CPR Learning Objectives Week 11

Isovolumetric phase (both valves closed) is to isometric\ isotonic contraction as aortic valve opening is to isometric/isotonic

Isometric/ Isotonic

Developing force is to isometric contraction as shortening is to?

Isotonic contraction

Explain why a swallowed sharp object might pierce the heart and into what chamber it could enter

It can penetrate the L. atrium since its anterior to the esophagus

Identify & describe the structure and function of postcapillary venules

FUNCTION: Collect blood from the capillary network and facilitate entry of immune cells (WBC) from lumen into CT b/c desmosomes are easier to reform than tight junctions STRUCTURE: has an endothelial lining (high cuboidal in nature), basal lamina and pericytes; "loosest" zonula occludens SITE OF ACTION OF VASOACTIVE AGENTS: Histamine & Serotonin (acts on blood vessels to loosed bonds and WBC can slip through spaces to go into surrounding tissue)

Identify & describe the structure and function of arterioles

FUNCTION: Flow regulators for the capillary beds by contracting smooth muscle in arteriole walls = inc. vascular resistance = dec. blood to capillaries (DETERMINES BP b/c R inversely proport. to 1/D^4) STRUCTURE: Smallest arteries at <0.1 mm in diameter T. Intima - Emdothelium T. Media - 1-2 layers of smooth muscle T. Adventitia - Ill-defined and merges with surrounding CT

Describe the effects of hypertension on cardiac muscle and smooth muscles in the vessel walls

HTN can cause damage to smaller BVs by scarring, hardening, narrowing BVs and eventually becoming less elastic

Describe the partitioning of the bulbus cordis and truncus arteriosus by the aorticopulmonary septum

Happens in the 5th Week BULBAR RIDGES form w/in BULBUS CORDIS (middle 1/3) TRUNCAL RIDGES form w/in TRUNCUS ARTERIOSUS due to ridges growing towards each other and spiral around each other in 180 degree motion. Fusion leads to AORTICOPULMONARY SEPTUM (divides truncus arteriosus & bulbus cordis into pulm. trunk and ascending aorta)

Describe the typical branching pattern of the aortic arch in the superior mediastinum

Has 3 branches: 1. Brachicephalic trunk (R. Subclavian & R. Common Carotid) 2. L. Common Carotid 3. L. Subclavian

What cardiac pathologies involve negative inotropes?

MI, cardiac failure

Indomethacin (Indocin)

Prostaglandin inhibitor (NSAID); closes ductus arteriosus

Describe the relationships of the esophagus, trachea and thoracic duct in the superior mediastinum

The ESOPHAGUS is posterior to the THYMUS (which is anterior to the superior mediastinum and behind the manubrium). The TRACHEA is adjacent to the right of the esophagus and posterior to the thymus. ESOPHAGUS - Continues from pharynx (C6), enters thorax thorough superior thoracic aperture, passes through diaphragm (T10) & ends at cardiac sphincter THYMUS - Involutes after puberty (replaced by fat) -Artery: Internal Thoracic & Ant. Intercostal -Vein: BC vein, Internal Thoracic, & Inf. Thyroid -Lymph: Parasternal, BC lymph, Tracheobronchial TRACHEA - Continuation of larynx from C6 and stops at Plane of Ludwig to separate into R & L bronchi -Aorta and Azygos veins cross over it

Identify & describe the structure and function of medium veins

-Represent most of the names veins; usually accompanied by arteries and have a d = 10 mm and recognized by valves (folds of T. Intima) STRUCTURE: Supported by fibroelastic CT (prevent backflow/regurgitation of blood) T. Intima - endothelium, thin subendothelial CT T. Media - Circularly arranged smooth muscle cells T. Adventitia - Thicker than T. Media

Describe the structure and functions of vascular endothelial cells

-SIMPLE SQUAMOUS EPITHELIUM (in vessels, tight junctions, & gap junctions) -CONTINUOUS layer of FLATTENED, ELONGATED & POLYGONAL cells lined up in LONG AXES in direction of blood flow -On LUMINAL SURFACE, receptors and surface adhesion molecules FUNCTION: permeable barrier that controls composition of interstitial fluid (brain, lung vs. inflamm. site), moves inflammatory cells into tissue and has a VEGF for angiogenesis in embryogenesis

List the structures that are found at the plane of Ludwig

-SVC goes through pericardium -Includes AORTIC ARCH, TRACHEA BIFURCATION, & PULM. TRUNK BIFURCATION

Describe the changes that may be seen in the walls of muscular arteries and arterioles as a result of hypertension

-Seen when there's 1. symmetrical hypertrophy in smooth muscles in T. Media 2. A lot of reduplication of IEL 3. Fibrous thickening of T. Intima - ALL LEAD TO Dec. LUMINAL DIAMETER OF SMALL ARTERIES/ARTERIOLES = Inc. VASCULAR RESISTANCE

Describe the subdivisions of the mediastinum and their boundaries

5,6,8,9,19-22 Mediastinum = Thoracic area between the two pleural sacs (contains major organs except lungs and highly mobile) with an imaginary plane across the thorax (Plane of Ludwig) ANTERIOR boundary - Angle of louis (manubriosternal joint) and 2nd costal cartilage at Plane of Ludwig (covers manubrium) MIDDLE boundary - Heart POSTERIOR boundary- T4/5 IV disc at Plane of Ludwig (covers T1-T4 vertebrae) Superior Mediastinum SUPERIOR boundary - Aortic arch, 1st rib, T1 INFERIOR boundary - Everything below Plane of Ludwig (T5-T9 vertebrae)

Cardiac Performance (Function) Curve

A Ventricular Function Curve whose y-axis is STROKE WORK (or Stroke VOLUME) and x-axis is RIGHT ATRIAL PRESSURE; can be done clinically; easier to measure RAP a than EDV

Explain how a cervical rib can lead to thoracic outlet syndrome

A cervical rib can compress the subclavian a./v. or brachial plexus significant to C8-T1

Effect of NE on isometric contraction

A chance in contractility means that at every length, the muscle develops more isometric tension with NE present, increasing the peak isometric tension

Inotropism (contractility)

A change in active force development in the absence of a change in preload (i.e. resting muscle length)

Describe the function of von Willebrand factor

Binds clotting factor VIII, platelet adhesion to site of endothelial injury

Identify & describe the structure and function of the myocardium

Consist of cardiac muscle; PRINCIPAL COMPONENT of the heart - in the ATRIA, it's THINNER than the ventricles and gets blood fro LARGE VEINS, delivering it to ADJACENT VENTRICLES (LOW PRESSURE) - in the VENTRICLES, it's THICKER because of HIGH ORESSURE needed to move blood through the pulmonary and systemic circulations

Explain which part of the myocardium will be affected if any of the coronary arteries is occluded

Coronary sulcus

Describe the anatomy of the great vessels, heart chambers and their relationships to one another and to adjacent structures

GREAT VESSELS: Base has LA, proximal pulm. v., part of R. atrium and proximal SVC/IVC; Apex has LV at 5th intercostal space from midsternal RELATIONSHIP: Ant. penetrating wound would puncture the RV. LA is ant to esophagus, so if someone swallowed something sharp it would puncture the LA. Enlarged LA = stenosed esophagus (difficulty swallowing) = dysphagia. WIDTH of heart is DIAPHRAGMATIC MARGIN < one hemithorax (1/2 thoracic diameter). If not, CARDIOMEGALY! -Chest radiograph showing heart = CARDIAC SILHOUETTE

Describe the origin of the greater, lesser and least splanchnic nerves

GREATER - From T5-9 (might be some variation) --> celiac gang LESSER - From T10-11 --> aortico-renal gang LEAST - From T12 (not always there) --> renal plexus

Know the factors that contribute to the formation of turbulent flow

Generally, blood flow is laminar (straight arrows pointing to one direction) Turbulent flow: when rate of blood flow becomes too high, blood flow passes by an obstruction in a vessel and makes a sharp turn (straight arrows try and go through an obstruction and squiggle to different directions) Reynolds number (Re) = measure of tendency for turbulence to occur; If >200-400, turbulence happen and you can hear ejection murmurs, carotid bruits; Re = (VDp)/n V = mean velocity D = vessel diameter p = blood density n = blood viscosity

resting tension

Force required to stretch a resting muscle to different lengths.

Define "lymph"

a colorless fluid containing white blood cells, that bathes the tissues and drains through the lymphatic system into the bloodstream.

Describe the term "aneurysm"

a localized weak spot or balloon-like enlargement of the wall of an artery

pericardial cavity

a potential space between the parietal pericardium and visceral layer

Describe the different classes of blood vessels and how their morphology is suited to their various functions.

aorta divides into a set of ARTERIES which branch repeatedly to form 1ST ORDER ARTERIOLES (r = 30 um), 2ND ORDER ARTERIOLES, 3RD ORDER ARTERIOLES and then 4TH ORDER ARTERIOLES (r = 5 um), which branch to form CAPILLARIES (r = 3 um) and converge to form 4TH ORDER VENULES (r = 5 um), 3RD ORDER VENULES, 2ND ORDER VENULES, and 1ST ORDER VENULES (r = 30 um), which drain into PERIPHERAL VEINS and into the CENTRAL VEINS which empty into the ATRIA. Each blood vessel (except for capillaries) have 3 layers: T. Intima (endothelial cells), T. Media (2 layers of elastic membrane with smooth muscles)and T. Adventitia (CT mainly collagen)

Describe the location of the heart in the mediastinum

in the middle mediastinum

Change in blood volume or venoconstriction/venodilation or slowing HR --> changes VR --> changes EDV --> changes PRELOAD. What does this affect?

inc. VR = inc. EDV (shifts to right) = inc. preload = inc. SV dec. VR = dec. EDV (shifts to left) = dec. preload = dec. SV --> AFTERLOAD stays constant

Change in aortic pressure or total peripheral resistance causes change in AFTERLOAD

inc. afterload = inc. aortic pressure (shifts up) = dec. shortening b/c not enough active isometric tension = ventricles eject less blood = dec. SV = dec. EF. LVEDV stays constant (steep wise) but elevates as afterload increases

Define a portal circulation and state its significance

liver gets O2 blood via hepatic artery and dO2 nutrient rich blood from the spleen/stomach/intestines via the portal vein - digestive products can be further processed in the liver

isotonic contraction

muscle shortens because muscle tension exceeds load; length shortens but tension stays the same and overtime shortening decreases until it can't shorten anymore; muscle fibers contract against afterload

List the subdivisions of the tubular heart

Truncus Arteriosus Bulbus Cordis Primitive ventricle Primitive Atrium Sinus Venosus CEPHALIC ARTERIAL end - Continuous with aortic sac CAUDAL VENOUS end - Opens into sinus venosos from placenta, embryo, and yolk sac

Differentiate between the pathways used by the two types of visceral afferent fibers (carrying pain versus physiologic sensation) from the heart to the CNS

Visceral afferent (pain): move with heart sympas through cardiac plexus --> cardiopulm. nerves --> sympa chain and WRC --> spinal cord segments (T1-4 or 5) Visceral afferent (physiological reflexes like stretch): move with para fibers --> vagus nerves --> brainstem cardiovasc. centers

Decrease in ventricular compliance would pathologically cause?

Ventricular hypertrophy due to uncontrolled HTN

What other parameters are equivalent to SV and EDV?

Ventricular pressure, CO, Stroke work <— contraction Central venous pressure, RA pressure, EDV, EDP <— muscle fiber length (PRELOAD)

List the negative inotropic agents.

Verrapamil (Ca channel blocker), propranolol (B receptor blockr

Describe the course of the pain fibers from the heart to the CNS

Visceral afferent (pain): move with heart sympas through cardiac plexus --> cardiopulm. nerves --> sympa chain and WRC --> spinal cord segments (T1-4 or 5)

Draw, in correct temporal relationship, the pressure, volume, heart sound, and ECG changes in the cardiac cycle

*** Look back at notes when you've drawn it out, 7-37

Identify the three types of capillaries in electron photomicrographs

****REVIEW WHEN YOU SEE THIS QUESTION****

Identify the major anatomical features of the mediastinum, heart, and great vessels in radiographic images, CT and MRI (DLA)

***GO OVER ON DLA SLIDE

Describe the relationships of the phrenic nerves to the aortic arch and the root of the lung

***REMEMBER: C3, 4, 5 keeps the diaphragm alive - ENTRANCE: superior mediastinum b/w subclavian a. & root of BV vein, moves along pericardium and through diaphragm -INNERVATION: Sensory & motor to the diaphragm

Describe the concept of left and right dominance as it relates to the blood supply of the heart

***REMEMBER: Dominance depends on which coronary a. supplies the posterior interventricular artery (PIV/PDA) --> Right is 60% of time, Left is 30%, co-dominance is 10% R. DOMINANCE - RCA gives rise to PIV => RCA supplies most of posterior wall L. DOMINANCE - PIV comes from circumflex branch of LCA, but can also come from AIV=> LCA supplies most of posterior wall

Describe the relationships of the vagus nerves to the aortic arch, the root of the lung and the esophagus

***WANDERER NERVE -Moves along common carotid a. and breaks up into branches in esophagus (ESOPHAGEAL PLEXUS) -Moves toward abdomen through diaphragm as ANT. VAGAL TRUNK (L. vagus) and POST. VAGAL TRUNK (R. vagal) -INNERVATION: parasympa & visceral afferent to thoracic viscera

Compare and contrast normal myocardium to the one with ischemic changes

***p. 40-41 The ischemic myocardium seems to have more plaque and/or more fat stores/fibrous granulation tissue due to some form of damage. Cardiac myocytes and neutrophil infiltrates increase exponentially in number

List the normal openings in the diaphragm and their approximate vertebral level

**REMEMBER: I 8 10 Eggs At 12 T8 - IVC (right) T10 - Esophageal hiatus (left) T12 - Aorta (midline)

Identify & describe the structure and function of muscular (medium)/distributing/named arteries

- MOST ABUNDANT IN THE BODY -Have more SMOOTH MUSCLES in T. MEDIA than elastic fibers -As they get SMALLER than elastic fibers, dec. elastic fibers = makes EEL between T. MEDIA & T. ADVENTITIA (KEYWORD: EEL = muscular arteries) -SIGNIFICANCE: Needed as a muscular conduit to move blood from elastic vessels to smaller vessels

Describe the path of blood flow through the heart

--> SVC/IVC --> RA -(tricuspid valve)--> RV -(pulm. semilunar valve)--> pulmonary a. --> pulmonary arterioles, capillaries, venules --> pulmonary v. --> LA -(bicuspid/mitral valve)--> LV -(aortic semilunar valve)--> ascending aorta (subclavian, common iliac, brachiocephalic)/descending aorta --> systemic arterioles, capillaries, venules --> SVC/IVC

Describe the course of the right and left recurrent laryngeal nerves in the thorax

-Comes from either side of the vagus nerve -L. RECURRENT = AORTIC ARCH -R. RECURRENT = R. SUBCLAVIAN A. -INNERVATION: intrinsic muscles of voice box (larynx)

Identify & describe the structure and function of large (muscular) veins

-Have a d = >10 mm (ex. SVC & IVC & hepatic portal vein) T. Intima - endothelium, subendothelial CT T. Media - Thin circularly arranged smooth muscles, CT, collagen fibers, fiibroblast T. Adventitia - THICKEST LATER of LONGITUDINAL SMOOTH MUSCLE BUNDLES, collagen, elastic fibers, fibroblast

Identify & describe the structure and function of the endocardium

-INNER LAYER of endothelium -has SUBENDOTHELIAL CT - subendothelial layer important for CONDUCTION of the heart -has PURKINJE FIBERS

Identify & describe the structure, function and localization of Purkinje fibers

-LARGE SIZE, LARGE ROUND NUCLEI, & PALE NATURE due to HIGH GLYCOGEN and LESS MYOFIBRILS

Describe the partitioning of the atrioventricular canal

-This happens during the 4th week -AV ENDOCARDIAL CUSHIONS form from CARDIAC JELLY and NEURAL CREST CELLS. Forms on the DORSAL and VENTRAL WALLS of AV canal -ENDOCARDIAL CUSHIONS grow towards each other and FUSE, dividing the canal into R&L AV CANALS to form AV VALVES. There is partial separation of the PRIMITIVE ATRIUM from PRIMITIVE VENTRICLE

Identify & describe the structure and function of elastic (large) arteries

-has LARGE NUMBER of ELASTIC FIBERS in T. MEDIA (40-70 layers) -ELASTIC FIBERS in CONCENTRIC LAYERS (ex. shingles on a roof) -FENSTRATIONS (regulate nutrient diffusion) - VASCULAR SMOOTH MUSCLE b/w ELASTIC FIBERS - Structural significance: Vessels expand to accommodate for the large volume of blood during systole & elastic recoiling needed for intravascular pressure

Identify & describe the structure and function of the epicardium

-visceral layer of SEROUS PERICARDIUM -one layer of MESOTHELIAL CELLS -has a layer of CT & ADIPOSE TISSUE -home to BV & nerves going to the heart -lines inner PERICARDIUM surrounding the HEART -has a PERICARDIAL CAVITY

Describe the four normal constrictions of the esophagus

1. C6 - Pharyngoesophageal 2. Thoracic (aortobronchial) 3. T4/5 - Left main bronchus 4. T10 - Diaphragmatic at inferior esophageal sphincter (hiatus)

List & describe the three types of capillaries

1. Continuous/Somatic Capillary - Control diffusion, endocytosis and exocytosis 2. Fenestrated/Visceral Capillary - Needed for greater exchange; presence of thin, non-membranous diaphragm across fenestrations 3. Discontinuous/Sinusoidal - Allows passage of macromolecules due the varying enlarged size of fenestrations

Describe the anatomical explanation of the three cardinal signs of cardiac tamponade (Beck's triad)

1. HYPOTENSION due to dec. CO 2. DISTANT HEART SOUND due to excess fluid buldup 3. distended neck veins (JVD) due to diastole filling

Leukocyte exudation (Inflammation in Post-Cap Venules)

1. Margination, rolling, and adhesion 2. Diapedesis (transmigration across the endothelium) 3. Migration toward a chemotactic stimulus 4. Phagocytosis

Describe the development of the interatrial septum

1. SEPTUM PRIMUM grows from atrium roof to endocardial cushions 2. FORAMEN PRIMUM - Space b/w inferior edge of septum primum and endocardial cushions 3. inc. SEPTUM PRIMUM growth = closing of FORAMEN PRIMUM 4. FORAMEN SECUNDUM - Simultaneously perforations appear in septum primum 5. SEPTUM SECUNDUM grown downward, and overlaps foramen secundum 6. Opening b/w free edges septum secundum & septum primum = FORAMEN OVALE; septum primum acts like a thin & flexible flap for the foramen ovale -Opens when RA pressure > LA pressure, which allows blood to shunt from RA to LA and bypass non-functional lungs

How can you increase afterload?

1. When aortic pressure is inc. (elevated MAP) -LV has to have a tension with pressure > aortic pressure (80 mmHg) -Inc. aortic pressure = inc. ventricular tension = inc. workload -TPR also close approx. of afterload 2. When systemic vascular/total peripheral resistance is increased, resulting in inc. resistance and dec. compliance 3. In AORTIC STENOSIS - pressure overload on the left ventricle

As the resting muscle fiber is stretched, tension increase. What reason leads to this conclusion?

1.Length-dependent change in sensitivity of the myofilaments to calcium. (As muscle length↑, ability of TN-C to bind Ca ↑. ) 2.Optimize overlap between actin and myosin filaments. (as in skeletal muscle)

Describe the typical arrangement of elastic fibers in elastic arteries

40-70 layers: concentric arrangement of layers with smooth muscle wedged in between each elastic fiber (elongated nuclei) and fenestrations

Describe the formation of the oblique and the transverse pericardial sinus

12,25 TRANSVERSE PERICARDIAL SINUS (communicates with both sides of the pericardial cavity) -Formed by degeneration of central part of dorsal mesocardium -In adult: pericardial reflection located POSTERIOR to aorta and pulm. trunk, ANTERIOR to SVC, SUPERIOR to LA (good place for cardiothoracic surgeons to separate arteries from veins, allowing isolation for temporary ligation) OBLIQUE PERICARDIAL SINUS (area b/w pulm. veins) -PRIMORDIAL PULM. VEINS persistently become incorporated into the walls of the LA to form the oblique sinus. Limited by reflection of serous pericardium onto the back of the heart

Describe five types of atrial septal defects

29-32 1. OSTIUM SECUNDUM DEFECT - Defect in center of atrial septum at the foramen ovale; results from abnormalities of septum primum or septum secundum; AV valves normal; does NOT require antibiotics for invasive procedures; 90% of ASDs 2. ENDOCARDIAL CUSHION DEFECT w/ FORAMEN PRIMUM DEFECT - Septum primum isn't fused with endocardial cushions, causing patent foramen ovale defect; often seen with ant. cusp of mitral valve as there's failed fusion of the endocardial cushions leading to AV valve defects, causing intracardiac shunting of blood from L to R 3. SINUS VENOSUS DEFECT (in sinus venarum) - There's either an incomplete resorption of R. horn of sinus venosus into RA, abnormal development of septum secundum or both, causing intracardiac shunting of blood from L to R 4. COMMON ATRIUM - Found in patients with ostium primum, ostium secundum and sinus venosus defects and they have complete absence of interatrial septum

Describe the developmental mechanisms underlying ectopia cordis, persistent truncus arteriosus, and transposition of the great arteries, tetralogy of Fallot, total anomalous pulmonary venous return

7,12-16 1. ECTOPIA CORDIS -Normal: Heart in middle mediastinum -Abnormal: a. THORACIC - Heart is partly/completely outside on thoracic wall as a result of faulty developmetn of STERNUM & PERICARDIUM b/c of failure of complete fusion of LATERAL FOLDS when forming thoracic wall (4th week), causing widely separated halves of sternum (nonfusion) and open pericardial sac b. ABDOMINAL - Heart protrudes through diaphragm into abdomen -Result: death within a few days after birth 2.PERSISTENT TRUNCUS ARTERIOSUS - Failure of neural crest cells migration --> failure in forming aorticopulm. septum (One great vessel is made = mild cyanosis) -VSD always present b/c truncus arteriosis straddles it -DiGeorge syndrome (chromo. 22; 22q11; CATCH 22) 3. TRANSPOSITION OF GREAT VESSELS - Switching of aorta and pulmonary trunk due to faulty neural crest migration = absent spiral twist movement of aorticopulm. septum => SEVERE CYANOSIS -LETHAL (unless they have VSD, ASD, PDA) -Maternal diabetes 4. TETRALOGY OF FALLOT - Due to ant. superior displacement of bulbar septum (infidubulum) --> unequal division of truncus arteriosus into small pulm. trunk and large aorta on top of intraventricular septum, getting blood from both ventricles, leading to PULM. STENOSIS, RV HYPERTROPHY (increased workload), membranous VSD, OVERRIDING AORTA -DiGeorge, Down's, & Fetal Alcohol Syndromes -Tet Spells 4. TOTAL ANOMALOUS PULMONARY VENOUS RETURN (TAPVR) - Abnormal drainage of pulm. v. into systemic circulation --> SEVERE CYANOSIS immediately after birth -Common in SVC, BC vein, Coronary sinus, IVC, Portal/hepatic v. -LETHAL (unless they have ASD, VSD or PDA, then they have a chance at surgery)

Identify & describe capillaries

7-9 microns in diameter -Single layer of endothelial cells and basal lamina -Possibly encircled by Rouget cells FUNCTION: allows exchange of material and different levels of metabolic exchange found here

Aortic Dissection Risk Factors

ABC: Atherosclerosis/ Aging/ Aortic aneurysm Blood pressure high/ Baby (pregnancy) Connective tissue disorders (eg Marfan's, Ehlers-Danlos)/ Cystic medial necrosis

Outline the embryologic basis common aortic arch anomalies of double aortic arch, right aortic arch, and anomalous right subclavian artery (DLA)

ANOMALOUS R. SUBCLAVIAN A. Normally formed proximally from R. 4th a. R. dorsal a. and R. 7th intersegmental a. form distal part of subclavian a. Pathology: Obliteration of R. 4th arch and proximal r. dorsal aorta, with persistence of distal R. dorsal aorta -Anomalous a. crosses midline behind esophagus and could compress it (not tight enough for clinical symp.) DOUBLE AORTIC ARCH Normally L. 4th arch and aortic sac form proximal side and L. dorsal aorta forms distal side Pathology: persistence of R. dorsal aorta b/w origin of 7th intersegmental a. and its junction w/ L. dorsal aorta (doesn't disappear) -Vascular ring goes around esophagus and trachea, which compresses them ==> problems with swallowing and breathing RIGHT AORTIC ARCH Normally L. 4th arch and aortic sac form proximal side and L. dorsal aorta forms distal side Pathology: persistence of entire R. dorsal aorta and abnormal involution of distal L. dorsal aorta (L. SUBCLAVIAN made by L .4th arch, L. dorsal aorta and intersegmental a.) TYPE I (w/o RETROESOPHAGEAL COMPONENT) - Ligamentum arteriosum passes from R. pulm. a. to R. arch TYPE II (w/ RETROESOPHAGEAL COMPONENT) - Original small arch involutes, leaving R. arch posterior to esophagus. Lig. arteriosum binds to distal arch and forms a ring that can compress trachea and esophagus)

Describe the arterial supply and venous drainage of the heart

ARTERY - R. Coronary (RA, SA/AV nodes, Post. 1/3 interventricular septum, most of RV and part of LV) - L. Coronary (LA, LV, Ant. 2/3 interventricular septum, AV Bundle of His, bundle branches) - Circumflex a. rarely supplies SA/AV nodes VEIN - Coronary Sinus receives blood from 1. Small Cardiac (follows R. marginal a.) 2. Great Cardiac (follows ant. interventricular a.) 3. Post. L. Ventricular 4. Middle Cardiac (follows post. interventricular a.) 5. Oblique of LA -Ant. Cardiac drains straight into RA

Describe the surface projections of the heart and the heart valves

AV VALVES - bound to fibrous skeleton and pressure changes opens/closes them; closed by papillary muscles and tendinous cords (CONTRACTION OF PAP. M. --> PULLS ON TENDINOUS CORDS --> NO EVERSION OF VALVE CUSPS TO ATRIA (Systole)) SEMILUNAR VALVES -Aortic: R, L, posterior w/ 2 coronary cusps -Pulmonary: R, L, anterior (no associated vessels)

How do you calculate total tension?

Active tension + passive tension

Describe the azygos system of veins and their typical pattern of drainage

Additional drainage supply with unpaired structure that forms a pathway b/w SVC and IVC in case there's a clot in the IVC -TARGET: back, thoracoabdominal wall, mediastinal viscera -roots of IVC/renal veins + ascen. lumbar & subcostal veins = azygos and hemiazygos -HEMIAZYGOS: inferior L. half of body -ACCESSORY HEMIAZYGOS: upper left side (T5-8) --> both cross over to join azygos -AZYGOS: R. side of body in posterior mediastinum --> inferior T8 vertebrae --> goes over root of right lung at T4 --> drains into SVC

EDV is to preload as the aortic valve open is to..?

Afterload

Explain the significance of angiotensin converting enzyme in pulmonary capillary endothelial cells

Angiotensinogen (with Renin) --> Angiotensin I --> Angiotensin II, which can 1. Constrict vascular smooth muscle --> Inc. Afterload 2. Stimulate aldosterone secretion --> Aldosterone --> inc. water and Na+ retention --> Inc. Preload

Describe the subclavian artery and its branches

Ant. scalene muscle divides it into 3 parts & later becomes the axillary a. ** REMEMBER VIT C&D (Vertebral a., Internal thoracic a. Thyrocervical trunk, Costocervical trunk & Dorsal scapular a.)

Anticoagulants, antithrombogenics and prothrombogenic. What is the difference between these three factors?

Anticoagulant (Thrombomodulin) - Stop platelet aggregation and stop blood coagulation so unobstructed blood flow happens Antithrombogenic (Prostacyclin) - Stops platelet aggregation and releases clotting factors Prothrombogenic (von Willebrand factor) - Allows clot formation

Identify the auscultation sites for heart valve sounds and explain why these auscultation points differ from the anatomical location of the valves

Aortic LOCATION - Post. to L. sternum at 3rd intercostal AUSCULTATION - R. sternal border at 2nd intercostal Pulmonary LOCATION - L. 3rd costal cartilage AUSCULTATION - L. costal border at 2nd intercostal Tricuspid LOCATION - Behind sternum at 4th & 5th intercostal AUSCULTATION - L. sternal border at 5th intercostal Mitral LOCATION - Behind sternum at 4th costal cartilage AUSCULTATION - 5th left intercostal in midclavicular

SV (amount of blood ejected) is determined by how far ventricular muscle cells are able to shorten during contraction, depending on length-tension relationship and the load against when they shorten. Once shortening happens, then what occurs shortly after?

Aortic valves close and the cardiac cells relax isometrically, ventricular wall tension and intraventricular pressure decrease during isovolumetric relaxation

auricle

Appendages of the atria & associated with aorta and pulm. trunk anteriorly

Define the terms "arteriosclerosis" and "atherosclerosis"

Arteriosclerosis: Hardening of the arteries (old age) Atherosclerosis: condition in which fatty deposits called plaque or ATHEROMA build up in the vascular lumen and weaken the T. Intima

Three types of cardiac muscle

Atrial = contract like skeletal muscle except, the duration of contraction is much longer. Ventricular = same as atrial Specialized = fibers exhibit either automatic rhythmic electrical discharge in the form of action potentials or conduction of the action potentials through the heart. This is the excitatory system that controls the rhythmical beating of the heart.

Describe the structure and function of intercalated discs

Attachment site between cardiac muscle cells; under microscope, it appears to be densely stained linear structures oriented transversely to the muscle fiber and consist of short segments arranged in a step-like fashion

If heart murmurs are SYSTOLIC and have a CRESCENDO-DECRESCENDO sound to the LEFT, what could that possibly be? RIGHT? What if the sound is HOLOSYSTOLIC?

CD LEFT: Flow, Aortic stenosis, Hypertrophic obstructive cardiomyopathy HOLO LEFT: Mitral regurgitation, Mitral valve prolapse, VSD CD RIGHT: Pulmonic stenosis HOLO RIGHT: Tricuspid regurgitation

Describe the anatomy of the heart chambers.

CHAMBERS: L. pulm surface has LV and LA; R. pulm surface has RA and RV RA - Gets blood from SVC/IVC/coronary sinus. CRISTA TERMINALIS (muscular ridge) separates smooth post. atrium from rough pectinae muscle. INTERATRIAL SEPTUM -> OVAL DEPRESSION (FOSSA OVALIS) RV - MODERATOR BAND important for conduction (contains BUNDLE OF HIS); Smooth part = Infundibulum (Conus Arteriosus), but Rough part = Trabeculae carnae. Tricuspid valve leaflets have tendinous cords bound to Ant., Septal and Post. Papillary muscle LA (most posterior but ant. to esophagus) - Gets O2 blood from 4 Pulm veins (2 left and 2 right). INTERATRIAL SEPTUM -> OVAL IMPRESSION (FOSSA OVALIS) LV (more muscular and thicker walls) - Mitral valve leaflets have tendinous cords bound to Ant. & Post. Papillary muscles, with THIN trabecular carnae

Describe the structure and function of cardiac muscle

Cardiac muscle tissue works to keep your heart pumping through involuntary movements. This is one feature that differentiates it from skeletal muscle tissue, which you can control. It does this through pacemaker cells, which control the contractions of your heart. The individual cardiac muscle cell (cardiomyocyte) is a tubular structure composed of chains of myofibrils, which are rod-like units within the cell. The myofibrils consist of repeating sections of sarcomeres, which are the fundamental contractile units of the muscle cells

Explain how cardiac pain differs from intercostal pain/pleural pain /bronchial pain

Cardiac pain (MI) - Severe CHEST HEAVINESS/pressure for > 20 min, SWEATING, CLENCHED FIST, CRUSHING PAIN RADIATES TO ARM, NAUSEA Pleural pain - PNA, PE, Viral resp. infection. ACUTE SHARP PAIN with BREATHING, COUGHING, MOVEMENT Intercostal pain - SHARP PAIN in THORAX (unilaterally worsens with chest wall movements, including breathing) Pericardial pain - PERICARDITIS, continuous CENTRAL CP (can radiate to both shoulders; might alleviate by sitting up)

What is the difference between stenosis and incompetence?

Caused by FAULTY VALVES - TURBULENCE = NOISY STENOSIS - Opened valve that's NARROW = higher pressure to push blood through narrow opening INCOMPETANCE (REGURGITATION) = Closed valve that's LEAKING

Describe the process of "endothelial activation" and its clinical significance

Change in functional properties in response to various stimuli Induced endothelial activation include bacterial and viral antigens, cytotoxins, complement products, lipid products and hypoxia. Activated endothelial cells exhibit new surface adhesion molecules and produce different classes of cytokines, lymphokines, GFs and vasoconstrictor/vasodilator molecules as well as those controlling blood coagulation.

Contractility

Change in performance at a given preload or afterload. Change in force of contraction at any given sarcomere length. Acute changes in intracellular calcium and drugs can alter the contractility. Contractility affects the rate at which a muscle can develop active tension. Ejection fraction is the best index of contractility.

Levine sign

Clenched fist held over the chest to describe ischemic chest pain.

Describe the embryologic origin of and clinical presentation of coarctation of the aorta

Congenital narrowing of segment of aorta (mostly seen at arch); more males than females, and in 15-20% of Turner syndrome pts. -THEORIES: 1. abnormal involution of small distal L. dorsal aorta 2. muscle tissue of ductus incorporates into aortic wall = constricts when ductus closes at birth -LOCATIONS (always opposite of ductus) a. PREDUCTAL (proximal to ductus) - before birth, blood goes to ductus to desc. aorta to lower body b. POSTDUCTUL (distal to ductus) - development of collateral circulation during fetal life so blood goes to lower body -COLLATERAL PATHWAY: Ant. intercostal a. shunts blood through subclavian as follows --- subclavian -> internal thoracic a. -> ant. intercostals -> post. intercostals -> desc. aorta

If heart murmurs are DIASTOLIC and have a DECRESCENDO sound to the LEFT, what could that possibly be? RIGHT? What if the sound is DECRESCENDO-CRESCENDO?

D LEFT: Aortic regurgitation DC LEFT: Mitral stenosis, Austin-Flint D RIGHT: Pulmonic regurgitation DC RIGHT: Tricuspid stenosis

Describe the difference between dextrocardia and situs inversus

DEXTROCARDIA - when the heart is on the opposite or right side of the chest (L-loop positions apex to the right and may be in isolation) DEXTROCARDIA & SITUS INVERSUS - Abdominal organs are also found on the opposite side of the body with the heart

Describe the function of the ductus venosus, foramen ovale and ductus arteriosus. Explain the mechanisms causing their closure at birth

DV - A shunt that allows oxygenated blood in the umbilical vein to bypass the liver -Closes 2-3 months later FO - An aperture in the muscular tissue between the left and right atrium that allows blood to cross the atria and bypass pulmonary circulation -Closes. Pressure reversal causes flap over foramen to close DA - A shunt between the pulmonary artery and the aorta -Closes due to pressure differences, inc. O2 tensions, dec. prostaglandins; muscular wall vasoconstriction

How does decreasing contractility affect isometric tension?

Decreased contractility is due to a Ca channel blocker ( - inotropy)

During systole/diastole, the ventricular fibers are stretched to develop a degree of tension to begin relaxation/contraction. To eject blood, the heart has to develop a tension (isometric/isotonic contraction) that will cause the ventricular/aortic pressure to exceed the ventricular/aortic pressure so that the valves will open/close, and then the myocardial fibres will have to shorten (isometric\sotonic contraction) to eject the blood.

Diastole; contraction; isometric; ventricular; aortic; open; isotonic

__________ inhibits Na-K-ATPase —> ↑ intracellular Na —> dec. extrusion of Ca by Na\Ca exchanger —> ↑ cystolic Ca —> ↑Ca pumped back into SR —> ↑ Ca in SR for cardiac contraction —> ↑ heart contractility. What drug uses this mechanism?

Digoxin

List the positive inotropic agents.

Dobutamine, Isoprenaline, Digoxin

Describe the embryological origin and clinical presentation of patent ductus arteriosus

Ductus arteriosus essential shunt for fetal life (function closes within first few days; anatomically closes in 12th week); PDA more frequent in females than males and associated with maternal rubella and down syndrome -Failure of DA to involute/close due to failure of CONTRACTION of MUSCULAR DUCTUS WALL -FINDING: premature infants, infants at high altitudes, HYPOXIA, low birth weight) -Dx: EKG/Color flow; Doppler -Tx: Indomethacin

Describe the progressive changes in maternal blood volume, cardiac output, and peripheral resistance during pregnancy and at delivery

During pregnancy, CO begins to steadily increase between conception and 20 weeks, but plateaus at CO = 7 L/min, which is related to increases in SV and HR. Blood volume also increases, but peripheral resistance decreases very early during pregnancy and continues to decrease during the second and third trimester. At delivery, CO increases by 70%, with SV increasing due to an inc. in preload (due to venous return) and possible increase in peripheral resistance

Describe the fetal cardiovascular response to acute hypoxia

EARLY GESTATION: Immature response to acute hypoxia. TACHY, no inc. peripheral vascular resistance to maintain ABP LATE GESTATION: acute hypoxia - CV response to sustain perfusion and CO. Not an ALL OR NONE response, but TITRATED to degree of hypoxia ***REMEMBER: VeroniCa HaTed BReAD ACUTE HYPOXEMIA: VASOCONSTRICTION, HTN, BRADY - dec. blood O2 levels (hypoxemia) - CHEMORECEPTOR REFLEX: vasoconstriction in nonvital peripheral areas (kidney, GI, lower extrem) so there's more blood to vital organs (adrenal glands, heart & brain), resulting in HTN --> baroreceptor mediating VAGAL response --> BRADY (maintains CO in EDV) --> fetal HR decelerates (seen by EKG and HR)

List the most common heart defects in Down's syndrome

Endocardial cushioning defects ==> ATRIVENTRICULAR SEPTAL DEFECT (AVSD) - Most frequent in Trisomy 21 (large defect in atrioventricular wall) -primum type ASD & membranous type VSD -always affects AV valve w/ common AV valve (most severe) -Incomplete form = ASD or VSD with defective AV valve (usually ant. cusp of mitral valve) ISOLATED ASD/VSD PATENT DUCTUS ARTERIOSUS TETROLOGY OF FALLOT

List the cardiac structures derived from the neural crest cells

Endocardial cushions (in outflow tract), bulbar ridges, truncal ridges, spiral septum, membranous interventricular septum, semilunar valves, AV valves, pharyngeal arches

How does exercise affect the pressure-volume loop?

Exercise --> inc. sympathetic activity --> stimulates B1 receptors and acts on a-receptors --> inc. venomotor tone and contractility --> inc. venous return --> inc. EDV --> inc. preload --> very large inc. SV

Describe fetal circulation and discuss the changes that occur at birth

FETAL CIRCULATION -Placental circulation supplies the fetus with O2 blood, leading to little pulm. blood flow since the liver and the lungs are non-functioning at this stage. BEFORE BIRTH, blood is shunted in 4 ways: 1. umbilical v. from placenta 2. ductus venosus bypassing liver sinusoids 3. foramen ovale bypassing lungs 4. ductus arteriosus --> aorta --> O2 blood in systemic circulation AT BIRTH (NEONATAL CIRCULATION), dec. pulm. circulation pressure = inc. systemic pressure and inc. O2 tension, so.. 1. contraction & fibrosis of umbilical v. = Lig. teres hepatis (liver) 2. closure of ductus venosus = Lig. venosum 3. closure of foramen ovale = fossa ovalis and limbus of fossa ovalis 4. closure of ductus arteriosus = Lig. arteriosum at plane of Lugwig (T4-5)

Explain the consequences of failure of the ductus arteriosus and the foramen ovale to close, and if pulmonary vascular resistance fails to decrease in these failures and in R to L shunt

Failure of DA closing -> Patent Ductus Arteriosus (PDA) - Left to right shunt where the DA stays open after birth because the muscular wall doesn't vasoconstrict, leading to excessive blood in pulm. circulation; inc. pulm. resistance Failure of FO closing -> Patent FO (PFO) -Most patient asymptomatic, but can present with ischemic stroke (paradoxical embolism); increased prevalence in pts < 55 yo who've had a CRYPTOGENIC STROKE (stroke w/o cardioembolic/large vessel source) In R --> L shunt: PVR fails to decrease after birth --> presence of hypoxemia. Will see CYANOSIS, TACHYPNEA, RESP. DISTRESS. -Cardiac Findings: Loud, single S2 or harsh systolic murmur secondary to tricuspid regurgitation

Describe the importance of the aortic sinuses (of Valsalva) for continuous myocardial perfusion

Fills after ventricular contraction, closing valves and filling coronary arteries

Describe the significance of valves in blood vessels

Folds of the T. Intima, supported by fibroelastic CT that prevent backflow/regurgitation of blood

Laplace's Law and Hypertension

Heart needs higher LV pressure = more wall stress to exceed higher aortic pressure so the aortic valve opens and ejects SV. -Chronic HTN: heart compensates by thickening its walls (concentric hypertrophy) increasing h in

Discuss hypertension and list the vessel that is a major determinant of blood pressure

Hypertension (high blood pressure) is seen in patients with a systolic BP > 130 bpm & a diastolic BP > 80 bpm Major determinant of BP: Arterioles

Describe the innervation and arterial supply of the fibrous pericardium

INNERVATION: Somatic sensation by phrenic nerve (C3-5) ARTERY: -ascending aorta --> subclavian (internal thoracic to musculophrenic and pericardiophrenic branches), inferior phrenic -descending (thoracic) aorta

Describe the intercostobrachial nerve and its clinical significance in relation to the upper limb and myocardial infarction

INTERCOSTOBRACHIAL NERVE (T2) intercostal nerve joins/overlaps distribution of medial cutaneous nerve of arm responsible for referred pain to the upper limb during MI

At one set of systole, ventricular muscles have isometric tension and intraventricular pressure increases. What does increase in intraventricular pressure do?

If intraventricular pressure > aortic pressure (afterload), aortic valves open, cardiac muscle shorten (isotonic), ventricular ejection happens (cardiac muscles in active tension and shortening).

Describe the classification of arteries.

If they're LARGE = ELASTIC arteries (aorta, pulmonary arteries, aortic branches - brachiocephalic, common carotid, subclavian, common iliac) If they're MEDIUM = MUSCULAR arteries (brachial a., radial a., femoral a., tibial a.) SMALL arteries ARTERIOLES

Discuss the relative differences in oxygen saturation and pressure in the fetus and how these values change at birth

In FETUS: Pressure - Pulm. circulation -> high pressure -> RA,RV > LA,LV O2 Sat - Maintained by O2 In Neonate: Pressure - Inc. systemic resistance -> inc. O2 tension -> vasoconstriction (no low resistance in placenta); dec. pulm. resistance -> pulm. vessel vasodilate -> inc. blood flow to LA; reduced blood flow to RA after occlusion of umbilical v.--> LA, LV > RA, RV O2 sat increases after birth

Internal elastic membrane

In arteries an arterioles, a sheet-like layer (lamella) of fenestrated elastic material in the subendothelial layer of the T. intima

External elastic membrane

In arteries, a layer of elastin that separates the T. Media from the T. Adventitia

Contrast the blood flow pattern in the fetus with that of a normal neonate

In the fetus, the umbilical v. bypasses the liver with deO2 blood, the ductus venosus by passes the liver to deliver deO2 blood into the IVC, the foramen ovale bypasses the lungs with O2 blood and the ductus arteriosus goes straight to the descending aorta with O2 blood to the body In a neonate, the umbilical cord is cut off --> vasoconstriction of placental vessels--> red blood flow to RA --> inc. in systemic resistance --> LV pumps against resistance --> LA pressure > RA --> FO closes --> dec. pulm resistance & pulm. a. pressure --> RV perfuses lungs --> lungs become functional. Inc. O2 tensions to peripheral tissues --> dec. prostaglandins --> vasoconstriction of muscular wall --> DA closes --> systemic and pulm. circulation run in parallel; DV closes in 2-3 months

Change in altering sympathetic activity or specific drugs that change inotropic state changes CONTRACTILITY

Inc. contractility = steeper ESPVR = more muscles can shorten = inc. SV and EF = + inotropy Afterload and Preload stay constant

Stretching myocardial fibers with increase/decrease active tension to a point.

Increase

Sympathetic activity via activation of B1 receptors can...

Increase inotropy as a inotropic B1 agonist. The major factor that regulates Ca entry into cells is norepinephrine (or epinephrine) acting upon β1 receptors. The resulting increase in cAMP activates PKA which phosphorylates L- type Ca channels thus increasing their permeability to Ca which increases Ca influx. Ca release from SR Activation of β1 receptors via increased PKA will also result in phosphorylation of sites on the SR which leads to increased Ca release.

Describe the changes in the structure of a valve in a vein that may result in varicose veins

Increased intraluminal pressure causes loss of support by the vessel wall, which leads to reverse blood flow due to a damaged valve

Frank-Starling Law

Increased preload = inc. stretch = inc. EDV = inc. active tension = inc. contractility = inc. ejection = inc. SV; mechanism - ↑Ca sensitivity of TN-C, and ↑ actin-myosin interaction

Identify and describe the structure of the tunica intima

Innermost later of the vessel with 1. one layer of SQUAMOUS EPITHELIAL CELLS 2. BASAL LAMINA 3. SUBENDOTHELIAL LAYER (LCT with smooth muscle cells, IEL and fenestrations)

Describe the clinical significance of the transverse pericardial sinus

It's a good place to put a clamp around the proximal aorta & pulmonary trunk

List left-to-right shunts in congenital heart defects and explain why they are generally acyanotic

L to R shunt (BACK LEAK) - blood goes from systemic to pulm. circulation due to DEFECT OF HEART WALL -Pulm. flow > systemic flow; inc. volume in R. heart = damage to pulm. vasculature = PULM. HTN and if UNTREATED, workload on RV inc. = RV HYPERTROPHY ACYANOTIC - No flow of deO2 through systemic circulation Types: 1. VSD - Ventricular septum is open, so O2 blood from LV goes into RV 2. ASD - Atrial septum is open, so O2 blood from LA goes into RA 3. PDA - Ductus arteriosus essential shunt for fetal life; PDA more frequent in females than males and associated with maternal rubella and down syndrome -Failure of DA to involute/close due to failure of CONTRACTION of MUSCULAR DUCTUS WALL -FINDING: premature infants, infants at high altitudes, HYPOXIA, low birth weight) -Dx: EKG/Color flow; Doppler 4. AVSD

Describe the fate of the sinus venosus

L. HORN of SINUS VENOSUS -Mostly obliterated (degenerates) and the remnants become the coronary sinus & the oblique vein of LA R. HORN of SINUS VENOSUS -Seen as SINUS VENARUM (opening of SVC, IVC and coronary sinus) and becomes smooth-walled part of RA

Base of heart

L. atrium and proximal parts of pulm. v.; part of R. atrium an proximal parts of SVC/IVC

Apex of heart

L. ventricle; found at 5th intercostal space 8-9 cm from midsternal line

Describe the anatomical location, mechanism and clinical sequences of thoracic duct laceration

LARGEST LYMPH VESSEL IN BODY (AVOID DURING SURGERY!!!) LOCATION: Starts: abdomen as confluence/cistera chyli --> moves to the right --> moves through aortic hiatus --> moves b/w azygos & aorta (left), esophagus (ant.) & vertebral column (post.) --> crosses midline at T5 to left of thorax --> enters root of neck --> drains at junction of l. subclavian v. and l. internal jugular v. MECHANISM: Caries lymph from the whole body except R. HEAD, R. NECK, R. UPPER LIMB, R. THORAX (they go to R. Lymphatic Duct) CLINICAL SEQUENCE: THORACIC DUCT LACERATION due to pathology in lungs, great vessels, etc., trauma, injury during surgery, but regardless it presents with CHYLE (mix of lipids, proteins, lymphocytes) in the thorax (CHYLETHORAX), mediastinum (CHYLEMEDIASTINUM), & pericardium (CHYLEPERICARDIUM)

Relationship between LVEDV & LVEDP

LVEDV changes LVEDP, but LVEDP is also related to stiffness of the myocardium, which can cause pathological issues. If EDV = 120 m", stiffer ventricle has higher pressure = dec. compliance = inc. LVEDP = mitral valves close earlier = less filling = dec. LVEDV = dec. SV

Describe the changes in the structure of elastic fibers of tunica media that may lead to formation of aneurysm

Laceration of the T. Intima --> blood tracks into T. Media --> Dissection b/w middle and outer thirds of media --> hematoma burst through T. Adventitia --> possible death

Eisenmenger syndrome (Reversal of shunt)

Large VSD, PDA & AVSD = excess volume through R. heart & pulm circuit = progressive damage to pulm. vasculature = PULM. HTN -Pulm. Circuit P >> Systemic Circuit P = REVERSAL OF BLOOD FLOW from R to L -LATE CYANOSIS (BLUE KIDS) = deO2 from R to L in systemic circulation -1-2 years: VSD, PDA & AVSD, few decades: ASD

Most of the posterior surface of the heart is formed by the...

Left atrium

Why is the peak isometric curve important?

Limits how far shortening can occur and sets the limit to how much blood can be ejected by a single contraction; in the heart, it's equivalent to the ventricular pressure developed in ventricles and called ESPVR (defines max pressure that can be generated at any given volume under given inotropic state)

Explain the presence of longitudinal muscles in the tunica adventitia of large muscular veins

Longitudinal smooth muscle in veins (T. Adventitia)==> veins in muscles help blood move to ONE DIRECTION when we walk and moving, were contracting muscle, so muscles squeeze veins to go to one direction. In IVC we don't have same muscular support. When we lie down, it helps to have those muscle to constrict so blood is shunted in one direction

Describe the expected auscultation sounds that define mitral stenosis, mitral insufficiency, aortic stenosis, and aortic insufficiency.

MITRAL STENOSIS (Opening Snap!; Early DIASTOLIC with presystolic kick w/o A. Fib; heart between S1 & S2) - Delayed rumbling mid-to-late diastolic murmur -LA pressure > LV pressure, especially in diastole -low LVEDV = impaired filling = low SV = low CO = low aortic diastolic pressure MITRAL INSUFF. -Regurgitation (PAN SYSTOLIC): During systole, the LV ejects blood back into the LA and the aorta = inc. LA pressure (v-wave); dec. aortic pressure and LV pressure = ESV dec. = dec. outflow resistance = inc. EDV = inc. SV = no isovolumetric phases involved -Holosystolic, high-pitched "blowing murmur"; loudest in apex and moves towards axilla; significantly elevated LA pressure during ventricular SYSTOLE and loudest just before S2 -Valve prolapse: Late state crescendo with mid-systolic click (MC) due to sudden tension of chordae tendineae AORTIC STENOSIS (SYSTOLE; most common) - During ejection, there's difficulty ejecting blood out aortic valve b/c its stenosed = high resistance level; LV pressure > aortic pressure during ventricular SYSTOLE; CRESCENDO-DECRESCENDO murmur heard between S1 and S2, but doesn't go pass S2; LA pressure elevated -inc. ESV = no change EDV = dec. SV -CRESCENDO-DECRESCENDO SYSTOLIC ejection murmur (age-related calcification) -High LVEDV = high peak systolic pressure (reduced FILLING) AORTIC REGURGITATION -During ventricular relaxation, the aortic valve doesn't close properly, so blood flows back from the aorta to the LV = Regurgitation = RAPID drop of aortic pressure in diastole, SLOWER drop in LV during relaxation = dec. diastolic pressure and inc. aortic pressure; LA pressure inc. because blood is backing up = inc. LVEDPV = inc. SV = No isovolumetric phases involved -High pitched "blowing" early diastolic DECRESCENDO murmur; long diastolic murmur; head bobbing (severe)

Describe the two types of ventricular septal defect

MUSCULAR (SWISS CHEESE) VSD - No muscular septum = common ventricle; can happen anywhere in the septum in isolation or simultaneously MEMBRANOUS VSD - Most common; no membranous septum = incomplete closure of IV foramen BOTH - More common in males than females and accounts for about 25% congenital HD. Causes INTRACARDIAC SHUNTING of blood from L to R

Describe the partitioning of the common ventricle

MUSCULAR INTERVENTRICULAR (IV) SEPTUM -first thing to develop and form from MYOCYTES OF PRIMITIVE VENTRICLE; has a CONCAVE SUPERIOR free edge to form the IV foramen -ventricular dilation => inc. size of septum IV FORAMEN - Allows for communication b/w RV and LV -bulbar ridges + muscular IV septum + endocardial cushion = MEMBRANOUS IV SEPTUM (later fuses with AORTICOPULMONARY SEPTUM. Once it's formed, it closes the IV foramen, so now the pulm. trunk has to communicate with the RV and the aorta has to communicate with the LV

Contrast the relationship between pressure and flow into and out of the left and right ventricles during each phase of the cardiac cycle

Mid-late ventricular diastole (relaxation) -> P wave (FILLING) AV VALVES: Open SV VALVES: Closed ATR>VENT. Pressure ART>VENT. Pressure Isovolumetric contraction (SYSTOLE) -> P wave (S1 = LUB, atrial curves/filling, LARGE DRUM--> longer) AV VALVES: Closed (large) SV VALVES: Closed ATR<VENT. Pressure ART>VENT. Pressure Mid to late ventricular systole (contraction) -> QRS complex (EJECTION) AV VALVES: Closed SV VALVES: Open ATR<VENT. Pressure ART<VENT. Pressure Isovolumetric relaxation (DIASTOLE) -> T wave (S2 = DUB, atrial curves/ejection, SMALL DRUM) AV VALVES: Closed SV VALVES: Closed (small) ATR>VENT. Pressure ART<VENT. Pressure

Identify and describe the structure of tunica media

Middle later with circumferentially layers of VASCULAR SMOOTH MUSCLE (makes up extracellular components) In ARTERIES --> relatively THICK layer, extending from the IEL to the EEL. -Elastin, reticular fibers and proteoglycans are in between the smooth muscle cells and T. Media -Elastin lamellae are FENESTRATED in circular concentric layers

Swiss cheese VSD

Muscular VSD

Discuss Marfan's syndrome and effects on cardiovascular system

Mutation in Fibrillin-1 (FBN1) causes this CT disorder. Found in association with aortic dissection

Mode of Action of NE and EPI in increasing contractility

NE, EPI —> B1 cardiac receptors —> adenylate cyclase —> ↑cAMP —> PKA —> ↑iCa (phosphorylation) —> ↑Ca transient —> ↑ CICR —> ↑ cytosolic of Ca —> ↑ force of contraction —> ↑SV

Describe the splitting patterns of the second heart sound

NORMAL (PHYSIOLOGICAL) => LUB, DUB, DUB -Inspiration = drop in intrathoracic pressure = inc. venous return = inc. RV filling = inc RV SV = delayed closure of pulm. valve -Aortic valve closes BEFORE pulm. valve during inspiration = inc. thoracic volume = splitting of S2 b/c there's a transient drop in blood to LA and inc. blood ot RA PATHOLOGICAL: 1. WIDE SPLITTING - Delay RV emptying -Possibly Pulm. Stenosis, RBBB 2. FIXED SPLITTING -ASD: L2R shunt = inc. RA & RV volumes = inc. pulm. valve flow = delay in pulm. valve 3. PARADOXICAL SPLITTING -Normal order of valve closure reversed (P2 occurs B4 delayed A2). -Inspiration = P2 closes later and moves closer to A2 = eliminates split usually heard in expiration paradoxically -Possibly aortic stenosis, LBBB

Explain how coarctation of the aorta results in a difference between femoral and radial pulses and notching of the ribs.

NOTCHING: Ribs haven't ossified yet, so inferior rib notching on lower border happens in about 75% of adults with coarctation as a result of inc. vessel size due to inc. pressure of intercostal collaterals (seen at 3rd to 8th ribs) PULSES: Extremely STRONG RADIAL PULSE and HTN, but delay exist b/w femoral pulse and brachial/radial pulse, so SIGNIF. WEAKER FEMORAL PULSE

Nervi Vasorum (Vascularis)

Network of autonomic nerves that control contraction of the smooth muscle in the vessel wall

What shifts the tension-length profile upwards?

Norepinephrine because it stimulates sympathetic B1 receptors for contraction and increases amount of force from muscle fibers with the same length and preload (increased contractility = + inotropy)

Describe the changes seen in the tunica intima in the process of atheroma formation

Normally: LDL has triglycerides and lipids (insoluble in water) PROBLEM: 1. excess LDL = free radical production from endothelial cells = LDL oxidizes 2. oxidation = inc. migration of monocytes in T. Intima (become macrophages) 3. smooth muscle cells move from the T. Media to the T. Intima (subendothelial CT) 4. SMC and macrophages eat up oxidized LDL = make FOAM CELLS 5. SMC increases & releases collage and other ECM = T. Intima now thick = makes FATTY STREAKS 6. Fatty Streaks ==> fibrofatty plaques (thanks to SMC's cytokines) --> moves to lumen and presses the T. Media down RESULT: Luminal obstruction; weak vascular walls (aneurysm)

Identify and describe the structure of tunica adventitia

OUTERMOST CT LAYER -Made of a FEW ELASTIC FIBERS and LONGITUDINALLY COLLAGENOUS TISSUES, which merge with LCT surrounding the vessel -Can be relatively THIN in most arteries to THICK in veins (major component of vessel wall) -In both arteries and veins, there's VASO VASORUM an NERVI VASORUM (VASCULARIS)

Explain the significance of lymphatics in metastasis of cancer

Obstruction of lymphatics: A rare cause of edema caused by tumor cells or chronic inflammation that occludes the vessels.

Laplace's Law

P=2Th/r; pressure = 2(tension)(wall thickness)/radius Converted to T = Pr/2h; Tension (wall stress) = (pressure)(radius)/2(wall thickness)

Describe the paraxiphoid and apical approach to pericardiocentesis for the alleviation of cardiac tamponade

PARAXIPHOID- tip of xiphoid (or b/w xiphoid and L. costal margin) angled toward L. shoulder APICAL - L. 5th and 6th intercostal space

Describe the anatomical location, mechanism and clinical sequences of pericarditis, pericardial friction rub and pericardial effusion

PERICARDITIS - Inflammation of pericardium due to trauma, infection, renal failure, post MI, post-op, etc. --> pericarditis leads to PERICARDIAL FRICTION RUB - Sound due to roughness of parietal lining from inflammation --> can also lead to PERICARDIAL EFFUSION - excess fluid buildup in pericardial space (could be slow or fast) due to (besides pericarditis) CT disease, hypothyroidism ---> no growth metabolism, protein synthesis, fat, protein, etc. metabolism ---> dec. elastin & collagen fibers

Summarize the major events in the transformation of the pharyngeal arch system into the adult arterial pattern. (DLA)

PHARYNGEAL ARCHES - 4th week development; One of the components of the pharyngeal apparatus (responsible for formation of the face and neck) -Includes Aortic arches, cartilage, muscle and nerves. The aortic sac contributes a branch to a new arch, making 5 pairs of arteries (there's really 6 but #5 is incompletely formed and regresses) -Aortic arch system begins in 6th week 1st arch: obliterated at Day 27 before the 6th is formed (small part stays to form maxillary a.) 2nd arch: later disappears (remainders are hyoid & stapedial a.) 3rd arch: COMMON CAROTID a. (1st part of internal carotid) 4th arch: on left (part of aortic arch); on right (most proximal subclavian a.) 5th arch: either incomplete formation or regression or never forms 6th arch (PULM ARCH): on right (proximal part ---> proximal R. pulm a.; distal part degenerates); on left (proximal part ---> proximal L. pulm a.; distal part is ductus arteriosus) -Distal aortae becomes DESCENDING AORTA from caudal part; R. side disappears b/w origin of 7th intersegmental a. and junction with L. dorsal aorta) -Recurrent Laryngeal n. (branches of vagus) originally supplied 6th pharyngeal arches, but as heart descends, nerves hook around 6th aortic arch and ascend to larynx. On right (when distal part of 6th and 5th arch disappear, nerve hooks around r. subclavian a.); on left (doesn't move up b/c distal part of 6th arch is ductus arteriosus => LIGAMENTUM ARTERIOSUM)

What are the pharyngeal arches and name the components that make up the arches.

PHARYNGEAL ARCHES - 4th week development; One of the components of the pharyngeal apparatus (responsible for formation of the face and neck) -NEURAL CREST CELLS move into future head and neck regions and add on to the formation of arches (numbered in craniocaudal sequence and contains representations of all the germ layers) -Components: AORTIC ARCHES (from aortic sac[most distal truncus arteriosus]; supplies pharyngeal arches and enters/connects to dorsal aorta[paired structures running through length of embryo]; arches and vessels in cranial -> caudal direction, CARTILAGE (forms skeleton of arch), MUSCLE (forms primordium of muscles in head and neck), NERVE (supplies mucosa and muscles from each arch)

Explain why the pain of a myocardial infarction maybe referred to the upper limb

Pain from ischemia/noxious stimuli referred to thoracic wall & medial aspects of upper limb sharing same spinal ganglion and dorsal horn with visceral afferents from heart SO, cardiac pain is referred to T1-T4 dermatomes on thorax, supplied by somatic afferents in intercostal nerves

In the pressure-volume loop, diastolic filling is the same as what in tension-length loop?

Passive stretch

List the pericardial coverings of the heart

Pericardial sac: FIBROUS PERICARDIUM (FP) - defines boundaries of middle mediastinum; continuous with great vessels' T. Adventitia; base bound to central tendon of diaphragm SEROUS PERICARDIUM (SP) - PARIETAL lines FP; VISCERAL (epicardium) covers the heart

Positive/negative inotropic inc./dec. Vmax

Positive: inc. Negative: dec.

High endothelial venules (HEV)

Post capillary venules in lymph system with prominent cuboidal/columnar endothelial cells and ovoid nuclei FUNCTION: Ports of entry for lymphocytes into lymphatic organs & recruit lymphocytes; Plays an important role in "homing effect" in lymphoid organs (lymph nodes), which is the site where lymphocytes enter a lymph node from circulation Allows circulation from blood into the cortex and medulla and into the lymphatic vessels. HEVs are a good indicator of a lymph node.

Preload/Afterload

Preload affects the amount of blood going into Right ventricle. Afterload is the systemic resistance after leaving the heart.

For preload to occur, which has to be smaller or greater: preload or afterload?

Preload has to be greater and afterload has to be smaller

Differentiate between the systemic and the pulmonary circulation

Pulmonary - moves blood from right side of heart through the lungs; creates a link with the gas exchange function of the respiratory system. Systemic - moves blood from left side of heart to the rest of the body

Describe the two pathways of circulation (ANAT)

Pulmonary circulation: conveys blood from the heart to the lungs and from the lungs to the heart Systemic circulation: conveys blood from the heart to other tissues of the body and fro: other tissues of the body to the heart

Prostaglandins

Purpose: Allows continued patency while awaiting surgery (needed if you need ductus to stay open for surgery toward TAPVR, CoA or transposition) MOA: A group of bioactive, hormone-like chemicals derived from fatty acids that have a wide variety of biological effects including roles in inflammation, platelet aggregation, vascular smooth muscle dilation and constriction, cell growth, protection of from acid in the stomach, and many more.

List right-to-left shunts in congenital heart defects and explain why they are generally cyanotic

R to L shunt - deO2 blood goes from pulm. to systemic circulation to bypass lungs and return to body -CYANOTIC: decrease in O2 blood in systemic circulation at birth or infancy (BLUE BABIES) -Blue discoloration of skin and mucous membranes b/c of high deO2 in blood = DEOXYGENATION -MILD = PERIPHERAL (only extremities/fingers) -SEVERE = CENTRAL (around core, lips, & tongue) Types: 1. PERSISTENT TRUNCUS ARTERIOSUS 2. TRANSPOSITION OF GREAT VESSELS 3. TRICUSPID ATRESIA 4. TOTAL ANOMALOUS PULMONARY VENOUS RETURN (TAPVR)

Describe the formation of the right and left atria

RA formation - R. HORN of SINUS VENOSUS enlarges simultaneously with the PRIMITIVE ATRIUM, and they engulf/absorb/swallow the R. horn to form the RA, and later becomes the SINUS VENARUM (smooth part of RA). The PRIMITIVE ATRIUM forms the ROUGH WALLED AURICLE LA formation - PRIMORDIAL PULM. VEINS form the LA as they persistently become incorporated into the walls of the LA, forming the OBLIQUE PERICARDIAL SINUS. Most of the wall is smooth. The PRIMITIVE ATRIUM forms the ROUGH WALLED AURICLE

Understand how and why left sided and right sided events differ in their timing

RA systole precedes LA systole, whereas contraction in RV starts after LV. however since pulm. arterial pressure < aortic pressure, RV ejection begins before LV During expiration, semilunar valves close at the same time During inspiration, aortic valve closes slightly before pulm. valve. Pulm. valve closes slower because of lower impedance (obstruction) of pulm. vascular tree Overtime, the outputs measures of the ventricles are equal

Describe the extent and attachments of the fibrous pericardium (pericardial sac)

Rigid Type I collagen fibers; continuous with T. Adventitia of great vessels; base attached to central tendon of diaphragm

Describe the timing and causes of the four heart sounds

S1 ORIGIN: AV valves closed LOCATION: mitral valve region NORMAL? yes, splitting is pathological and occurs in conduction defects on one side of the heart S2 ORIGIN: Semilunar valves closed LOCATION: L. upper external border NORMAL? yes -4 splitting patterns (GO OVER!!!) S3 (VENTRICULAR KENTUCKY GALLOP RHYTHM) ORIGIN: Early diastole in rapid ventricular filling; difficult to hear (low frequency) LOCATION: NORMAL? In children, young adults, and pregnant woman --> yes In adults, abnormal (dilated ventricles, inc. filling pressure => mitral regurgitation or HF (LV failure)) MECHANISM: blood rushes into ventricles from atria (recoil vibration) S4 (ATRIAL GALLOP RHYTHM;TENNESSEE) ORIGIN: Late diastole/atrial systole (atrial kick), just before S1 LOCATION: Apex with pt. in L. lateral decubitus position NORMAL? no, regardless of age (high atrial pressure, ventricular hypertrophy, STIFF L. ventricular wall due to inc. ventricular diastolic stiffness = dec. compliance)

Describe the conducting pathway of the heart

SA NODE (pacemaker b/w SVC and RA/ + sympa, - para) --> AV NODE (inferior interatrial septum near coronary sinus) --> BUNDLE OF HIS (common) --> BUNDLE BRANCHES (L: divides to 6 branches for IV septum and LV & R: supplies IVS and RV with moderator band and trabecula) --> PURKINJE FIBERS

Describe the development of the heart valves

SEMILUNAR VALVES - 3 swelling of SUBENDOCARDIAL CUSHION tissue around orifices of aorta (AORTIC VESTIBULE) and pulm. trunk (INFUNDIBULUM). It's hollowed out and reshaped to form the three thin-walled cusps ATRIOVENTRICULAR (AV) VALVES - Localized proliferations of ENDOCARDIAL CUSHION tissue around AV canals

Describe the clinical signs, causes and presentation of thoracic outlet syndrome

SIGNS: -if in SUBCLAVIAN A./V. = thrombosis, embolization -if in NERVES (C8-T1) = sensory deficit, muscle wasting of hand CAUSES: extra rib bound to C7 and rib 1, muscle abnormalities, trauma, tumor PRESENTATION: -if NEUROLOGICAL = pain, paresthesia, paresis/paralysis -if VASCULAR = pallor, pulselessness, poikilothermia (cold), edema (venous compression)

Identify and describe the structure, function and location of fenestrated (visceral) capillaries

STRUCTURE: Continuous basal lamina and tight junctions in between endothelial cells, but fenestrations (80-100 nm wide) on endothelial cell membrane with a lot of pinocytotic vesicles FUNCTION: Needed for greater exchange; presence of thin, non-membranous diaphragm across fenestrations except the glomerular capillaries LOCATIONS: peptide-secreting endocrine organs, ciliary process (eye), choroid plexus, glomeruli, lamina propria of GI tract

Identify and describe the structure, function and location of continuous (somatic) capillaries

STRUCTURE: Continuous basal lamina with uninterrupted endothelium; tight junctions in between cells FUNCTION: Completely controls diffusion, endocytosis and exocytosis; the vessels that make barriers in organs (brain, thymus, lung, testis, etc.) LOCATION: CT, muscle tissue, nerve tissue, exocrine gland, cerebral cortex

Identify and describe the structure, function and location of discontinuous (sinusoidal) capillaries

STRUCTURE: Discontinuous basal lamina and no tight junctions, but large fenestrations and very separate wide gaps SIGNIFICANCE: Allows passage of macro molecules with varying and large fenestrations LOCATIONS: Liver, spleen, bone marrow

Identify & describe the structure and function of muscular venules

STRUCTURE: Found distally to post capillary venules -1-2 layer of vascular smooth muscle in T. Media -Thin T. Adventitia -No pericytes

List the structures found in the superior, anterior, middle and posterior mediastinum and their relationships to one another

SUPERIOR - Esophagus, thoracic duct, thymus, trachea, aortic arch and major vessels, L & R brachiocephalic veins (posterior to sternoclavicular joints; subclavian + internal jug. veins = BC veins), SVC, pulmonary arteries, nerves (vagus, recurrent laryngeal, phrenic) ANTERIOR - Thymus, lymph nodes, CT MIDDLE- Heart (ascending aorta, intrapericardial SVC, pulmonary trunk), main bronchi POSTERIOR - Sympathetic chain, esophagus, esophageal plexus, azygos venous system, descending thoracic aorta, thoracic duct

List the surfaces and margins of the heart and the chambers/structures that contribute to them

SURFACES -Anterior (Sternocostal): formed mainly by R. ventricle -L. Pulmonary: faces L. lung & made of L. ventricle and part of L. atrium -Diaphragmatic (Inferior): formed mainly by L. ventricle -R. Pulmonary: faces R. lung & made of R. atrium MARGINS -R. margin = R. Pulmonary surface -L. Margin = L. Pulmonary surface -Inferior (acute) = sharp edge b/w ant & diaphragmatic surfaces -Obtuse = separates ant & L. pulmonary; round in nature & extends from L. auricle to cardiac apex

Stroke work vs. Kinetic work

SW - Contracting and pumping blood into aorta and pulmonary artery; SW = PV = (force)(blood volume) = (SV)(MAP) KW - Accelerating the blood through the valves into aorta and pulmonary artery (about 1% of total work done)

Describe the sympathetic, parasympathetic and sensory innervation of the heart

SYMPATHETIC -Pregang sympa: cell bodies in intermediolateral cell columns (T1-4 or 5) -Pregang fibers enter sympa chain via WRC and can 1. Synapse at T1-4 chain gang 2. Ascend chain & synapse at cervical gang -Postgang sympa: cell bodies in cervical and upper thoracic chain gang -Postgang fibers carried in cardiac component of cardiopulm. nerves to cardiac plexus -Cardiopulm. Nerves: Stop at SA/AV nodes, common bundle, bundle branches, atrial & ventricular muscle cells PARASYMPATHETIC -Pregang para: cell bodies in vagal nuclei -Pregang para fibers branch from vagus nerves (upper & lower cervical branches and recurrent branches) to VAGAL CARDIOPULM. BRANCHES (PSNS) -Postgang para: cell bodies in atrial wall & interstitial septum near SA/AV nodes, near common AV bundle, bundle branches, atrial muscle cells and along coronary a. SENSORY INNERVATION Visceral afferent (pain): move with heart sympas through cardiac plexus --> cardiopulm. nerves --> sympa chain and WRC --> spinal cord segments (T1-4 or 5) Visceral afferent (physiological reflexes like stretch): move with para fibers --> vagus nerves --> brainstem cardiovasc. centers

Changes in LVEDV following an increase in afterload and during the next cycle. What does this mean?

Starling's Law can compensate for a fall in SV by increasing SV on the next cycle SV: 2 < 1 = 3 Afterload: 1 < 2 = 3 Preload: 1 = 2 < 3 In Loop 1 - Normal In Loop 2 - First contraction against inc. aortic pressure from the same LVEDV = inc. afterload = dec. SV = inc. LVEDV = inc. preload = more tension being made = larger SV

Identify and describe the structure of lymphatic vessels

Starts off as blind-ended lymph capillaries and dump into circulation (unidirectional valves). Skeletal muscles next to them contract to speed up flow and filament bundles anchor the vessels to CT -No clear separation into tunics -No tight junctions -Not in nervous tissue, bone marrow, cartilage -Can cause edema

Vaso Vasorum

Supplies blood to the vascular walls themselves in the T. Adventitia

State the features that distinguish the pulmonary and systemic circulations

Systemic circuit (The LV pumps out an equal volume of O2 blood to the rest of the body. The blood flows through the aorta, which gives off several major arteries. Repeated branching gives rise to millions of capillaries where the ultimate function of the CVS is fulfilled - the delivery of O nutrients to the tissues and the removal of waste products. The deoxygenated blood returns to the RA via a convergent system of veins that drain into the SVC & IVC) Pulmonary circuit (The RV contracts and pumps dO2 blood through the pulmonary artery, which divides and supplies the lungs. Inhaled O blood returns to the LA through the pulmonary veins)

Cardiac myocytes are invaginated with

T-tubules

Name the cells found in various tunics

T. ADVENTITIA - unmyelinated nerves, blood vessels, myelinated nerves, fibroblasts, elastic fibers and collagen fibrils, DCT T. MEDIA - (8-40 layers) EEM, smooth muscle cells, elastic lamella I. INTIMA - endothelial cells, basal lamina, IEM

Identify & describe the structure and function of small arteries

T. Intima = endothelial cells, minimal subendothelial CT, IEL T. Media = 3 - 8 layers of smooth muscle cells in a circular fashion T. Adventitia = CT with Type I Collagen, thin ill-defined sheath that blends in with surrounding CT

List the three layers (tunics) forming the walls of arteries and veins

T. Intima, T. Media, T. Adventitia

Describe the arterial supply, innervation, venous and lymphatic drainage of the thoracic and abdominal portions of the esophagus

THORACIC -Artery: Thoracic a., bronchial a. -Innervation: Esophageal plexus, Sympa. trunks -Veins: Azygos v., hemiazygos v. -Lymph: Thoracic duct, Post. Mediastinal n. ABDOMINAL: -Artery: L. Gastric a., L. Inferior phrenic a. -Innervation: Vagal trunks, Greater splanchnic nerves -Veins: L. Gastric v. -Lymph: L. Gastric n.

Describe the anatomical locations of the transverse and oblique pericardial sinus

TRANSVERSE Anterior - Aorta and pulm. trunk Posterior - SVC Superior - R. Pulm. a. Inferior - Atria OBLIQUE Anterior - L. atrium Posterior - pericardium

Identify & describe the structure and function of the aortic valve

The aortic valve has 3 layers: 1. Fibrosa - from DICT of skeletal rings with COLLAGEN and ELASTIC FIBERS, covered in ENDOTHELIAL cells. Needed for TENSILE STRENGTH and continues into the CHORDAE TENDINAE 2. Spongiosa - CORE OF VALVE; LCT with loose COLLAGEN and ELASTIC FIBERS; SHOCK ABSORBER = dampens vibrations and function continues with FLEXIBILITY/PLASTICITY to CUSPS 3. Atrialis (Ventricularis) - next to ventricular/atrial surface, covered in ENDOTHELIUM, DCT with organized COLLAGEN and ELASTIC FIBERS, EXTENSION and RECOIL allows VALVE FUNCTION

Describe the organization of the cardiovascular system

The cardiovascular system consists of: • Four chambered heart which acts as a dual pump (two pumps: right ventricle (RV) & left ventricle (LV). Each pump is filled from chambers, right atrium (RA) & left atrium (LA)) • Blood and lymphatic vessels It is subdivided into two circuits : • Systemic circuit • Pulmonary circuit

Preload

The degree of tension, stretch or load on the ventricular muscle when it begins to contract/at the end of diastole. It cannot be measured directly. Instead indices such as LV EDV and LV EDP are measured directly. The preload can be explained on the basis of change in sarcomere length.

Why is kinetic energy important when valves are stenosed?

The heart has to work harder to push blood through the narrowed valves

Explain why the output from the left heart must be more or less the same as the output from the right heart

The left heart pumps out blood to the aorta and then to the rest of the body, so more output of blood is needed to supply bloodto organ systems

Afterload

The load that the heart must eject blood against. It is the pressure in the aorta leading from the ventricle. The afterload of the ventricle corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. The best 'marker' of afterload is systemic vascular resistance also called total peripheral resistance.

In a normal vs. dilated heart, what has the same according to Laplace's Law?

The same ventricular pressure in which the ventricle needs inc. tension in a dilated heart = has to work harder to eject the same blood volume into aorta = larger afterload

Explain why velocity of flow is slower in capillaries

The total cross sectional area of the capillaries is greater than the total cross sectional area of the arteries of any other part of the circulatory system The velocity of blood flow is inversely proportioned to the total cross-sectional area of blood vessels. As the total cross-sectional area of the vessels increases, the velocity of flow decreases. Blood flow is slowest in the capillaries, which allows time for exchange of gases and nutrients.

Peak zisometric tension

The total tension developed (active and passive); The amount of active tension developed by a cardiac muscle during an isometric contraction depends on the initial myocardial muscle length. Stretching the resting myocardial muscle fibre before it contracts will increase the amount of tension it can develop.

Laplace's Law and Hypertension in Athletes

They also develop LV hypertrophy because the wall tension has to > than non-athletic individuals. The ventricular radius during cardiac cycle is smaller, hence why tension is smaller, making ejection easier

What type of enzyme does pulmonary endothelial cells make?

They make ACE (stops Angiotensin I from becoming Angiotensin II)

Describe the structure and functional significance of Weibel Palade bodies

They're ROD-SHAPED INCLUSIONS that STORE VON WILLEBRAND FACTORS (glcoproteins) Found in heart, elastic/muscular arteries, small arteries and arterioles, but NOT IN CAPILLARIES

Describe the clinical significance of the oblique pericardial sinus

This is a cul-de-sac made when SP reflects onto pulmonary v.

Know the various phases of ventricular systole and ventricular diastole

V. SYSTOLE - Isovolumetric Contraction, Rapid and Reduced Ventricular Ejection V. DIASTOLE - Isovolumetric Relaxation, Rapid and Reduced Ventricular Filling

Explain the fate of vitelline, umbilical and cardinal vessels (Reading Assignment; see end of lecture packet)

VITELLINE VEINS - Carry deO2 blood from umbilical vesicle to heart. -R. VITELLINE => forms most of hepatic portal system and terminal portion of IVC -L. VITELLINE => regresses UMBILICAL VEINS - R. and cranial part of L. umbilical DEGENERATES -Caudal L. umbilical is the TRUE umbilical vein that carries O2 blood from the placenta to the embryo -Connected to IVC via ductus venosus; large venosus shunt made w/in liver and shunts blood to embryo's heart, bypassing the liver's capillaries COMMON CARDINAL VEINS - Return deO2 blood from embryo's body to heart -forms major venous drainage system of embryo -Anterior = drains cranial -Posterior = drains caudal -Ant + Post = common cardinal vein

Describe the significance of valves in lymphatic vessels

Valves prevent backflow of the lymph, which helps with a unidirectional flow

Describe the functions of vaso vasorum and nervi vascularis

Vaso Vasorum - Small blood vessels that supply the vascular walls themselves Nervi Vasorum - A network of autonomic nerves that controls contraction of the smooth muscles in the vessel walls

Vasconstriction vs vasodilation in epithelial cells

Vasoconstriction (Endothelin) ACE --> dec. luminal diameter --> inc. vascular resistance --> inc. systemic BP Vasodilation (Nitric Oxide) inc. relaxed smooth muslce --> inc. luminal diameter --> dec. vascular resistance --> dec. systemic BP

active tension

When a muscle is stimulated to contract whilst its length is held constant

Define cardiac tamponade

When an injury to the heart causes blood to flow into the surrounding pericardial sac, which compresses the heart to a point where it won't adequately fill. Usually the result of penetrating trauma like a stab wound.

Identify the intervals of isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid ventricle filling, reduced ventricular filling and atrial contraction (systole)

atrial contraction - A. SYSTOLE; late ventricular diastole (atrial depol. In P wave) isovolumetric contraction - V. SYSTOLE; mitral valve closes (S1; ventricular depol. in QRS complex) rapid ejection - V. SYSTOLE; aortic valve opens (70% of blood emptying during 1/3rd) reduced ejection - V. SYSTOLE; aortic valve slowly closes but still open (30% of blood emptying during next 2/3rds) isovolumetric relaxation - V. DIASTOLE; aortic valve closes rapid ventricle filling - V. DIASTOLE ; mitral valve opens reduced ventricular filling (diastasis) - V. DIASTOLE; mitral valve slowly closes but still open

Write down the basic law of flow

blood flow = change in pressure / resistance

Describe the origin of the extracellular matrix in the blood vessel wall

book

endothelial activation

change in functional properties in response to various stimuli

Aortic dissection

diagnosis in which the arterial wall splits apart

Austin Flint murmur

diastolic murmur caused by regurgitation on anterior mitral valve leaflet -> sign of severe aortic regurgitation -> need to replace aortic valve

Coronary sulcus (atrioventricular groove)

encircles junction of atria and ventricles

List the 3 layers of the heart

endocardium (T. Intima), myocardium (T. Media), epicardium (T. Adventitia)

varicocele

enlarged veins of the spermatic cord near the testicles

Apply the law of flow to explain the pressure changes seen across the circulation

if pressure is different, the resistance must be different; in left ventricle, pressure is higher than in the right so resistance in the left must be higher in order to keep blood flow the same

interventricular sulcus

overlies the interventricular septum that divides the right ventricle from the left

Describe the origin of elastic and reticular fibers of the tunica media

p. 18-20

ventricular function curve

relation of the increase in SV as EDV increases, all other factors being equal; Any graph whose x-axis is a function of myocardial muscle fibre length and whose y-axis is a reflection of contractile energy

Tet spells

results from a transient increase in resistance to blood flow to the lungs with increased preferential flow of desaturated blood to the body. Tet spells are characterized by a sudden, marked increase in cyanosis followed by syncope, and may result in hypoxic brain injury and death. Older children will often squat during a tet spell, which increases systemic vascular resistance and allows for a temporary reversal of the shunt.

Filarial

roundworm parasite that blocks the host's lymphatic system causing swelling

Circulation through fetal/primordial heart

sinus venosus --> primordial atrium ------> primordial ventricle via SA valves and AV canal --> bulbus cordis and truncus arteriosus --> aortic sac --> pharyngeal arch arteries --> dorsal aortae for distribution to the embryo, umbilical vesicle and placenta

Pericytes (Rouget cells)

spider-shaped stem cells help stabilize capillary walls, control permeability, and play a role in vessel repair; save integrity of BBB

Explain the significance of vascular endothelial growth factors (VEGF) produced by endothelial cells

stimulates endothelial cells to multiply and restore endothelial lining; important in angiogenesis. embryogenesis, vascular trauma, tumor, etc. for tissue regeneration and repair

pericardial cavity

surrounds the heart

Describe "lymphedema"

swelling of the tissues due to an abnormal accumulation of lymph fluid within the tissues

esophageal varices

swollen, varicose veins at the lower end of the esophagus

Define systole and diastole

systole (heart contraction) and diastole (heart relaxation)

List the major functions of the cardiovascular system

• Distribution of O2, nutrients (e.g. glucose, amino acids)and hormones to all body tissues • Transportation of CO2 and metabolic waste products (e.g.urea) from the tissues to the lungs and excretory organs • Distribution of water, electrolytes and hormones throughout the body • Contributing to the infrastructure of the immune system • Regulation of body temperature • Involved in several homeostatic mechanisms: Regulation of B.P., homeostatic adjustments to altered body states

In contrast to skeletal muscle, cardiac muscle:

• Form Branching network of cells (separated by intercalated discs) • Low resistance gap junctions which allow APs to spread from cell to cell. • Two syncytium - atrial and ventricular which are connected via the specialized conducting system. Atria contract ahead of ventricular contraction. • Tetanic contractions are not possible because of long refractory period of cardiac APs

Define cardiac output and stroke volume. Explain how SV is calculated. Know normal values.

•Cardiac Output (CO) - The total volume ejected by ventricle per unit time (mL/min) = SV • HR - From RV & LV, CO = 5 L/min •Stroke Volume (SV) - Volume of blood ejected by the ventricle on each beat (mL) = EDV - ESV - SV(normal) = 70 - 80 mL; SV(athlete) = 100 - 125 mL

Factors or drugs which increase contractility (inotropism) by ↑[Ca++]

•↑iCa •↑Rate of uptake of Ca into SR → ↑ stored Ca in SR • Inhibiting Ca - ATPase pump • Inhibiting the Na - Ca exchanger