Physiology DES

Biruk A. (balemaye@sgu.edu) & Sami Ahmed. (sahmed10@sgu.edu)

• Blood vessels to each organ are arranged in parallel which means that each
organ receives its blood simultaneously

• Amount of blood received related to metabolic needs  except Kidneys (gets

20% uses 6%. The large amount of the blood is required in order to filter out
waste (urea, excess Na+, etc.)
Important Facts

– The lung receives 100% CO from the RV

– Heart receives more O2 but less blood because it has a high O2 extraction

• Exceptions to parallel arrangement of blood flow (portal system):

– Liver – has direct arterial supply via the hepatic artery but 70% of its blood
supply comes from the hepatic portal vein, which is venous blood drained from
the gut and spleen
– Kidney – afferent arterioles supply the glomeruli and efferent arterioles carry
venous blood from the glomeruli; these efferent arterioles then supply O2 and
nutrients to the kidney tubules
– Brain – a portal system exists between the hypothalamus and the pituitary
gland which function to transport hypothalamic hormones to the pituitary

• Bronchi gets O2 blood but dumps deoxygenated blood back into the pulmonary
veins; this will decrease the partial pressure in the pulmonary veins
 The resting membrane
potential is unstable
and fluctuates between
-60 and -40 mV;
known as the
pacemaker potential
or the slow diastolic
potential

Action potential:
Phase 4 –
Inward If current is due to Na current; these channels open when the inside is
relatively negative (Normally Na opens to response to a depolarization of
the cell)
Inward Ica current is due to opening of the T-type Ca channels (T because
they open transiently); these open when the pacemaker potential becomes less
negative (ie they open in response to a depolarization and contribute to the
depolarization)

If channels open – inwared Na current – depolarization – open t-type Ca

channels – Ica – more depolarization
Phase 0 –
If channels start to close
When the membrane reaches -40mV, L-type Ca channels open and Ca
enters causing the upstroke of the action potential (depolarization
causes Ca to come in, not Na like in other tissues)

Phase 3 –
As Ca channels start closing, the K channels start opening
As membrane becomes repolarized the if channels start to open again
When fully opened, the membrane starts to spontaneously depolarize
again
Important Points

• HR is set by the fastest pacemaker – the SA node.

• However, the major innervation of the heart (PSNS – Vagus nerve) keeps it at lower rate

• AV node is the connection between the atria and the ventricles (but conduction is slow)
This delay allows time for the atria to complete their contraction before the ventricles are
stimulated to contract
– Delay allows time for the atria to completely contract and complete its filling
of the ventricles before they contract

– Delay is due to slow rate of rise of the AV action potential and higher electrical
resistance between cells (less gap junctions)

– Advantages: if the atria develop an abnormally fast rhythm due to disease, many
of the atrial depolarizations reaching the AV node will find the AV in refractory
(protects the ventricles)
Normal HR  60-100 bpm
> 100 bpm = Tachycardia
< 60 bpm = Bradycardia
Did you forget about
action potentials?

1 70 bpm

2 100 bpm

3
60 bpm

4 120 bpm

5 150 bpm
Did you forget about
action potentials?

1 70
70bpm
bpm

2 100 bpm

3
60 bpm

4 120 bpm

5 150 bpm
 QRS wide > 120ms (0.12s)

Tip: Whenever QRS

>120ms therefore the
problem is in the
ventricles

<120ms look at the atria

Impulse spreads slowly through the ventricles from one myocyte to the
next (through gap junctions) because the conducting system is not
working

QRS complex is widened and there is no coordinated spread of APs

Contractions of the heart are weaker

A block in both bundles will lead to a 3rd degree block

Did you forget about
action potentials?

1 Mobitz type I

2 Atrial Fibrillation

3
Ventricle Fibrillation

4 Mobitz type II

5 3rd degree AV block

Did you forget about
action potentials?

1 Mobitz type I

2 Atrialfibrillation
Atrial Fibrillation

3
Ventricle Fibrillation

4 Mobitz type II

5 3rd degree AV block

Classic Q

1 Mobitz type I

2 Atrial Fibrillation

3
Ventricle Fibrillation

4 Mobitz type II

5 3rd degree AV block

Classic Q

1 Mobitz type
Mobitz type II

2 Atrial Fibrillation

3
Ventricle Fibrillation

4 Mobitz type II

5 3rd degree AV block

LV >> aortic pressure during
Systole

The LV has to contract harder

to pump blood through the
narrow valve

Crescendo-decrescendo
systolic ejection murmur.
Pumping the blood out is
normal but due to the valve
insufficiency, blood pools back
into the ventricle so the aortic
pressure drops (seen in
diastole)

Early diastolic decrescendo

murmur
During diastole atria has to
pump blood through the narrow
mitral/bicuspid valve

LA pressure >> LV diastole

pressure

Late diastolic decrescendo

murmur
During systole when the LV
contract, some of the blood will
enter the LA due to mitral valve
insufficiency, so the LA
pressure rises

Holosystolic/Pansystolic
murmur
Q

80y old male comes to your office complaining of dyspnea on exertion and
syncope during extreme workouts . Upon auscultation you hear a cresendo-
decresndo systolic murmur on the right 2nd intercostal space that radiates to the
carotids. How would his wigger’s diagram look?

1 LV systolic pressure >> Aortic pressure

2 LA pressure >> LV diastole pressure

3
LV diastolic pressure >> Aortic pressure

4 Aortic pressure >> LV systolic pressure

Q

80y old male comes to your office complaining of dyspnea on exertion and
syncope during extreme workouts . Upon auscultation you hear a cresendo-
decresndo systolic murmur on the right 2nd intercostal space that radiates to the
carotids. How would his wigger’s diagram look?

1 Mobitz
LV typepressure
systolic I >> Aortic pressure

2 LA pressure >> LV diastole pressure

3
LV diastolic pressure >> Aortic pressure

4 Aortic pressure >> LV systolic pressure

 Cardiac Pump

• Ca2+ goes through the L type channels and activates ryanodine receptors which
releases Ca2+ into the cytosol known as Calcium induced Calcium release
• Ca2+ binds to troponin C and starts the cardiac contraction.
• Regulation of cardiac contraction (Inotropy)
• Ca2+ entry through L type channels Epinephrine and Norepinephrine
• Ca2+ release from SRB1 receptors ( camp)
• Ca2+ binding to troponin C increased H+ inside the cell will decrease
troponin C for Ca2+ affinity
• Ca2+ uptake by SERCA more sequestered more will be released
• Ca2+ efflux from the cell inhibited by digoxin which results in  contraction
Cardiac Performance
Systolic(ventricular) function curve

• Systolic performance means the overall force generated by the

ventricular muscle during systole. This is determined by the number
of cross-bridges cycling during contraction.
• The greater the number of cross-bridges cycling, the greater the
force of contraction.
• The number of cross-bridges cycling is determined by two
independent variables: the amount of preload on the muscle and the
level of contractility.
• These two factors are summed together to determine the overall
force of ventricular contraction.
• The greater the contraction the greater the pressure developed
inside the ventricles the larger the stoke volume and the bigger
the cardiac output
Systolic(ventricular) function curve
preload

• Is the load or stretch on the ventricular muscle at the end of

diastole.
• Can be measured by either Left ventricular end-diastolic volume
(LVEDV) or Left ventricular end-diastolic pressure (LVEDP)
• Starlings Law: the bigger the end diastolic volume  the bigger end
diastolic pressure the bigger the preload the bigger the stroke
volume
• In a normal heart, increased preload increases
sarcomere length toward the optimum actin-
myosin overlap. This results in more cross-
linking and a more forceful contraction during
systole.
Contractility
Starling Curve

• Y axis: contractive energy

» Ventricular pressure
» Stroke volume
» Cardiac output
» Stroke work
• X axis: indices of the preload
» Atrial pressure
» Filling pressure
» Venous return

Positive Inotropes: contractility e.g catecholamine, digoxin

Negative Inotropes:  contractility e.g MI, B blockers, Ca2+ channel blockers
PARASYMPATHETIC doesn’t have much effect in contractility
• Sympathetic +inotropic, + chronotropic
• Parasympathetic: -ve chronotropic
Stroke volume loop

• After load :represents the force that the muscle must generate to
eject the blood into the aorta for left ventricle.
• Increases during hypertension and aortic stenosis. Decreases
during hypotension

Area under the curve: stroke work

 Altered states
Stroke-volume loop changes

Increased preload
• Increase in venous return
• Venous contraction(sympathetic action)
• Arterial dilation
• Decreased Thoracic pressure (during inspiration)
• Decreased Atrial pressure
• Increase blood volume
• stroke volume, ejection fraction
Increased afterload Increased Contractility
• Hypertension • Refer earlier slides
• Aortic stenosis • stroke volume, ESV
• Vaso(arterial) contraction
• stroke volume, ESV, EF
Altered states
Compensation

• Exercise: increase in contractility and preload

• Aortic insufficiency: increased preload

• HF: decreased contractility

Decreased contractility  decreased stroke volume

Compensation increase preload increase stroke
volume
Questio

The diagram represents a LV Pressure-Volume Loop. How would

increased sympathetic activity alter this loop? Sympathetic activity
would…

A. Shift E downwards
B. Shift C to the right
C. Shift F to the left
D. Increase X
E. Shift A downwards
Question

• Which of the following changes would most likely

immediately alter the loop to ABC'D'E'F (broken line)?

(A)Increased arteriolar constriction

(B) Increased contractility
(C) Reduced venous compliance
(D)Increased venodilation
(E) Increased heart rate
Nitroglycerin, a drug used to treat angina is effective in
this condition because its most prominent effect is to…

A. Increase preload
B. Increase afterload
C. Increase contractility
D. Decrease preload
E. Decrease afterload
F. Decrease contractility
qUESTION

• Which of the following changes represents

a person with transplanted heart (no
autonomic innervation) and exercising ?

D: No change in contractility
but increased in afterload
• Which of the following changes represents
MI

F: decreased in contractility
• A change in Ejection fraction without
changing preload is represented by?

C: increased contractility
Which of the following sets of changes would be expected in
response to this increased sympathetic output?
Which of the following sets of changes would be expected in a
patient with atherosclerosis?