Anatomy

1
Anatomy PhysiologyBio 2402 Lecture

• Instructor Daryl Beatty
• Day 3 Class 3
• The Heart, Cardiac Muscles Rythym

2
Review

• Look back at Clotting and control of clotting

3
Blood Disorders

• Disorders of the Erythrocytes
• Polycythemia
• Anemia

4
Anemias Symptoms

• Lethargy
• Loss of stamina energy
• Winded rapid respiration
• Pallor
• Depressed metabolic rate

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Anemias Types (655)

• Hemorrhagic internal bleeding
• Hemolytic anemia erythrocytes rupture
  prematurely
• Aplastic anemia Red marrow not functioning,
  (drugs, radiation, virus,)
• - It also results in loss of immunity and
  clotting.
• - Treatment with cord blood or bone marrow
  transplant

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Polycythemia

• Excessive levels of RBCs
• Polycythemia Vera Type of Bone Marrow cancer
• Count may be 8-11 M vs. 4-5 M cells/ ul
• Hematocrit may reach 80
• Blood volume may double
• Treated remove blood and replace with saline

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Polycythemia

• Excessive levels of RBCs
• Secondary Polycythemia 6-8 M RBCs/ul commonly
  those living at high altitudes.

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Hemostasis Three steps(663)

• Vascular Spasm Step 1
• What is a muscle spasm?
• Structure of the vessel? Smooth muscle in wall
• Reaction to injury spasm
• Reduces diameter
• Cuts flow almost instantly

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Hemostasis Step 2

• Platelet Plug Formation Step 2 (665)
• Smooth vessel walls do not attract platelets
• (Blood vessels platelets both charged)
• Rough surfaces cause platelet adhesion
• Once attracted, they release serotonin (enhance
  the vascular spasm)
• Also, ADP, Thromboxane A (prostaglandin)
• Within one minute this occurs
• Platelet plug will stop very minor leaks
• If a severe cut, we move to step 3.

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Hemostasis Step 3

• Coagulation Page 664
• Very complex about 30 substances
• Good illustration of irreducible complexity
• 13 clotting factors most from liver
• About 30 total chemicals

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Coagulation -Two triggers

• Intrinsic
• Extrinsic

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Hemostasis Summary

• Coagulation Page 664
• Very complex about 30 substances
• 13 clotting factors most from liver
• About 30 total chemicals
• Illustration of irreducible complexity
• Contrast to adaptation of sickle cell to
  P.falciparum (Malaria).

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Hemostasis Clinical Application

• Drugs may interfere with clotting (can be good or
  bad)
• Aspirin Often recommended for those over 50,
  reduces stickiness of platelets.
• Coumadin Maintenance for those prone to
  clotting and in atrial fibrillation
• Plavix Newer maintenance drug
• Heparin Used in IV lines and blood collection
• Typically suspend these before surgery

14
Hemostasis Clinical Application

• Larger cuts stimulate faster clotting
• Major arterial bleeding has too much pressure for
  clotting (aneurisms and trauma lethal)

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Bleeding Disorders (667-8)

• Thromboembolic Conditions
• (Defined as formation of undesired clots)
• Thrombus (Stationary clot) obstructing flow
• strokes, heart attacks, DVTs
• Atheroschlerosis plaque deposits
• Embolus portion of a thrombus which has broken
  free into the blood flow, (or any other material
  that can obstruct flow.)

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Bleeding Disorders (667-8)

• Thromboembolic Conditions
• TYPES
• DIC Disseminated intravascular coagulation

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Bleeding Disorders (667-8)

• Thromboembolic Conditions
• Thrombocytopenia (668)
• Spontaneous bleeding widespread
• Caused by bone marrow suppression
• Sign - Platelet count of lt50,000/ul
• Platelet transfusions for temporary relief.

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Bleeding Disorders (667-8)

• Hemophilia
• Hemophilia A most common
• Genetic expressed mainly in males
• Hemophilia C less common, both sexes
• Symptoms joints debilitated, bleeding, bruising
• Genetic defect of clotting factor.
• Treatment Plasma transfusions, Synthetic
  factors now available.

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Bleeding Disorders (667-8)

• Role of impaired liver function
• Synthesizes the pro-coagulants
• Also produces bile
• Bile is important in fat absorption
• Vitamin K from bacteria is fat soluble, and hence
  hard to absorb with poor fat digestion.

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Steps in Healing 1. Clot retraction

• Platelets contain contractile proteins (Actin
  Myosin) and growth factors for vessel repair
• Begins rapidly within about 1 hour
• Review Primary Secondary Unions

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Steps in Healing 2. Fibrinolysis (Pg 666)

• Define Fibrinolysis - Breaking up the clot
• Plasminogen is in the clot (inactive form)
• Plasmin is a protein digesting enzyme
• TPA Tissue Plasminogen Activator released about
  2 days later from the cells of the endothelium of
  the vessel.

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Clinical Application

• TPA Tissue Plasminogen Activator
• Clinical Application TPA also used in ischemic
  strokes and some heart attacks
• Must be given in first 4 hours
• What happens if TPA given in hemorrhagic stroke?

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Undesired Clotting

• Why would plaque initiate clotting?

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Factors Limiting Clot Formation

• Homeostasis
• Removal of clotting factors quickly
  (concentration away from site)
• Inhibition of clotting factors must reach a
  critical concentration to trigger the sequence.

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Factors Limiting Clot Formation

• Platelet charge () repels vessel wall
• Natural Anticoagulants
• Antithrombin III prevents Thrombin activity
• Prostacyclin inhibits platelets from sticking
• Heparin- from endothelium and Basophils masts
• Vitamin E Inhibits platelets (but some
  studies have not shown it to reduce heart
  attacks, as aspirin will).

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Factors Limiting Clot Formation - Application

• Blood flow prevents coagulation
• DVT Deep vein Thrombosis from sitting
• Blood transfusion Storage
• Citrate or oxalate is used to bind Ca.
• Heparin is used in IV lines. -

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Review of Cardiac Blood Flow

• Be able to trace flow, from start to finish

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Review of Cardiac Blood Flow

• Pulmonary Systemic Circuits
• Thickness of each chamber (also pg 685 TR) Why?

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Review of Cardiac Blood Flow

• Function of chordae tendineae and papillary
  muscles?
• What opens and closes the valves?

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Micro-structure of Cardiac Muscle

• Why do the fibers branch?
• (See Picture - Page 690)

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Overview of Cardiac conduction - Autorythmicity

• l

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Contractile Fibers

• Compare and contrast to skeletal muscle
• Similarities
• Depolarize - electrically excitable
• Review of Resting Membrane Potential
• Why is the outside of the Cell Membrane ??
• What is depolarization??
• What ion causes it to happen??
• What are the K and Na found?
• What is the role of Ca?

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Contractile Fibers

• Compare and contrast to skeletal muscle
• Role of Calcium
• Sarcoplasmic Reticulum releases large amounts of
  Ca to effect the muscle contraction.

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Contractile Fibers

• Contrasts of Cardiac with skeletal muscle
• Means of Stimulation
• Skeletal must be stimulated by nerves
• Cardiac is innervated (Vagus), but has
  automaticity or autorythmicity

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Contractile Fibers

• Contrasts of Cardiac with skeletal muscle
• Metabolic rate
• Larger amount of mitochondria (10-15X) What is
  the benefit of this?

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Contractile Fibers

• Contrasts of Cardiac with skeletal muscle
• Organ vs motor unit contraction
• Intercalated discs - for conduction to allow
  coordinated contraction (skeletal works as motor
  units).

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Contractile Fibers

• Contrasts of Cardiac with skeletal muscle
• Length of refractory period
• 250 ms, vs. 1-2 ms in skeletal
• WHY? Prevents tetanic contractions or
  fibrillation
• Illustration raise hands in sequence or
  Squirming bag of worms

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Contractile Fibers

• Contrasts of Cardiac with skeletal muscle
• Depolarization is very different, due to several
  different types of ion channels for K, Na, Ca
• Skeletal muscle more explosive rapid. Why
  would cardiac need to be slower?
• Heart never uses anaerobic metabolismWhy is this
  important?
• Strength of contraction can be varied, by the
  amount of Ca allowed in.

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Sequence of Contraction

• Page 690-2
• RMP?
• Page 691 picture

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Sequence of Contraction (691)

• 1. Na Channels open (Na enters)
• 2. Slow Ca channels open (Ca enters)
• 3. Ca concentration opens Ca channels causing
  contraction

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Plateau Phase (691)

• 1. Calcium slowly entering
• 2. Potassium slowly leaving the cell
• 3. Protracted, sustained contraction

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Sequence of Repolarization (691)

• 1. Potassium channels open(also slower, like
  Ca)
• 2.Potassium/Sodium
• pump restores the RMP

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Summary

• Concentration of Ca entering determines Ca in
  the SR and the force of contraction (Hence
  efficacy of Ca channel blockers)
• Entire sequence is about 300 ms (0.3 sec)
• Limiting factor of maximal heart rate
• Cardiac muscle is not all-or-none like skeletal
• Slower, consistent contraction

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Summary

• What will Calcium Channel blockers do?(2
  effects)

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Summary

• Very high rate of metabolism
• Always aerobic
• Variable force
• Calcium plays a role in depolarization

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Control system - Autorythmic Fibers

• See figure 18.14 on page 694
• These fibers have an unstable resting potential
  due to Na Ca leakage in.

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Control system - Autorythmic Fibers

• See figure 18.14 on page 694
• These fibers have an unstable resting potential
  due to Na Ca leakage in.

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Control system - role of instability of RMP

• Sinoatrial node (SA)
• Inherent rate of 100 BPM
• Sinus Rhythm Hearts pacemaker
• Location Upper RA
• Fastest cells in system

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Control system -

• Atrioventricular Node (AV)

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Control system -

• Atrioventricular Node (AV)
• Impulse is delayed here 0.1 second (Why?)

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Control system -

• Atrioventricular bundle (Bundle of His)

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Control system -

• Atrioventricular bundle (Bundle of His)
• The only electrical connection between atria and
  ventricles
• Rapidly conducts through Right Bundle branch,
  (RBB), Left Bundle Branch (LBB) and Purkinje
  fibers

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Control system -

• Right Bundle branch, (RBB), - stimulates septal
  cells
• Left Bundle Branch (LBB) septal cells
• Purkinje fibers- most important, stimulates most
  of the ventricular walls, and first stimulates
  the papillary muscles (why?)

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Control system -

• Time required 220 ms from SA node to complete
  depolarization.
• Longer time indicates conduction defect

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Control system - Clinical Applications

• Arrhythmias
• Uncoordinated atrial and ventricular contractions

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Control system - Clinical Applications

• Ectopic Foci Depolarization (beat) originates
  someplace other than SA node.
• May be triggered by high caffeine or nicotine
• Most common cause is low oxygen to a region of
  the heart
• Premature Ventricular contractions (PVCs) most
  serious.

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Control system - Clinical Applications

• Ventricular Tachycardia rapid rate stimulated
  by ventricular ectopic foci.

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Control system - Clinical Applications

• Ventricular Fibrillation
• This is the quivering of muscle uncoordinated
• No pumping is occurring
• Use of defibrillator is indicated here

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Control system - Clinical Applications

• Congestive Heart Failure
• Walls thinning, loss of strength
• May be on either side (r or l)
• If on left, fluid builds up in lungs (why?)
• Treatment
• Digitalis (From poisonous Foxglove family of
  plants) slows the rate, but increases strength
  (contractility)

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ClinicalWhat is a Heart attack?

• (Page 692 Btm Left)
• Ishemia results in
• anaerobic metabolism - lactic acid formation
• Rising acidity hinders ATP cannot pump out
  Ca, then
• Gap junctions close - cells electrically
  isolated, and
• If ischemic area is large, pumping action
  impaired.