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Lesson outcomes

Cardiac 1. Describe the Mechanical events


Cycle: occurring during a Cardiac cycle
2. Discuss the Pressure and Volume
Heart as a changes in various Cardiac
chambers
pump 3. Discuss the determinants of
cardiac output, stroke volume,
heart rate and venous return
Conduction System
SA Node- Pacemaker
AV Node- Delay
Purkinje Fibers

Atria contract before Ventricles… This


allows atria to work as “primer pumps”
allowing ventricles to fill adequately
before pumping the blood out
The Heart Valves
Only allow one-way traffic

1. Atrioventricular valves (Atria  Ventricles)


• Left: Mitral
• Right: Tricuspid
2. Semilunar valves: (Ventricles 
Aorta/Pulmonary Artery)
• Left: Aortic
• Right: Pulmonary
Cardiac Cycle
Cardiac Cycle: The events that occur Sequence of one
from the beginning of one heartbeat to the diastole (relaxation)
beginning of the next followed by one systole
• Initiated by : spontaneous generation of (contraction)
an action potential in the sinus node
(SA node), the action potential travels • Atrial cycle
from here rapidly through both atria • Ventricular cycle
and then through the A-V bundle into
the ventricles 1 Cardiac Cycle
= 1 Heartbeat
• There is a delay of 0.1 second during
passage of the cardiac impulse from the Heart rate =75
atria into the ventricles beats/min

• This allows the atria to contract ahead Duration of each


of ventricular contraction, thereby cardiac cycle?
pumping blood into the ventricles 60 sec/75 = 0.8 sec
Ventricular Ventricular
filling ejection
Duration of Cardiac Cycle
Duration decreases with increasing heartHeart
rate…rate too high CO
HR 60/min = 60s/60 = 1.0 s drop because hear
HR 100/min = 60s/100 = 0.6 s cannot filled with blood
HR 200/min = 60s/200 = 0.3 s
Cardiac Cycle is shortened at the expense of diastolic period
This means that the heart beating at a very fast rate does not
remain relaxed long enough to allow complete filling of the
cardiac chambers before the next contraction
Pressure and
Volume events
during cardiac
cycle
Left
side

Pressur
e
change
s

Volume
changes
• Arterial START Cardiac Cycle
pulse and Events
pressure 1. Electrical events
• Venous – ECG
pulse and 2. Mechanical
pressure events – Systole
•(usually
Valve very
closure  and diastole
low) 3. Hemodynamic
Turbulence 
Heart sound events
• Pressure
• Valve changes 
opening  Flow changes:
usually silent
Diastole SA Systole
node
fires
1 2 3 4 1 2
Atrial Isovol. Ventr.
Isovol. Ventr. Relax. Rapid Filling Slow Filling Ventr. Ejection
Diastasis Systole Contr.
Atrial Systole
1. Rise in atrial pressure
2. “a” wave of venous pulse (due to atrial contraction,
backpressure go back to jugular vein)
3. Incr. blood flow to ventricle
4. Rise in intraventricular volume (30% of ventricular
filling)
Isovolumetric Ventricular Contraction
1. Rapid increase in intraventricular pressure
(without a change in ventricular volume because
all valves are closed)
2. Intraventricular pressure exceeds atrial pressure
 Closure of the A-V Valve  First heart sound
(S1) Ventricular Ejection
1. Ejection begins when the intraventricular
pressures exceed the pressures within the aorta
and pulmonary artery, which causes the aortic
and pulmonic valves to open
2. Blood continues to flow into the atria from their
respective venous inflow tracts and the atrial
Isovolumetric Ventricular Relax
1. Intraventricular pressures fall sufficiently, the aortic and
pulmonic valves abruptly close causing the second
heart sound (S2)
2. Ventricular volumes remain constant because all valves
are closed
3. Atrial pressures continue to rise because of venous
return Rapid Filling
1. Ventricular pressures fall below their respective atrial
pressures  the AV valves open and ventricular filling
begins
2. This causes a rapid fall in Atrial Pressure
3. Ventricular filling is normally silent (When a third heart
sound (S3) is audible, it may represent tensing of
chordae tendineae and AV ring during ventricular
relaxation and filling) Slow Filling
1. Ventricles continue to fill with blood and expand, the
intraventricular pressures rise. This reduces the
pressure gradient across the AV valves so that the rate of
filling falls
2. In normal, resting hearts, the ventricle is about 70-90%
Pressure Changes
in left side of the
heart

Pressure Changes
in right side of the
heart
S1 : heart at beginning of
In Summary… atrial systole
S2: aortic & pulmonary valve
close (beginning of diastole)
Between s2 & s1: diastole
* Check carotid pulse
Arterial pulse
Pressure
wave changes in
Aorta are
transmitted
down the
arteries

Pressure changes in Right


Atrium are reflected in the
Jugular Vein, giving rise to
central venous pulse
Cardiac Output and its Regulation
Cardiac Output
The amount of blood pumped
Stroke Volume
per minute
Cardiac Output = HR x SV 80

*Left and Right side are the


SAME
Average HR is 70/min 120 40
Average SV is 80 ml
Cardiac Output = 70 x 80
Cardiac Output = 5.6 L/min
Transplant heart: resting Heart rate = 100
Normal : 70 EDV =120 ml ESV =40 ml
Normal: Constant parasympathetic influence
on SAN

When exercise? EDV-ESV=120-40 = 80 ml


Circulating epinehrine can still increase HR
Heart Rate - determined by:
Autonomic 1. Sympathetic : Increased HR
Nervous System 2. Parasympathetic : Decreased HR
Hormones and 1. Circulating catecholamine: Increased HR
Ions 2. Thyroid hormones: Increased HR
3. ↓ Potassium (K+) : Increased HR
Physical Factors 1. Age
2. Exercise
3. Temperature (Fever)

Chronotrophy: Heart Rate


(parasym & sym effect almost same)
Inotrophy: Force of Contraction
(sympathetic more effect)
Dromotrophy:conduction speed at
AV Node
Lusitrophy: how quicky the heart
muscle econtract
Stroke Volume- determined by
Preload
“Stroke Volume”Increased preload (venous
determined by: return) will
(Increase,increase increase stroke volume (Frank-Starling law
) of the heart)
Afterload Elevated afterload (the aortic pressure during
(Increase,Decrease) systole) reduces stroke volume
Ventricular Factors increasing ventricular contractility
Contractality (inotropy) increase stroke volume
Regular Exercise Regular exercise training increases stroke
Venous Return volume Frank Starling Law
Determined By: “The stroke volume increases in response to an
1) Blood Volume increase in the end diastolic volume when all other
2) Venous Tone factors remain constant”
3) Resp. Pump
4) Muscle Pump How?
The increased volume of blood stretches the
ventricular wall, causing cardiac muscle to
In Summary…
Cardiac Cycle as Pressure-Volume
Loop

Left ventricular pressure-


volume (PV) loops are
derived from pressure and
volume information found in
the cardiac cycle diagram.
 Inotropy  Compliance
(Systolic (Diastolic
dysfunction)
Shift to right dysfunction)
Shift to left & up

100 100
Pressure

Pressure
(mmHg)

(mmHg)
50 50

0 0
0 50 100 150 0 50 100 150

Volume (ml) Volume (ml)

ESV ESV EDV ESV EDV EDV

Stroke Volume? Stroke Volume?

e.g., ventricular failure e.g., ventricular


hypertrophy
Ejection Fraction
(EF)

• Fraction of blood ejected from a ventricle with each


contraction
Echocardiograph
How to calculate?
y
• SV/EDV = 80/125 = 0.64 (or 64%)
Ejection
Pumping Ability of the
Fraction (EF) Level of Heart Failure
Heart
%
55% to 70% Normal -
40% to 54% Slightly below normal Usually sub-clinical
35% to 39% Moderately below normal Mild heart failure
Moderate-to-severe Heart
<35% Severely below normal
failure
Question
At which stage of cardiac cycle,
ventricular pressure is the highest?
• Isovolumic relaxation
• Isovolumic contraction
• Ventricular ejection
• Rapid filling

A 40-year old woman A 57-year old man


suffers from light- complains of an irregular
headedness and heartbeat. An ECG reveals
recurrent syncope. In atrial fibrillation. Which of
emergency ward, she is the following is most likely
given atropine. How to accompany this
atropine will relieve her condition?
symptoms?
• Increased venous A wave
• Increased heart rate
• Increased left atrial
• Increased force of pressure
contraction
• Decreased heart rate
• Increased stroke
volume • Increased stroke volume
• Increased PR interval