary oedema- o SOB during exercise
emergency valve repair! o Fainting, dizzy
o Chronic- eventually, dilation of o Tired
Left ventricle, HF. o Chest pains (reduced flow
EXAMINATION
o
OF A MURMUR
Progressive exertional coronary arteries)
x
dyspnoea o Chest infections- due to bronchial
o (Systemic emboli/stroke, chest vein ruptures, congention,
pain
Inspection, AF, less common
palpation, than
auscultation pulmonary infarction.
stenosis)note when maximum
Time a murmur, o Coughing up bloody sputum.
o
intensity. and radiation COMPICATIONS
COMPICATIONS
SYSTOLIC o AF- due to faulty LA
o o AF- due to faulty LA
Pansystolic? o HF: orthopnoea, PND
o o HF: orthopnoea,
Ejection PND
systolic? o Stroke/emboli- due to AF
o
DIASTOLICStroke/emboli- due to AF o Fatigue and cold hands- low CO
o o Fatigue and cold (start
Early diastolic? hands-from
low CO SIGNS
SIGNS 2nd sound) o Malar flush
oo Bibasal crackles- pulmonary
Mid diastolic? o Pulse: small vol/ AF
oedema o Evidence emboli- ischaemic
o LA enlargement- parasternal bowel/ leg etc
heave o JVP raised
o LV dilation- thrill at apex o Swollen liver
o Look for things eg. Rheumatoid MURMUR
arthritis, EhlersDanlos, o MID DIASTOLIC (blood from A
oesteogenesis imperfect (blue to V, before V contract- blood fills
sclera) ventricles in diastole, as in
MURMUR systole, pumps to body.)
o PANSYSTOLIC MURMUR at o At APEX (M area)
AORTIC STENOSIS x AORTIC REGURG x
- -
- Mitral Stenosis, can cause pulmonary hypertension, which can cause Tricuspid regurgitation
- Trauma or infective endocarditis
- Rheumatic fever
- Blood goes from RA to RV, but in systole, RV is meant to squeeze it into the lungs and it goes
back into RA, pressure on venous system of body- portal hypertension.
-ISCHAEMIC
IVDU? Infective
HEART endocarditis?
DISEASE- Basics x
SYMPTOMS
o Fatigue
Result of
o anOedema
imbalanceandbetween Myocardial oxygen supply and demand
ascites (peripheral)
Term covers
o Hepatic pain- liver capsule stretched.
o Angina
MURMUR
o ACS
o PANSYSTOLIC MURMUR
o Anything
o that reduces
Loudest blood edge
at L sternal supplyintoinspiration
heart! (T)
Due too No radiation
o Atherosclerosis
o of coronary arteries (COMMON)
Investigations
o Coronary artery spasm
o Emboli
o Aortic stenosis (supplies coronary arteries)
o Hypertrophic obstructive cardiomyopathy
o Arrythmias- cause dec coronary perfusion.
o Anaemia
o Syndrome X- normal coronary arteries- but abnormal small vessels.
Risk Factors
o Age- Raised cholesterol, hypertension, cigarettes over time.
o Male / post-menopausal women
o Family Hx- below 50 / hypercholesterolemia.
o Cigarettes (x3)- after 10 years same as non-smoker
o Blood lipids- HDL protective, LDL and Triglycerides inc risk
o Hypertension- (also a risk of stroke and renal failure)- drugs decrease risk heart disease by 16%
o DM (2x risk major ISH event)
o Race- Asian- more DM.
o Weight: overweight 2x risk IHD. (increased BP, total cholesterol, insulin resistance, decreased HDL,
dec exercise)
IHD Investigations
o EGC- ACS
o Exercise ECG- look for 1mm ST depression
o ECHO: assess ventricular function- an exercise stress echo can be used to look at areas of
hibernating myocardium- where reduced bloodflow in exercise, as decreased coronary reserve
in a territory- if improve at rest- good for intervention.
o Nuclear Imaging- Radioactive isotope (thallium) injected during exercise and image after.
Isotope taken up by healthy myocardium- infarction are cold spots. Adenosine can give
pharmatological stress instead.
PATHOLOGY OF ATHEROSCLEROSIS- Basic x
TREATING IHD (Basic) x
Slowly progressive, focal proliferation of connective tissue in arterial intima. Begins in early life. High lipid
- GENERAL
levels.
o Inc exercise, (better collaterial circulation heart, and for VD) smoking stop, diet,
LDL main athrogenic lipid
weightloss
Plaques- mostly made of COLLOGEN synthesized by smooth muscle cells.
- 1. ENDOTHELIAL DYSFUNCTION- associated with high cholesteriol, inflammation, and shear forces.
oDRUGS
2. MACROPHAGES enter arterial wall, between endothelial cells, take up lipids and become FOAM
- oANTIPLATELET
CELLS.
o All patients ASPIRIN 75mg Daily- lowers risk subsequent MI and death
o 3.o FOAM
RiskCELLS ACCUMULATE
of GI bleed- melena,intakesubendothelial zone- forms FATTY STREAKS
with food, PPI
o 4.o FOAM CELLS/MACROPHAGES
CLOPIDOGREL release toxic products-
if aspirin contraindicated lead to aggregation)-
(inhibits platelet PLATELET ADHESION, MUSCLE
mostly used postCELL
PROLIFERATION, THROMBUS FORMATION
NSTMI/angioplasty.
5. Becomes organized- ATHEROSCLEROTIC CAP with FIBROUS CAP.
- oBETA-BLOCKERS
o 6.o Progressive enlargement,
Reduce Sympathetic and narrowing of lumen- exertional angina.
tone.
o 7.o RUPTURE-
Negativecause sudden(reduce
ionotropes thrombuscontractility)- reduce oxygen demand
o Neg Chronotripoc (HR)- reduce oxygen demand
Atherosclerosis
o is Increase
initiatedperfusion of ischaemic
by inflammatory area- decreasing
processes HR, increases
in the endothelial cells of diastole-
the vesseltime
wallfor
in coronary
response to
retained (LDL) blood flow.
o Contraindications? Asthma, PVD with skin ulceration, 2 nd and 3rd degree heart block.
Lipoproteinsoin the blood survival
Improve vary in size. Some data suggests that small dense LDL particles are more prone to
post-MI
pass between o the Goodendothelial cells,
in chronic going
heart behind
failure- the cellular
shouldnt monolayer
be given in acute. of endothelium.
- NITRATES
LDL particles and their content are susceptible to oxidation by free radicals- risk is higher while in the wall than
o Cause peripheral vasodilation- especially in veins
while in the bloodstream.
o Reduces venous return, and ventricular pre-load.
o Reduction
However, LDL particles in a
have heart wallof
half-life distension- decreases
only a couple of days,o2and
demand of heart(LDL
their content wall-particles
angina relief.
typically carry
o fat
3,000 to 6,000 Nitrates are converted
molecules, including:to NO- which phospholipids,
cholesterol, results in an increased intracellular
cholesteryl cyclic guanosine
esters, tryglycerides & all other
fats in the watermonophosphate
outside cells, to cGMP in smooth
the tissues of themuscle. This stimulates
body) changes calcium
with time. Oncebinding processes
inside the and LDL
vessel wall,
free calcium
particles can become vaaliable
more prone to trigger muscle contraction is reduced.
to oxidation.
o Nitrates and rest relieve angina in minutes.
Endothelial cells
o respond
Longer by attracting
acting monocyte
nitrates can white for
be effective blood cells,
hours. causing them
(isosorbide to leave
dinitrate, the blood by
metabolized stream,
penetrate into the arterial
liver walls and
to isosorbide transform into
mononitrate- themacrophages.
main active metabolite- helps avoid bad 1 st pass
metabolism.
o Adverse effects due to arterial dilation- headaches, flushing, hypotension, fainting
- CALCIUM CHANNEL BLOCKERS
o Calcium antagonists inhibit influx of calcium into myocyte during action potential and relax
peripheral smooth muscle.
o Reduced afterload (so less myocardial oxygen demand), reduce HR, increase coronary
vasodilation.
o Therefore reduce angina
o Useful in coronary artery spasm
o Dihydropyridines (Nifedipine) may be combined with a beta blocker, as they cause
peripheral vasodilation and reflex tachycardia.
o Diltiazem has slight neg iontropic and chronotropic effect- if on betablocker- needs
monitoring for bradycardia
o Al CCB are net iotrope to a degree- be careful in impaired LV function (even through
amilodipine good in HF)
o Headache, dizziness, flushing, constipation, gravitational oedema.
- K CHANNEL ACTIVATORS
o Nicrorandil- has arterial and venous vasodilating properties
o Useful if refractory to other anti-anginal agents.
- STATINS
o HMG-CoA REDUCTASE INHIBITORS
o Lipid lowering therapy
o Help stabilize plaques- reduce freq of acute coronary events.
o If IHD, and cholesterol normal, still should be on statin.
DIAGNOSING ACSx
- After acute MI
o Up to 18hrs: No macroscopic or microscopic changes
o 24-48hrs (2 days): Pale oedematus muscle (macro), (micro) oedema, acute inflammatory
cell infiltration, necrosis of myocytes.
o 3-4 days: yellow rubbery centre with haemorrhagic border (macro), (micro) Obvious
necrosis and inflammation, early granulation tissue.
o 3-6 weeks: Silvery scar becoming rough and white, (micro) dense fibrosis.
- Cardiac Enzymes
o Intracellular enzymes that leak out of infarcted myocardium into bloodstream
o CREATININE KINASE (peak 1 day)
Peaks in 24hrs
Cardiac enzyme, also produced by skeletal muscle and brain.
CK-MB can be requested if in doubt- a myocardium-bound isoenzyme, specific heart
muscle damage.
Site of infarct related to serum level of enzyme.
Used to assess reinfarction in patients who have elevated troponin from a previous
MI
o ASPARTATE AMINOTRANSFERASE (peak day 1-2)
o LACTATE DEHYDROGENASE (peak day 1-2)
o TROPONIN I or T (8-12hrs)
Good markers of cardiac damage
Proteins involved in myocyte contraction
8-12hrs post MI most reliable
MANAGEMENT HYPERTENSION- Basic
THIAZIDE DIURETICS
o Lower body sodium stores- BP falls as dec in blood vol, venous return and CO.
o Gradually the CO returns to normal, but the hypotensive effect remains as peripheral
resistance decreases
o Side effects: GOUT, impaired glucose tolerance.
o Low doses (2.5mg bendrofluthiazide) cause little biochemical disturbance without loss of
anti-hypertensive effect. High doses not usually needed.
POTASSIUM-SPARING DIURETICS
o Diuretic induced hypokalaemia.
BETA-BLOCKERS
o Decrease CO, so initially cause fall in BP
o CO returns to normal, but peripheral resistance is set to a new lower level so BP remains
low.
o Renin levels are reduced.
o Side-effects: Provokes asthma, and heart block. Neg ionotrope. Cold hands and fatigue.
CALCIUM CHANNEL BLOCKERS
o Calcium antagonists.
ACUTE CORONARY o SYNDROMES: (Nifedipine)- good vasodilating drugs that can cause reflex tachycardia.
Dihydropyridines
Pathophysiologyo Diltiazem- neg ionotrope, and chronotrope- contraindicated in HF
o Amlodipine- safe in HF
ACUTE CORONARY SYNDROMES:
o Flusing, headache, oedema, constipation
Affects 7% population
o Dont use verapamil with beta-blocker.
Pathophysiology
Increases with age, males, post-menopause
ACE INHIBITORS
RF: smoking, hypertension,
Inhibit diabetes,
renin-angiotensin-aldosterone axis
o Affects 7% population
cholesterol, family.
Increase in vasodilating bradykiin
o Increases with age, males, post-menopause
About 20%o ofMore
all deaths in UK
effective in yonger patients with higher renin levels- best
RF: smoking, in young white
hypertension, diabetes, cholesterol,
After MI-o30-60%
Gooddeath
in HF,before hospital,
proteinurig 10%
nephropathy, diabetes family.
in hospital,
o 20%Dry within
cough 2 years (HF to
(secondary or bradykinin),
MI) Hyperkalaemia, Transient worsening in serum
About 20% of all deaths in UK
Variant Angina? Vasospasm
creatinine (GFR)- as intraglomerular pressure falls, Acute renal failure (if sepsis,
After MI- 30-60% death before hospital, 10% in
Stable angina? Fixed Plaque renal artery stenosis)
hypovolumeia, hospital, 20% within 2 years (HF or MI)
ACS: thrombosis
o overelectrolytes
Monitor ruptured complex
until dose titrated. Variant Angina? Vasospasm
plaque
ANGIOTENSIN II RECEPTOR BLOCKERS Stable angina? Fixed Plaque
o Block rein angiotensin system- similar to ACE
ACS: thrombosis over ruptured complex plaque
CONSEQUENCES oOF CORONARY ARTERY
Good if chronic OCCLUSION
cough on ACE- dont effect bradykinin production
o CV protective effect
CONSEQUENCES OF CORONARY ARTERY OCCLUSION
o
LEFT CORONARY ARTERY
MINOXIDIIL
Supplies
o Potent vasodilator,
LAD and dec Major
Circumflex: PVR- can cause reflex tachycardia- use beta-blocker
Fluid retention o LEFT CORONARY ARTERY
contribution
o to LV and (use diuretic)
RV perfusion
o RIGHT CORONARY
o Hirsutism ARTERY Supplies LAD and Circumflex: Major
Occlusion causes inferior MI. contribution to LV and RV perfusion
o RIGHT CORONARY ARTERY
Main Supply to RV and AV node
Occlusion causes inferior MI.
o LAD ARTERY
Main Supply to RV and AV node
Occlusion causes Anterior MI
o LAD ARTERY
Supplies LV, Septum and RV
Occlusion causes Anterior MI
o CIRCUMFLEX ARTERY
Supplies LV, Septum and RV
Causes lateral MI
o CIRCUMFLEX ARTERY
Causes lateral MI
FACTORS LIMITING OXYGEN SUPPLY
ATRIAL TACHYCARDIA
SYSTOLIC FAILURE
Treat the
o CAUSE (IHD/valve)
o Pathophysiology (DD)
o Precipitating events (arrhythmias)
AFTERLOAD REDUCTION rapidly improves LV function
and CO in the failing heart.
But may cause Hypotension.
PRELOAD REDUCTION: relieves symptoms (eg.
Pulmonary oedema), but CO is not increased.
Non-invasive monitoring and less frequently pulmonary
artery catheterization- may be required to measure
filling pressures, CO, vascular resistance.to optimize HF
CLINICAL FEATURES treatment.
ALPHA
ALPHA RENIN-ANGIOTENSIN
RENIN-ANGIOTENSIN
SYMPATHETIC
SYMPATHETIC ACTIVATION
ACTIVATION
ACTIVATION
ACTIVATION
BETA
BETA
SYMPATHETIC
SYMPATHETIC
ACTIVATION
ACTIVATION
(Betablockers) ALDOSTERONE:
ALDOSTERONE:
(Betablockers) (spironolactone)
(spironolactone)
Fluid retention
Fluid retention
ARTERIAL
ARTERIAL (diurteics)....... PRELOAD
VASOCONSTRICTIO (diurteics)....... PRELOAD
VASOCONSTRICTIO INCREASED!
INCREASED!
N
N (venodilators)
(venodilators)
(arterial
(arterial
INCREASES
INCREASES vasodilators)
vasodilators)
CONTRACTILITY
CONTRACTILITY
and HR ANGIOTENSIN
ANGIOTENSIN II:II:
and HR (angiotensinII receptor
(angiotensinII receptor
blockers)
blockers)
ARTERIAL
ARTERIAL
INC
INC AFTERLOAD
AFTERLOAD VASOCONSTRICTION......
VASOCONSTRICTION......
AFTERLOAD
AFTERLOAD INCREASED!
INCREASED!
Renal artery...
Renal FLUID
artery... FLUID
RETENTION
RETENTION
heart- More Work
heart- More Work PRELOAD
PRELOAD INCRESED
INCRESED
and
and oxygen
oxygen
consumption
consumption
heart-
heart- More Work
More Work
and oxygen
and oxygen
consumption
consumption
heart-
heart- More Work and
More Work and
INC
INC Myocardial
Myocardial oxygen consumption
oxygen consumption
Damage
Damage
INC Ca2+ Overload
INC Ca2+ Overload
INC
INC Myocardial
Myocardial
INC energy deficit
INC energy deficit Damage
Cardiac Damage
Cardiac INC Ca2+ Overload
INC Ca2+ Overload
Remodelling
Remodelling INC energy
INC energy deficit
deficit INC Myocardial
INC Damage
Myocardial Damage
INC Ca2+
INC Overload
Ca2+ Overload
Cardiac
Cardiac INC energy deficit
INC energy deficit
Remodelling
Remodelling Cardiac Remodelling
Cardiac Remodelling
Reduced
Reduced CO
CO
Reduced
Reduced CO
CO Reduced CO
Reduced CO
Cardiovascular compensatory mechanisms and the detrimental positive feedback effects they exert in
HF.
WORRYING SIGNS: LV failure and cardiac dysrrythmia. WORRYING SIGNS: LV failure and cardiac
Central crushing heavy chest pain, (over 20mins) dysrrythmia.
Radiating to L arm/jaw Central crushing heavy chest pain, (over
SOB, nausea, sweating, vomiting, palpitations, anxiety 20mins)
RISK Radiating to L arm/jaw
o Smoking, obesity, DM, Hypertension, cholesterol, SOB, nausea, sweating, vomiting,
family, previous IHD. palpitations, anxiety
SIGNS Typically, episodes of angina, occurring
o Same as STEMI at rest or minimal provocation, with poor
o Patients tend to be older with more co-morbidities response to GTN.
than STEMI More frequent and painful than usual.
o ST DEPRESSION, INVERTED T WAVES RISK
o CARDIOMEGALY , FAILURE (CXR) o Smoking, obesity, DM,
o ELEVATEED TROPONIN (12hrs after worst pain) Hypertension, cholesterol,
ACUTE TREATMENT (MONAC) family, previous IHD.
M: DIAMORPHINE 2.5-5mg IV SIGNS
O: OXYGEN 15l/min o ST DEPRESSION, INVERTED T
N: NITRATES: GTN: 2 puffs every 5 mins until no WAVES
pain- if still pain, give IV unless hypotensive. o Dynamic ECG changes over
A: ASPIRIN 300mg time
C: CLOPIDOGREL 300mg o Signs of previous MI?
o Troponin not elevated.
FONDAPARINUX (anticoagulate) ACUTE TREATMENT (MONAC)
Beta-blocker- Bisoprolol 10mg STAT- beware in M: DIAMORPHINE 2.5-5mg IV
COPD, hypotension, failure O: OXYGEN 15l/min
RISK STRATIFY: for ones needing bed in CCU, N: NITRATES: GTN: 2 puffs
catheterization or glycoprotein inhibotors. every 5 mins until no pain- if still
SECONDARY PROHHYLAXIS (BAN SCAR)- same as pain, give IV unless hypotensive.
STEMI A: ASPIRIN 300mg
o B: BETA BLOCKERS C: CLOPIDOGREL 300mg
o A: ACEi - PLUS! BETA-BLOCKERS to limit
o N: Nitrates (symptoms) ischemia
o S: STATIN - FONDAPARINUX (disrupt thrombus)
o C: Clopidogrel 1yr
o Same further management as
o A: aspirin lifetime
NSTEMI
o R: Risk factors (smoking, DM, obesity, BP,
cholesterol)
COMPLICATIONS- same as STEMI, but less common SECONDARY PROHHYLAXIS (BAN SCAR)-
o Dysrhythmias same as STEMI
AV Block, Bradycardia, VF/VT PERICARDITIS
LVF
Valve prolapse Pleuritic chest pain
Ventricular septal rupture Worse on laying flat and deep inspiration
Ventricular aneurysm formation Relieved by sitting forward, recent viral
Pericarditis, Dresslers syndrome (pericarditis- illness
STABLE ANGINA
SIGNS?
o May be none
Retrosternal chest discomfort occurring predictably upon o Pericardial rub
exertion ECG
Relieved by rest and nitrates. o Saddle shaped ST segments in
SYMPTOMS most leads
o Central, heavy chest pain BLOODS
o Lasting under 20mins- radiating to L.arm and jaw o
o Precipitated by exertion, relieved by rest, or GTN in High WCC
under 5 mins Inflammatory markers
o SOB, nausea, sweating, palpitations. ECHO
o Tachycardia, cool, sweaty, clammy, pallor- normal after o Pericardial Effusion
episode. TREAT
ECG o Acutely- reassurance and
o Transient ST-depression during pain anaelgesia
o Flat or inverted T-waves o Paracetamol, NSAIDS
o Signs of previous MI o Should settle 2-4 weeks
Cardiac markers not elevated!
PRIMARY PROPHYLAXIS- kind of the same.
o B: BETA BLOCKERS
o A: ACEi
o N: Nitrates (symptoms)
o S: STATIN
AORTIC DISSECTION
Aortic dissection occurs when a tear in the inner wall of the aorta causes blood to flow between the
layers of the wall of the aorta, forcing the layers apart.
Severe characteristic chest or abdominal pain- "tearing" with other symptoms from decreased blood
supply to organs.
Aortic dissection is a medical emergency and can quickly lead to death, even with optimal treatment, as
a result of decreased blood supply to other organs, cardiac failure, and sometimes rupture of the aorta.
More common: high blood pressure, known thoracic aortic aneurysm, Marfan syndrome, EhlersDanlos
syndrome.
The treatment of aortic dissection depends on the part of the aorta involved.
Surgery in dissections that involve the aortic arch, while dissections further away from the heart treated
with blood lowering BP (systolic under 100)
SYMPTOMS
o Sudden onset, severe chest pain
o Anterior or interscapular
o Tearing in nature
o Dizziness, breathlessness, sweating, neurological deficits
RISK FACTORS
o Smoking
o Obesity
o DM
o High BP
o Increased Cholesterol
o Family history
o IHD
SIGNS
o Unequal radial pulses
o Tachycardia
o Hypertension/ Hypotension
o Difference in brachial pressures of over 15mmHg
o Aortic regurg
o Pleural Effusion (left more than right)
o Neurological defects from carotid artery dissection
INVESTIGATIONS
o ECG normal/ show LV strain or ischemia.
o CXR widened mediastinum over 8cm (rare)
o Blood can track down and cause irregularity of aortic knuckle and small left pleural effusion
o ECHO: shows aortic root leak, aortic valve regurg, pericardial effusion
o Consider MRI/CT
ACUTE TREATMENT (HYPOTENSIVE? Treat as shock)
o Senior help!!!
o OXYGEN (15/min)
o CANNULA (2 large bore)
o BLOOD: X-MATCH 6units
o OPIDOIDs (anaelgesia)
TREATMENT
o Surgery: for type A (Ascending aorta)
TACHYARRYTHMIAS EMERGENCY!!! ADULT TACHYCATRDIA WITH PULSE ALGORHYTHM
Irregular
IRREGULAR, NARROW
COMPLEX TACHCARDIA
Probably AF
o Beta blocker
o Diltazem
TACHYARRYTHMIAS
TACHYARRYTHMIAS
SINUS TACHYCARDIA
Worrying Features
Decreased GCS
Dec BP (systolic under 90)
Chest Pain
HF
Causes
FAST AF
Common
o Sinus Tachycardia
o Fast ventricular rate in AF
o SVT
o Atrial Flutter
o Physiological: shock, sepsis
Uncommon
o SVT
VT
o Re-entrant tachycardia (Wolf-Parkinson)
Ask about
Onset
Associated Symptoms (chest, SOB, dizziness,
palpitations, facial flushing, headchaes)
VT (pulseless/pulse)
Previous
PMHx: Cardiac (IHD, valve lesions, HTN), Thyroid, DM
Drugs: Cradiac, Levothyroxine, salbutamol,
anticholinergics, caffeine, nicotine
Smoking, Alcohol, Drugs
Observations: UNSTABLE?
ECG:
A re-entrant tachycardia
Due to accessory conduction pathway (bundle of kent) between atria and ventricles.
SHORT P-R INTERVAL and DELTA WAVE
Avoid Digoxin and verapamil
Refer to cardiologist for ablation
WORRYING SIGNS
o HF
o Hypotension
o Decreased GCS
o Chest pain
o PULSELESS!!!!!!!!
SYMPTOMS
o SOB
o Palpitations
o Dizziness
o Chest Pains
o ARREST!!!
RISK FACTORS
o IHD
o Trauma
o Hypoxia
o Acidosis
o Long QT
COMPLICATIONS
o May deteriorate into VF or other
dysrhythmia
SIGNS
o Tachycardia
o Anxiety
o Pallor
o Hypotension
o Decreased GCS/ shock
Investigate
o ECG: Broad complex tachycardia
o Absence of p waves
o Rate over 150
o Check U&E urgent! Especially K! and
MG2+!
o Cardioversion the main priority
Acute Treatment
o Pulseless VT? Call arrest team, commence
ALS after precordial thump
o Pulse? Oxygen, large bore cannula
o Drugs: SOTALOL, AMIODARONE
o DC CARDIOVERSION
o Possible SVT with bundle branch block? Or
VF? Treat as VT
Chronic Treatment
o Implantable cardiovertor/ defib
VASOVAGAL ATTACKS
o IF SYSTOLIC OVER 200, DIASTOLIC 120 o IF SYSTOLIC OVER 200, DIASTOLIC 120
o Sit up o Sit up
o OXYGEN (15l)- if SOB/ sats under 94% o OXYGEN (15l)- if SOB/ sats under 94%
o MONITOR o MONITOR
Pulse oximiter Pulse oximiter
BP BP
Defib leads- if unwell Defib leads- if unwell
o Request full set OBS and ECG o Request full set OBS and ECG
o Bried HX / NOTES/ Ask staff o Bried HX / NOTES/ Ask staff
o Examine o Examine
RS, CVS, abdo, EYE RS, CVS, abdo, EYE
o Rule out serious causes, establish likely o Rule out serious causes, establish likely causes-
causes- is it new?? is it new??
o DO NOT GIVE STAT DOSE ANTI- o DO NOT GIVE STAT DOSE ANTI-HYPERTENSIVE
HYPERTENSIVE WITHOUT SENIOR REVIEW WITHOUT SENIOR REVIEW
o Further treatment o Further treatment
o ACCESS o ACCESS
FBC, U&E, markers, TFT, glucose, FBC, U&E, markers, TFT, glucose,
cortisol cortisol
o Consider urgent CXR o Consider urgent CXR
o Urinalysis and bHCG (if childbearing age) o Urinalysis and bHCG (if childbearing age)
o Senior advice reassess, ABC o Senior advice reassess, ABC
Everyone
o HYPERTENSIVE 160/100 (aim for 140/90)
or (150/90 if over 80)
o TYPE2 DIABETES: if end organ damage aim
for under 130/80- microalbuminuria, or eGFR
under 60, retinopathy, Hx TIA/stroke
o TYPE1 DIABETES:
o HYPERTENSIVE PATIENTS: with existing
cardiovascular disease/end-organ damage,
or predicted 10year risk CV disease over
20%
Over
Over
Under 55
Under 55 55/Black
55/Black
A C
A&C A&C
A, C, D A, C, D
CARDIAC HISTORY AND EXAMINATION
A: ACEi / Angiotensin receptor blockers (RAMIPRIL)
C: Calcium Channel Blockers (AMLODIPINE,
INSPECTION
OVERALL:
o ECG monitor suggestive? Pain? Cannula? Malar flush? (mitral stenosis), tachypnea (HF),
Cyanosis (HF), Forceful neck pulsations eg. Carotid (aortic regurg), ankle oedema (HF)
HANDS:
PALPATION
ARMS:
o Radial pulse: rate, rhythm, character
ASCULTATION
o A, P, T, M
o Roll to axilla, mital area for mitral stenosis (diastolic)
Places to Listen
Splitting of Heart sounds (LUB SPLAT): Extra sound after S2 is called P2, Normal finding in
inspiration
Loud S1 (LUUBB!dub) Mitral stenosis- narrowed valve, shuts quicker, louder sound
Soft S1 (lubDUB) Mitral regurg, valve not completely closed
Soft S2 Aortic stenosis (reduced valve movement)
Wide fixed splitting of S2 ASD
Prosthetic heart sounds Metallic clicking sound
Aortic stenosis
A bit quiteter
Heard in apex, radiates to axilla
Causes
o Rheumatic heart disease, IE, IHD, Post-MI, Cardiomyopathy, AF, Congenital
DIASTOLIC MURMURS
Aortic regurgitation
Mitral stenosis
o Mid diastolic murmur (click whoosh)
o Associated with AF
o Lay on LHS, listen to mitral area
o Caused by rheumatic fever
Aortic regurg
o Early diastolic murmur
o High pitched, starts loud and lets quitter
o Heard sitting up and forwards at L sternal edge, patient holding breath at end of expiration.
Opening snap
o Mitral stenosis
o High pitched snap after S2
Ejection click
o Aortic valve opening
o Aortic stenosis
o Heard in aortic area after 1st heart sound
Mid-systolic click
o Mitral valve prolapsing
o Halfway through systole, pressure in ventricles risen to such a level to prolapse the mitral
valve
Pericardial friction rub
o Acute pericarditis
o Scratching sound in systole or diastole
o Can vary hr to hr
o When inflamed, vicsceral and parietal pericardium rub together
o Heard sitting forwards, expiration and hold breath.
Remember
o lEEEft sided noises- heard in expiration
READING AN ECG
The ECG represents electrical activity, primarily from the L.Ventricle, as it has more muscle mass than
the RV.
The ECG therefore tells you little about the RV.
This is important as RV infarcts can occur, and can be missed if you dont request specific RHS leads.
They have a high rate of death, so important not to miss them.
Suspect RV INFARCTS in patients who are VERY HYPOTENSIVE with little in the way of ST
CHANGES in the ECG, or minor ST CHANGES in the inferior leads.
The ECG electrodes are place primarily across the anterior chest wall.
The ECG is therefore very good at detecting ischemia originating from the LAD and RCA territories, as
they supply they supply areas of the heart well covered by the ECG electrodes.
However, they may miss ischemia originating from the Circumflex artery, which is poorly represented
by ECG electrodes.
Leads 1 and AVL that look at the lateral wall of the LV may give some indication but changes are
subtle.
For this reason, posterior infarcts are missed on ECG
If you see ST DEPRESSION across V1-V3, ask for posterior leads, ST elevation in V4, V5, V5 will
become evident.
Ie. While a normal ECG in the setting of chest pain is reassuring, its NOT a definitive indication that
ischemia and infarction are absent.
If the history and context fit, then treat patients as if they do have ischemia- you can repeat the ECG
every 20mins
Remember: we often see NSTEMIS with NORMAL LOOKING ECGs.
If you were to treat fast AF that was broad with DIGOXIN or BETA-BLOCKER, you can make AF worse.
They act on AV NODE ONLY!
If you block the AVNODE in the presence of an accessory pathway, the only way the beat can get to
the ventricles is the accessory pathway.
WHAT???!??!
HEART BLOCK
The first sign to look for is a p wave, they doesnt have a QRS complex following
Then decide what type
If no impulse arrives in the ventricle, after a period of time, a ventricular escape response takes over,
and this is ALWAYS REGULAR.
Therefore, complete heart block always has a regular ventricular rhythm.
1st DEGREE
o Prolonged P-R
o Over 0.2secs
o Fibrosis of the AVN, increases risk of further block in 20% cases
o Every p wave followed by a QRS complex.
2nd DEGREE
o MOBITZ 1 (WENKEBACH)
PR progressively lengthens, until one P wave fails to conduct
The cycling of lengthening and dropping is irregular
Irregular conduction through the AV node, so ventricular rhythm irregular too.
If you look at the rhythm strip, and see the ventricular rhythm is irregular, it has to be
Wenkebach, after youve realized it must be a block because there are p waves
without a QRS.
o BOBITZ 2 (2:1)
Regular pattern to non-conducted p-waves.
P-R interval in conducted beat is always the same.
Regular conduction through the AV node.
Regular ventricular rhythem
COMPLETE HEART BLOCK
o Lack of any relationship between p and QRS
o REGULAR VENTRICULAR RHYTHM
In 2:1 block and Complete block are treated the same.- They are paced.
ECG and TERRATORIES
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
An occlusion of the LAD at the beginning (ie proximal) is a lot worse, as the territory is septal,
then also a lot of the ventricles too- so more likely to lead to HF. V1 and V2 is bad.
Occlusion distally results in a small loss of territory- so low risk of HF.
ST CHANGES
ST ELEVATION
o MI, Pericarditis, Scarring, aneurysm.
ST DEPRESSION
o Ischemia strain (LVH)
o Repolarisation abnormalities (BBB)
o Digitalis effect
T WAVE INVERSION
o Ischemia
o Repolarization abnormalities (BBB)
o Changes in posture normal.
DEFINITIONS
QUICK CHECK
RATE
RHYTHEM
AXIS
P WAVES
P-R INTERVAL
QRS COMPLEX
ST
Q-T interval
T WAVES
RATE
RHYTHEM
SINUS
o P before every QRS and at fixed interval from it.
P BEFORE EVERY QRS
P-R NORMAL
P-R CONSTANT
ATRIAL FIBRILLATION
o No P waves, irregular QRS
ATRIAL FLUTTER
o ECG shows presence of flutter waves
o Baseline adopts a saw-tooth appearance
o AV flutter may occur with a fixed degree of block (3:1 block)- ie for every 3 flutter
waves, a QRS
o May have variable block
HEART BLOCK
o 1st: prolongued P-R interval (over more than 5 small squares), constant P-R interval
o 2nd WENKE: P-R lengthens, then drops a QRS
o 2nd MOB2: P-R might be normal, but every 2 or so, theres a p with no QRS.
o 3rd p waves and QRS totally dissociated. Mark the p waves, then try to line up with
QRS
CARDIAC AXIS
P WAVES
Q WAVES
R, and S WAVES
QRS DURATION
ST SEGMENT
QT INTERVAL
T WAVE
SHOCKABLE
o VF
o VT
NON-SHOCKABLE- need to reverse the cause of the arrest, and start CPR
o PEA
o ASYSTOLE
o P wave ASYSTOLE: only p waves, can respond to cardiac pacing
ATRIAL FLUTTER
WENKEBACH
VT
VF