cardiovascular physiology and monitoring tariq alzahrani m.d assistant professor college of medicine...
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Cardiovascular Physiology and Monitoring Tariq Alzahrani M.DAssistant Professor College of Medicine King Saud University
Coronary Circulation Blood Supply RCA LCA
Conduction System SAN AVN
Coronary Perfusion Pressure (50-120mmHg)
ADBP – LVEDP
Cardiac Cell Types• Electrical cells Generate and conduct impulses rapidly• SA and AV nodes• Nodal pathways• No contractile properties
• Muscle (myocardial) cells Main function is contraction• Atrial muscle• Ventricular muscle• Able to conduct electrical impulses• May generate its own impulses with certain types of stimuli
PURKINJE FIBERS
BUNDLEBRANCHES
Sino-atrial(SA) node
Atrio-ventricular (AV) node
INTERCALATED DISC (TIGHT JUNCTION)
Nerve impulse Terminology• Resting state The relative electrical charges found on each
side of the membrane at rest • Net positive charge on the outside • Net negative charge on the inside
• Action PotentialChange in the electrical charge caused bystimulation of a neuron
Action Potential Terms• DepolarizationThe sudden reversal of electrical chargesacross the neuron membrane, causing thetransmission of an impulse• Minimum voltage must be met in order to do this
• Repolarization Return of electrical charges to their originalresting state
Automaticity (P Cells)• Prepotential, Resting Potential,
Diastolic Depolarization• Action Potential• Repolarization
Factors That Affect Automaticity:Sympathetic and parasympathetic outflow will affect the prepotential phaseTemperatureRA and SAN stretchHormonesDrugs
Distribution Of P Cells
Conduction SpeedA-V nodal conduction:One way conductionA-V nodal Delay (0.1 sec)
Factors Affecting Conductivity:Sympathetic and vagal infuinceTemperatureHormonsIschemiaAcidosisDrugs
MEM
BRAN
E P
OTE
NTI
AL (m
V)
-90
0
0
12
3
4
TIME
PHASE0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot (outward K+ current)
2 = Plateau (inward Ca++ current)
3 = Repolarization (outward K+ current)
4 = Resting Potential
Mechanical Response
(outward K+ current)(inward Na+ current)
MEM
BRAN
E P
OTE
NTI
AL (m
V) 0 0
-50 -50
-100 -100
SANVENTRICULULARCELL
ACTION POTENTIALS
0
12
3
4
4
0 3
Cardiac MyocyteStructureCa++ ReleaseExcitation-Contraction
Coupling
The Fibrous A-V Ring
THE ANATOMY OF BLOOD VESSELS
• Layers:1. Tunica interna (intima)
2. Tunica media
3. Tunica externa (adventitia)
Comparison of Veins and Arteries
Arteries: Veins:
The Distribution of Blood
Cardiac Output CO = SV x HR• The amount of blood ejected from theventricle in one minute• Stroke volume Amount of blood ejected from the ventricle inone contraction• Heart rateThe # of cardiac cycles in one minute
Determination of Stroke Volume• Preload Amount of blood delivered to the chamber Depend upon venous return to the heart Also dependent upon the amount of blood delivered to the
ventricle by the atrium• Contractility The efficiency and strength of contraction Frank Starling’s Law• Afterload Resistance to forward blood flow by the vessel walls
• End-diastolic volume (110-120 mL)• End-systolic volume (40-50 mL)• Stroke volume (70 mL)• Ejection fraction (60%)
Pressure-Volume Loops
Volume Load ►
Pressure Load ►
Regulation of Cardiovascular System
• Neural Mechanisms–Vasoconstriction
–Vaosdilation
–Baroreceptors
–Chemoreceptors
Nerve Supply of the Conduction System
SANReceives right vagal and right sympathetic supply
AVNReceives left vagal and left sympathetic supply
The rest of the conduction system receive sympathetic supply (like ventricle)
HORMONAL REGULATION
• Epinephrine & Norepinephrine– From the adrenal medulla
• Renin-angiotensin-aldosterone– Renin from the kidney– Angiotensin, a plasma protein– Aldosterone from the adrenal cortex
• Vasopressin (Antidiuretic Hormone-ADH) _ ADH from the posterior pituitary• ANP from RA
BP (Kidney) Renin
Angiotensinogen (renin substrate)
Angiotensin
Aldosterone
Kidney
sodium & water retention
Vasoconstriction
Venoconstriction
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
HypothalamicOsmoreceptors
BP via Posterior Pituitary Vasopressin (ADH)
Vasoconstriction WaterVenoconstriction Retention
VASOPRESSIN(ANTIDIURETIC HORMONE)
How To interpret ECG?
1. Rate?
2. QRS Duration?
3. Stability?
ECG limb leads
Normal ECG
• P wave corresponds to depolarization of SA node
• QRS complex corresponds to ventricular Depolarization
• T wave corresponds to ventricular repolarization
• Atrial repolarization record is masked by the larger QRS complex
Measurements
Small square = 0.04 sec.
Large square = 5 small square = 0.2 sec.
One second = 5 large square.
One minute = 300 large square.
P duration = 3 small sqs = 0.12 sec.
P height = 3 small sqs = 0.12 sec.
QRS duration=3 small sq=0.12 sec.
P-R interval = 5 small sq = 0.2 sec.
Remember This 3, 3, 3 and 5
Right ventricular hypertrophy (precordial leads)
Left ventricular hypertrophy (precordial leads)
QRS voltage decrease
• Myocardial infarction (decrease of excitable myocardium mass)• Fluids in the pericardium (short-circuits of currents within pericardium)• Pulmonary emphysema (excessive quantities of air in the lungs)
J-point:
ST-segment shift –sign of current ofinjury
-Time point of completeddepolarization (zero reference)-The junction of the QRS and the ST segment
Injury currents: constant source
• Mechanical trauma• Infectious process• Ischemia
• Ischemia= ST depression or T-wave inversion Represents lack of oxygen to myocardial tissue
• Injury = ST elevation -- represents prolonged ischemia; significant when > 1 mm above the baseline of the segment in two or more leads
• Infarct = Q wave — represented by first negative deflection after P wave; must be pathological to indicate MI
What part of the heart is affected ?II, III, aVF =
Inferior Wall
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Which part of the heart is affected ?
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
• Leads V1, V2, V3, and V4 =
Anterior Wall MI
What part of the heart is affected ?
I, aVL, V5 and V6 Lateral wall of left
ventricle
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
• I, aVL, V5 + V6 = Lateral Wall = Circumflex Artery Blockage
RateIf regular: Divide 300/ number of large squares between 2 Rs = HR
If irregular: count number of complexes in 6 sec. and multiply by 10
- Normal 60 -100
- Bradycardia < 60
- Tachycardia > 100
P = Sinus
No P = Non sinus
Rate > 100.
QRS: Narrow.
Stable or unstable.
Rate < 60.
QRS: Narrow.
Stable or unstable.
Sinus tachycardia.
PSVT.
Atrial flutter.
Atrial fibrillations.
Sinus bradycardia.
1st degree HB.
2nd degree HB.
Complete HB.
Supraventricular Rhythm
Supraventricular Rhythm: Tachycardia
Sinus Tachycardia
Paroxysmal SVT
Supraventricular Rhythm: Tachycardia
Atrial Flutter
Supraventricular Rhythm: Tachycardia
Atrial Fibrillations
Supraventricular Rhythm: Tachycardia
Supraventricular Rhythm: Bradycardia
Sinus Bradycardia
Normal Sinus Rhythm
Supraventricular Rhythm: Bradycardia
1st Degree HB
Supraventricular Rhythm: Bradycardia
2nd Degree HB: Mobitz 1 Wenckebach.
Progressive lengthening of the P-R interval with intermittent dropped beat.
Supraventricular Rhythm: Bradycardia
Sudden drop of QRS without prior P-R changes
2nd Degree HB: Mobitz 2
Supraventricular Rhythm: Bradycardia
3rd Degree HB
The right bundle brunch block (precordial leads)
Left bundle branch block (precordial leads)
Characteristics of PVCs• QRS prolongation due to slower conduction in
the muscle fibers• QRS high amplitude due to lack of synchrony of excitation of RV and LV which causes partial neutralization of their contribution to the ECG• QRS and T-wave have opposite polarities, again
due to slow conduction which causes repolarization to follow depolarization.
Ventricular Rhythm
Idioventricular Rhythm.
Ventricular Rhythm
Accelerated Idioventricular Rhythm.
Ventricular Rhythm
Ventricular Rhythm
Pacer Rhythm
Ventricular Rhythm
Stability
* Stable patient: think of drug therapy.
* Unstable patient: think of electric therapy.
Treatment
Supraventricular Rhythm:
Stable = Drugs
Adenosine.
B blocker.
Ca channel blocker.
Digoxin.
Unstable = Electric
DC, Synchronized
Treatment
Ventricular Rhythm:
Stable = Drugs
Amiodarone.
Lidocaine.
Procainamide.
Unstable = Electric
DC, Non Synchronized
Normal Venous Tracing
a ► Atrial Contraction
c ► Isometric (V) Contraction
x ► Mid-Systole
v ► Venous Filling (Atrial)
y ► Rapid Filling (Ventricular)
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