Test 1 (Part 3) Flashcards
(125 cards)
1
Q
Hemostasis
A
- The steps taken by the body to LIMIT BLOOD LOSS
- Hemostasis is not confined only to the production of a BLOOD CLOT!
2
Q
Hemostasis Cont
A
Composed of Four Steps:
1) Vascular Spasm
2) Formation of a Platelet Plug
3) Formation of a Blood Clot
4) Repair of Damage
3
Q
Platelets
A
- A cell Fragment
- Derived from Megakaryocytic
- Normal Range: 150,000 to 300,000/ um^3
- Spontaneous Bleeding doesn’t occur until we reach 25,000 to 50,000 Platelets
4
Q
Production of Platelets
A
THROMBOPOIETIN (TPO)
- Protein Hormone
- Chromosome 3
- Amine Terminal is like ERYTHROPOIETIN (EPO)
- Carboxyl End: PROLOGS HALF-LIFE
- Produced in EQUAL Amounts by LIVER and KIDNEY
Platelets = Thrombocytes
- Have Mitochondria and part of the old Endoplasmic Reticulum
THROMBOPOIETIN: Can make ALL CELL LINEAGES!!!!!
5
Q
Production of Platelets Cont
A
Production of Platelets Control of Thrombopoietin secretion:
- CONTINUALLY Secreted
- Platelets bind Thrombopoietin (MPL) Receptor!!!!!
MPL Receptor: is expressed on the Platelets and Thrombopoietin
*** Trigger of Erythropoietin was Hypoxia!!!
6
Q
Thrombopoietin
A
- Binds to the MPL (CD-100) Receptor
- Found on Platelets, Megakaryocytic, and other Hematopoietic Cells
****JAK2/ STAT5
***Phosphorylation and subsequent transcription and Translation of various genes
7
Q
Control of Thrombopoietin Secretion
A
1) High Number of Platelets:
- Lots of TPO bound to MPL Receptor on Platelets
- INTERNALIZE TPO and Destroy it!!!
- Not much free to act on MEGAKARYOCYTES
2) Low Number of Platelets:
- Little bound to Platelets
- Not being destroyed
- LOTS FREE (more free to act on Megakaryocytes)
8
Q
Production of Platelets Cont
A
Thrombopoietin:
- INCREASE Differentiation of Stem Cells and Maturation Rate
- EFFECTS ON ALL CELL LINEAGES!!!!!!!
- A Mutation in the TPO Receptor or platelets has recently been implicated in causing POLYCYTHEMIA VERA- the platelets are UNABLE to INTERNALIZE and DETROY the TPO, so its action becomes CONTINUOUS!!!!!
- May INCREASE Platelet Function!!!
9
Q
Platelets
A
1) Actin and Myosin
- Cell Contraction
- Empty Vesicles**
2) Mitochondria (ATP and ADP**)
3) Remnants of the ER (Ca++ Storage)
4) Cyclooxyrgenase (COX1)
- Thromboxane A2**
5) Fibrin Stabilizing Factor (Clot Stability)**
6) Platelet Derived Growth Factor (Repair)**
7) Serotonin (5-HT)
**= INSIDE VESICLE!!!
10
Q
Platelets
A
On Cell Membrane:
1) Glycoproteins
- When activated, STICKY!!!
2) Phospholipids
- Platelet Factor 3
3) Receptors for COLLAGEN
11
Q
Describe the production of Platelets
A
1) Platelets are cell fragments derived from Megakaryocytic
2) Production of Platelets is controlled by Thrombopoietin
- Under normal conditions, TPO is continually secreted by the Liver and Kidney, but destroyed by the Platelets
- If Platelet levels drop, there is less destruction of TPO, so TPO can act
- TPO acts on ALL CELL LINEAGES
3) Platelets contain MITOCHONDIRA, ACTIN, MYOSIN, Cyclooxygenase 1, and Vesicles containing, among other things SEROTONIN!!!
12
Q
Compare and Contrast Thrombopoiesis and Erythropoiesus
A
ERYTHROPOIESIS:
1) Hormone:
- Erythropoietin
2) Source of Hormone:
- Kidney
3) Trigger for Hormone Release:
- Low O2 delivery to Kidney
4) Control fo [Hormone] Blood:
- HIF accumulation in Renal Cell
5) Receptor:
- EPoR
6) Cells Expressing Receptor:
- Pluripotent Stem Cell, RBC precursors
7) Effect:
- Pluripotent Stem Cell: Division with one daughter cell committed to Erythroid Lineage
- Increased erythroid lineage division and Maturation speed
THROMBOPOIESIS:
1) Hormone:
- Thrombopoietin
2) Source of Hormone:
- Liver, others?
3) Trigger for Hormone Release:
- Constitutive (Constant)
4) Control fo [Hormone] Blood:
- Internalization and Destruction of TPO by Circulating Platelets
5) Receptor:
- MPL
6) Cells Expressing Receptor:
- Platelets**, Pluripotent Stem Cell, All HEMATOPOIETIC Cell Lines
7) Effect:
- Increased division and maturation of ALL BLOOD CELL LINEAGES
13
Q
Hemostasis (Step 1)
A
Step 1- VASCULAR SPASM
- Spasm may be strong enough where we don’t have any Blood Loss
PRIMARY CAUSES:
1) Myogenic:
- Direct response to Injury
- No neurons, reflexes Involved
2) Platelet Factors:
- Serotonin
- Thromboxane A2
***VASCULAR SPASM is INDEPENDENT of what the Brain is telling IT!!!
FACTORS CONTRIBUTINF TO THE SPASM:
- A Neural Reflex initiated by the Mechanical Injury and Pain
- Neither NECESSARY or SUFFICIENT for SPASM to OCCUR
***If we get rid of NOCICEPTORS, the Vascular Spasm will still occur!!!
14
Q
Describe the Initiation and Function of Vascular Spasm
A
1) Myogenic response to Injury- Vascular Smooth Muscle Contracts on own
2) Serotonin (5HT) and Thromboxane A2 from Platelets contributes
3) Minor contribution from a Neural Reflex
4) Reduces blood loss by Slowing/ Stopping blood flow out
15
Q
Hemostasis (Step 2)
A
Step 2- Formation of a Platelet Plug
A) With damage to Vessel Wall:
- COLLAGE Exposed
- Platelets will bind to COLLAGEN (2 step process)
1) Part I: VON WILLEBRAND FACTOR- Plasma Protein
- Bind between Collagen and Platelet (receptor)
- Binding of Platelet Receptor (INTEGRIN) to Collagen
B) Activation of Platelet
- Platelet Swells
- Extends Podocytes
Formation of Platelet Plug:
1) Platelets Swell
2) Contraction
- Force the vesicles out of the Platelet and release its contents into the area
3) Granules leave Platelet
4) Platelets stick to vessel wall and to each other (Thromboxane A2 and ADP)
- Platelet cell membrane becomes Increasingly Sticky
- Other platelets become attracted to the Sticky Platelet and then they themselves becomes ACTIVATED
- ***PLATELET PLUG stops bleeding from Small Breaks, Nose and Skin
- May be all that is required to stop bleeding
16
Q
Describe the formation and function of the Platelet Plug
A
1) Formation of the platelet plug is initiated by exposed collagen on damaged blood vessels binding to receptor on the platelet
2) This triggers platelet activation and aggregation
3) Platelets swell and stick to one another
4) Plugs the “Hole” in the vessel
5) If the cut is small enough, the platelet plug may be all that is required
17
Q
Hemostasis (Step 3)
A
Step 3- Blood Coagulation
3 Essential Steps:
1) Formation of Prothrombin Activator
2) Activation of Thrombin
3) Creation of Fibrin from Fibrinogen
***CLOT CREATION!!!!!
CLOT RETRACTION:
1) Get rid of excess fluid within Clot
2) Solidify CLOT
3) Platelets required
- Bind Firbin Polymer together
- Actin and Myosin in Platelet- Contraction
4) Also requires CALCIUM
18
Q
The Blood Clot
A
- Platelets are bound to Fibrin and these Platelets will contract and pull the Fibrin strands together!!!
19
Q
Hemostasis (Step 4)
A
Step 4- Repair of Damage
SECRETED BY PLATELETS:
- Platelet-derived Growth Factor
- Stimulates Fibroblast to grow into area
- Fibroblasts differentiate into Smooth Muscle, etc… to Close Hole
***Causes tissue healing by causing tissue Invasion by Fibroblasts into the damaged area
20
Q
Getting Rid of the Clot
A
1) Plasminogen
- Made by Liver
- Floating in Plasma
- Not ACTIVE FORM
2) Activation of Plasminogen
- TISSUE PLASMINOGEN ACTIVATOR!!!!!!
- Released by DAMAGED TISSUE
- Activation is Inhibited by tPA INHIBITOR (Blood)!!!!!!
***tPA was released when the vessel was damaged by the tPA Inhibitor stopped the tPA from doing its job, and therefore the Clot will stick around longer!!!
21
Q
Endothelial Cells
A
- When we get healing, the Endothelial cell lining will be intact and give off Thrombomodulin
- Thrombin binds to Thrombomodulin and then becomes an Antigoaculant!!!!
22
Q
Describe How Clots are Removed (tPA, tPA Inhibitor, Protein C)
A
1) Relies on delayed activation of a Fibrinolytic Enzyme (Plasmin) that is found in the blood in an Inactive form (Plasminogen)
2) Plasminogen is prevented from becoming active by a Plasmin Inhibitor, while activation requires tissue Plasminogen Activator (tPA) released from the Damaged Tissue
3) The binding of Thrombin to Thrombomodulin activates Protein C, which inactivates the Plasmin Inhibitor
4) Once the inhibitor is inactivated, tPA can convert Plasminogen to Plasmin
5) Plasmin breaks down FIBRIN to remove the Clot
23
Q
Preventing Clot
A
1) Blood Vessels
- Smooth Surface: Prevents Platelets from RUPTURING
- Membrane Proteins:
A) GLYCOCALYX: repels Platelets
B) THROMBOMODULIN: Changes Thrombin Activity
2) Chemicals which LIMIT CLOTTING
A) Fibrin:
- “Binds” Thrombin and prevent it from working
B) Prostacyclin (PGI2)
- Made at time of Injury by Endothelial Cells - Vasodilation - Limit Platelet Aggregation
C) Antithrombin II
- When Thrombin binds to it, works as Antigoaculant
D) Heparin
- Derived from Mast Cells - Increases Antithrombin efficacy
**Activated Protein C—–> Inactivation of VIIIa and Va —-> INHIBITION of Further FIBRIN Creation
24
Q
Describe the System which limit Clotting (Fribin, Prostacyclin, Antithrombin III, Protein C)
A
- Because the enzymes of the Clotting Cascade are always present in the Blood, we have to work to prevent clotting that is NOT REQUIRED
- Factors that Limit Clotting Include:
A) Smooth Endothelial Lining of the VesselsB) Continuous flow of blood (preferably not Turbulent)C) Platelet repelling action of the GLycocalyxD) A variety of Endogenous Anti-Coagulants, including Fibrin, Heparin, Prostacyclin, and Anti-Thrombin IIIE) Protein C, when activated, inactivates factors V and VIII
25
Cardiovascular System
- Primitive vertebrate cardiovascular plan begins Mid-Week 3 and present by Week 4
- First SYSTEM TO FUNCTION!!!
- Early development necessary because of RAPID GROWTH
- Embryo can no longer meet nutritional or Oxygen needs by Diffusion
- Requires both PUMP, TUBING, and DELIVERY SYSTEM (Heart, Vessels, Blood)
- Begins with Cardiac Progenitor cells in Epiblast migration to form PRIMARY HEART FIELD (PHF)
26
Establishment and Patterning of PHF
- Progenitor Heart cells have migrated and formed the horsehsoe- shaped primary heart field (PHF).
- As they migrated, PHF Cells we specified to form Left and Right sides of the heart and form the ATRIA, LEFT VENTRICLE, and Part of the RIGHT VENTRICLE.
- The remainder of the RIGHT VENTRICLE and the Outflow tract consisting of CONUS CORDIS and TRUNKS ARTERIOSUS are formed by the Secondary Heart Field (SHF)
27
Patterning of Cardiac Progenitor Cells
- Occurs at the same time that Laterality (lift-right sidedness) is established
- Pathway is expressed in Lateral Plate mesoderm on the Left Side and involves a number of SIGNALING Molecules, including SEROTONIN (5HT), which result in expression of the Transcription Factor, PITX2, the Master Gene for LEFT Sidedness. (SSRIs and Heart Defects)
- This pathway specifies the Left side of the body and also program sHeart Cells in the primary and SHFs
- The right side is Specified as well, but genes responsible for this patterning have not been completely determined
- Disruption of the Pathway on the left results in Laterality Abnormalities, including many heart defects
28
Endocardial tubes
- Once cells establish the PHF, they are induced by the underlying Pharyngeal Endoderm to form Cardiac Myoblasts and Blood Islands that will FORM BLOOD CELLS and VESSELS by the process of VASCULOGENESIS
- With time, the ISLANDS UNITE and form a HORSHOE-SHAPED Endothelial-lined tube surrounded by the Myoblasts
- This region is known as the CARIOGENIC REGION
29
Repositioning of Heart and Pericardial Cavity and Septum Transversum
- Endocardial tubes fuse to form a single primitive Heart Tube
- Structures go from the Anterior of the Head to the Inferior of the Head
1) Pericardial Cavity
2) Endocardium
3) Myocardium
4) Epicardium
30
Vascular Circuits
- Embryonic Circuit
- Series of Aortic Arches that connect to Dorsal Aortae
- Dorsal Aortae subdivide into Smaller Vessels to Supply Embryo
- Blood Drained by Anterior and Posterior Cardinal veins
- Common Cardinal vein
**UMBILICAL Artery and Vein: Take oxygenated blood from mom and give it to baby while taking deoxygenated blood from baby and giving it to mom
**VITELLINE Artery and Vein: Play important role in blood circulation to and from the Yolk Sac
31
Extra embryonic Vascular Circuits
- "Nutritional" Circuits
1) VITELLINE- Supply and drain Yolk Sac, "Nursery fro Blood Cells"
2) Umbilical Vein carriers Oxygenated Blood from the Palcenta
- Umbilical (Placental)
32
Major Trends in Development
- Heart is converted into a 2-Chambered and then a 4-Chambered Structure
- Extraembryonic Circuits are lost
- Ex: Vitalline (Before Birth) and Umbilical (After Birth)
- Embryonic vascular circuit separates into Systemic and Pulmonary portions
- Systemic Aterial Outfliw----> LEFT
- Systemic Venous Return ----> RIGHT
33
Embryonic Structure Versus Adult
EMBYRONIC:
1) Sinus Venous
2) Primitie Atrium
3) Primitive Ventricle
4) Bulbus Cordis
5) Truncus Ateriosus
ADULT Equivalent:
1) (Sinus Venous)-----> Smooth part of Right Atrium (Sinus Venarum), Coronary Snus, Oblique Vein of left Atrium
2) (Primitie Atrium) ----> Trabeculated part of Right and Left Atria (Auricles)
3) Primitive Ventricle-----> Trabecualted part of Right and Left Ventricles
4) Bulbus Cordis -----> Smooth part of Right Ventricle (Conus Cordis), Smooth Part of Left Ventricle (Aortic Vestibule)
5) Truncus Ateriosus ----> Aorta, Pulmonary Trunk
34
Heart Formation
- Umbilical Vein, Vitelline Veins, and Common Cardinal All provide something to the Fetus and Heart
***Site of Apoptosis: Programed Apoptosis to kill off some of the tissue around the Heart to give it more Space!!!
35
How to Think of the Heart
The heart is a House with:
1) 4 Rooms (Chambers)
2) 4 Doors (Valves)
3) 4 Big hallways (Vessels)
4) 4 Small Hallways (Vessels)
- Ex: Coronary Arteries
36
Aortic Arches
- there are a variety of Molecular signals from the Anterior Endoderm to specify and initiate Endocardial tube Development
- Once the Endocardial tubes fuse, the Venous end is specified by RETINOID ACID (RA)
- Lower RA concentrations in more Anterior Structures (Ventricles and Outflow Tract) specify them as Anterior Structures
- Importance of RA in Cardiac signaling is Important for Incidence of CONGENITAL Abnormalities
***SEPTUM TRANSVERSUM!!!!
37
Day 22 and 23 of Heart
DAY 22:
- Most of the Growth in the Heart will take place in the Ventricles and the Outflow tract
- Truncus Antibiosis and Bulbus Cordis
- Ventricle
- Atrium
DAY 23:
- Cardiac Folding: The parts that are growing the fastest are folding more ANTERIORLY
- PITX2 regulates the Cardiac Folding or Looping!!!!!!
- Bulbus Cordis
- Ventricle
- Atrium
**Cardiac Looping is dependent on LATERALITY Pathway and Proper Expression of transcription Factor PITX2!!!!!
***The Fulcrum for the bending around in the LV!!!!!
38
Dextrocardia
- Heart bends to the LEFT instead of the RIGHT
- Heart displaced to the RIGHT with Transposition of Heart and Great Vessels
- Most common POSITIONAL ABNORMALITY
- During Gastrulation or later during Cardiac Looping
Can be Found:
- By itself
- With other laterality sequence issues
0 with SITUS INVERSUS
***Reverses the names but he Flow would be the SAME!!!
39
Partition of Atrioventricular Canals
- After folding, Atrium and Ventricle are separated by narrow AV Canal
- Dorsal and Ventral blocks of tissue GROW TOGETHER
- ENDOCARDIAL CUSHIONS
- Divide single AV Canal into separate RIGHT and LEFT AV Canals
- Canals (and their valves) REGULATE blood flow from Atria to Ventricles!!!!!
40
Atrioventricular Communis
- The formation and fusion of Endocardial Cushions is the CRITICAL FIRST STEP in the development of the 4-Chambered Heart
- Large communication between Chambers that occur when the CUSHIONS FAIL TO FUSE!!!!
41
Common AV Canal
- Enlarged Pulmonary Trunk
- Less resistance in the Pulmonary circulation than in the Systemic Circulation
***There is less resistance in the Pulmonary circulation compared to the Systemic Circulation so then you get an enlarged Pulmonary Trunk
**They put a and around the Pulmonary Artery which doesn't allow the artery to expand and therefore the blood will go more towards the Systemic Circulation
42
Correction of Common AV Canal
- Doctors will perform a single procedure to take the Pulmonary Artery Band off, close the holes between the Upper Chambers and the Lower Chambers of the Heart, and construct Two Valves out of the Single Existing Valve to make the Heart Function NORMALLY
- This limits the amount of blood sent to the Lungs making it LESS CONGESTED
43
Formation of Interventricular Septum
- Two Parts
- MUSCULAR PORTION develops in the MIDLINE on the Floor of the Primitive Ventricle
- Grows UPWARD towards ENDOCARDIAL CUSHIONS and Down-Growing BULBAR RIDGES!!!!!
- The Muscular Portion does make it all the way toward the Endocardial Cushion
- This hole gets filled in by a Membranous Tissue so there are two Parts to the Septum:
1) Muscular Part
2) Membranous Part
44
Ventricular Septal Defects (VSDs)
- 25% of all CONGENITAL HEART DEFECTS
- Opening between Left and Right Ventricles, associated SHUNTING of BLOOD
- 4 toes based on Position and Severity
- MOST VSDs occur in MUSCULAR PORTION (these Spontaneously Close unless they're Very Large)!!!!!!!!
- MEMBRANOUS Defects are more commonly CORRECTED SURGICALLY!!!!
45
Case #1
- Had VSD
- Initially with inflation of the Lungs, RV Pressure Decreases
- With Increased Blood Flow through Lungs, Increased Blood Flow to Left Heart, LV Pressure Increases
- With VSD, Left-To-Right SHUNTING (ACYANOTIC)
- Causes Increased work by RV, HYPERTROPHY and eventually, RIGHT-to-LEFT SHUNTING----> CYANOSIS
- Rate DEPENDS on SIZE of VSD!!!!
46
Does a VSD cause Conduction?
- It is rather surprising to not CONDCTION Defects are not common in VSDs
- In fact it can be termed RARE. VSD, however large may be, usually spares the Conduction System. This is simply due to the fact that Developmentally the Two Systems, Ventricular Septum and the Electrical System of the Heart, come from DIFFERENT EMBRYOLOGICAL Precursors and are simply ANCHORED TOGETHER
- If the IV Septum is nor formed properly, the bundle of His and its Major Right and Left branches are SIMPLY DISPLACED and are not DESTROYED, they tend to occupy one of the rims of VSD.
- Further, a VSD located Peripherally and Distally towards the APEX has little impact on the Conduction Tissue as it has already FANNED OUT and SMALL little twigs are affected, while Central, Proximal, and Basal VSDs can have more Significance
47
Formation of the Atrial Septum
- There is a hole that form in the Atrial Septum, and this happens because we want the Blood to go from the RA to LA and then to the Ventricle and out!!!!
**WE NEED TO HAVE A FUNCTIONAL VALVE BETWEEN THE RA and LA!!!!
- An Atrial Septum is built so that there is an opening, but when the Child is born the Valve needs to CLOSE and STAY CLOSED!!!
- If there is a failure to close, then this could cause so many problems!!!
1) Foramen Secundum ---> FORAMEN OVALE!!!!!
2) Valve of Foramen Ovale (Derived from Septum Primum)
3) Septum Secundum (Upper Limb)
4) Septum (Lower Limb Secundum)
48
Before Birth vs After Birth with Foramen Ovale
Before Birth:
- Right Atrium: HIGHER PRESSURE
- Left Atrium: LOWER PRESSURE
- Septum Secundum
- Foramen Ovale
- Septum Primum
- SHUNT
After Birth:
- Right Atrium: LOWER PRESSURE!!!!!!
- Left Atrium: HIGHER PRESSURE!!!!!!!
- Septum Secundum
- Fossa Ovalis
- Septum Primum
***The Higher Pressure in the Left Atrium causes the Foramen Ovalis to CLOSE!!!!
1) LIMBUS: Septum Secundum
2) Fossa Ovale (Floor): Septum Primum
3) Valve of Fossa Oale: Septum Primum
4) Fossa Ovale: Floor is Septum Secundum
49
Atrial Septal Defects
- ASD: Fairly common, present in 10 to 15% of patients with Congenital Cardiac Anomalies
- Osmium (Foramen) Primum Defects: Similar to Endocardial Cushion Defects
- SECUNDUM TYPE: Involve Foramen Ovale and Septum Primum
- SINUS VENOSUS: Usually Near Opening of SVC
50
Remember Holt-Oram Syndrome?
- Mutation in TBX5 Gene, associated with FORELIMB Development
- Although the abnormality of the Upper Extremities is more Extensive in some cases, the Characteristic findings in the Holt-Oram Syndrome (HOS) are Thumb Anomaly and Atrial Septal Defect!!!!
- Can also have VSD!!!!!!
51
Major Trends in Development
- Heart is Converted into a 2-Chambered and then a 4-Chambered Structure
- Extraembryonic Circuits are LOST!!!!
- Embryonic vascular circuit separates into Systemic and Pulmonary Portions!!!
- Systemic Arterial Outflow---> LEFT
- Systemic Venous Return ---> RIGHT
52
Changes in Sinus Venosus
- Opens initially into DORSAL Wall of PRIMITIVE ATRIUM
- Left and Right Horns are EQUAL in SIZE!!!
- Right Horn enlarges as Blood is SHUNTED from Left to Right
- Shunts involve "Nutritional" Vascular Circuits and Embryonic Circuits!!!!
- Move all Systemic Inflow to the Right Side!!!!!
- There are the Nutritional Circuits: VITELLINE and UMBILICAL!!!!
- (Intra) Embryonic Circuit: CARDINAL VEINS!!!!
53
Shunt 1- Vitelline Veins
- Liver develops in SEPTUM TRANSVERSUM
- Veins become incorporated into LIVER as HEPATIC SINUSOIDS, HEPATIC VEINS, part of IVC and some of the Veins that DRAIN the GI Tract!!!!
***Liver will start to develop in the areas of the Vitelline Veins (and they make the Hepatic Sinusoids)
*** Vitelline System is essentially lost except for pieces of it that we can use!!!
54
Shunt 2- Umbilical
- Loses direct connection with HEART (Ligamentum TERES HEPATIS)
- Would you want a direct Connection with the Heart?? NO!!!!!!
- Joins Large Venous Shunt- DUCTUS VENOUSUS
- Connects Umbilical Vein with IVC
- BYPASSES the Liver and Diverts OXYGENATED BLOOD into the HEART!!!!!
55
Ductus Venousus
- Connects Umbilical Vein with IVC
| - BYPASSES the Liver and Diverts OXYGENATED BLOOD into the HEART!!!!!!
56
So What Happens to the Sinus Venous?
- Loss of Vitelline Veins; Re-used as part of the GI SYSTEM
- Re-routing of Umbilical Vein to utilize the Ductus Venous to by-pass the Liver yet not have a direct Connection to the Right Atrium
- So what happens to the Cardinal System that drains blood from the Embryo itself into the Primitive Heart?
57
Shunt 2
- Anterior Cardinal Veins becomes CONNECTED!!!!
- ANASTOMOSIS becomes Left Brachiocephalic Vein
- Right Anterior Cardinal and Common Cardinal become SVC!!!!!!!!!!
**If ABOVE Diaphragm, everything on the Left Side goes to the Superior Vena Cava
*** If BELOW Diaphragm, everything on the Left Side goes to the Inferior Vena Cava
*****SHUNITNG of Blood means that the RIGHT HORN becomes MUCH LARGER!!!!
**Superior Vena Cava: Head and Neck
**Inferior Vena Cava: Placenta and Caudal regions of Embryo
**Coronary Sinus: takes all the Blood from the Heart itself and dumps it back into the Right Atrium!!!
Three Things Dump into Right Atrium:
1) Superior Vena Cava
2) Inferior Vena Cava
3) Coronary Sinus
58
Sinus Venosus
- Smooth part of Right Atrium
- Coronary Sinus
- Oblique Vein of Left Atrium
- CRISTA TEMRINALIS marks division between Embryonic Sinus Venous and Embryonic Primitive Atrium (Auricles)
59
Formation fo Aorticopulmonary Septum
- Partition of the AV canal will for BICUSPID and TRICUSPID Valves
- Partition of the TA will form the Aortic and pulmonary Semilunar Valves
60
Neural Crest Cells
*** NERUAL CREST Cell invade Ridges that form in BULBUS CORDIS and TRUNKS ARTERIOSUS!!!!!!
- Kids with Neural Crest Defects will have problems with their Hearts:
- Ex: Skin Pigmentation and Heart Defects
61
Partitioning of the Great Vessels
- The SEPTUM is a SPIRAL!!!
- AORTA and PULMONARY TRUNK SPIRAL around each other so we have to make some cuts in the OUTFLOW TRACK!!!!!!
1) Truncal Ridge
2) Bulbar Ridge
3) Bulbar Ridge
- Distal part of AP Septum (Bulbar Ridge) must contact Endocardial Cushions and IV Septum
- More complex Developmental Process = INCREASED Possibility errors!!!!!
SLIE 75-77 of CARDIAC COLE LECTURE!!!!
62
Eisenmenger's Syndrome
- Equal division of TRUNKS, Incomplete fusion of Bulbar Ridges Inferiorly ---> VSD!!!!
- Initial Left ---> Right Shunt, Increased PULMONARY BLOOD FLOW and HYPERTENSION!!!!
- Proliferation in Intima and Media to Narrow Lumen
- Increased Pulmonary Resistance causes RIGHT --> LEFT Shunt and CYNAOSIS!!!
63
Tetralogy of Fallot
1) Pulmonary Stenosis
2) VSD
3) Overriding Aorta
4) RIGHT Ventricular Hypertrophy
64
Case #2
- Tetralogy of Fallot
65
Transposition of the Great VEssels
- Coronary arteries are detached from the AORTIC Valve and Connected to the PULMONIC Valve
SLIDE 85 of CARDIAC COLE LECTURE!!!
66
Development of the Arterial System
- 6 pair of Arotic Arches
- Connect Aortic Sac/ TA to Dorsal Aortae
- Pharyngeal Arches (Organize Development of Head and Neck)
67
Derivative of Aortic Arches
I: Contribute to Maxillary VEINS
II: Produce Stapedial and Hyid Arteries
III: Common Carotid Arteries and Proximal Portion of the Internal Carotid Arteries
IV: On the LEFT SIDE, it persists, connecting the VENTRAL AORTA to the DORSAL AORTA, forming the AORTIC ARCH. On the RIGHT it forms the PROXIMAL Portion of the RIGHT SUBCLAVIAN Artery***********
V: Rudimentary and do not develop into any known vessels
VI: The proximal portions develop into the RIGHT and LEFT pulmonary Arteries, while the Distal Portion of the LEFT Aortic Arch artery develop uno the DUCTUS ARTERIOSUS*********
68
Ductus Arteriosus
- Potency in uteri is promoted by Continual production of PROSTAGLANDIN E2 (PGE2) by the DUCTUS
- Psotaglandin Antagonism, such as maternal use of Nonsteroidal Anti-Inflammatory Medications (NSAIDS), can cause fetal closure of the Ductus Arteriosus
- Prostaglandins are utilized to maintain the potency of the Ductus Arteriosus until Surgical Ligation is Performed
- When surgical Ligation is not indicated, Prostaglandin Inhibitors (Ex: Nonsteroid Anti-inflammatory Drugs (NSAIDS) are used to close the DUCTUS ARTERIOSUS!!!
- Can put a COIL or a CLIP on the Ductus Arteriosus if NSAIDS do not work!!!!
SLIDE 89 - 91 CARDIAC COLE LECTURE!!!
69
Pulmonary veins
- Form independently, are not made
- Venous drainage channels from the Lungs converge to form SINGLE VESSEL ---> LEFT ATRIUM
- As ATRIUM EXPANDS, tissue of the vein is Incorporated into the wall!!!!
***Develops from the Lungs and grow towards the Heart and come into contact with the LEFT ATRIUM. NOT PART of the HEART DEVELOPMENTALLY!!!
70
Total Anomalous Pulmonary Venous Return (TAPVR)
- TAPVR is a RARE Congenital Malformation in which all FOUR PULMONARY VEINS do NOT connect normally to the LEFT ATRIUM
- Instead all FOUR PULMONARY VEINS drain abnormally to the RIGHT ATRIUM by way of an ABNORMAL (Anomalous) CONNECTION!!!
- TAPVR is CLASSIFIED into different types, based on how and where the Pulmonary Veins drain to the HEART:
1) SUPRACARDIAC TAPVR: The Pulmonary Veins drain to the Right Atrium via the Superior Vena Cava
2) CARDIAC TAPVR: The Pulmonary Veins come together behind the Heart and then drain to the Right Atrium through the Coronary Sinus
3) INFRACARDIAC TAPVR: The Pulmonary Veins drain to the Right Atrium vis the hepatic (liver) veins and Inferior Vena Cava
***If the child survives, they must have an Atrial Septal Defect so that the Blood can get to the OTHER SIDE!!
71
TAPVR
- All types of TAPVR have to have an ASD
- Because none of the Pulmonary Veins connect normally to the LEFT SIDE of the Heart, Blood must be Shunted from the Right Atrium across the ASD
- ABSENCE of an ASG in TAPVR is NOT COMPATABLE WITH SURVIVAL!!!
72
Malformation of the Bloods Vessels
- Vena Cavae: relatively Common. Duplications or persistence of Left Instead of Right Segments
- PDA
- Double Aortic Arch
- Right Aortic Arch
- Coarctation of the Aorta
73
Right Aortic Arch
- Persistence of Right 4th Arch Distal to the Right Subclavian
- Left segment Caudal to Left Subclavian disappears
- Isolated
- SITUS INVERSUS COMLEX!!!!
74
Double Aortic Arch
- Segment of Right 4th Aortic Arch CAUDAL to the Right Subclavian Persists
- VASCULAR Ring around Trachea and Esophagus
**Get Vascular Ring around the Esophagus and Trachea that can Compress the Esophagus and Trachea, so solid food becomes a problem
75
Contraction of the Aorta
- Coarctation of Aorta Distal to the LEFT SUBCLAVIAN
- Typically new the DUCTUS ARTERIOSUS: Postductal ("Adult") or Preductal ("Infantile")
- Collateral Circulation often includes the ITA and Branches
***Blood runs through the Internal Thoracic Artery and runs through the Anterior Intercostal Arteries to the Thoracic Aorta!!!!
***So the Arteries will become Dilated and the ribs will DISTAL WAVY PATTERNS from the Blood Vessels!!!
76
Case #3
- Blood was getting out of the Aortic Arch but not getting into the DESCENDING AORTA!!!
77
Ectopic Cordis
- Heart outside of the Thoracic Cage
78
Depolarizing Cardiac Muscle
- Just like Skeletal Muscle, Cardiac muscle WONT CONTRACT unless it has been DEPOLARIZED by an ACTION POTENTIAL FIRST
- In the Heart, the Specialized tissue of the SA NODE and the AV MODE spontaneously DEPOLARIZE and GENERATE the Action Potentials that causes the Cardiac Muscle to CONTRACT
- Under normal conditions, the SA Node is FASTER to each threshold than the AV Node, and therefore it serves as the PACEMAKER!!!!
- After the SA node generates the Action Potential, too things happen at about the same time:
1) The AP DEPOLARIZES the ATRIA using the Gap Junctions between the CARDIAC Muscle Cells
2) The AP travels to the AV Node via the INTERNODAL PATHWAY!!!
79
What ECG wave occurs when the Sodium Influx is occurring in Atria Myocytes?
- P WAVE!!!!!
80
Depolarizing Cardiac Muscle Cont
- The CONDUCTION VELOCITY is the AV mode is Slow, so there is a "PAUSE" between the Depolarization of the ATRIA and that of the VENTRICLES, leading to the PR INTERVAL!!!!!
- Once the AV Node transmits the AP to the Ventricles, specialized Cardiac Muscle (The Bundle Branches and Pukinje Fibers) transmit the AP to the Ventricle, DEPOLARIZING the:
1) SEPTUM
- Stiffened Septum is like the backbone for the Ventricular Contraction and then starting from the bottom up, it is effectively squeezing the blood out of the Ventricle
2) Free wall of both Ventricles tarting from the APEX back up!!!!
81
What wave is positive and the hight peak?
- R WAVE!!!!
82
What event begins after the wave comes from from the R Wave?
- VENTRICULAR REPOLARIZATION!!!!!
**Pulseless Electrical Activity: Next to Dead. Normal heart electricity but Mechanical events are all MESSED Up!!!
83
Summary: Depolarizing Cardiac Muscle
1) Both the SA Node and the AV Node can generate Spontaneous Action Potentials
2) Under normal conditions, the SA Node is FASTEST and Serves as the NORMAL PACEMAKER for the Heart
3) When the SA NODE fires, the AP is spread through the Atria (Gap Junctions)
4) The AV Node receives the Depolarization fro the SA Node via the Internodal Pathway
5) The AV Node is slow to conduct the AP to the Ventricle, so there is a very brief "Pause"
6) The Ventricles are the DEPOLARIZED
7) The Ventricles DEPOLARIZE, but the last to DEPOLARIZE are the first to REPOLARIZE!!!!!
84
Definitions
Systole: the CONTRACTION of the Heart. It can be divided into ATRIAL SYSTOLE (the Atria are Contracting) and VENTRICULAR SYSTOLE (The Ventricles are Contracting)
Diastole: the RELAXATION of the Heart. It common to refer to Ventricular Diastole, but eh Atrial do relax too!
Blood Presure: shows as two number, the Systolic Pressure (the Pressure during Contraction) and the Diastolic Pressure (the Pressure at the End of DIASTOLE). t is always written as Systolic/ Diastolic
85
Atrial Systole
- Since the Atria DEPOLARIZE First, they contact first- this INCREASES the Pressure in the ATRIA
***Atrial Pressure INCREASES as the Atria CONTRACT!!!!
***The Ventricular Pressure INCREASES as Blood is Pushed from the Atria into the Ventricles!!!!!
- Ventricle Pressure line is right below the Atrial Pressure line
86
Ventricular Systole
- After the Atria contract and begin to Relax, the Ventricles start to Contract
- The pause while the AV Node was slow gives the Atria time to do their job before the Ventricles start to CONTRACT!!!
- Because the SEPTUM was DEPOLARIZED First, it also CONTRACTS FIRST!!!
- This "STIFFENS" it!
- The walls of the Ventricles Contract Next, squeezing the Blood in the Chambers
- This INCREASES the Pressure in the Ventricles
**Contraction of the Ventricles will begin shortly after the QRS Complex. There is a BIG INCREASE in Ventricle Pressure!!! With Ventricle contraction, the Atrial Pressure Increases with a little Glitch as well from the "Back Pressure" from the Ventricle (PASSIVE PRESSURE CHANGE)
87
Why is Atrial Pressure Increasing during Ventricular Systole?
- Blood continues to return to the Heart during the Period of Ventricular Systole, but cant move into the Ventricles because of the Ventricular Contraction. This causes the Atrial Pressure to Increase!!!
88
Ventricular Diastole
- The Relaxation of the Ventricles begins, causing a DECREASE in the VENTRICULAR PRESSURE!!!
89
What are the Pressure in the Ventricle at the Lowest and Highest
Highest: above 120 mm Hg
- Because it has to just exceed Atrial Pressure
Lowest: around 0 mm Hg
90
Atrial Systole
- The pressure in the Atria exceed the tin the Ventricle and FORCES the Blood in the Atria to move into the Ventricle
1) Aortic Pressure: Quite a bit ABOVE the Atrial and Ventricular Pressures sot that it can drive the Blod out of the Periphery
2) Ventricular Pressure: Starts to rise dramatically
3) Atrial Pressure: Has a little blimp and then stays leveled
4) Ventricular Volume: Stays about level
***The Atria basically "Top Off" the Ventricles, so the Volume Change is creatively Small!!!
91
Ventricular Systole
- After the Atria CONTRACT and Beign to RELAX, the Ventricles start to CONTRACT
- Almost immediately, the Ventricular Pressure exceeds the Atrial Pressure, causing the AV Valves to Close, Preventing Blood from Flowing back into the Atria!!!
******The FIRST HEART SOUND ("lub") is associated with the closure of the AV VALVES!!!!!!
- The contract of the Ventricles continues, building pressure in the Ventricles...
In any blood being ejected now?
- NO, the pressure in the Ventricle must exceed the Pressure in the Pulmonary artery and Aorta before the valves leaving the ventricles will OPEN!!!
- Ventricle VOLUME remains constant, while the Ventricular Pressure INCREASES Dramatically!
* ******* This is the period of ISOVOLUMETRIC CONTRACTION!!!!!
92
What actually makes the sound of the First Heart Sound?
- The sound is the result of Blood in the Atria hitting the Closed Valves as it tries to ENTER the VENTRICLE. That impact creates Vibration in the Cardiac Tissue that can be heard!!!
93
Ventricular Systole Cont
What Pressure does the L and R Ventricle have to reach before the Valves Open?
- Normal Aortic Pressure is 120/70
- Normal Pulmonary Artery pressure is 25/15
- The Ventricular Pressure must EXCEED the DIASTOLIC PRESSURE on EACH SIDE to OPEN THE VALVE!!!
- When the Ventricular pressure exceeds that in the Artery, the valve is "Forced" OPEN!!!
- The Blood is then EJECTED from the VENTRICLE into the ARTERY
- Once the Ventricular Pressure EXCEEDS the Aortic Pressure, the Aortic Valves open and Blood is Ejected from the Ventricle
- This ends the period of ISOVOLUMETRIC Contraction, indicated by the Black Bars!!!
SLIDE 38 of CARDIAC CYCLE LECTURE!!!!
94
Ventricular Systole Cont
- Blood is EJECTED until the Ventricle begins to RELAX and PRESSURE within the Ventricle begins to DECREASE!!!!
- As the Volume in the Ventricle starts to Decrease, the Pressure starts to dip slightly
- The Ventricles will EJECT 60 to 70% of the blood inside them during Systole!!!
95
Ventricular Diastole
- When the Pressure in the Ventricle DROPS below the Arterial Pressure, the Aortic and Pulmonary (Pulmonic) valves CLOSE!!!!!
- Now we are relaxing the HEART!!!
- The CLOSING of the Aortic Valve produces the DICROTIC NOTCH int eh Aortic Pressure Wave!
- The Atrial Pressure shows a Similar "Wiggle"
- The SECOND HEART SOUND is associated with the CLOSING of the AORTIC and PULMONARY VALVES
- It is produced when the Blood in the AORTA/ PULMONARY Artery BACKFLOWS and "Bounces" off the closed valves...
Why does the Blood "Backflow" when the valves close?
- When the valves close, the FORCE driving the blood forward (the Pressure in the Ventricle) is "CUT-OFF" from the blood and gravity is FREE to PULL the Blood Back DOWN!!!
- We now begin a period in which NO BLOOD ENTERS or LEAVES the VENTRICLE while it is RELAXING (Both the AV and Aortic Valves are CLOSED)
- This is the Period of ISOVOLUMETRIC RELAXATION!!!
96
Ventricular Diastole Cont
- When the ATRIAL Pressure exceeds the Ventricular Pressure, the AV Valves WILL OPEN, and Blood will MOVE FROM the Atria to the Ventricles (Note that the Atria are almost certainly NOT contracting at this point!!!)
- At this point the Ventricles are filling up with Blood and will continue to until the Next Contraction
What Pressure does the Left and Right Ventricle have to be at for the Blood to Enter the Atria?
- The VENTRICULAR Pressure must be LOWER than all the PRESSURE during DIASTOLE for blood to MOVE from HIGH Pressure to LOW Pressure!!!
- Because the Ventricular Pressure and Volume are both VERY LOW when the AV Valves Open, Blood flows into the Ventricles VERY RAPIDLY!!!!!!
- The Blood Rushing into the Ventricle during the RAPID FILLING PHASE creates the THIRD HEART SOUND!!!!!!
- This sound is NORMAL in CHILDREN, but may or may not be heard in ADULTS!!!
97
Ventricular Diastole Cont.
Why is the Aortic Pressure Still Dropping?
- The Blood is leaving the Aorta and flowing into the Smaller Vessels in the Periphery. The rate of this PERIPHERAL RUN-OFF is determined by the RESISTANCE to BLOOD FLOW!!!!!
- The A WAVE is the Pressure Wave created by the ARTERIAL CONTRACTION. Since there is NO VALVE between the Atria and Great Veins, the Pressure is REFLECTED BACKWARDS!!!!!!!!!!
- The C WAVE is the Pressure wave created by the period of ISOVOLUMETRIC CONTRACTION in the Ventricles- there is BULGING of the WALL back into the ATRIA!!!!
- The V WAVE is the Pressure wave created as Blood RETURNS back to the HEART but cant enter the VENTRICLE!!!!!
- There is a FOURTH HEART SOUND that may be heard during the Atrial Contraction. It is the RESULT of that last little bit of Blood being SQUEEZED into the Ventricle! Like the Third Heart sound, it is normal in Children but NOT greatly HEARD in a Normal Adult
98
The four normal heart sounds (even S3 and S4 are heard in Normal adults when the Right equipment is used) are the result of blood moving in the EXPECTED DIRECTIONS:
MURMUR is heard either:
1) Blood is moving in a Direction it SHOULDN'T be moving
2) Blood is having a HARD TIME Moving in the Direction it Should be Moving!!!!
99
To Cause a SYSTOLIC MURMUR
MURMUR is heard when either:
1) Blood is MOVING in a DIRECTION it SHOULDN'T be MOVING, in this case, back into the ATRIA, caused by regurgitation (MITRAL REGURGITATION)
2) Blood is having a HARD TIME Moving in the direction it should be moving in. In this case the blood cant get into the Aorta/ Pulmonary Artery due to STENOSIS!!!!!
100
To Cause a DIASTOLIC MURMUR
MURMUR is heard when either:
1) Blood is moving in a Direction it SHOULDN'T be MOVINg, in this case, BACK into the AORTA or PULMONARY ARTERY, caused by Regurgitation (AORTIC REGURGITATION)
2) Blood is having a HARD TIME moving in the Direction it SHOULD be Moving, in this case the Blood CANT GET INTO the VENTRICLE due to STENOSIS!!!!!
101
Cardiac Electrophysiology
- Ventricles, Atri, and Purkinje system have stable resting potentials, rapid upstroke and long duration
1) Phase 0: Rapid upstroke caused by CROSSING THRESHOLD and VOLTAGE Gated Na+ channels OPENING
2) Phase 1: A small DEPOLARIZATION is caused by START of Na+ gates CLOSING and some K+ gates OPENING
3) Phase 2: PLATEUA PHASE is sustained by SLOW Ca2+ CHANNELS OPENING and CLOSING of SPECIAL, VOLTAGE Gated K+ Channels
4) Phase 3: DEPOLARIZATION is caused by SLOW Ca2+ Channels CLOSING and SPECIAL K+ Channels Opening
5) Phase 4: The RESTING POTENTIAL and is SUSTAINED by HIGH K+ CONDUCTANCE
102
Action Potentials in the Sinoatrial Node
- Resting membrane potential (Phase 4) gradually DEPOLARIZES until it reaches THRESHOLD and "Fires". This INTRINSIC, spontaneous DEPOLARIZATION makes the SA node and the PACEMAKER and is said to exhibit AUTOMATICITY
- The AV NODE is Similar but the Phase 4 DEPOLARIZATION is SLOWER so it normally does not REACH THRESHOLD before being stimulated by an Action Potential ORIGINATING in the SA Node
103
Action Potentials in the Sinoatrial Node
1) Phase 0: due to opening of SLOW Ca2+ GATES and CLOSING of SPECIAL K+ Gates
2) Phase 3: due to CLOSING of Ca2+ GATES and the OPENING of SPECIAL K+ Gates
3) Phase 4: due to OPENING of SPECIAL (Funny) VOLTAGE GATED Na+ Gates tat open when the membrane is REPOLARIZED
- No Phase 1 and 2 due to SCARCITY of traditional, VOLTAGE Gated Na+ Channels
104
Latent Pacemakers
- Will naturally DEPOLARIZE to reach Threshold without electrical Stimulation
- AV NODE is similar to SA NODE but with a SLOWER DEPOLARIZATION during PHASE 4 so if it takes over, the rate is MUCH SLOWER
- BUNDLE of HIS and PURKINJE FIBER will remain POLARIZED but if not STIMULATED for an extended period of time will begin to SPONTANEOUSLY DEPOLARIZE during Phase 4! The rate of the Bundle and Purkinje Fibers is SLOWER than that of the AV NODE!
105
Conduction Velocity
- The HIGHER the INWARD (Fast Na+) or SLOW Ca2+, the FASTER the VELOCITY
- Ex: The steeper the Phase 0 Slope, the FASTER the Velocity
- Also, BIGGER the FIBER the FASTER the TRANSMISSION of AP and therefore FASTER the VELOCITY
****Purkinje (and Atrial pathways) > Atrial and Ventricular Muscle > AV Node
***Delay in AV allows Atria to EMPTY into VENTRICLES before VENTRICLES Contract!
106
Excitability and Refractory Periods
- Ability to generate an AP
- REFRACTORY PERIOD is when the Electrolyte Gates have not reset sufficiently to allow a Second AP to be GENERATED
- REFRACTORY PERIOD is important to HELP PREVENT ARRHYTHMIAS!!!
107
Autonomic Effects
- CHRONOTROPIC EFFECT changes rate of Depolarization of SA NODE and therefore Heart Rate (HR)
1) Positive = Faster
2) Slower = Negative
- DROMOTROPIC Effect is SPEED of CONDUCTION!!!
108
Autonomic Effects
1) PARASYMPATHETIC (Vagus)
- To AV and SA Nodes and to insignificant extent to CONTRACTILE MYOCYTES
- Neurotransmitter is ACETYL CHOLINE (ACh)
- Receptor is MUSCARINIC
2) Decrease OPENING of Special (funny) Na+ Gates during Phase 4 in SA and AV Nodes
- DECREASE Depolarization Rate
- DECREASE HR: Negative Chronotropic Effect
3) Decrease Conduction Velocity through AV Node
*****More Parasympathetic effects on the Phase 4 means a longer Phase 4!!!!!!!
109
Autonomic Effects
1) SYMPATHETIC to all of Heart
- Neurotransmitter is NOREPINEPHRINE
- Receptor is Beta-1
2) Increase Opening of SPECIAL Na+ (funny) Gates
- INCREASE rate of Depolarization
- INCREASE HR: Positive Chronotropy
3) INCREASES Conduction Velocity through the AV Node
110
Excitation- Contraction Coupling
- ACTION POTENTIAL spreads, as in SKELETAL MUSCLE
111
Contractility
- CONTRACTILITY is how hard the Cardiac Muscle contact when STIMULATED
- REFERRED to as ISOTROPY
A) POSITIVE INOTROPY = Increased Force of CONTRACTION
B) NEGATIVE ISOTROPY = DECREASED Force of Contraction
- Generally PROPORTIONAL to amount of Ca2+ AVAILABLE to TROPONIN on the ACTIN FILAMENTS
112
Effects of the Autonomic Nervous System- Sympathetic
- SYMPATHETIC STIMULATION of the VENTRICULAR and ATRIAL myocuytes vis NOREPINEPHRINE and BETA-1 causes MORE Ca2+ to enter Interstitial Space during AP and also causes more Ca2+ to be SEQUESTERED in SR!!!!
- POSITIVE Inotropic Effect
- What would the blocking of Beta-1 receptors do?
113
Parasympathetic
- PARASYMPATHETIC SYSTEM Innervates the Atria but only SPARSELY Innervates the VENTRICLES
- PARASYMPATHETIC Stimulation WEAKLY INHIBITS SYMPATHETIC Stimulation and thus has a NEGATIVE INOTROPIC EFFECT!
114
Effect of Heart Rate
- INCREASE HR causes more Ca2+ to accumulate and remain Intercellularly (sequestered in the SR)
- therefore more Ca2+ released per AP and STRONGER CONTRACTION
115
Cardiac Glycosides
- DIGOXIN (Cardiac Glycoside) BLOCKS Na+/ K+ ATPase Pump!!!!!!!!!!!!!
- Intracellular Na+ Concentration INCREASES causing the EXTRA to INTRACELLULAR Gradient to Decrease
- Na+/ Ca2+ EXCHANGER is therefore LESS EFFECTIVE causing INTRACELLULAR Ca2+ Concentration to INCREASE
- More available Ca2+ during CONTRACTION has a POSITIVE INOTROPIC EFFECT without INCREASING Energy demand
116
Definitions
PRELOAD:
- The amount of WALL TENSION in the Right Ventricle right BEFORE Contraction is INITIATED
- Less accurate is the Pressure in the Chamber just BEFORE CONTRACTION
- Least accurate is the Volume in the Chamber just BEFORE Contraction
* * All are INTERACTED but differ DEPENDENT on the SIZE of the Ventricular Chamber
- Ex: A Dilated Chamber has a GREATER WALL TENSION for the same Chamber Pressure as a Non-Dilated Chamber
117
Definitions
AFTERLOAD:
- The amount of Chamber PRESSURE that must be delivered to cause EJECTION of Blood
- A Little Greater than but essentially equal to that of the AORTA or PULMONARY ARTERY
118
Definitions
1) Sarcomere Length:
- The length of the Sarcomere determines the amount of Actin/ Myosin OVERLAP
- The MORE EFFICIENT the Overlap, the GREATER the Tension that can be developed when Contraction is INITIATED
2) Velocity of Contraction:
- Greatest if AFTERLOAD is 0 and is INVERSELY PROPORTIONAL to AFTERLOAD
119
Frank-Staling (Length Tension Relationship)
- The GREATER the PRELOAD the more efficient the Initial Overlap of ACTIN and MYOSIN causing MORE FORCEFUL CONTRATION
- The greater the PRELOAD the greater the FORCE of CONTRACTION, STROKE VOLUME, EJECTION FRACTION, and CARDIAC OUTPUT
120
Stroke Volume, Ejection Fraction, and Cardiac Output
1) END DIASTOLIC VOLUME (EDV) = The Amount of Blood in the VENTRICLE just BEFORE CONTRACTION
2) END SYSTOLIC VOLUME (ESV) = The Amount of Blood LEFT in Ventricle following CONTRACTION
3) STROKE VOLUME (SV) = The Amount PUMPED OUT per BEAT
****SV= EDV-ESV
****Ejection Fraction= SV/EDV
**** Cardiac Output = SV x HR
121
Stroke Volume
1) Stroke Volume (SV) = The Amount of Blood PUMPED OUR with each BEAT
2) CARDIAC OUTPUT = Stroke Volume x Heart Rate
3) EJECTION FRACTION = Fraction or Percent of Blood PUMPED OUT with EACH BEAT
122
Frank-Starling
- Changing the ISOTROPY of the Heart will Change the position of the RELATIONSHIP
- Positive influences will INCREASE the Stroke Volume, Ejection Fraction, and Cardiac Output
- A negative INOTROPIC Influence will DO THE OPPOSITE
123
Ventricular Pressure- Volume Loops
1) Increased Preload
2) Increased Afterload
3) Increased Contractility
124
Cardiac Work
- Work per Heart Beat
- Stroke Volume x Aortic Pressure
- STROKE WORK dependent on:
A) AFTERLOAD
B) DIAMETER of Chamber (Greater Diameter = Less Efficient)
C) INOTROPIC State
- Minute work is HOW MUCH work per minute and is therefore DEPENDENT on HEART RATE (= Stroke Work x Heart Rate)
125
Measurement of CO
- Three ways to MEASURE:
1) FICK
2) THERMODILUTION
3) DYE
- All 3 rely on PUTTING a KNOWN QUANTITY of material into the Blood and Measuring how much is DILUTED. The more Diluted it becomes in the Blood, the GREATER the CO and can be CALCULATED!
1) FICK:
- Add )2 vis LUNGS (O2 Consumption) and measure O2 difference BEFORE and AFTER Lungs
2) THERMODILUTION:
- Add Cold Fluid in PULMONARY ARTERY and MEASURE Downstream how much it cools the blood
3) DYE
- Add a quantity of Dye and measure how much the Color Change is DOWNSTREAM
