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287 Cards in this Set

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What layers make up the pericardium?
An outer Fibrous Pericardium

An inner Serous Pericardium (Inner Visceral Layer and Outer Parietal Layer)
There are three divisions
The Pericardium is associated with several structures on its Anterior, Lateral and Posterior sides. They are:
Anterior: Two Pleural Sacs and The Surface of the sternum + 4th and 5th intercostal spaces (@ deviation of the pleura)

Posterior: Esophagus, Descending Aorta, Thoracic Aorta, Main Bronchi

Lateral: Drapes of the Mediastinal Pleura which overlay the Phrenic N. and Pericardiacphrenic Artery and Vein
The Pericardium maintains its position in the thorax via attatchments from:
Anterior: Anchoring sternum via Sternocardial Ligaments

Posterior: Anchoring to the Tracheal Bi-furcation thru Membranous CT
The Pericardium is continous with what fascia superiorly?
Pre-Tracheal Fascia
The Pericardium receives its cirulation via:
Arteries: Pericardiacophrenic Arteries, Musculophrenic Arteries, Branches of the Thoracic Aorta (Bronchial, Esophageal, and Superior Phrenic) and Coronary Arteries (The Visceral Layer of the Serous Pericardium only)

Veins: Internal Thoracic Veins and Tributaries of the Azygos System
The Pericardium is innervated by:
The Phrenic N. in the Fibrous and Parietal Layers

The Cardiac Plexus in the Visceral layer
Remember that the Fibrous and Parietal Layers are the only ones that have pain sensation...
The Fibrous Pericardium is composed of?
Dense Connective Tissue
What is the function of the fibrous pericardium and what specializations does it contain?
It functions to keep the heart in a relative position within the Thorax and also limit the ammount of distension that it can accomplish during contraction.

The layer is thus quite inelastic
The Fibrous Pericardium fuses with what structures to maintain its position in the Thorax?
Superiorly: The Adventita of the Superior Vena Cava, Ascending Aorta, Pulmonary Arteries

Inferiorly: Central Tendon of the Diaphragm
What structure is Parietal Layer closely adherent to?
The Fibrous Pericardium
The Visceral Layer is bound loosely to the heart through what underlying structures?
Loose CT
Adipose Tissue
Blood Vessels
The Visceral Layer of the Heart encases the entire heart except for a very small area known as the Irregular Area. Where is this located?
Myocardium contacts the Fibrous Pericardium between the Vena Cava and Pulmonary Veins.
What is the Pericardial Cavity
This is a potential space that is formed in the gap between the Parietal and Visceral Layers of the Serous Pericardium
What are the basic features of the Cardiac Muscle?
Nuclei, Size, Connections, Impulse Conduction?
They contain one centrally located nuclei
It is striated just like skeletal muscle
The cells are much smaller than skeletal muscle
The many cells seen in a cross section are connected via Intercalated Disks
They contain T-tubules in a Diad association with the Z-lines
They are DEPENDANT on Extra-Cellular Ca+
What are the three components of the Intercalated Disks?
1. Fasica Adherens (Transverse Component)
Actin Filaments insert from end Sarcomeres
Do NOT occur in a belt pattern but sparsely
2. Macula Adherens (Trans. and Lat.)
Contain desmosomes and anchor cells together firmly using Intermediate Filaments
3. Gap Junctions (Lat. Component)
Allow for the spread of depolarizing impulses across Myocardium
What specializations to Cardiac T-tubules posess?
They are much larger in diameter than their skeletal counterparts and contain much greater concentrations of EC Ca+
What role does EC Ca+ play in the Strength of Cardiac Contraction?
Cardiac Muscle cells contract through a Calcium triggered Calcium Release Mechanism...In other words the EC calcium introduced into the cell stimulates the release of Intracellular Ca from the SR...This essentially exponentially increases the ammount of Ca+ in the Cardiac cells at contraction as opposed to muscle cells who use Na+ to accomplish the SR release.
What is the role of the Endocardium?
This layer lines the interior of the Heart and prevents clot formation on the underlying Collagenous Structures that make up the cores of Valves, Septum and Chordae Tendinae.
What special structures are located in Subendothelium?
The Purkinje Fibers that run in the interventricular space
The CT Skeleton of the heart has two important structures called the?
Annuli Fibrosi- create the CT cores of Valves

Chora Tendinae- connect papillar muscles to valves.
What are the two area of the Right Atrium ?
Sinus Venarum- Derived from the embryonic Sinus Venosus it is the smooth part of the posterior Atrial wall that receives the Vena Cava and Coronary Sinus

Pectinate Muscles and the Auricles- Muscular portion of the Atria that is divided from the Sinus Venarum by the Crista Terminalis
What structures does the Left Atrium Receive?
The Four Pulmonary Veins
Muscular irregularities on the interior surfaces of ventricles are known as?
Trabeculae Carnea
What specialized structures are located in the Right Ventricle?
Septomarginal Trabeculum or Moderator Band-makes a bridge for the R. Branch of AV bundle to the Anterior Papillary Muscle

Conus Arteriosus- Cone-shaped pouch that leads in the the pulmonary trunk
When compared to the interior of the R. Ventricle the Left Ventricle:
Has much finer and more numerous Trabeculae Carnae
A wall that is up to 2X thicker
The Left Ventricular wall contains a smooth passsageway in its lumen that leads into the:
Ascending Aorta
The depression located on the Interatrial Septum is known as the?
Fossa Ovalis...a remnant of the embryonic Fossa Ovale and Valve
An Atrial Septal Defect has what consequences? What percentage of the population does this malformation affect?
Blood is shunted from Left to Right causing an overload in the pulmonary system and enlargement of the Right heart compartments and Pulmonary Trunk. This affects Approx. 25% of people
The Interventricular Septum is composed of 2 parts:
A musclar part derived from embryological Ventricle

A Membranous Part in the superior and posterior portions of the septum
Where to Interventricular Septal defects commonly occur?
In the Membranous Portion of the Septum
Cardiac Formation begins at what week in Developmet? What events mark this time period?
4 weeks...Cardiac Tube Looping
In the normal looping pattern the Cephalic or Superior portion of the tube moves _______ while the Caudal or Inferior portion of the tube moves _______?
The Cephalic portion grows anteriorly and caudally at a slight angle to the right moving into position to become the future ventricle

The Caudal portion moves posteriorly and crainally at a slight angle to the left.
A reversal of the this looping process will lead to a condition known as?
Dextrocardia where the heart lies on the Right side of the chest.
During Cardiac Septation the nerual crest cells migrate to what structures to proliferate?
Conotruncal Ridges located along the Conus Cordis and Truncus arteriosus.
The Aorticopulmonary Septum or Conotruncal Septum divides the heart tube into two parallel tubes the:
The Aorta and The Pulmonary Trunk
In the condition known as Transposition of the great vessels what abnormalities are seen?
The Aorta opens into the R. Ventricle

This is due to failure of the Aorticopulmonary septum to develop in a spiral fashion.
What is the most common cause of Cardiac Failure in Newborns
Failure of the Aorticopulmonary Trunk to develop in a spiral fashion.
The Atrioventricular Septum and Interventricular Septum develops from?
4 Endocardial Cushions or Atrioventricular Cushions...1 Post, 1 Ant, 2 Lat.
What is the most common cardiac malformation?
When the membranous portion of the interventricular septum fails to develop and Ventricular Septal Defects Occur.
Describe the structures and events that lead up to Atrial Septum formation.
Septum Primum forms small hole called Osteium Primum or Foreamen Primum

The Ostium Secundum is created via apoptosis of the Septum Primum

Septum Secundum begins forming to the right of the Septum Primum...this structure contains the Foreamen Ovale.

The Septum Primum and Secundum partially overlap each other and at birth the arrival of oxygentated blood and increased pressure causes the two to slam together and eventaully close permanantly.
Describe the flow of blood through the heart including the entering and exiting vessels:
From SVC, IVC, Coronary Sinus and Anterior Cardiac Veins to the R. Atrium....Thru the Tricuspid Valve into the R. Ventricle...Thru the Semilunar Valve into the pulmonary trunk thence pulmonary arteries...Oxygenated blood form the lungs enters into the L. Atrium via 4 Pulmonary Veins...Thru the Mitral Valve into the L. Ventricle...Thru the Semilunar valve and into the Ascending Aorta.
Which cusp of the Tricuspid valve is associated with the Moderator Band?
the Anterior Cusp
What is the most commonly diseased valve of the heart?
Mitral Valve
What does prolapse of the valve and the subsequent Hemodynamics of blood do to the endothelium?
Causes erosion and thus and irregular surface. Allows transient bacteremias to colonize the surface of the heart easier.
What is the purpose of the Aortic Sinuses and where are they located?
The Aortic Sinuses are located just behind the cusps of the Aortic Semilunar valves on the aortic side...They allow the blood pumped out by the left ventricle to pool and then fill the Coronary Arteries.
The Myocardium and Epicardium are supplied which arteries?
Coronary Arteries
There are two branches of the coronary arteries both a left and a right...each of these gives of subsequent branches, name them:
Left: Right Marginal Artery and Posterior Descending Artery (Usually)

Right: Circumflex Artery and Anterior Descending Artery

There is an SA Nodal Artery that is given off 60% of the time by the R. Coronary and 40% of the time by the L. Coronary
How do we determine heart dominance?
By locating the Posterior Descending Artery and determining it source i.e. the L. or R. Coronary Artery
Where are the 3 common sites for occlusion to the hearts blood supply?
L. Anterior Descending Artery
Right Coronary Artery
Circumflex Artery
What role does heart dominance play in assessing the severity of Coronary Artery occlusion?
This artery determines which artery functionally supplies more of the heart the left or the right and thus if an occlusion is opposite of heart dominance then the outcome is generally better (but not much)
What is the main venous drain for the heart?
3 major veins: Great Cardiac Vein, Anterior Interventricular Vein and Middle Cardiac Veins
All feeding into the coronary sinus
Anterior Cardiac Veins...
Provide very small caliber venous drainage of the heart and drain directly into the R. Atrium.
In fetal circulation Arteries and Veins are named for the direction of blood flow in relation to?
The Fetus
What are the three vessels of the umbilical cord?
2 umbilical arteries which carry unoxygenated blood AWAY from the fetus to the mother.

1 Umbilical vein carrying Oxygenated blood TO the fetal heart.
From what embryonic structures do the Medial Umbilical Ligaments form?
Umbilical Arteries
From what arteries to the Umbilical Arteries branch off of?
The Internal Iliac Arteries
From what embryonic structure does the ligamentum teres form?
The Umbilical Vein
Describe the flow of Fetal blood through the heart:
The Umbilical Vein bypasses the live and feeds Oxy-Hb into the IVC whcih feeds into the right atrium and mixes with Deoxy-Hb coming down from the SVC (Shunted Blood)...Blood can then flow 1. Thru the Foreamen Ovale and into the L. Atrium or 2. To the R. Ventricle to be shunted to the Aorta via the Ductus Arteriosus.
The Cardiac Plexus can be described in its fiber content as:
A mixture of Sympathetic and Parasympathetic Fibers
Soma from Sympathetic N. originate in?
The Lateral Horns of spinal segements T1-T5 or from Cervical Nerves
Where do Pre-ganglionic Sympathetics Synapse?
in one of 8 Superior Thoracic Paravertebral Ganglion or one of 3 Cervical Ganglion
What structures do Post-Synaptic Sympathetics travel to in the heart?
To the SA and AV Nodes as well as the Coronary Arteries.
What net effect does the Sympathetic System have on your body and what NT does it use?
Sympathetics utilize Nor-Epi and Epi to stimulate the cardiac system thus increase HR, increase contraction strength and dilate coronary arteries.
Parasympathetic Fibers to the heart come mainly from?
Cranial N. 10 or the Vagus N.
The Vagus N. passes thru the neck associated with what other structures?
The Internal Jugular Veins and The Common Carotids.
The Vagi give off two recurrent branches they are?
The R. and L. Recurrent Laryngeal Branches.
Which Recurrent Laryngeal N. never enters the Mediastinum?
The Right
The Vagus N. delivers _____ to the Cardiac and Pulmonary Plexus.
Pre-Synaptic Parasympathetic N. Fibers....They do not synapse until they are within the organ walls!
The Anterior and Superior Vagal trunks arise from?
The Vagus N.
The Parasympathetic System uses what NT to cause what Net Effect on the heart.
It uses Acetyl-Choline to depress the cariac system. It slow the HR, Decreases the force of contraction and Constricts the Coronary Arteries.
Visceral pain associated with the heart follows the path of?
Sympathetic Nerves responding to Ischemia ...Thus the associated pain is seen in dermatomes C8-T5.
The Sinoatrial Node or SA is also known as?
The pacemaker of the heart
Where is the SA Node located?
Between the SVC and the Superior end of the Crista Terminalis
The SA Node conducts impulses through the wall of the R. Atria via:
Internodal Fibers
The AV Node conducts impulses thorugh:
The Membranous part of the Interventricular Septum.
The AV Node splits into:
Right and Left Bundle Branches

The Right Bundle passes through the Moderator Band
What structures do Post-Synaptic Sympathetics travel to in the heart?
To the SA and AV Nodes as well as the Coronary Arteries.
What net effect does the Sympathetic System have on your body and what NT does it use?
Sympathetics utilize Nor-Epi and Epi to stimulate the cardiac system thus increase HR, increase contraction strength and dilate coronary arteries.
Parasympathetic Fibers to the heart come mainly from?
Cranial N. 10 or the Vagus N.
The Vagus N. passes thru the neck associated with what other structures?
The Internal Jugular Veins and The Common Carotids.
The Vagi give off two recurrent branches they are?
The R. and L. Recurrent Laryngeal Branches.
Which Recurrent Laryngeal N. never enters the Mediastinum?
The Right
The Vagus N. delivers _____ to the Cardiac and Pulmonary Plexus.
Pre-Synaptic Parasympathetic N. Fibers....They do not synapse until they are within the organ walls!
The Anterior and Superior Vagal trunks arise from?
The Vagus N.
The Parasympathetic System uses what NT to cause what Net Effect on the heart.
It uses Acetyl-Choline to depress the cariac system. It slow the HR, Decreases the force of contraction and Constricts the Coronary Arteries.
Visceral pain associated with the heart follows the path of?
Sympathetic Nerves responding to Ischemia ...Thus the associated pain is seen in dermatomes C8-T5.
The Sinoatrial Node or SA is also known as?
The pacemaker of the heart
Where is the SA Node located?
Between the SVC and the Superior end of the Crista Terminalis
The SA Node conducts impulses through the wall of the R. Atria via:
Internodal Fibers
The AV Node conducts impulses thorugh:
The Membranous part of the Interventricular Septum.
The AV Node splits into:
Right and Left Bundle Branches

The Right Bundle passes through the Moderator Band
Nodal Fibers are derived from:
Caridac Muscle cells that have become specialized to conduct impulses through the heart instead of contract. They are generally smaller than cardiac muscle cells.
What is the bundle of His?
This is the Common AV bundle that splits into the Left and Right AV bundle after passing through the Atrioventricular septum.
Purkinje Fibers are located in what layer of the heart?
They run through the Subendothelial layer of the Ventricles.
What specializations do Purkinje Fibers posess?
They lack T-tubules and have little to no cytoplasmic myofibrils thus they have no no contractile function...They do however transmit impulses about 4 times faster than cardiac muscle.
The Heart displays "En Passant Innervation" what does this mean?
1 Nerve innervates many cells along its path.
What Lymphatics do the superficial tissues of the chest drain into?
Axillary and Internal Thoracic Nodes
What Lymphatics do the Deeper Tissues of the chest drain into?
Internal Thoracic, Intercostal and Diaphragmatic Nodes collect the Lymph and they all drain into the Lymphatic Duct
What Lymphatics does the heart drain into?
Into the Left and Right collecting ducts and then into the Inferior Tracheobronchial and Brachiocephalic Nodes
Deep Lymphatics run where?
They follow the air passageways.
What Lymph Nodes merge to form the Right and Left Bronchomediastinal Trunks?
The Brachiocephalic and Posterior Mediastinal Nodes
What merges to form the Intercostal and Diaphragmatic Nodes?
The Right and Left Bronchomediastinal Trunks and the Internal Thoracic Duct.
What portions of the body does the Thoracic Duct drain?
It drains the entire body except for the right side of the head, neck, upper limbs, thorax and right upper surface of the liver.
Where does the Thoracic Duct drain into the Venous System?
at the junction of the Internal Jugular and Subclavian Veins
From the surface where would one estimate the Superior Border of the Heart and the Origins of the Great Vessels?
At the 2nd Intercostal Space...Behind the sternum and one fingers breadth to either side of the sternum.
From the Surface where would one estimate the location of the Inferior Border of the Heart?
At the 5th Intercostal Space...behind the sternum and one fingers breadth to the right and one hands breadth to the left
From the surface where would one estimate the location of the Superior Vena Cava?
Behind the 3rd Costal Cartilage...on the Right Side of the sternum
From the surface where would one estimate the location of the Pulmonary Trunk?
The upper portion of the 3rd Costal Cartilages...on the left side...It bi-furcates superiorly just deep to the 2nd Costal Cartilages.
From the Surface where would one estimate the location of the Aorta?
The 3rd Intercostal Space to the left of the Sternum.
Where does the Mediastinum make contact with the Costal Cartilages?
At Costal Cartilages 2-4
What Costal Cartilages indent the Left Pleura?
Costal Cartilages 4-6
From the Surface where can the Anterior Inferior Border of the Pleura of the lungs be located?
It crosses Costal Cartilages 8 at the mid-line.
From the surface where can the Lateral Inferior Border of the Pleura of the Lungs be located?
It crosses Rib 10 at the Mid-Axillary Line
From the surface where can the Posterior Inferior Border of the Pleura of the Lungs be located?
Crosses Rib 12 on the back
From the surface where can the Pleura of de-flated lungs be located?
Approximately two ribs higher than the pleura at their previous locations so...6, 8, and 10.
From the surface where can the Horizontal Fissure of the Right lung be located?
It Begins deep to the Mid-Axiallary Line at Ribs 5 and runs to the sternocostal joint at Rib 4
From the Surface where can the the Oblique Fissures of the Right and Left lung be located?
It begins adjacent to the spine 3 and passes deep to Rib 6 at the Mid-Clavicular lines.
Where is the general location of the Thymus?
It is located deep to the Manubrium and extends downwards to rest on the Mediatinum lying Anterior to the Pericardium.
What is the blood supply to the Thymus?
It is supplied by the Internal Thoracic Arteries and Drained by The Internal Thoracic Vein and Brachiocephalic Vein.
What are Ausculation Points?
They are areas where sounds from each valve can be heard the most distinctly on examination b/c the blood flow is close to and directed at the chest wall.
What is the Ausculation Point for the Pulmonary Valve?
Deep to the 3rd Sternochondral Joint on the Left Side of thesternum.
Where is the Ausculation Point for the Aortic Valve?
It lies deep to the sternal body at the 3rd intercostal space to the left of the sternum.
Where is the Ausculation Point for the Mitral Valve?
It lies deep to the sternal body adjacent to the 4th intercostal space left of the sternum.
Where is the Ausculation Point for the Tricuspid Valve?
Lies behind the Sternal Body adjacent to the 5th intercostal space on theright side of the sternum.
What keeps impulses from traveling backwards up the purkinje fibers and bundle of His to the Atria?
The AV valves are surrounded by an "insulation" of CT Sheet...Annuli Fibrosi
How fast can the SA Node Fibers conduct impulses?
3/10 m/s
How many pathways can impulses take via internodal fibers?
3....Anterior, Posterior, Middle.
How is the delay between Atrial Contraction and Ventricular Contraction Caused?
By the AV Node which is composed of Transition Fibers
What special features of Transition Fibers allow them to delay impulses?
They are smaller in diameter and contain fewer gap junctions which effectively increases their resistence.
What is the Bundle of His composed of?
Purkinje fibers
How fast can a Purkinje Fiber conduct impulses?
1.5 - 4 m/s
How is it that Purkinje Fibers conduct impulses at such great speeds?
They have an increased number of gap junctions.
Explain Automatic Rythmicity:
this is a feature possessed by all cardiac cells but especially in the SA Node

The SA Fibers are essentially leaky for
Na+ and generally have a membrane potential of about -55 to -60 mV vs -80 to -90
What happens when Na+ leakage into SA Nodal Fibers increases the membrane potential to -40 mV?
Ca+ channels open and allow an influx of Ca and Na and generate an action potential.
How is the action potential generated in SA Nodal Fibers stopped?
Ca+ channels are only open for a small ammount of time and then proceed to close...at the same time K+ channels open and allow a efflux of K+ Hyperpolarizing the cell.
How many contractions does the SA Node generate per minute?
Generally about 70-80
What is an Ectopic Pacemaker?
an ectopic pacemaker is an instance when some other object besided the SA Node has taken over rythmically controlling the heart.
What is Strokes-Adams Syndrome?
If there is a sudden loss of SA to AV transmission of impulse then the ventricles cease to beat for several seconds...As a result of hypoxia the body passes out...soon the AV Node will begin to automatically regulate Ventricular contraction again albeit at a slower rate of about 40-60 bpm.
Explain the appearence of the "Plateau" in the action potential of Cardiac muscle vs. the spike in action potential of skeletal muscle.
In Cardiac Cells Fast-Na+ channels open leading to the rapid spike in Action Potential after that Ca+ channels open which stay open slightly longer and allow an influx of both Ca+ and Na+ sustaining contraction. To aid in sustaining contraction the Cell membrane become less permeable to K+ immediately following contraction to slow repolarization.
Do Hyper- and Hypo- Calcemia affect Heart Rates?
Yes, Cardiac Muscle is DEPENDANT on EC Ca+ Concentrations
What does net effect does Nor-epinephrine and Epinephrine released by the Sympathetic system have on the heart?
These substance lead to an increase in
Ca+ permeability thus shortening the time it takes to reach threshold...Nor-Epi can also help the uptake of Ca+ thus increase intra-cellular storage and increase contractile capability.
How long is an action potential delayed in the A/V Nodal Fibers?
approx. 1/10 of a second
When we are looking at an EKG what we are seeing is a recording of?
Changes in conductivity of the skin!
What is the P Wave?
It is the event that immediately precedes Atrial Contraction.
What is the QRS Complex?
It initiates depolarization of the Ventricles...it is the largest event on the EKG...Series of 3 waves in succession.
What is the T Wave?
It represents the repolarization of the Ventricles
What is Heart Sound 1?
This is the "Lub" sounds at the beginning of Ventricular Contraction that we say corresponds with closing of the AV valves (Mitral and Tricuspid)
What is Heart Sound 2?
This is the "Dub" sound at the end of Ventricular Contraction that we say coresponds to the Aortic Valve closing
What is Heart Sound 3?
We assume that this sound correlates to the Period of Rapid Filling of the ventricles during the first 1/3 of Diastole.
What is Heart Sound 4?
We assume that this sound correlates to the Period of Slow Filling in which the atria contracts.
What are the stages of Ventricular Contraction and Relaxation?
Isovolumetric Contraction
Ventricular Ejection-Rapid and Slow
Isovolumic Relaxation
Ventricular Filling- Rapid and Slow
What is Pre-load?
This corresponds to the pressure upon the Ventricles just prior to contraction i.e. at the end of diastole...it is = to the End-Diastolic Volume
What is After-load?
This corresponds to the pressure that the heart exerts upon contraction...it is roughly equal to the pressure of the Aorta which it is trying to overcome.
What is effeciency of the heart?
it is the ratio of work to total chemical energy input...it is generally about 20-25% but can fall as low as 5-10%
What is the Cardiac Index?
It is cardiac output / body SA....it is roughly = to 3
What factors could change the cardiac index?
Changing Contractile Strength of heart
Autonomic Regulation
Metabolic Activity
The condition of the conducting vessels
Ultimately depends on Venous Return*
What does the Frank-Starling Law say?
It says that Venous Return takes into account all factors that can affect the Cardiac Output/Index thus what the veins return = what the heart pumps out.
What is the Frank-Starling Mechanism?
This is the changes in the heart that adjust its function to match the ammount of Venous Return...More blood to the R. Atrium stretches it and thus the sarcomeres and thus it increases contractile strength of the heart and the cardiac output!
What is the Bainbridge Effect?
Along with the Frank-Starling Mechanism..when the R. Atria is stretched it MIGHT see a coupled Increase in Heart Rate and thus increased cardiac output.
What is the main reason that a person would experience CHRONICALLY elevated cardiac outpt?
There is a pathologically related function that causes a decrease in overal periphreal resistence thus increasing venous return! i.e. an AV Fistula or Anemia...
What is an AV Fistula?
A condition where Arterioles by-pass capillary beds and run straight into venules and thus the blood flows much faster and increases venous return...decreases periphreal resistence...
What is the effect of BeriBeri?
BeriBeri is a thyamine defeciency...it commonly causes periphreal vasodialation and thus decreases periphreal resistence...CHRONICALLY eleveated Cardiac Output!
What is the effect of Hyperthyroidism?
In this condition the Thyroid Hormones increase the metabolic rate to such an extent that tissue requirements demand stronger heart contractions and faster heart beat...this causes a general decrease in Periphreal Resistence...CHRONICALLY elevated Cardiac Output!
What problems can lead to a decrease in Cardiac Output?
A decrease in pumping effectiveness
MI, Valvular Disease, Infection
or
A Problem in the Periphreal System to Decrease Venous Return
Blood Loss, Hemorrhage,Acute Vasodilation or Obstructions in Venous System
Through what two mechanisms is the Cardiac Output controlled nervously?
Sympathetics
Parasympathetics
What is Limitation?
The downfall of the heart is that it requires time to supply itself with O2 and Nutrients via Coronary Arteries...During Systole Coronary Arteries Collapse and thus decreasing the ammount of time spent in systole decreases the flow of blood to the Myocardium weakening it...
What happens during the inhibition of Sympathetics?
Sympathetics are ALWAYS discharging at constant rates thus their inhibition is accompanied by a decreased HR, Sympathetic Tone and strength of contraction...overall decreased Output of 30%!
What effect does Acetycholine released by Parasympathetics have on the heart?
AcH causes an increased membrane permeability to K+ which leads to hyperpolarization and slower rythmicity.
Why do Parasympathetics play little to no role in decreasing the contractile strength of the heart?
Because the fail to innervate the Ventricles which ultimately determines contractile strength...
What is Hyperkalemia? Its' Consequences?
This is an increase in the concentration of K+. this causes inhibition of depolarization and mimics a hyperpolarized state and weakened contractions.
What is the cause of dilated cardiomyopathy?
Chronic Hyperkalemia which leads to a dilated, soft and flaccid heart.
Why should K+ be "Slow Pushed" when administered to a patient?
Because too much K+ can lead to complete blockage of the conduction b/t Atria and Ventricles and cause FATAL Arrythmias.
What does Hypercalcemia Cause?
It mimics a depolarized state in the heart and leads to spastic contractions and increasing excitability and HR...
What does Hypocalcemia Cause?
It generally mimics Hyperkalemia...Hyperpolarized state...leads to Dilated Cardiomyopathy like symptoms.
What effect does Temperature have on heart rate and why?
Increasing Temps lead to increasing HR and conversely Decreasing Temps lead to Decreasing HR...This is due to the Q10 principles and rxn rates...
An EKG is?
A overall measurement of net electric potential!
What are the two ways to record EKG's?
via oscilloscope or stationary pen and paper that moves with change in electrical impules = Rythym Strip...
Why is Chart Speed so important and what are the averages?
Chart speed affects the way the rythym strip looks and thus affects proper diagnoses...avg. chart speeds are 5-10 cm/s
What does the PR/PQ Interval measure?
Conduction time b/t Atrial contraction and Ventricular contraction...
What does the ST segment measure?
the time between ventricular depolarization and ventricular repolarization.
What does the QT Interval measure?
The beginning of ventricular depolarization to the END of repolarization.
What does the RR Interval measure?
It measures the time from one ventricular contraction to another ventricular contraction...
When is the only time that waves are produced on the EKG?
during times of partial polarization or depolarization...
What does Einthovens Triangle represent?
electrode attatchment points...
What does Einthovens law state?
That the net sum of voltages of the QRS complex from Leads I and III = Lead II
What is the difference between an Augmented Unipolar Lead and regular Leads I-III?
There are two leads connected to a - terminal and 1 to a positive...aVR, aVL, aVF...
Precordial Leads are located on the:
Chest at positions V1-V6
What is the mean QRS Vector?
this is averages of 2 Leads plotted on a Vectocardiogram and is normally = to about 59 degrees...or relatively the angle of the heart in the chest...
What is a right axis deviation and what might cause this?
A Mean QRS Vector with an angle of greater than 160 degrees...it may be from overload of the pulmonary system...pulmonary obstruction etc.
What is a right axis deviation and what might cause this?
A mean QRS Vector with an angle of les than 40 degrees...it may be from overload of the left system...hypertension or aortic stenosis
What problems will affect the appearence of P Waves in an EKG?
Anything that changes conduction...A problem with Internodal Fibers, SA Node or Av Node will cause an INCREASE in the PR interval...
What factors might be associated with a changing of the mean QRS value?
Changes in Heart orientation such as occur in normal breathing.
Changing body position
Changes in the size of the heart...i.e. Hypertrophy leading to a shift to the corresponding side
Damage to Conduction of the Bundle Branches leading to one ventricle contracting before the other
Damage to Ventricular Muscle such as in M.I.'s
Why does damaged heart muscle cause a change in the mean QRS values?
Dead heart muscle gives the appearence of always being depolarized b/c they have no functional Na+/K+ Pumps...
What is the Current of Injury?
The constant flow of energy from dead muscle to healthy muscle...
How might one pinpoint an area of the heart affected by an infarct?
locating the J-point and knowing the angle of our viewing lead and point us towards the dead portion...+ points to healthy and - points to dead
What are some typical non-cardiac changes in an EKG?
Pericardial Effusion- conductor
Pleural Effusion- conductor
Emphysema- insulation
What is the most common T-Wave abnormality and how is it cause?
Inversion of the T-wave...caused by prolonged depolarization...A L or R Bundle Block, Mild Ischemia or Athletes with slow HR.
What is the effect of Digitalis Toxicity?
It decreases rates of depolarization and thus is useful for people who have premature Ventricular Contraction though too much is toxic and can block all conduction...inverted T-Wave is the first warning of this...
What are the two types of Arrythmia's and which one is worse?
Regular Irregular
Irregular Irregular- Serious!
In the case of an SA block:
There is NO atrial contraction and the AV takes over the pacemaking of the ventricles...Ventricular Escape!
In the Case of an AV block internodal fibers are blocked and can be so to a varying degrees including:
1 degree: Abnormally long PR
2 degree: M1~ PR progressivley lengthens and leads to a QRS drop
M2~ PR is abnormally long and QRS drops at random
3rd degree: Complete blockage of Fibers...AV node takes over pacemaking
What is generally the cause of premature contractions?
An ectopic pacemaker has developed somewhere in the heart.
In premature atrial contraction PAC what is seen?
PR interval is decreased followed possibly by a prolonged heartbeat...so a net Irregular TP...
In Premature Nodal Contractions PNC what is seen?
the AV Node doesn't delay long enough so the QRS wave is superimposed upon the P which may or may not be seen!
In Premature Ventricular Contraction PVC what is seen?
The PR interval is shortened and the QR complex is prolonged...possible T-wave inversion because of delayed conduction and repolarization in ventricles!
What is Paroxysmal Tachycardia?
Rapid Rythmical discharges spreading in all directions of the heart...Can last for minutes or hours...can be stopped by Vagal Stimulation (Carotid Rub)
What is Atrial Flutter?
It is a condition where one side of the atria is contracting while the other side is relaxing (within same atria)...very high contractile speeds of up to 200 bpm
Might see and inversion of P-Wave superimposed over the T-wave
What is Ventricular Fibrillation?
this is erratic, arrythmic Ventricular contraction or Systole without Diastole...Very little blood is pumped and it is fatal without immediate treatment...Defibrillation is the cure...Associated with Irregular QRS complexes!
What is Cardiac Arrest?
This is complete cessation of rythmical impulse in the heart. CPR!!!
Blood flow to tissue if often associated with?
The minimal requirements for sustaining life...
How is acute control of blood flow to the body regulated?
By constriction or dilation of the Arterioles and Metarterioles...primarily Microcirculatory Changes!
How is chronic control of blood flow to the body regulated?
Overtime you can completely change the type (size) of the vessels and number of vessels running to tissues to meet supply and demand.
What are some ways that Humoral Regulation INCREASES blood flow?
Via Oxygen demand to tissue...increase metabolism, increase O2 use = increase blood flow...supply and demand
AND
Through Vasodilation...decreases periphreal resistence and thus blood flow to tissue!
What are some substances that are responsible for Vasodilation humoraly?
CO2, Lactic Acid, K+, H+, Histamine and Adenosine.
What is the most important vasodilator for local blood flow to tissue?
Adenosine
What is Hyperemia?
Excess Blood Flow
Active: Increase in activity of tissue
Reactive: After blood supply has been blocked for a while it increases to recover
What does Autoregulation of Blood Flow accomplish?
This mechanism attempts to keep all values at a constant or normal level...There are factors that can change circulation but these are normally transient changes...
What are some compensatory mechanisms to Vasodilation?
Metabolic: Increased pressure caused by the increase flow of blood in response to low nutrients causes Vasoconstriction
Myogenic: Increased pressure on the smooth muscle causes secondary contraction and thus decreased flow...conversely low flow/pressure causes SM relaxation
What are glomeruli?
These are capillary tufts that filter bloow
What is Tubloglomerular feedback?
this is a mechanism in the kidney that controls blood flow using the Juxtaglomerular apparatus (Barorecepters)
What is the Macula Densa?
This is a specialized region in the wall of the distal convoluted tubule right next to the glomeruli...it functions as a Chemoreceptor for Na+ concentrations
Why is Renin produced and what is its function?
Renin is produced in response to drops in Blood pressure and it works to activate Angiotensin II.
What is Angiotensin II
It is a VERY potent Vasoconstrictor
The Chemosensitive area of the brain monitors what?
Increasing levels of CO2 and H+ which will cause Vasodilation.
Most mechanisms that promote vasodilation in the body involve what substance?
NO
NO is released simply through blood flow via what mechanism?
Increased blood flow increases Endothelial Sheer...damaging Endothelium and releasing NO
What causes vasodilation and associated erection of the penis?
NO
What Arterial pressure is essential to maintain adequate tissue perfusion?
60 mm Hg
Chronically comprimising tissue perfusion leads to?
Creating larger or more vessels to that tissue and thus increasing flow
If Arterial pressure is CHRONICALLY too high to a certain tissue it leads to:
Decreasing size and number of vessels to that tissue
In cases where O2 concentration is low:
The body creates vasculature
Angiogenesis is promoted by what factors?
Vascular Endothelial Growth Factor
Fibroblast Growth Factor
Angiogenin
Angiogenesis is associated with dissolvment of the:
basement membranes of endothelial cells follow by rapid production/division...BM "Sprouts" out and forms small tubes until they contact other vasculature forming Vascular Loops!
Name the Humoral Regulators with Vasoconstricting Effects:
Epinephrin and Nor-Epi
Angiotensin II
Antidihuretic Hormone (ADH)
Endothelin
Prostaglandins F series and Thromboxane A2
Nor-epinephrine Vasoconstricts by interacting with:
Alpha Adrenergic Nerves
What is the most potent Vasoconstrictor?
Antidihuretic Hormone (ADH)...
What does Antidihuretic Hormone do?
It works to increase water absorption in the renal tubes...retention of water
What is Endothelin?
It is a vasoconstrictor produced by damaged endothelial cells and causes vasoconstriction at the LOCAL site of injury!
Name the Humoral Regulators with Vasodilating Effects:
Bradykinin
Histamine
Prostaglandins E Series
Describe the activation of Bradykinin
Kallikrein is an actively circulating molecule that is inactive...activated by damage/rupture of cells and inflammation...Kallidin is released and converted by tissue enzymes into Bradykinin
What is the primary function of Bradykinin?
It is a powerful Vasodilator that causes leaky vessels allowing Macrophage migration in damage...it lasts only a short while as Carboxypeptidases break it down!
Why does Histamine cause pain?
Because a long with Vasodilation it can cause damage to some nerve endings.
When is the heart adequately perfused?
Only during Diastole!
Where is the pressure greatest during Myocardial contraction?
Subendocardium...thus most susceptible to anoxic damage!
What is the most common Coronary Heart disease?
Ischemic Heart Disease
What is the most frequent cause of Ischemia in Cardiac Tissue?
Atherosclerosis
What causes Atherosclerosis?
Genetic predisposition...High Cholesterol leading to plaques which cause Thrombus which release emboli and create Thromboembolic Disease!
What causes the pain we call Angina?
The build-up of Lactic-Acid and Histamine released when cells are damaged
What causes "Transient Episodes" of Ischemia?
Coronary Artery Spasms
Coronary Artery Spasms are induced by?
Extreme Emotional Outbreaks
Exercise
Where is Angina Felt?
Around the sternum radiating to the Left shoulder.
What are two common treatments of Angina?
Nitroglycerin and Aspirin
Sympathetic Stimulation of alpha receptors causes?
Usually periphreal Vasoconstriction
Sympathetic Stimulation of Beta 1 Receptors causes? Beta 2's?
Beta 1 = increase heart rate and strength

Beta 2= Vasodilation
What is the use of Beta Blockers?
These decrease Sympathetic Stimulation to the heart and thus they can decrease arrhythmias...they are very specefic for B1 or B2
Why is Ischemia in the heart bad?
It leads to decreased Cardiac Output and
Venous and Pulmonary Pooling leading to Pulmonary Edema
It can also cause Fibrillation if damage occurs in the conduction systems
The heart can potentially Rupture due to the weakened dead cells
Why is it so important that one rest after an M.I.?
Because there is a zone of dead cells and a zone of DAMAGED cells that will recover so long as there is suffecient O2...Increasing their workload increases their O2 needs and decreases the chances that they will maintain adequate O2 to recover...Dead Zone Grows!
What happens to Dead Myocytes?
They are phagocytosed and replaced by Scar Tissue...Collagen...This is called Metaplasia
Why does the Myocardium Hypertrophy around the Scar Tissue over the following months?
Becuase scar tissue has no Contractile function and the muscle around it must hypertrophy to maintain regular function.
What is the difference between Humoral and Nervos Controls?
Humoral is for local changes while Nervous is more Systemic
What is the most important regulator of circulatory pressures?
The Sympathetic Nervous System
What does the Somatosympathetic Reflex do?
this insures that anytime we are exercising or experience pain that Sympathetic stimulation will occur and increase blood pressure
Parasympathetics primarily innervate?
The atria
There are 4 main areas of the Vasomotor area of the brain they are:
Vasoconstrictor area: Use sympathetics to vasoconstrict
Vasodilator Area: Inhibit Vasoconstrictor area to yeild dilation
Sensory Area: Relex control via Baroreceptors of vasoconstriction and dilation
Vagal Center: Control Parasympathetics
Where are Baroreceptors located?
In L. Arteries such as the Aorta, Carotids and Pulmonary Arteries
What are Baroreceptors used for?
To control Transient and Acute changes in pressure such as when you change positions
Chemoreceptors in the walls of some vessels monitor?
Concentrations of O2, CO2 and H+...Ionic Concentrations
Hypoxia and Hypercapnia detected by Chemoreceptors stimulate what reaction?
Increase Arterial Pressures...vasoconstrict and sympathetic stimulation
What is the CNS Ischemic Response?
An event triggered by cerebral ischemia that elevates pressures substantially via vasoconstriction
Hypercapnia in CNS triggers what response?
Periphreal Vasodilation to promote blood flow...
What is the Cushing Response?
It is a detection of increased CSF pressure that prevent movement of nutrients across systemic capillaries...It initiates Vasoconstriction to increase pressure and overcome the CSF pressures allowing diffusion
What is Vasovagal Syncope and what causes it?
Fainting...This is due to activation Cortical Override and subsequent Vasodilator reflexes in the brain which decreases BP and O2 supply
What is Pressure Diuresis?
Increased excretion of fluid by kidneys
What is Pressure Natriuresis?
Excretion of salt through the kidneys
It is impossible to change Arterial Pressures long term without altering either:
Water or Salt concentrations in the body
What is the best kidney mechanism to increase arterial pressure?
Increasing salt content which increases water reabsorbtion and retention
What does an increase in Osmolarity cause?
It stimulates the Hypothalmus to produce Antidihuretic Hormone which causes absorbtion of Water by renal tubules.
Hypertension is defined by blood pressures that near what?
90 mm Hg in Diastole
135 mm Hg in Systole
Why does Chronic Hypertension shorten lifespan?
It increases the workload on the heart
It causes increased damage to the vessels
It can cause Infarts in the brain
It can damage the kidney Glomeruli
What is Toxemia of Pregnancy
It is a thickening of glomerular membrane due to an Autoimmunity disorder which decreases filtration...body responds by increasing pressures...Hypertension
What is Neurogenic Hypertension?
A result of anxiety and sympathetic stimulation...Can lead to chronic hypertension as damage from acute phases slowly begins to add up
What changes are seen in Spontaneous Hereditary Hypertension?
Increased preglomelular renal resistence
Decreased permeability in the glomerular membrane
What is the most common cause of all hypertension?
Essential Hypertension
What causes Essential Hypertension?
There is a strong hereditary component that leads to a failure in the kidneys to secrete salt and water at normal pressures and thus the pressure must be raised in order for excretion to occur.
What are the two major categories of essential hypertension?
Salt Sensitive...restrictive diet helps
Non Salt Sensitive...Diet has little to No effect
What are some treatments for Essential Hypertension
Drugs to increase renal blood flow...Vasodilators
Decreasing resorption of salt and water through natriuretics and diuretics
Diuretic drugs
What are the primary substances that the Kidneys use to work in the body?
Renin, Angiotensin and Aldesterone