Transcript heart anatomy & arrhythmias

OVERVIEW OF THE HEART
ANATOMY
And
ARRHYTHMIAS
Presented by Linda and Livia
www.vancouverhearthealth.com
ANATOMY
 The size of a fist
 Weighs between 250 and 350 grams
 It has 4 chambers
Two superior chambers called Atria
Right Atrium (RA) and Left Atrium (LA)
Two inferior chambers called Ventricles
Right Ventricle (RV) and Left Ventricle (LV)
 Sulci define the boundaries of the 4 chambers
 Coronary sulcus separates the atria from the
ventricles
 Interventricular sulcus separates the left and
right ventricles
 Sulci contain major arteries and veins for heart
circulation
 The heart has 3 layers:
Pericardium – tough membranous sac that
encloses and protects the heart (outermost layer of
the heart)
A thin layer of clear pericardial fluid inside the
pericardium lubricates the external surface of the heart
as it beats
Inflammation of the pericardium - Pericarditis
Myocardium – thickest layer of the heart made of
pure muscle and it gets damaged during a heart
attack. It is responsible for contraction and
relaxation of the atria and ventricles.
Epicardium – covers the outside of the myocardium. It is
a thin layer made of connective tissue and fat.
Endocardium – innermost thin layer of tissue that
lines the heart's chambers and valves. The cardiac
conduction system is located in this layer of the
Overview of Valves and Blood Flow
Heart Chambers, Valves, and Blood
Flow
 The heart is a two pump system
The right side of the heart collects blood from the
periphery and pumps it through the lungs – called
Pulmonary circuit
The left side of the heart collects blood from the
lungs and pumps it throughout the body – called
Systemic circuit
 The left ventricle pumps the blood against the
greater resistance to the body (more
muscular)
 The right ventricle pumps the blood a relative
short distance through the pulmonary circuit
(less muscular)
Valves
 The heart has 4 valves
Atrioventricular valves:
Tricuspid valve – controls the blood flow from RA to RV
Bicuspid valve – controls the blood flow from LA to LV
These valves prevent the retrograde blood flow during ventricular
contraction
Semilunar valves:
Pulmonary valve – lies between the RV and the
pulmonary artery
Aortic valve – lies between the LV and the aorta
The cusps of the semilunar valves prevent the back-flow of blood
from the arteries to the ventricles
Blood Flow
 Venous blood flows into the RA via the
superior and inferior vena cava, coronary
sinus, and anterior cardiac veins
 The RA free wall contracts, and blood flow
moves through the tricuspid valve into the RV
 The RV free wall contracts, the tricuspid valve
closes, and blood flows through the
pulmonary valve into the pulmonary artery
and the branches of that system
 Blood ultimately reaches the alveolar
capillaries, where gas exchange occurs
 Blood flows back to the LA via the pulmonary
veins
 The LA free wall contracts, and blood flows
through the bicuspid valve and into the LV
 The LV free wall contracts, the bicuspid valve
closes, and blood flows through the aortic
valve into the aorta and its branches, where it
is distributed to the coronary circulation and
the systemic circulation
Heart Blood Supply
 Only the endocardium gets direct blood supply
 The myocardium is too thick to permit
adequate diffusion of nutrients and oxygen to
the cardiac muscle cells and epicardium
 Coronary arteries originate from the aortic
sinus at the base of the aorta
Left coronary artery (LCA)
Right coronary artery (RCA)
 LCA goes towards the left side of the heart
before branching into
Left anterior descending (LAD) coronary artery
Circumflex artery (CxA)
 The LAD artery supplies blood to the
interventricular septum and anterior walls of both
ventricles
 The CxA branches toward the left margin of the
heart in the coronary sulcus and supplies
blood to the laterodorsal walls of the LA and LV
 Both the LAD and CxA curve around the left
ventricular wall and supply small branches that
interconnect with the RCA
 The RCA supplies blood to the right side of the
heart as it follows the AV (atrio-ventricular)
groove
 It then curves to the back of the heart giving off a
posterior interventricular artery (posterior
descending artery - PDA)
 The RCA and PDA have numerous branches
that supply blood to the anterior, posterior,
and lateral surfaces of the RV and to the RA
 After circulating through the coronary artery
system and the myocardial capillaries, it is
collected by the cardiac veins
 The blood then travels a path similar to that of
the coronary arteries but in the opposite
direction
 On the posterior side of the heart, the cardiac
veins form an enlarged vessel → coronary
sinus, which empties the blood into the RA
 The smaller anterior cardiac veins also empty
directly into the RA
Conduction System of the Heart
 Cardiac muscle has intrinsic properties → no
need for neural stimulation
 Cardiac cells interconnect end to end and form
intercalated discs
these discs allow electrical impulses to spread from cell
to cell and cause the myocardium to act as a single unit
 Components of the Conduction System:
Sinoatrial node (SA node)
Atrioventricular node (AV node)
AV bundle (Bundle of His)
Right and Left bundle branches
Purkinje Fibers
 The electrical impulse starts at the SA node
(intrinsic pacemaker)
 The cells depolarize spontaneously at 60 to 80
beats per minute at rest
 Electrical activity goes rapidly to AV node via
internodal pathways through both atria
 Depolarization spreads more slowly across
atria. Conduction slows through AV node to
allow the atria to contract and fill the
ventricles
 Depolarization moves rapidly through
ventricular conducting system to the apex of
the heart
 Depolarization wave spreads upward from the
 Sympathetic nerves and hormones
(neropinephrine and epinephrine) stimulate
the atria and ventricles of the heart to beat
faster → chronotropic effect
and more forcefully → inotropic effect
 Parasympathetic nerves control the atria and
slow the heart rate
ECG changes during electrical
events in the heart
 The SA node initiates a depolarization wave at
regular intervals in the atria which is
represented by a P wave on an ECG
 The P wave represents both depolarization and
contraction of atria
 When the wave of atrial depolarization enters
the AV node, depolarization slows producing a
brief pause – time it takes for the blood to
enter the ventricles
 Depolarization conducts rapidly through the
Bundle of His and its subdivisions and into
Purkinje fibers
 Depolarization of the ventricular myocardium
records as a QRX complex
 The horizontal segment of baseline that follows
the QRS complex is the ST segment
 ST segment is horizontal, flat, and most
importantly, it is normally level with other
areas of the baseline
 If the ST segment is elevated or depressed
beyond the normal baseline level, this is
usually a sign of serious pathology that may
indicate imminent problems
 ST segment represents the initial phase of
ventricular repolarization
 The final T wave represents the final “rapid”
phase of ventricular repolarization
What Is Arrhythmia?
 Abnormal
rhythm of the heart
 It
can feel like a temporary pause and be so
brief that it doesn't change your overall heart
rate
 Or
it can cause the heart rate to be too slow or
too fast
What are the signs of Arrhythmia?

If brief it can have almost no symptoms → it can feel
like a skipped heart beat that you barely notice

Or it can feel like a fluttering in the chest or neck

If it lasts long enough the heart may not be able to
pump enough blood to the body → it can cause
tiredness and light-headedness, or the person may
pass out

Tachycardia can lead to decreased cardiac out (heart
is not able to pump blood effectively) → can lead to
shortness of breath, chest pain, light-headedness or
loss of consciousness. In severe cases it can cause
heart attack and death.
Different Types of Arrhythmias
 Pacemaker of the heart → SA node → initiates
depolarization of the myocardium
Beats at its own inherent rate of 60 bpm to 100 bpm
 Bradycardia → slow heart rate < 60 bpm
Common in athletes → ↑ stroke volume, ↓ heart
rate
Increased vagal stimulation → release of hormones
that slow down the heart rate
Patients who receive drugs to slow down the heart
rate
Individuals who have disease of the sinus node
Symptoms: tiredness, dizziness, light-headedness
or fainting
Treatment: electronic pacemaker
 Types of Bradycardias:
Sick Sinus Syndrome:
“malfunction” in the SA node → it fires too slowly due to
increasing age or disease
some medications can slow your heartbeat
Solution:
treatment with medication or with an electronic pacemaker
 Heart Block:
Interruption of the electrical signal to the lower chambers
of the heart
It may develop as a side effect of certain heart
medications
It may be idiopathic in nature
Or may be due to other forms of circulatory diseases:
coronary artery disease
cardiomyopathy
rheumatic heart disease
uncontrolled or untreated high blood pressure
primary conduction system disease
Complete AV block (3rd degree block) is usually due to a
complication of a heart attack, but may the result of a
heart surgery or infections of the heart muscle
 Symptoms:
Llight-headedness, fatigue, or fainting
Diagnosis:
By ECG
Treatment:
Implanting an electronic pacemaker
 Tachycardia → fast heart rate → > 100 bpm
Causes:
stimulation of the heart by sympathetic nerves
increased body temperature
or toxic conditions of the heart
Factors that affect SNS stimulation of the heart:
blood loss that results in a shock or semishock
weakening of the myocardium
 Supraventricular Tachycardia (above the
ventricle)
rapid heartbeat in the atria or AV node
Atrial flutter
Atrial fibrilation
Paroxysmal supraventricular tachycardia
Wolf-Parkinson-White Syndrome
 Atrial Flutter → 250 to 350 atrial depolarization
per minute
Due to back-to-back identical atrial depolarization
waves
Usually not life threatening
Can cause chest pain, faintness, or others more
serious problems
 Atrial Fibrillation → multiple foci discharge
rapidly at 350-450/min
Very common dysrhythmia
Results in ↓ cardiac output
Usually not life threatening
Causes light-headedness or palpitations
It increases the risk of stroke
 Symptoms of Atrial fibrillation:
Irregular and fast heart beat
Heart palpitations and rapid thumping in the chest
Chest discomfort, chest pain or pressure
Shortness of breath, particularly with exertion or
anxiety
Fatigue
Dizziness, sweating, or nausea
Light-headedness or fainting
 Causes of Atrial fibrillation:
In most cases idiopathic in nature
Age
High blood pressure
Infection or inflammation of the heart
Valvular heart disease
Ischemic heart disease
Cardiomyopathy
Conduction system disease
Overactive thyroid
Pulmonary embolism
Hypoxia
Holiday heart syndrome
 Treatment of Atrial fibrillation
Blood thinners to decrease the risk of stroke
Rhythm control therapy:
medication to prevent atrial fibrillation from occurring
electrical cardioversion
ablation
maze procedure
Rate control therapy:
medication to slow down the heart rate:
Digitalis
Calcium channel blockers (diltiazem and verapamil)
Beta-blockers
 Treatment of Atrial fibrillation
Blood thinners to decrease the risk of stroke
Rhythm control therapy:
medication to prevent atrial fibrillation from occurring
electrical cardioversion
ablation
maze procedure
Rate control therapy:
medication to slow down the heart rate:
Digitalis
Calcium channel blockers (diltiazem and verapamil)
Beta-blockers
 Paroxysmal supraventricular tachycardia →
140-250/minute
Involves atria or AV node
Usually occurs in young, healthy people
May be distressing and can cause weakness during
the paroxysm
Rarely life threatening
 Can occur with digitalis toxicity and WolfParkinson-White Syndrome
 The following increases your chance for PSVT:
Alcohol use
Caffeine use
Illicit drug use
Smoking

Symptoms:
Anxiety
Chest tightness
Palpitations and rapid pulse
Shortness of breath
Dizziness and fainting
 Treatment:
Valsalva maneuver
Cough while sitting with your upper body bent
forward
Splashing ice water on face
Ablation
Cardioversion
Medications
Pacemaker
Wolf-Parkinson-White syndrome
Ventricular Arrhythmias
 Premature Ventricular Contractions
 Ventricular Tachycardia
 Ventricular Fibrillation
 Long QT syndrome
 Premature ventricular contractions → a site in
the ventricle fires before the next wave of
depolarization from the sinus node reaches
the ventricle
These are bizarre looking complexes
Relatively benign → often occurs in healthy hearts
during rest and exercise → occasional PVC's
Causes: cigarettes, excessive coffee intake, lack of
sleep, various mild toxic states, and emotional
irritability
Many PVC's may be markers of underlying cardiac
disease such as infarcted or ischemic areas of
the heart and can develop into lethal ventricular
fibrillation
 Ventricular tachycardia → three or more
consecutive ventricular beats at 100 bpm or
faster
Non-sustained ventricular tachycardia lasts less
than 30 seconds
Sustained ventricular tachycardia lasts more than
30 seconds
Wide QRS complex, AV dissociation
A serious condition → occurs due to considerable
ischemic damage that is present in the ventricles
→ initiates the lethal condition of ventricular
fibrillation
Treatment: ICD, ablation, medications - quinidine
 Ventricular fibrillation → 250-350/minute
Serious of all cardiac arrhythmias
If not stopped within 1 to 3 minutes it is fatal
It's not a coordinate contraction of all the ventricular
muscle at once
The ventricular chambers neither enlarge nor
contract but remain in an indeterminate stage of
partial contraction → loss of consciousness
within 4 to 5 seconds due to lack of blood flow to
the brain
 Causes:
Sudden electrical shock of the heart
Ischemia of the heart muscle
 Treatment:
CPR
Defibrillation
 Long QT syndrome
Normal QT interval is less than half of the R-to-R
interval at normal rates
Usually hereditary due to mutations of sodium or
potassium channel genes
Acquired forms include hypomagnesemia,
hypokalemia, or hypocalcemia, or excess
amounts of antiarrhythmic drugs such as
quinidine or some antibiotics
Symptoms:
no major symptoms present
fainting and ventricular arrhythmias due to
exercise, intense emotions, or when startled by a noise
Treatment:
magnesium sulfate for acute LQTS
beta blockers, or ICD for long term LQTS
Long QT syndrome
Delayed repolarization of ventricular muscle can lead to ventricular
arrhythmia called Torsades de pointes → if unresolved, it can lead
to a deadly arrhythmia
What to do if you think you have
an undiagnosed Arrhythmia?
 Check
your heart rate and blood pressure on
regular basis
 Check
your family history
 Screening
→ looking for disease before there
are symptoms
 Seek
medical help → your family doctor
 Your
doctor will review your medical history
including a physical exam
 He/she
may send you for further testing
including:
An electrocardiogram (ECG)
Exercise electrocardiogram (Stress test)
Holter monitor
How is Arrhythmia Treated?
 Life-style
changes
Avoiding stress, cutting out alcohol and caffeine,
eating healthy diet, being more physically active
 Medications
Digitalis/digoxin, beta blockers, calcium channel
blockers
 Surgery
or other non-surgical techniques
Ablation
Cardioversion therapy
Implantable pacemaker
Ventricular resection or remodeling
THE END