1. Cardiovascular System:
The Heart

2. Heart Size, Shape, Mass About the size of a closed fist:
3.5” wide (at widest pt) X 5” long. 2.5” thick
Cone-shaped: Base & Apex
8 oz in adult females, 10 oz in adult males
8 oz = hamburger weight

3. Heart Location
In the mediastinum (tissue between sternum & vertebral column)
2/3 of its mass is left of midline
A cone lying on its side:
Base is toward your right shoulder, apex points to your left hip
Anterior surface - deep to sternum
Inferior surface – on diaphragm
Right border – against right lung.
Left border (pulmonary border) – against left lung
Notice esophagus between heart & vertebral column - think “heartburn”
Because heart lies between two rigid structures, the vertebral column and the sternum, external compression on the chest can be used to force blood out of the heart and into the circulation. (CPR)
2007 japanese study - chest compression alone is equally as effective if niot better than chest compression w mouth to mouth lung ventilation

4. Fibrous, Serous (Visceral & Parietal)
pericardium

5. Fibrous & Serous pericardium
What if the heart were just beating without this serous pericardium?
Rubbing up against the fibrous pericardium - friction burn?
What if the pericardium were inflamed? Pericarditis - take an aspirin, call me in the morning
Cardiac tamponade - too much fluid in the pericardial cavity - from chronic pericarditis
Pericardium – the sac that surrounds, protects, anchors heart to diaphragm. It is composed of 2 layers - the fibrous & serous (visceral & parietal layers) pericardium

6. The FIBROUS Pericardium
Can you figure out what part of the heart we are looking at in the picture on the right?
FIBROUS PERICARDIUM
Outermost layer
Tough, inelastic, dense irregular CT
Prevents overstretching of heart
Anchors heart to diaphragm. Prevents rising of heart

7. The SEROUS PERICARDIUM
SEROUS pericardium: thinner, delicate, inner layers that form a fluid-filled sac. It has 2 continuous layers:
Parietal layer: is adhered to fibrous pericardium
Visceral layer aka “Epicardium”: is adhered to heart
The pericardial cavity is filled with Pericardial fluid. The pericardial cavity is the space between parietal & visceral layers.
The pericardial fluid PREVENTS FRICTION
Double-bag it - like groceries. One layer will rip, 2 won’t
Base of pericardium fused with the central tendon of the diaphragm
Pericardium is attached to central tendon of diaphragm
Fluid is from leakage from myocardial capillaries & drained by the lymph

8. Systemic & Pulmonary Circulations
Two closed circulatory systems:
Body
Lungs
The output of one becomes the input of the other with each beat of the heart
Circulation makes a cross -
Horizontal (lungs) & vertical (body)

9. Blood Flow Within the 4 Heart Chambers

10. FYI: is it just a pump?
Anthroposophical medicine - enlivens the blood with spiraling hemodynamics.
What does the heart do? It pumps – faster, slower, stronger, weaker.

11. Cardiac Output (CO)
Total volume of blood in the body is approximately 5L. CO is typically about 5L/min
CO= Amount of blood pumped by left or right ventricle PER MINUTE
CO depends on Heart Rate & Stroke Volume
HEART RATE ie number of beats per minute. Normal is 75BPM
STROKE VOLUME ie. the amount of blood ejected from one Ventricle PER BEAT. Normal is 70ml/beat in a 70 kg healthy man
Preload - think rubberband or water balloon
Think of squeezing a water bottle - if sqeeze stronger, more will squirt out than if squeeze gently
Cardiac reserve - difference between CO at rest & max CO (4-5x more is possible)
Heart pumps 5 L blood
PER MINUTE

12. Electrical activity of the heart

13. Autorhythmic vs Contractile myocytes
Assuming the coronary arteries are supplying oxygen, how does the coronary artery
In skeletal muscle, each cell had a nerve supplying it - imagine if the heart had a nerve to each cell?
The Heart has 2 kinds of cells:
Autorhythmic myocytes (purple circle / yellow cell) spontaneously depolarize and generate action potentials
Contractile myocytes (pink cells) contract together to pump blood as the action potential spreads across them

14. The Sinoatrial (SA) Node or Pacemaker
Autorhythmic fibers have much higher resting membrane potential than “working fibers’ or contractile fibers -60 vs -90
-60 to -45 If channels open (funny current) Na/K channel that is more permeable to Na - net positive influx
-45 T-type Ca channels open (Transient) -open & close for a very short time
-35 voltage gated L-type Ca channels open & cause action potential spike to 0 mV
The SinoAtrial (SA) node is an area of modified cardiac myocytes within the R atrium.
Cells here spontaneously depolarize (become more positive) 100 x/min
Pacemaker potential: the spontaneous depolarization from -60 to -35mV that precedes the action potential
Action potential: the depolarization that occurs after threshold of -35 mV

15. Action Potential at the SA Node
CaT = transient - open & close quickly
CaL = long - open & close slowly
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel = HCN4 excpressed in heart generates funny current
HCN has dual activation by voltage and by cyclic nucleotides
SA node cells do not “rest”
Na+ channels spontaneously open at -60mV. (If –funny current)
Na+ leaks into SA node cells which initiates the pacemaker potential
2 Ca2+ channels open. One at low voltage, one at high voltage.
Ca2+ enters the cell, causing part of pacemaker potential & then the action potential
At 0mV, K+ channels open
K+ exits cell which repolarizes the cell membrane to -60mV

16. Features of Cardiac Contractile Cells
Exhibit branching
Intercalated disks: at end of each myocyte, its sarcolemma thickens
Stair-step appearance
2 disks are held together by Desmosomes
Gap junctions connect cytoplasm of adjoining cells
Striated/Sarcomeres: same structure as skeletal muscle cells: bands & zones of actin &myosin, z-discs, m-lines
Sarcoplasmic reticulum: smaller w less Ca2+ reserve
T-tubules: 1 per sarcomere. located at the z-disk
Mitochondria: Larger, more numerous (25% of cytosol)
One central nucleus: cardiac myocytes are shorter in length
Intercalate - “insert between”
WHY BRANCHING? Have a conical strucutre.
Goal is to spread the AP in a circular direction - so need BRANCHING or else would just have long cells that radiate out from the central SA NODE.
GAP JUCTIONS only work to spread AP because cells are shorter in length

17. Positive ions pass from SA to Contractile Cells through Gap Junctions
In a skeletal muscle, the depolarization = ion flow is triggered by a neurotransmitter
In cardiac muscle, ion flow is initated by pacemaker cell
Gap junction: a channel formed between two cells by 2 adjoined connexons. Connects cytoplasm of 2 cells, allowing ions & small molecules to pass through to adjoining cells quickly.
Positive ions (Ca2+ & Na+) pass from the autorhythmic cells, through gap junctions, to enter the adjacent contractile cells

18. Contractile Cell Depolarization – Fast Na Channels
Gap Junction: Positive ions (Na+ & Ca2+ enter through gap junctions which triggers:
Rapid Depolarization: Fast voltage-gated Na+ channels on the sarcolemma open. The cell instantly becomes positive on the inside.
Plateau Phase: at +20mV Ca2+ & K+ channels open. Influx and efflux of positive ions is balanced so AP graph plateaus.
In myocardial cells, magnesium is a cofactor for the sodium-potassium adenosine triphosphatase enzyme[6] and antagonizes both the L-type and T-type calcium channels in the atria

19. Action Potential Plateau & Repolarization
Ca2+ channels and K+ channels are open at the same voltage (+20 mV).
Thus, Ca2+ enters the cell, while K+ leaves. Influx and efflux of positive ions is equal, the cell does not become more positive or negative, creating a plateau in the AP graph.
Ca2+ channels close, while K+ channels remain open and K+ keeps leaking out so the cell becomes more negative inside, or, repolarizes

20. Calcium-Triggered Calcium Release – plateau and contraction
Na+ & Ca2+ influx from an adjacent cell changes voltage
Voltage-gated Ca channels on cell surface open & Ca enters the cell from Extra Cellular Fluid
Calcium-triggered calcium release: Ca entering cell binds to ryanodine receptors, which are Ca channels on the sarcoplasmic reticulum
Sarcoplasmic Ca stores are released into cell.
Ca binds to troponin, tropomyosin moves off myosin binding sites, myosin binds to actin & the sarcomeres shorten…
Xanthines like caffeine and pentifylline activate it by potentiating sensitivity to native ligand Ca.

21. cardiac excitation-contraction coupling

22. Action potential vs contraction
The action potential is generated first in the SA node.
Then the action potential spreads to contractile myocytes.
After the contractile myocytes depolarize, the sarcomeres shorten and a contraction is generated.

23. Tetanus
Unlike skeletal muscle, cardiac muscle cannot enter tetanus (sustained contraction).
The cardiac cell has a refractory period that is almost as long as the entire muscle twitch
You can ‘fit’ another action potential into a skeletal muscle contraction. Cardiac muscle is still in plateau when muscle contraction is already ending

24. Sympathetic & Parasympathetic
Heart rate REGULATION

25. HR slows due to Vagus Nerve (Ach): Parasympathetic
Max heart rate about 200bpm
The Vagus nerve (Parasympathetic) innervates SA, AV nodes & atrial myocardium.
It releases ACETYLCHOLINE which binds to muscarinic receptors on cardiac mm.
Binding of Ach to muscarinic receptors causes K+ to leave the cells. Thus:
SLOWS rate of depolarization of SA & AV nodes, thus HEART RATE DECREASES
The Vagus N. slows SA node to make the normal HR. Normal HR = BPM.
(Contractile Fibers: little effect on contractility because does not innervate ventricles)

26. HR & Contractility increase due to Sympathetic Nerves (NE)
Max heart rate about 200bpm
Sympathetic “Cardiac Accelerator Nerves” innervate SA & AV nodes, and most of the myocardium. They release NOREPINEPHRINE which binds to β1 receptors. Binding of NE to β1 enhances Ca2+ entry to cell, thus, at:
SA & AV nodes, it speeds rate of depolarization so HEART RATE INCREASES
Contractile Fibers,more crossbridges form and CONTRACTILITY INCREASES
(simple tachycard), (paroxysmal), (flutter), 350+ (fibrillation)

27. Inputs affecting Heart Rate
Input to the Cardiovascular Center in medulla oblongata comes from:
Brain - cortex, limbic system (eg anxiety), hypothalamus
Sensory Receptors - proprioceptors (limb position), chemoreceptors, baroreceptors (artery & vein stretch, blood pressure changes)

28. Chemical & Other Regulation of HR
INCREASES HEART RATE & CONTRACTILITY
Hormones:
Epinephrine
Norepinephrine
Thyroid hormones
Cations:
Ca2+
Other:
Increased body temperature (fever, exercise)
TACHYCARDIA: increased resting heart rate (>100bpm for adult)
DECREASES HEART RATE & CONTRACTILITY
Cations:
K+ blocks generation of AP (Hyperkalemia)
Na+ blocks Ca inflow during AP
Other:
Decreased body temperature (hypothermia)
BRADYCARDIA: decreased resting heart rate (<50bpm for adult)
Epi & norepi from adrenal medulla
Hyperthyroid sx = inc hr

29. Damage to the pacemaker, or having Ectopic pacemakers produces Arrhythmias

30. The Cardiac cycle & EKG

31. Sequence Of Cardiac Conduction & Contraction
The Sinoatrial (SA) node generates action potentials (AP)
AP propagates through walls of both atria via gap junctions.
ATRIA CONTRACT
Atrioventricular (AV) node in inter-atrial septum slows AP conduction
AP can only pass from atria to ventricles through AV bundle (Bundle of His)
AP propagates down inter-ventricular septum to apex via Right and left bundle branches
Purkinje fibers conduct AP from apex up walls of ventricles.
VENTRICLES CONTRACT.
Fibrous skeleton of heart electrically insulates atria from ventricles
Pacemaker potential = resting potential to threshold
After threshold is an action potential
Why would the contraction start at the apex of the heart & not at the bundle of his? To pump blood upwards

32. ECG & Cardiac Cycle P- atrial depolarization
QRS complex: Q- septal depolarization, R- early ventricular depolarization, S- late ventricular depolarization
T- ventricular repolarization

33. Cardiac Depolarization
Large P waves: enlargement of atria
Large R waves: enlarged ventricles
SA node: bpm
Atrial cells: bpm
AV node: bpm
HIS bundle: bpm
Bundle branch: bpm
Purkinje cells: bpm
Myocardial cells: bpm

34. FYI: EKG leads Electrodes are placed on:
arms & legs (limb leads: I, II, III, AVR, AVL and AVF)
6 positions on chest (chest leads: V1, V2, V3, V4, V5, V6).
limb leads provide views of cardiac activity in frontal plane
chest leads provide views in horizontal plane
12 different tracings are produced
Can tell:
Abnormal conducting pathway
Enlarged heart
Damaged regions of heart
Cause of chest pain
12 tracings because measuring ecg between pairs of electrodes

35. Normal Lead II Tracing
movement of charges (ions) generate an electrical current
electrical currents from cardiac action potentials can be detected on the surface of the body
Electrocardiogram: recording of electrical signals.
Electrocardiograph: instrument used
Six second method. Obtain a six second tracing (30 five mm boxes) and count the number of R waves that appear within that 6 second period and multiply by 10 to obtain the HR/min

36. Cardiac Cycle = one heartbeat
Systole= Contraction
Diastole = Relaxation
Cardiac cycle = one heartbeat:
systole & diastole of atria +
systole & diastole of ventricles

37. Cardiac Cycle S2
In skeletal muscle where CICR was first discovered, however, the primary mechanism of physiological Ca2+ release is not CICR, but direct protein-protein interaction between the voltage sensor of the t-tubule membrane, the dihydropyridine receptor (DHPR), and the Ca2+ release channel of the SR membrane, the ryanodine receptor (RyR). The coordination may require Ca2+, but in that case, some other stimulus or stimuli must be provided simultaneously, which is not CICR by definition. We then learned that the initial source of calcium (to cause opening of ryanodine receptors) was quite minimal. In fact, we learned it was an L-type calcium channel voltage sensor touching a ryanodine receptor. S1
1) START: Passive ventricular filling. 80% of the ventricle fills at rest, or DIASTOLE. Approximately 105mL.
2) Atria contract & pump 25mL (20%) more into ventricles so the End Diastolic Volume is about 130mL.
3) QRS - ventricular DEPOLARIZATION.
4) Isovolumetric Ventricular contraction - AV valves shut (ventricles are exerting force but not shortening)
5) Ventricular ejection or SYSTOLE. SL valves open as ventricular pressure exceeds aortic/pulmonary pressure
6) 70mL ejected into aorta & pulm trunk. Volume remaining in each ventricle(~60mL) is End Systolic Volume

38. Closing Valves Produce Heart Sounds – S1 & S2
Heart VALVES

39. 4 Heart Valves: 4 Fibrous rings (valve annuli)
4 Dense connective tissue rings surround
the valves & are fused together. Creates an electrical barrier. Electrical insulation. Prevents valve overstretching

40. Fibrous Skeleton Of The Heart
Annulus
*Rings prevent valve overstretching
*Act as electrical insulation between atria & ventricles
Insertion points for cardiac muscle fibers
The 4 rings merge with the interventricular septum

41. Heart Valves: 2 AV & 2 Semilunar valves
Atrial contraction first
Ventricular contraction (systole) second
Semilunar valves - ventricles are pushing blood up to the moon.
When the 2 atria contract: AV or atrioventricular valves (tricuspid + mitral) valves open
When 2 ventricles contract: Semilunar (aortic+ pulmonic)valves open

42. Atrioventricular or “AV” Valves, S1
AV valves: TRICUSPID & BICUSPID VALVES
When AV valves are Open, during ventricular filling:
Atria are pumping blood into ventricles
Valve cusps project into ventricle
Chordae tendinae are slack & papillary muscles relaxed
When AV valves are Closed, during ventricular contraction, S1:
AV cusps meet & close
chordae tendinae are taught & papillary muscles contracted
**AV valves prevent backflow of blood to atria when ventricles are contracting

43. Chordae tendinae & papillary muscles of AV valves
Structures on Mitral & tricuspid valves only
When atria contract, chordae tendinae are slack, hanging threads of connective tissue
When ventricles contract, blood pushes up against bottom of valve leaflets causing them to close & balloon up, like a parachute.
Papillary muscles contract, pulling on chordae tendinae to keep valve closed

44. Semilunar (SL) Valves, S2
Semilunar Valves = AORTIC & PULMONARY VALVES
SL valves open when pressure in the ventricles exceeds pressure of blood sitting in the arteries
SL valves close when ventricles relax.
This creates the heart sound – S2
Prevent backflow of blood from arteries into ventricles
Look at shape in aorta - like a cup
Stenosis of the valve prevents it from opening all the way

45. Heart Sounds: S1, S2
Auscultation – listening to sounds within the body
First sound, S1, “lubb” is louder, longer
AV valves close due to
VENTRICULAR SYSTOLE / contraction
Second sound, S2, “dupp” is shorter, not as loud
Semilunar valves close due to
VENTRICULAR DIASTOLE / relaxation

46. Preload, Contractility, Afterload
Stroke volume

47. Stroke Volume (think “Beat volume”)
Stroke volume depends on:
PRELOAD - volume of blood in the ventricle before it contracts (ie end diastolic volume)
Frank-Starling law: increased venous return = increased stroke volume (because more ventricular stretch= greater contraction)
CONTRACTILITY (Inotropy) – muscular strength of the contraction
Positive inotropic agents  Ca2+ thus  # of cross bridges &  force of contraction: Ca, Epi, NE
Negative inotropic agents- # of cross bridges,  force of contraction: Ca channel blockers, ß-blockers
AFTERLOAD – the pressure behind the semilunar valves that must be exceeded for blood to be ejected from ventricles (ie mean arterial pressure)
SV is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat (called end-systolic volume) from the volume of blood just prior to the beat (called end-diastolic volume).
Afterload - hydrostatic pressure?ck The Frank-Starling mechanism As the heart fills with more blood, increases load experienced by each muscle fiber. stretches muscle fibers, increasing taffinity of troponin to Ca2+ ions causing a greater number of cross-bridges to form within the muscle fibers. This increases the contractile force of the cardiac muscle, resulting in increased stroke volume.
AFTERLOAD increased causes HYPERTROPHY

49. Coronary (cardiac) circulation
Blood flow and oxygen supply to the heart muscle
Coronary (cardiac) circulation

50. Coronary (Cardiac) Circulation
The myocardium (heart muscle) has its own blood supply, the coronary, or cardiac, circulation

51. Right Coronary Artery supplies Right & Back of heart
R atrium via Atrial branches
R ventricle, Lateral side via Right marginal branch
Posterior walls of 2 ventricles via Posterior interventricular branch

52. Coronary Veins
Coronary Sinus – a large vessel on posterior surface of the heart
Drains all deoxygentated myocardium blood into R atrium
Collects blood from
Great (front), Middle (back), Small (R) & Anterior (R) cardiac veins

53. Cardiac Circulation
2 Coronary arteries (R & L coronary aa) branch off from the ascending aorta
When ventricles contract, coronary arteries are squeezed shut
When ventricles relax, blood from the aorta rushes into the coronary arteries, oxygenating the myocardium

54. ATP synthesis
ATP production in cardiac myocytes is mostly made by AEROBIC cellular respiration in cardiac mitochondria
Aerobic ATP synthesis requires oxygen for oxidative phosphorylation of ADP to ATP
O2 is supplied by myoglobin in cardiac cells or hemoglobin from cardiac circulation
Some ATP is produced from creatine phosphate
If creatine kinase (CK-MB) is found in blood (leaked from damaged cells) it’s a sign of myocardial infarction
Creatine kinase catalyzes transfer of phosphate group to ADP to make ATP. Should only be found in cell
CK enzymes consists of two subunits, which can be either B (brain type) or M (muscle type). There are, therefore, three different isoenzymes: CK-MM, CK-BB and CK-MB.
CK-MB can be detected w/in 3-4 hrs post MI, peaks at around 18 hrs and gone by 72

55. Fuels for ATP production in Cardiac Myocytes
Fatty acids, the major cardiac fuel, are obtained from either lipoproteins or free fatty acids associated with albumin. The heart is the tissue with the most robust expression of lipoprotein lipase
Fuels at rest:
60% fatty acids
35% glucose
Fuels during exercise:
Above fuels +
Amino acids, ketone bodies & lactic acid from skeletal muscle

56. Coronary artery disease
Pain referring to neck or chin & down left arm -
MI tx may involve thrombolytic eg streptokinase or t-PA + heparin; angioplasty, CABG
Myocardial Ischemia: narrowed artery reduces blood/ oxygen supply (hypoxia), weakening myocardium & producing squeezing pain (angina pectoris)
Myocardial Infarction: blocked artery, complete obstruction of blood flow to myocardium resulting in distal tissue death

57. Angiogram, angioplasty, stent
Cathetetr from groid threaded to heart
Radioopaque mediium injected
Cn also be used to deliver fibrinolytic agents to dissolve clot

58. Reperfusion Damage
“Reperfusion” = reestablishing blood flow to myocardium after blockage of a coronary artery
Reperfusion damages heart tissue further due to formation of oxygen free radicals from reintroduced oxygen, and Ca2+, and activation of the immune system
Antioxidants like glutathione peroxidase, Catalase can mitigate the effects.
reperfusion after an ischemic insult of sufficient duration initiates an inflammatory response, beginning with complement activation, followed by the recruitment and accumulation of neutrophils into the reperfused myocardium.
generation during ischemia-reperfusion may come from several sources, including NOS activity, mitochondrial electron transport, multiple steps in the metabolism of arachidonic acid and, in some species, xanthine oxidase, which is produced by hydrolysis of xanthine dehydrogenase. In addition, the decreased intracellular pH accompanying ischemia may alter the binding of transition metals such as iron, increasing their participation in the Haber-Weiss reaction [21]. P450 enzymes and NAD(P)H oxidase are two additional potential sources of oxygen radicals whose contribution to enhanced radical production during CNS ischemia has not been systematically explored.

59. Stenosis & Insufficiency
Heart valve disorders

60. Heart Valve Disorders: Stenosis
Age-related Aortic stenosis is most common type
Mitral Valve Stenosis is most commonly due to Rheumatic fever wks after strep infxn - antibodies inflame the CT of joints, heart valves (usually mitral) and other organs.
Kids 5-15
inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
Fever joint pain
ECG shows shows long pr interval like ht block

61. Heart Valve disorders: Insufficiency
TRICUSPID INSUFFICIENCY - R ventricular dilation messes up anatomy of valve dt L ventricular dilation, R ventricular infarction, inferior MI, cor P
AORTIC INSUFFICIENCY - 50 aortic root dialtion of which 80% is idiopathic. aging, syphillitic aortitis, aortic dissection, osteogenesis imperfecta, SSRI’s, dopmine aginists, Systemic HTN, 15% bicuspidal aortic valve, 15% retraction of cusps from rheumatic endocarditis, collagen vascular dz, marfan’s, ehlers-danlos, ankylosing spond, lupus, ACUTE - infective endocarditis
Valve Insufficiency / incompetence – failure to close fully leads to backflow of blood (regurgitation). May be due to HTN, post-infection…

62. Heart Valve Disorders: Stenosis
AORTIC STENOSIS - age-related Calcification is most commong reason (>50%), calcification of congenital bicuspid aortic valve (30-40%), HTN, diabetes, hyperlioproteinemia, uremia all can speed up process. Acute Rheumatic fvr (10%) can scar
MITRAL STENOSIS - almost all from Rheumatic ht dz dt rhem fvr. - uncommon - calcification dt congenital. When severe, get Afib
TRICUSPID STENOSIS is rare & almost always together with mitral stenosis. Can also be dt carcinoid synd, endocarditis, lupus e, r atrial myxoma, congenital
TRICUSPID INSUFFICIENCY - R ventricular dilation messes up anatomy of valve dt L ventricular dilation, R ventricular infarction, inferior MI, cor P
AORTIC INSUFFICIENCY - 50 aortic root dialtion of which 80% is idiopathic. aging, syphillitic aortitis, aortic dissection, osteogenesis imperfecta, SSRI’s, dopmine aginists, Systemic HTN, 15% bicuspidal aortic valve, 15% retraction of cusps from rheumatic endocarditis, collagen vascular dz, marfan’s, ehlers-danlos, ankylosing spond, lupus, ACUTE - infective endocarditis
Stenosis (narrowing) – valve leaflets thicken, stiffen, or fuse together so it cannot fully open.
May be due to calcification, post-inflammation, scar formation, tumors, congenital
Age-related Aortic Stenosis from calcification is most common type

63. Heart Valve Disorders: Insufficiency w Regurgitation
Most common valves affected:
Mitral insufficiency – backflow of blood from L ventricle to L atrium
Mitral valve prolapse (MVP) – one or both valve cusps protrude into L atrium during ventricular contraction
Aortic insufficiency – backflow of blood from aorta into L ventricle

64. Congestive Heart Failure
In CHF, the heart is a failing pump:
Stroke Volume decreases, blood remains in ventricle (end systolic volume increases)
End diastolic volume increases gradually (ventricle enlarges)
If Left ventricle fails first,blood backs up into lungs, get Pulmonary edema
If Right ventricle fails first, blood backs up in body, get Peripheral edema
CHF may be due to: coronary artery disease, congenital defects, long-term high blood pressure (increases afterload), myocardial infarctions, valve disorders.
Either ventricles are too dilated & can’t contract or they can’t relax and let blood in