Physiology Exam questions

Physiology of the circulatory system

The 4 characteristics of heart tissue:

1. Conductibility
2. Excitability
3. Conductivity
4. Contractibility
Cardiac regulation is done via:
1. Humoral regulation i.e. epinephrine, vasopressin, Atrial natriuretic peptide ANP,
Angiotensin 2
2. Neural i.e. cardiovascular center in medulla, CN X vagus and CN 9 glossopharyngeal and
cardiac accelerator nerve (sympathetic)
3. Local regulation I.e. NO, histamine, thromboxane

66. Automatism heart. Gradient automatism?

 Automatism of heart - the ability of cells of the heart conducting system to produce
independently bioelectric impulses, that cause its excitement.
 Structures of conducting system have different degrees of automaticity. It is established
the so-called gradient of automaticity . It manifests itself in a reduced ability to
automatism of different structures of the conducting system according to their distance
from the sine-atrial node. Thus, if the sine-atrial node number of action potentials riches
the level of 60-90 imp / min, and in the cells of Hys node - 30-40 imp / min, so in the
fibers of Purkin'ye – less than 20 imp / min. Gradient of automaticity caused by different
spontaneous permeability cell membrane of conduction system to Ca2 +. Based on the
fact, that the sine- atrial node imposes its rhythm to the departments of conduction
system, that lying lower, it is called pacemaker or pacemakers of first order. Pacemaker
of second order is atrio-ventricular node. Pacemaker third order – it is Hys node and its
ramifications.

67. The action potential atypical cardiomyocytes mechanisms of physiological role?

Cardiomyocytes are striated, mononucleated cells which are connected by intercalated discs
that allow cardiac cells to contract in unison. They have T-tubules and sarcoplasmic reticulum
for Ca2+ releases.
Action potential changes the membrane potential of cardiomyocytes by opening Na and Ca
channels

68. Conducting system of the heart. The sequence and speed of conduction of excitation in the
heart?

sequence description speed

1. SA node (pace In right atrium, 90-60 bpm
maker) responsible for p wave
2. AV node (gate Creates a delay to 60-40 bpm
keeper) prevent blood back flow
from ventricles to atrium
3. Bundle of His In intraventicular septum 30-40 bpm
forms a left and right
branch
4. Purkinje fibers Branches from left and Less than 20 bpm
right branches of bundles
70. Formation of the propagation of excitation electrocardiogram heart?

P-Wave Atrial depolarization, both atriums contract

QRS Both ventricles contract i.e. depolarize
Complex
T-Wave Both ventricles relax/depolarize
RR interval should be consistent i.e. regular rhythm
If PR and QRS complex time is higher it could indicate dysrhythmia

71. Electrocardiographic leads?

Positioning of leads in the body:
The electrodes detect the charge on outside the cell during depolarization
72. Cardiac cycle, its phases and their physiological role? Diastole (S1) – Systole (S2)
Atrial Atrium contracts / P waves
Depolarization
Isovolumetric No blood ejected as the semilunar valves and AV valves are
contraction closed and ventricular volume unchanged – S1 (lub) sound i.e.
AV valves closing
Rapid ejection Ventricular pressure> aortic and pulmonary pressure –
(SYSTOLE) semilunar valves open ejecting blood
Reduced Due to reduced ventricular pressure
ejection
Isovolumetric semilunar valves close (S2 sound dub) marking the end of the
relaxation systole and beginning of diastole i.e. ventricle filling and
Ventricular
filling

74. The mechanism of influence of sympathetic/parasympathetic nerves on heart activity?

This is done to regulate blood pressure

Sympathetic Parasympathetic
Control Centre Medulla (cardiovascular Medulla (cardiovascular
center) center)
Sensors Baroreceptors: carotid Baroreceptors: carotid
sinus reflex and aortic sinus reflex and aortic
reflex reflex
Chemoreceptors: carotid Chemoreceptors: carotid
bodies and aortic bodies bodies and aortic bodies
acidosis or hypercapnia
(excess CO2 stimulates
Sympathetic response)
Nerve T1-T4 Sympathetic chain Vagus Nerve CNX
ganglia Right vagus innervate SA
node
 Left Vagus innervate AV
node
Neurotransmitter Norepinephrine Acetylcholine
Heart Rate Cardiac accelerator Decrease HR
nerves Decrease SA nodal
Increase HR discharge
Increase SA Nodal Decrease rate of
discharge depolarization through
Increase rate of heart
depolarization through
heart
Increase intracellular
Calcium
Increase ventricular
contraction force
Vasoconstrictor nerves
Constrict blood vessels

76. Humoral regulation of the heart?

a. Renin angiotensin aldosterone system
b. Epinephrine/norepinephrine system:
c. Antidiuretic hormone/Vasopressin: causes vasoconstriction which increases blood
pressure, released by hypothalamus from posterior pituitary in response to
dehydration or decreased blood volume
d. Atrial natriuretic peptide: lowers blood pressure by causing vasodilation and
promotes loss of salt and water in urine lowering blood volume
 Acetylcholine Epinephrine
Ionotropic effect -ve +ve
(strength of heart
contraction)
Chronotropic effect -ve +ve
(Frequency/Rate)
Dromotropic -ve +ve
(conductivity)
Pathmotropic effect -ve +ve
(Excitability)

73. Cardiac mechanisms of their origin. PCG its analysis?

Phonocardiography is a graphic recording of heart sound, there are 2 categories of sound
 Heart sounds: i.e. closing and opening valves, short duraction
  Murmurs: noisy characteristics with long duration i.e. turbulent blood flow
Heart sounds include:

 1st sound S1 (Lub): closure of mitral and tricuspid valve

 2nd sound S2 (Dub): Closure of aortic and pulmonary valve
 3rd sound: Blood rapid movement into relaxed ventricular chamber
 4th sound: Atrial contraction

Heart Occurs cause characteristics Duration Frequency ECG phonocardiogr

sound during sec Hz aphy
First Isometric Closure of Long soft low 0.1-0.17 25-45 R wave 9-13
contraction AV valve pitched sound
and –LUBB
ejection
period
Second Protodiastol Closure of Short, sharp 0.10.17 50 0.09sec 4-6
part of semilunar and high after T wave
isometric valves pitched DUBB
relaxation
Third Rapid filling Rushing of Low pitched 0.07-0.1 1-6 T to P 1-4
blood into
ventricles
fourth Atrial Contraction Inaudible 0.02- 0.02-0.04 P to Q 1-2
systole of atrial sound 0.04
musculature
 Cardiac
contraction mechanism
The cardiomyocytes are kept at a resting potential of -90mV by the Na/K pump. As the AP
travels down the membrane of the Cardiomyocyte the voltage gated Na+ channels get
activated and Na floods the cell (moving due to concertation gradient) this depolarizes the call
causing the membrane potential to go up from -90 to +25mV. The increase in potential causes
L-Type Calcium voltage gated channels to open up hence Calcium enters the cell. The Calcium
gated calcium channels on the sarcoplasmic reticulum opens up releasing Ca2+ into the
cardiomyocyte. The Ca2+ binds o the actin filament (thin) causing a conformational change
and exposing the binding sites, under the influence of ATP the myosin heads bind to actin
filament and does a “power stroke” hence the 2 filaments interdigitate.
77. Dependence of the heart to change the ionic composition of the blood?

Chemoreceptors, sensory receptors that monitor the chemical composition of blood, are
located close to the baroreceptors of the carotid sinus and arch of the aorta in small structures
called carotid bodies and aortic bodies, respectively. These chemoreceptors detect changes in
blood level of O2, CO2, and H_.
Hypoxia (lowered O2 availability), acidosis (an increase in H_ concentration), or hypercapnia
(excess CO2) stimulates the chemoreceptors to send impulses to the cardiovascular center.
In response, the CV center increases sympathetic stimulation to arterioles and veins,
producing vasoconstriction and an increase in blood pressure. These chemoreceptors also
provide input to the respiratory center in the brain stem to adjust the rate of breathing.

78. The mechanisms of self-regulation of heart: the law of Frank-Starling, effect Anrepa,
phenomenon Boudichi?

Frank-Starling: the greater the stretch in cardiac muscle the greater the force of Contraction
hence a Greater end diastolic volume (amount of blood in each ventricle at the end of
ventricular diastole) would increase the contractile strength of the ventricle and will increase
stroke volume (amount of blood ejected by each ventricle during each heart beat).
Stroke volume = End diastolic volume – End systolic volume (amount of blood remaining in
each ventricle a the end of ventricular systole)
Stroke Volume proportional to Preload (end diastolic pressure which is stretching the wall of
ventricle to their greatest) and preload is proportional to EDV therefore, increase in blood
volume in heart leads to increased stretch of myocardium which leads to increased force to
pump blood out.

Anrep effect: auto regulatory method In which myocardial contractibility increases with
afterload hence a sudden increase in afterload increases ventricular inotropy
Bowdtich effect: an autoregulation method by which myocardial tension increases with an
increase in heart rate (AKA Treppe effect). One explanantion is the inability of Na/K pump to
keep up with influx of Na at higher heart rates
79. Functional types of blood vessels? There are 5 types
1. Arteries: carry blood away from the heart to other organs. Large elastic arteries leave
the heart and divide into medium sized muscular arteries which in turn divide into small
arteries and then into arterioles
2. Arterioles: are small arteries that enter into tissues and then divide into capillaries
3. Capillaries: the thin walls of capillaries allow the exchange of substances between the
blood and body tissues – a group of capillaries reunite to form a venule
4. Venules: merge to form a larger blood vessels called veins
5. Veins: are blood vessels that convey blood from tissues back to the heart

Another way: Aorta, compressive/elastic arteries, Resistive/ muscular arteries,

exchange/shunts/ capillaries/ venules / veins

80. Arterial pulse mechanism of properties, methods?

Alternate expansion and recoil of elastic arteries after each systole of the left ventricle creates
a traveling pressure wave that is called a pulse. The pulse is strongest in the arteries close to
the heart
 Normal heart pulse rate: 70-80 beats/minute
 Tachycardia: over 100 beats/minute
 Bradycardia: less than 50 beats/minute

81. Blood pressure, factors that determine its value?

Blood pressure is the pressure in the arteries generated by the left ventricle during systole and
the pressure remaining in the arteries when the ventricle is in diastole.
Factors affecting blood pressure:
1. Smoking/ Caffeine/ alcohol: increase blood pressure
2. Age: may change stiffness of blood vessels causing hypertension
3. Medication/diet: salt raises blood pressure as It raises blood volume
4. Emotional state: Anger/stress raises BP while relaxation decreases BP
5. Blocked arteries by cholestrol
Normal blood pressure is 120mmHg (Systolic)/80mmHg (diastolic)
83. The method of recording blood pressure?
Manual recording of blood pressure:
1. Have patient relaxed, legs uncrossed and arm at heart level
2. Place stethoscope diaphragm on brachial artery once you hear a pulse, inflate the cuff
with the rubber bulb. Inflate until you can’t hear the brachial artery anymore (typically
around 180-200mmHg in the sphygmomanometer)
3. Once inflated, let the air out slowly using the air valve
4. 1st noise heard (Woof) is the systolic pressure and when you can’t hear the heart beat
it’s the diastolic pressure.
5. Blood pressure given in the form of systolic/diastolic pressure (mmHg) i.e. 120/70

84. Blood circulation in the veins. Factors that provide blood flow to the heart?
Venous blood flow to the heart depends on pressure difference between venules and right
ventricle, there are 2 methods that promote venous return and they are:
1. Skeletal muscle pump: peripheral veins have one way valves that direct blood away
from the limb and towards the heart, the veins undergo compression as the muscle
surrounding them contract and become decompressed as the muscle relax. This propels
the blood forward. Blood flow is unidirectional due to venous valves
2. Respiratory pump: based on alternating compression and decompression of veins.
During inhalation the diaphragm moves downward which cause a decrease in pressure
in the thoracic cavity and an increase in pressure in the abdominal cavity this results in
abdominal veins being compressed and blood moving from the compressed abdominal
veins to the decompressed thoracic veins and then into right atrium. The pressure is
reversed during exhalation and the valves in the veins prevent backflow of blood from
the thoracic veins to the abdominal veins

88. Characteristics of efferent humoral regulation of vascular tone in?

Neural control over blood pressure

85, 86, 87. Characteristics afferent link in the regulation of vascular tone? Characteristics
central element in the regulation of vascular tone? Characteristics of efferent neural link in the
regulation of vascular tone?
Chemoreceptors, sensory receptors that monitor the chemical composition of blood, are
located close to the baroreceptors of the carotid sinus and arch of the aorta in small structures
called carotid bodies and aortic bodies, respectively. These chemoreceptors detect changes in
blood level of O2, CO2, and H_.
Hypoxia (lowered O2 availability), acidosis (an increase in H_ concentration), or hypercapnia
(excess CO2) stimulates the chemoreceptors to send impulses to the cardiovascular center.
In response, the CV center increases sympathetic stimulation to arterioles and veins,
producing vasoconstriction and an increase in blood pressure. These chemoreceptors also
provide input to the respiratory center in the brain stem to adjust the rate of breathing.

vasoconstriction
1. Local: Vasoconstriction chemicals,
Thromboxane A2, superoxide radicals,
serotonin from platelets, endothelin from
endothelial cells
2. Humoral: Epinephrine/Norepinephrine,
vasopressin/Antidiuretic hormone,
Angiotensin 2/Aldosterone/ renin
3. Chemoreceptor reflex: Carotid/ Aortic
bodies – Acidosis/ Hypoxia/ Hypercapnia
→ CV in medulla → vasoconstriction
Vasodilation
1. Local: Vasodilating chemicals released by
metabolically active cells: K+, H+, Lactic
acid, adenosine from ATP, NO by endothelial
cells, Kinins and histamine
2. Humoral: Atrial Natriuretic peptide ANP
lowers BP via vasodilating and promoting
water and salt loss hence reducing blood
volume
3. Neural: Baroreceptor Reflex - ↑BP/↑ Stretch
of baroreceptors → ↑ Parasympathetic (i.e.
CNIX, CNX) → Medulla CV → ↑ Vegal
4. Bainbridge reflex: Atria stretch→ ↑HR efferent tone (CNX) → ↓Sympathetic tone →
→↑CO (CNX, prevents pulmonary ↓HR, ↓BP
edema)
5. Herring reflex: artificial increase in carotid
sinus causes stoppage of heart beat

89. Regulation of blood flow by changing the position of the body?

90. Regulation of circulation in exertion?
82. Lines blood pressure?