\

Approximated by EDV
Depends on : blood volume and venous tone .
Vasodilators decreases preload .
?????
Myocardial action potential
 Phase 0
rapid upstroke and depolarization
voltage-gated Na+ channels open.
 Phase 1
initial repolarizationinactivation of voltage-
gated Na+ channels.
Voltage-gated K+ channels begin to open.
 Phase 2
plateauCa2+ influx through voltage-gated
Ca2+
channels balances K+ efflux.
Ca2+ influx triggers Ca2+ release from
sarcoplasmic reticulum and myocyte
contraction.
 Phase 3
rapid repolarizationmassive K+ efflux due to
opening of voltage-gated slow K+ channels
and closure of voltage-gated Ca2+ channels.
 Phase 4
resting potentialhigh K+ permeability
through K+ channels.
 In contrast to skeletal muscle:

Cardiac muscle action potential has a plateau, which is

due to Ca2+ influx and K+ efflux.

Cardiac muscle contraction requires Ca2+ influx from

ECF to induce Ca2+ release from sarcoplasmic
reticulum (Ca
2+-induced Ca2+ release).

Cardiac myocytes are electrically coupled to each other

by gap junctions.
 Pacemake action potential
Occurs in the SA and AV nodes.
 Phase4
slow spontaneous diastolic depolarization due to If (funny
current).
If channels responsible for a slow, mixed Na+/K+ inward
current; different from I
Na+ in phase 0 of ventricular action potential.
Accounts for automaticity of SA and AV nodes.
The slope of phase 4 in the SA node determines HR.
ACh/adenosine the rate of diastolic depolarization and HR,
while catecholamines
depolarization and HR.
Sympathetic stimulation the chance that If channels are open
and thus HR.
 Phase0
upstrokeopening of voltage-gated Ca2+
channels.
Fast voltage-gated Na+ channels are
permanently inactivated because of the less
negative resting potential of these cells.
Results in a slow conduction velocity that is
used by the AV node to prolong transmission
from the atria to ventricles
 Phase1,2
absent
 Phase3
inactivation of the Ca2+ channels and
activation of K+ channels >K+ efflux.
 AV nodelocated in posteroinferior part of
interatrial septum.
Blood supply usually from RCA.
100-msec delay allows time for ventricular
filling.
 Pacemaker ratesSA > AV > bundle of His/
Purkinje/ventricles
 Speed of conductionPurkinje > atria >
ventricles > AV node.
 P waveatrial depolarization.
Atrial repolarization is masked by QRS complex.

PR intervaltime from start of atrial depolarization to start of

ventricular depolarization (normally < 200 msec).
QRS complexventricular depolarization (normally < 120 msec).
QT intervalventricular depolarization, mechanical contraction of
the ventricles, ventricular repolarization.
T waveventricular repolarization.
J pointjunction between end of QRS complex
and start of ST segment.
ST seg mentisoelectric, ventricles depolarized.
U waveprominent in hypokalemia, bradycardia
 ECG abnormalities
Ventricular vs Atrial
Atrial fibrillation
Atrial Flutter
Ventricular tachycardia
Ventricular Fibrillation
1st degree heart block
 2nd degree block mobitz type 1
Progressive lengthening of PR interval until a
beat is dropped (a P wave not followed by a
QRS complex)
Variable RR interval with a pattern (regularly
irregular).
2nd degree heart block - Mobitz type II
May progress to 3rd-degree block.
Often treated with pacemaker.
 3rd degree
(complete)
Atrial rate > ventricular rate
 Brugada syndrome
Autosomal dominant disorder most common
in Asian males.
ECG pattern of pseudo-right bundle branch
block and ST elevations in V1-V3.
risk of ventricular tachyarrhythmias and SCD.
Prevent SCD with implantable cardioverter-
defibrillator (ICD)
brugada
RBBB
 Wolff-Parkinson-White
syndrome
Most common type of ventricular pre-excitation
syndrome.
Abnormal fast accessory conduction pathway
from atria to ventricle (bundle of Kent) bypasses
the rate-slowing AV node .
ventricles begin to partially depolarize earlier
characteristic delta wave with widened QRS
complex and shortened PR interval on ECG.
May result in reentry circuit supraventricular
tachycardia.
 Atrial natriuretic
peptide
Released from atrial myocytes in response to
blood volume and atrial pressure.
Acts via cGMP.
Causes vasodilation and Na+ reabsorption at
the renal collecting tubule.
Dilates afferent renal arterioles and constricts
efferent arterioles, promoting diuresis .
contributes to aldosterone escape
mechanism.
 B-type (brain)
natriuretic peptide
Released from ventricular myocytes in
response to tension.
Similar physiologic action to ANP, with longer
half-life.
BNP blood test used for diagnosing HF (very
good negative predictive value).
Available in recombinant form (nesiritide) for
treatment of HF.
Baroreceptors and chemoreceptors
Receptors:
1. Aortic arch transmits via vagus nerve to
solitary nucleus of medulla (responds
changes in BP).

2. Carotid sinus (dilated region at carotid

bifurcation) transmits via glossopharyngeal
nerve to solitary nucleus of medulla (responds
to changes in BP).
 Baroreceptors
Hypotensiondecrease in arterial pressure decrease
in stretching decrease afferent
baroreceptor firing increase efferent sympathetic firing and
decrease efferent parasympathetic stimulation .
1. vasoconstriction
2. increase in HR
3. Increase in contractility
Increase in BP
Cardiac pressure
 PCWP ( UP TO 12 )
Pulmonary capillary wedge pressure (PCWP; in
mm Hg) is a good approximation of left atrial
pressure.
In mitral stenosis, PCWP > LV end diastolic
pressure.
OTHER USES???
Autoregulation