Cardiovascular Physiology

1
(No Transcript)
2
Cardiovascular Physiology

• Properties of the Cardiac Muscle

3
Properties of the cardiac muscle

1. Excitability
2. Conductivity
3. Contractility
4. Rhythmicity

4
Properties of the cardiac Muscle

• I. Excitability (Irritability)

5
I. Excitability (Irritability)

• the ability of cardiac ms to respond to
  adequate stimuli by generating an action
  potential followed by a mechanical contraction.

6
Relation between the action potential the
mechanical response

• The mechanical response consists of
  contraction (systole) relaxation (diastole).
• Cardiac ms begins to contract few
  milliseconds after the AP begins, continues to
  contract until few milliseconds after the AP
  ends.
• Duration of contraction
• ? 0.2 sec in arial muscle,
• ? 0.3 sec in ventricular muscle.

7
Relation between the action potential the
mechanical response (continued)

• Diastole begins at the end of the plateau.
• 2nd rapid repolarization is completed at
  about the middle of diastole.

8
Action potential of different types of cardiac
muscle
9
Action potential of ventricular muscle

• Ventricular ms has a RMP of 90 mV. (? 85 to
  95mV).
• The trans-membranous AP overshoots to a
  potential of (? 20mV).

10
AP of ventricular muscle (continued)
Trans-membranous AP of ventricular ms is
characterized by presence of 5 phases.

• Phase 0 Rapid depolarization.
• Phase 1 Rapid repolarization/
• 1st rapid repolarization.
• Phase 2 A plateau.
• Phase 3 Slow repolarization/
• 2nd rapid repolarization.
• Phase 4 Complete repolarization.

11
AP of ventricular muscle (continued)
1
2
3
0

• Phase 0 Rapid depolarization.
• op fast Na channels ? ? Na influx.
• Phase 1 Rapid repolarization/ 1st rapid
  repolarization.
• cls Na channels, ? K permeability, w Cl-
  influx.
• Phase 2 A plateau.
• op slow Ca2 channels (slow Ca2 Na
  channels) ? ? Ca2 influx, w slow op K channels.
• Phase 3 Slow repolarization/ 2nd rapid
  repolarization.
• cls slow Ca2 channels, w ? K permeability
  ? ? K efflux.
• Phase 4 Complete repolarization.
• actv Na K pump ? 2K in/ 3Na out.

4
12
Excitability changes during the action potential

• Passes through 3 periods
• 1. Absolute refractory period (ARP)
• 2. Relative refractory period (RRP)
• 3. Dangerous period (supranormal period)

13
Refractory Periods
14
1. Absolute refractory period (ARP)

• The excitability of cardiac ms is completely
  lost
• during this period, i.e. doesnt respond to
  2nd stimulus.
• V. long.
• Occupies the whole period of systole.
• Corresponds to the period of depolarization
  (phase 0),
• the first 2 phases of repolarization.
• Ht cant be tetanized (continuous
  contraction), as its
• ARP occupies the whole contraction phase.

15
2. Relative Refractory Period (RRP)

• The excitability of cardiac ms is partially
  recovered
• during this period, i.e. stronger stimuli
  than normal are
• required to excite the ms.
• Occupies the time of diastole.
• Corresponds to the 3rd phase of
  repolarization.
• Can be affected by the HR, temp., bacterial
  toxins,
• vagal stimulation, sympathetic stimulation
  drugs.

16
3. Dangerous Period (Supranormal)
The excitability of cardiac ms is supranormal
just at the end of the AP, i.e. weaker
stimuli than normal can excite the ms.
? result in ventricular fibrillation.
17
Factors affecting myocardial excitability

• 1. Cardiac innervation.
• 2. Effect of ions concentration in ECF.
• 3. Physical factors.
• 4. Blood flow.
• 5. Chemical factors (drugs).

18
Factors affecting myocardial excitability
(continued)

• 1. Cardiac Innervation
• Sympathetic NS ? ? excitability.
• Parasympathetic NS (vagus) ? ?
  excitability.
• 2. Effect of ions concentration in ECF
• ? Ca2 ? ? excitability.
• ? K ? ? excitability.
• 3. Physical factors
• ? temperature ? ? excitability.
• ? temperature ? ? excitability.

19
Factors affecting myocardial excitability
(continued)

• 4. Blood flow
• Insufficient bl flow to cardiac ms ?
  excitability
• myocardial metabolism for 3 reasons
• (1) lack of O2,
• (2) excess accumulation of CO2,
  
• (3) lack of sufficient food
  nutrients.
• 5. Chemical factors (drugs)
• Digitalis ? ? excitability.

20
Properties of the cardiac Muscle

• II. Conductivity

21
II. Conductivity

• the ability of cardiac ms fibers to conduct
  the cardiac impulses that are initiated in the
  SA-node (the pacemaker of the heart).

22
The direction of the impulse

• The impulse is conducted
• 1st ? Atrial spread
• from SA-node ? conductive tissue ?
• ventricles.
• 2nd ? Ventricular spread
• from apex of the heart ? base, via
• Purkinje fibers to the endocardial
• surface of ventricles.

23
The direction of the impulse (continued)

• N.B. LBB starts before RBB, as LV wall is
  thicker so the impulse
• needs more enough time to reach.
  Accordingly both ventricles
• will contract together.

24
Conduction of Impulse

• APs from SA node spread quickly at rate of 0.8
  - 1.0 m/sec.
• Time delay occurs as impulses pass through AV
  node.
• Slow conduction of 0.03 0.05 m/sec.
• Impulse conduction ? as spread to Purkinje
  fibers at a velocity of 5.0 m/sec.
• Ventricular contraction begins 0.10.2 sec. after
  contraction of the atria.

25
The conduction velocities of the impulse
SA-node 0.05 m/sec. AV-node
0.01 m/sec. (slowest)
Bundle of His 1.00
m/sec. Purkinje fibers 4.00
m/sec. . (fastest) Atrial Ventricular muscles
0.3 to 0.4 m/sec.
26
The conduction velocities (continued)

• The slowest conduction velocity in AV-node
• because it has few no. of
  intercalated discs.
• Importance to allow sufficient time
  for ventricles to be
• filled w bl before they contract.
• The fastest Conduction velocity in Purkinje
  fibers
• Importance to allow the 2 ventricles
  to contract at the same
• time simultaneously.

27
Factors affecting myocardial conductivity

• 1. Cardiac innervation.
• 2. Effect of ions concentration in ECF.
• 3. Physical factors.
• 4. Blood flow.
• 5. Chemical factors (drugs).

28
Factors affecting myocardial conductivity
(continued)

• 1. Cardiac Innervation
• Sympathetic NS ? ? conductivity.
• Parasympathetic NS (vagus) ? ?
  conductivity.
• 2. Effect of ions concentration in ECF
• ? Ca2 ? ? conductivity.
• ? K ? ? conductivity.
• 3. Physical factors
• ? temperature ? ? conductivity.
• ? temperature ? ? conductivity.

29
Factors affecting myocardial conductivity
(continued)

• 4. Blood flow
• Insufficient bl flow to cardiac ms ?
  conductivity
• myocardial metabolism for 3 reasons
• (1) lack of O2,
• (2) excess accumulation of CO2,
  
• (3) lack of sufficient food
  nutrients.
• 5. Chemical factors (drugs)
• Digitalis ? ? conductivity.

30
Properties of the cardiac Muscle

• III. Contractility

31
III. Contractility

• the ability of the cardiac muscle to convert
  
• chemical energy into mechanical work.

32
Contractility (continued)

• ? Myocardial fibers have Functional syncytium
  
• NOT anatomical syncytium, because they
  present
• in contact but NOT in continuity.
• ? Strength of myocardial contraction determines
  the
• heart pumping power.
• ? Mechanism of contraction depends on the
  contractile
• filaments, which contain the protein
  molecules (actin
• myosin).

33
Excitation-Contraction Coupling in Heart Muscle

• is the mechanism by which AP causes
  myofibrils of
• cardiac ms to contract.
• ? When AP passes over cardiac ms membrane, AP
  also spread to interior of cardiac ms fiber along
  membranes of transverse (T) tubules.
• ? Depolarization of myocardial cell stimulates
  opening of Ca2 channels in sarcolema.
• Ca2 diffuses down gradient into cell through T
  tubules.
• Stimulates opening of Ca2-release channels in
  SR.
• Ca2 binds to troponin stimulates contraction
  (same mechanisms as in skeletal ms).

34
Excitation-Contraction Coupling (continued)

• ? At the end of plateau of cardiac AP, i.e.
  during
• repolarization,
• Ca2 in sarcoplasm is rapidly actively
  transported
• pumped out of the cell via a Na-
  Ca2- exchanger,
• back into both SR T tubules.
• Resulting in cessation of the contraction
  until new
• AP occurs.

35
Excitation-Contraction Coupling (continued)
36
Factors affecting myocardial contractility
(Inotropic effectors)

• 1. Cardiac innervation.
• 2. Oxygen supply.
• 3. Calcium potassium ions concentration in
  ECF.
• 4. Physical factors.
• 5. Hormonal chemical factors (drugs).
• 6. Mechanical factors.

37
Factors affecting myocardial contractility
(continued)

• 1. Cardiac Innervation
• Sympathetic NS ? ? force of
  contraction.
• Parasympathetic NS (vagus) ? ? atrial
  force of contraction
• w no
  significant effect on ventricular ms.

38
Factors affecting myocardial contractility
(continued)

• 2. Oxygen supply
• Hypoxia ? ? contractility.
• 3. Calcium potassium ions concentration in
  ECF
• ? Ca2 ? ? contractility.
• ? K ? ? contractility.
• 4. Physical factors
• Warming ? ? contractility.
• Cooling ? ? contractility.

39
Factors affecting myocardial contractility
(continued)

• 5. Hormonal chemical factors (drugs)
• ve inotropics
• (Adrenaline, noradrenaline,
  alkalosis, digitalis, Ca2,
• caffieen,)
• -ve inotropics
• (Acetylcholine, acidosis, ether,
  chloroform, some
• bacterial toxins (e.g. diphtheria
  toxins), K, )

40
Factors affecting myocardial contractility
(continued)

• 6. Mechanical factors
• a. Cardiac ms. obeys all or none law
• i.e. minimal or threshold stimuli lead
  to maximal
• cardiac contraction, because cardiac
  ms. behaves as
• a syncytium.

41
Factors affecting myocardial contractility
(continued)

• b. Cardiac ms. cant be stimulated while it is
  contracted, because its excitability during
  contraction is zero due to long ARP, so it cant
  be tetanized.
• c. Cardiac ms. can perform both isometric
  isotonic types of contractions.

42
Factors affecting myocardial contractility
(continued)

• d. Starlings law of the heart
• Length-tension relationship
• Within limits, the greater the
  initial length of the fiber,
• the stronger will be the force of its
  contraction
• However, overstretching the fiber as
  in heart failure its
• power of contractility decreases
• i.e. within limits, the power
  of contraction is directly
• proportional to the initial length of
  the ms.
• Cardiac ms accommodates itself (up to
  certain limit) to
• the changes in venous return.

43
Factors affecting myocardial contractility
(continued)

• e. Cardiac ms shows staircase phenomenon
  (gradation),
• if providing all other conditions kept
  constant.
• i.e. if an isolated heart is stimulated by
  successive
• equal effective stimuli, the 1st few
  contractions
• show a gradual ? in the magnitude of
  contraction.

44
Properties of the cardiac Muscle

• IV. Rhythmicity (Automaticity)

45
IV. Rhythmicity (automaticity)

• the ability of cardiac ms to contract in a
  regular
• constant manner w/out nerve supply.
• ? Its myogenic in origin (i.e. not
  neurogenic).
• ? Its initiated by the pacemaker of the
  ht, the
• SA- node.

46
The pacemaker of the heart

• the SA- node.
• ? Contains the P- cells, which are probably
  the
• actual pacemaker cells.
• ? Has the fastest rhythm (rate of
  discharge) of all
• parts of the heart, 90 impulses/min.
• its fibers have an unstable
  RMP.
• ? Has spontaneous (w/out stimulation)
  depolarization,
• up to firing level.

?
47
Pacemaker potential

• ? Its RMP is (? -60 mV).
• ? Pacemaker tissue is characterized by unstable
  
• membrane potential, Prepotential.

?
-6
48
Pacemaker Prepotential
?

• ? Due to gradual state of
  depolarization
• Steady ? in K permeability
• (? K efflux), leading to
• ? intracellular negativity.
• Causing spontaneous leakage
• of membrane to Na w/out
• stimulation.
• ? (-60 mV to -55 mV).
• Which causes op of voltage
• gated transient Ca2 channels,
• leading to some Ca2 influx.
• ? (-40 mV).

-6
49
Pacemaker Action potential (AP)
-6

• ? Pacemaker Depolarization
• Opening of long lasting (fast) Ca2 channels.
• More Ca2 influx ? till reaching the potential,
  i.e. firing level point ? leading to
  depolarization.
• Opening of VG Na channels ? also contribute to
  the upshoot phase of the AP.

50
Pacemaker Action potential (AP) (continued)
-6

• ? Pacemaker Repolarization
• Opening of VG K channels.
• K diffuses outward (efflux), (so vity will go
  out of cell).
• ? Pacemaker Hyperpolarization
• excessive K effllux,
• (This will lead to hardship of K efflux
  in 2nd depolarization).
• Ectopic pacemaker
• Pacemaker other than SA node
• If APs from SA node are prevented from reaching
  these areas, these cells will generate
  pacemaker potentials.

51
??? Ca2 in
? K out
L Ca2
??? K out
L Ca2
T Ca2
-6
? Ca2 in
Na in
? K out
52
Factors affecting myocardial rhythmicity
(chronotropic effectors)

• 1. Cardiac innervation.
• 2. Effect of ions concentration in ECF.
• 3. Physical factors.
• 4. Chemical factors (drugs).

53
Factors affecting myocardial rhythmicity1.
Cardiac Innervation

• a. Sympathetic stimuli
• ? Tachycardia, by ? spontaneous
  depolarization of
• SA- node.
• How?
• ? SA- node membrane permeability to K ? less
  K efflux.
• ? membrane permeability to Ca2 ? more Ca2
  influx.
• As a result, the slope of depolarization ?,
  causing ? rate of SA- node firing ? HR.

54
Factors affecting myocardial rhythmicity1.
Cardiac Innervation (continued)

• b. Parasympathetic stimuli (vagus)
• ? Bradycardia, by ? spontaneous
  depolarization of
• SA- node.
• How?
• ? SA- node membrane permeability to K ? more
  K efflux.
• ? membrane permeability to Ca2 ? less Ca2
  influx.
• As a result, the prepotential slope ?,
  causing ? rate of SA- node firing ? HR.

55
(No Transcript)
56
Factors affecting myocardial rhythmicity2.
Effect of ion concentrations in ECF

• a. K ions
• If ? in ECF ? ? rhythmicity.
• If ? in ECF ? ? rhythmicity.
• (? stop heart
  in diastole)
• b. Na ions
• If ? in ECF ? innitiate rhythmicity, but
  cant
• maintain it.

57
Factors affecting myocardial rhythmicity3.
Physical factors

• a. Warming ? ? rhythmicity.
• b. Cooling ? ? rhythmicity.
• c. Exercise ? ? HR as a result of ? sympathetic
  n.
• stimulation ? vagal
  inhibition to
• SA- node.
• d. Endurance-trained athletes Resting
  bradycardia
• 
  due to high vagal activity.

58
Factors affecting myocardial rhythmicity4.
Chemical factors (drugs)

• a. Thyroid hormones catecholamines
• ? ? rhythmicity.
• b. Ach
• ? ? rhythmicity.
• c. Hypoxia
• ? ? rhythmicity.

59
Remember

• Intrinsic rhythmicity of denervated SA- node
  is ? 90
• impulses/min, while that of AV- node is ?
  60
• impulses/min.
• However, vagal tone controls SA- node to
  become 70
• impulses/min, AV- node to 40
  impulses/min.
• If SA- node activity is depressed by a
  disease, AV-
• node takes over becomes the pacemaker
  instead,
• leading to bradycardia.

60
(No Transcript)