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117 Cards in this Set

  • Front
  • Back
single layer of epithelial cells of the heart (outermost)
layer of cardiac myocytes and connective tissue (middle layer)
single layer of endothelial cells (inside layer)
the sac the heart sits in; composed of connective tissue with a few ml of fluid for lubrication
pericardial sac
when fluid collects inside the sac and the heart cannot fill or pump
cardiac tamponade
these allow for the unidirectional movement of blood in the heart
how do valves open and close?
pressure differences
valve that separates the left ventricle and left atria
mitral (bicuspid)
valve that separates right ventricle and right atria
what holds mitral and tricuspid valve leaflets in place?
chordae tendineae attached to papillary muscles
to allow for filling during ventricular relaxation and prevent blood from regurgitating into the atria during ventricular contraction
Purpose of mitral and tricuspid valves
why are the papillary muscle cells among the first to depolarize?
to tense the valve to prevent the valve from failing during ventricular contraction
during heart contraction, these allow blood to move from the ventricles into the pulmonary trunk and aorta;
during relaxation they prevent blood from moving back into ventricles
semilunar valves
During ventricular contraction when the semilunar valves open, why do their leaflets flap over the openings to the coronary arteries?
to prevent blood from entering during ventricular contraction because the pressure is too high; coronary arteries receive their blood during ventricular relaxation when semilunar valves are in the closed position
Striated muscle fibers associated with the heart; have actin and myosin arranged in sarcomeres; cells are shorter, branched, and have a single nucleus
*a cardiac muscle fiber is made up of many individual cells (not one cell, like skeletal muscle)
individual cells joined together to form a fiber or disc with numerous gap junctions
intercalated disc
what is the purpose of gap junctions in the myocardium?
electrical events in one cell are transmitted to others by means of gap junctions; AP in one cell can influence other cells and thus propagate from cell to cell throughout the heart by means of the gap junctions
Does the heart beat at a constant rate and volume?
-Heart is highly regulated.
-Rich neural innervation
-Responds to hormones.
these nerves release norepinephrine
sympathetic fibers
the receptors that norepinephrine and epinephrine bind to
beta-adrenergic receptors
this hormone is from the adrenal medulla, binds to the same recetors, thus acting like norepinephrine
what is the net result of beta-adrenergic receptor binding of norepinephrine/epinephrine?
increased heart rate and force of contraction
these neurons release acetylcholine
parasympathetic fibers
what does acetylcholine do?
binds to receptors that slow the heart
these drugs bind and block beta adrenergic receptors
beta blockers
-slow heart rate and reduce force of contraction
Why would it be a poor design to deliver blood to the heart muscle directly from the left ventricle?
too much pressure and coronary arteries would have to be huge provide a uniform and abundant blood supply to the myocardium deliver oxygen, nutrients, remove CO2 and other waste products
purpose of coronary circulation
results in more than one artery perfusing the same tissue
the leading cause of death in the US
coronary artery disease
what causes coronary artery disease (cardivascular disease)?
begins at an early age and develops over many years and considered a chronic inflammatory disease
high fat diet
high serum cholesterol (<160 mg/dL considered good)
high LDL
low HDL
smoking (increased fibrinogen levels in smokers, increases LDL and decreases HDL)
hypertension - especially elevated systolic pressure
stress, sedentary lifestyle, obesity, diabetes

sex differences
racial differences - low in Asians - probably due to diet
genetic differences
risk factors associated with CAD (CVD)
this is white, elevated and partially blocks the lumen - occur at bifurcations, curvatures, and at narrowings
these are thought to develop into plaque
fatty streaks
*fatty streak formation can start as early as 10
-occurs with 75% blockage of coronary artery
-ischemia and angina pectoris
first appearance of symptoms of CAD
1.if severe ischemia occurs,
2.necrosis of the myocardium results (MI)
3.plaques may become hemorrhagic
4.lead to thrombosis

3.plaques may calcify(dystrophic-causes inflammation from an area of unresolved healing)
4.core of plaque becomes necrotic, ruptures, and leads to thrombosis
pathogenesis of CAD
If a thrombus blocks the artery it can result in
sudden unstable angina or an MI
If a thrombus embolizes and blocks the coronary artery at a more distal site, this is called
acute coronary syndrome
1.drug Tx: nitroglycerin, beta blockers
treatment of CAD to restore blood flow
dilates arteries and reduce peripheral resistance
nitroglycerin (nitric oxide)
this drug reduces work load on the heart
beta blockers (slows heart and force of contraction)
these drugs prevent thrombosis
Ca channel blockers
-a less invasive procedure
-quick recovery
-local anesthesia

insert a catheter into the femoral, brachial, or carotid artery and snake it to coronary artery openings at base of aorta, cath. w/baloon pushes plaques against vessel wall, sometimes a stent is placed to prevent restenosis
-much more invasive
-major surgery through the sternum and opening of the pericardium and stopping the heart
-venous or arterial graft from leg
-sewn into the aorta and bypasses the blockage to the artery to restor blood supply distal to the blockage
coronary artery bypass graft (bypass surgery)
conditions which results when the blood supply is not able to meet metabolic demands of myocardium
inschemic heart disease (aka mycardial ischemia)
angina pectoris and myocardial infarction
symptoms of ischemic heart disease
Perception of pain in ischemic heart disease is thought to be related to what mechanism?
Lactic acid, the waste product of the glycolytic pathway to produce ATP, builds up when oxygen is not available and stimulates nerve endings.
Where is pain perceived from ischemic heart disease?
Angina or MI pain:
substernal, feeling of tightness, crushing pain, may radiate down one or both arms into neck and jaw
pallow, dyspnea, profuse sweating
in women: fatigue
means "to choke"
refers to chest pain or pressure associated with myocardial ischemia
radiates to jaw and left arm ("referred pain" travels common neurons from these areas)
what are the three kinds of angina?
classic angina
variant angina
unstable angina
-occurs in people with CAD in which exertion above normal activity increases metabolic needs of the heart, but demand exceeds supply
-with rest or vasodilator, chest pain diminishes (myocardial demand decreases)
classic angina (exertional, stable)
In an otherwise healthy individual,this results from coronary artery spasm (constriction) that results in myocardial ischemia; usually at night or at rest
-may occur in people without any evidence of CAD
-may occur in people who can run a mile without difficulty
unknown mechanism
variant angina (atypical)
-Occurs in people with a prior history of classic angina in which the pain does not subside at rest
-Occurs in people with a prior history of classic angina with activity which in the past did not result in angina
-or angina occurs even at rest
unstable angina
*a worsening of the normal pattern of angina pain
ischemic necrosis of myocardium, n usually results from prolonged ischemia - 20-40 minutes (depends on the amount of anastomoses).
Myocardial Infarction (MI)
this is influence by the extent, severity, and duration of ischemmic episode and the metabolic needs of the myocardium at the time of the event
size of infarct
*the larger the infarct the greater the loss of contractility
why do infarcts usually occur in the left ventricle?
left ventricle works the hardest
*MI results in decreased ventricular function
1.central area of necrosis
2.surrounded by an area of injury
3.which is surrounded by an area of ischemia
the sum of 1-3 determines amount or area of myocardial dysfunction from an MI
area of necrosis from MI is replaced by what?
scar tissue, since cardiac myocytes cannot regenerate
what is the significance of the negative impact of scar tissue in the myocardium?
scar inhibits tissue contractility and the significance of this depends on the amount of scar tissue formed; as contractility falls, heart failure ensues
what are the compensatory mechanisms initiated to maintain cardiac output?
peripheral vascular constriction
heart rate increase
renal retention of sodium and water
activation of renin-angiotensin system
-these range from sudden death to dysrhythmias, ventricular rupture, to no symptoms or vague symptoms such as fatigue or acute symptoms
-Acute symptoms include acute substernal pain, diaphoresis, dyspnea, nausea, vomiting, and anxiety
Clinical Manifestations of a Myocardial Infarction (MI)

*n depends on severity of infarct, previous physical condition, previous infarcts, location of infarct
-CBC elevated leukocytes
-elevated erythrocyte sedimentation rate
-myoglobin in serum
-Creatine Kinase (CK-MB)
-Troponin - (CTnT)
lab levels indicative of Myocardial Infarction (MI)
Why is cardia troponin (CTnT) the best marker of the occurence of an MI?
it is found only in cardiac cells; it is a regulatory protein that mediates contraction in cardiac muscle
a serum protein released by cells in response to acute injury, infection or other inflammatory stimuli
C-reactive Protein (CRP)
why is CRP significant?
people with athersclerosis make and release CRP, may serve as a predictor of CAD in addition to serum cholesterol levels, especially for people with low cholesterol.
CRP also promotes atherosclerosis formation

CRP>3mg/L is considered high risk for CVD
diseases in which valve function and the flow of blood through the heart is compromised; accompanied by
-cardiac muscle hypertrophy
valvular disease
heart valve orifice narrows and leaflets fuse; results in obstruction to blood flow

*chambers try to compensate for stenosis
when heart chambers must compensate for stenosis by increasing pressure this leads to a thickening of heart muscle fibers called
cardiac muscle hypertrophy
this results from scarring and retraction of the valve leaflets - retrograde flow of blood (regurgitation)
cadiac insufficiency
when stenosis and regurgitation occur simultaneously, the defect is called a...
mixed lesion and is considered to be an advanced disease
impairment of blood flow from the left atrium to the left ventricle
when valve cannot open during diastole.
mitral stenosis
-most common cause - scarring from rheumatic fever
-other cause - congenital stenosis, bacterial endocarditis
causes of mitral stenosis
-valve becomes funnel shaped
-rarely any symptoms until the valve orifice is decreased from 4-6 to 1-2 cm
-pulmonary symptoms are see first
-left atria dilates and hypertrophies
mitral stenosis
mitral stenosis leads to
1.pulmonary edema
2.increased pressure on right heart-right heart hypertrophy
3.progresses to right heart failure
if pulmonary hypertension is sufficient to cause blood to exit the pulmonary circuit
hemoptysis - blood in sputum
-Rare condition – occurs for the same reasons as mitral stenosis
-5% of all patients with rheumatic fever will develop tricuspid stenosis
tricuspid stenosis
Peripheral edema
jugular venous distension
symptoms of right heart failure
backflow of blood from the left ventricle across the mitral valve to the left atrium during ventricular systole because mitral valve fails to close
Mitral regurgitation and insufficiency
common: mitral valve prolapse, coronary artery disease and rheumatic valve disease
less common: include connective tissue disease, papillary muscle dysfunction (why?) and infective endocarditis
causes of mitral regurgitation and insufficiency
how is mitral regurgitation and insufficiency diagnosed?
-no symptoms for many years - then signs of congestive heart failure develop
-systolic murmur
-(with rupture of papillary muscle, onset is very rapid, and see sudden onset of pulmonary congestion and pulmonary edema)
-rare condition
-backflow of blood from the right ventricle across the tricuspid valve to the right atrium during ventricular systole and tricuspid valve fails to close
Tricuspid regurgitation
most common causes of this condition are enlargement of the right ventricle (many causes), rheumatic fever, bacterial endocarditis (IV drug abusers), diet medication called “phen-fen” (dexfenfluramine)
causes of triscupid regurgitation

*symptoms are the same as tricuspid stenosis
-both the conditions of narrowed mitral opening and failure of the mitral valve to close properly caused by rheumatic lesions
Mixed mitral stenosis and regurgitation

*symptoms are the same as those associated with either mitral stenosis or regurgitation
-condition is probably a congenital abnormality (women, or marfan syndrome)caused by a posterior displacement of the posterior cusp of the mitral valve
-large posterior leaflet bulges into the atrium during systole
-chordae and papillary muscles become stressed

-With time contraction of the papillary muscles decreases and regurgitation may occur as the condition progresses

-major complications are bacterial endocarditis or acute mitral insufficiency from chordae stretching and rupture
-give antibiotics prior to dental work
mitral valve prolapse

-patients usually free of symptoms until condition progresses with time
obstruction of outflow of blood from left ventricle to the aorta
-obstruction may be at the valve (semilunar), above the valve or below the valve
acquired; usually associated with rheumatic fever, degenerative calcific aortic stenosis (dystrophic), and bacterial endocarditis
-more common in elderly
aortic stenosis

*symptoms: chest pain, loss of consciousness, heart failure and pulmonary edema
-regurgitation is due to incomplete closure of the aortic semilunar valve
-occurs as a chronic or acute lesion depending on the disease process
-chronic lesions include lesions from rheumatic fever, syphilis, hypertension, connective tissue disorders and atherosclerosis
-acute lesions can result from aneurysm of the aorta, infectious endocarditis, and rheumatic fever
-dissecting aortic aneurysms dilate the valve ring and prevent aortic closure
n during systole, blood is ejected into the aorta, but some flows back into the ventricle during diastole

-atrial and pulmonary hypertension can develop
-Onset of heart failure indicated by fatigue, dyspnea, chest pain, pulmonary
Aortic regurgitation, insufficiency and incompetence

*Tx: valve replacement
-used to be a major cause of valve disease (still is in the 3rd world)
-acute phase
-chronic phase
occurs in 3% of group A Strep pharyngitis
-a hypersensitivity rxn (Type III) - deposit of antibody on antigens, also binds on valves induces inflammatory response
-acute: results in tissue damage, necrosis, scarring of mitral and aortic valves
-chronic: severe scarring of valves-->stenosis and insufficiency
Rheumatic fever
-Infection of the lining of the heart by bacteria(#1), fungi, rickettsiae, viruses and parasites
-Precipitating factors include contaminated needle usage, dental work or endoscopic procedures in persons with previously damaged cardiac valves
-Disease progresses very rapidly and causes valvular damage – tricuspid and mitral valves affected the most
-damage to the heart valve that results in endothelial damage and exposure of underlying basement membrane and if organisms are in blood they attach to fibrin deposit & proliferate
Infective endocarditis
what organism is implicated in infective endocarditis?
Staph. aureus

*produce friable structures that crumble off --> can embolize and colonize other sites like valve leaflets, peripheral sites
what can inflammation from bacterial endocarditis result in?
malalignment of the valves
fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss

Osler's node, Janeway's lesions, Roth's spots

presents acute and subacute(asymptomatic)
symptoms of infective carditis
painful, tender, red, subcutaneous nodules in the pads of the fingers
Osler's nodes
flat small irregular nontender red spots on the palms and soles
Janeway's lesions
retinal hemorrhages that have a white or yellow center
Roth's spots
severe and rapid development of symptoms including high fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss
-could be fatal within days
Acute Endocarditis
high IV dose, prolonged antibiotic therapy strong enough to penetrate the vegetation and reach the microorganism because valves have no vasculature - med. must diffuse from blood surrounding it.
-patient given a Picc catheter and antibiotics for 6 weeks or more
Treatment of Endocarditis
-initiated by damage to endothelial lining on valve
-damaged areas develop a sterile fibrin deposit
-circulating organisms colonize these fibrin deposits
-peripheral lesions result from bacterial emboli from the vegetations
-emboli can travel and colonize the CNS, pulmonary systems, etc, with the development of symptoms
pathogenesis of endocarditis
which organisms are implicated in bacterial endocarditis
Staphylococcus aureus - pathogen found on skin
– highly virulent
– seen in IV drug abusers

HACEK group - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella
– found in the oral cavity and seen following dental work
inflammatory processes of the myocardium that results in primary injury to cardiac myocytes
causes: include infections (viral, bacteria, fungi, protozoa and helminths), immune-mediated reactions (rheumatic fever, lupus, transplant rejection) and idiopathic causes
Literally means heart muscle disease, but has come to mean heart disease resulting from a primary abnormality in the myocardium, 3 kinds:
dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive cardiomyopathy
most common cause of sudden cardiac death in athletes; autosomal dominant disorder with defects to myosine, tropolyosin, and troponins
-results in enlarged heart w/enlarged left ventricle
-basic problem is inability to fill the hypertrophic left ventricle during diastole
hypertrophic cardiomyopathy

*symptoms are sudden reduce ejection fraction, harsh murmur, exertional dyspnea
– Patent ductus arteriosus (PDA)
– Atrial septal defects
– Ventricular septal defects
– Tetralogy of Fallot
– Transposition of the great vessels
Congenital Heart Diseases-an abnormality of structure or function of the heart, circulatory system or both
when the the ductus arteriosus doesn't close completely at birth and there is a shunt between aorta and pulmonic arteries
-blood flows from the aorta into pulmonary circulation
Dx: 2 weeks postnatally w/harsh murmur
-results in increased volume and pressure in the pulmonary system, (followed by CHF)
Patent ductus arteriosus (PDA)
fetal opening between atria doesn't close properly

-Right ventricular hypertrophy, respiratory infections, dyspnea, fatigability are seen with larger defects
atrial septal defects
-Most common congenital defect
-An opening in the septum that separates the left and right ventricle doesn't close properly
-usually requires surgery
ventricular septal defects
-Primary cause of cyanotic heart disease
-More common in males
-Involves the combination of pulmonary stenosis, ventricular septal defect, and hypertrophy of the right ventricle
-polycythemia (compensatory)
Tetralogy of Fallot
right & left heart get switched, and right heart cannot maintain systemic circulation
-corrective surgery asap
Transposition of the great vessels
inability of the heart to eject blood delivered by the venous system; common cause of death

CAD, malformation, persistent HTN
*(but not from other causes, like cardiac tamponade)
congestive heart failure (CHF)
acute or insidious onset
diastolic and/or systolic dysfunction

*VENOUS return stays the same or increases.
pathophysiology of CHF
– Reflex increased sympathetic activity – how does this occur? baroreceptors
– Release of renin – increases volume and return to heart – mechanism for release? RAA, & stimulate brain thirst centers
– Anaerobic metabolism by affected cells
– Increased extraction of oxygen from hemoglobin by peripheral cells
Systemic responses to decreased output from CHF
-Seen most often in patients with systemic hypertension
-Ventricle undergoes hypertrophy due to increased work load due to increased peripheral resistance
-wall enlarges --> chamber volume decreases -->ventricular compliance decreases --> CO declines

*ventricular contractilty is normal
Diastolic dysfunction with CHF

(Ventricle wall thickens)
Seen in patients with myocardial damage due to an MI
CO declines but venous return stays the same or increases --> volume of the ventricle increases

Hypertrophy of the ventricular wall does NOT occur

*Ventricular contractility impaired
Systolic dysfunction with CHF

Chamber gets huge (enlarged heart)
decrease CO --> lowers BP --> renin is released from kidney --> angiotensin --> ACE --> angiotensin II --> stimulates thirst center in brain, causes vasoconstriction, secretion of aldosterone

results: increased BP, expansion of blood volume (via aldosterone)
Renin-angiotensin-aldosterone system

* increases the workload on the already failing heart
Right heart failure follows left heart failure
Right heart failure follows left heart failure
why does an ANP draw confirm CHF?
Atrial natriuretic peptide is release from atrial cells when there is increased stretch due to increase blood volume, as in CHF
-Output of the left ventricle is less than the total volume of blood received from the right side of the heart through the pulmonary circulation
-Pulmonary circuit becomes congested
-Systemic blood pressure falls
-compensatory mechanisms initiated
-Major causes include MI, systemic hypertension, aortic stenosis and insufficiency, cardiomyopathy, mitral stenosis and mitral insufficiency
-Blood back into the left atrium due to left ventricular failure
-Blood volume in the lungs increases
-Above a critical point (25-28 mm Hg), fluid passes across the pulmonary membrane into the interstitial spaces around the alveoli and eventually into the alveoli
-Pulmonary edema results when pulmonary lymphatics are unable to handle the additional fluid volume
-Recall they can compensate up to 4X the lymph flow
-Acute pulmonary edema results as alveoli fill with fluid
-Microhemorrhages can occur and sputum may become rust-colored
-Hemosiderin-laden macrophages are present – known as heart failure cells
-With decreased CO, BP decreased and RAA system stimulated
-Sodium and water are retained -Sympathetic neural stimulation increases heart rate and peripheral vasoconstriction
-Blood volume increased
left heart failure
Output of right ventricle is less than the input from the system venous circuit.
-Systemic venous circuit is congested and output to the lungs decreases
-Primary cause of RHF is LHF
-Due to excessive pulmonary pressure generated by left heart failure
-Other causes include chronic obstructive lung disease, pulmonary embolus, right ventricular infarct, and congenital heart defects
-Right heart failure that results from lung disease is called cor pulmonale – common in patients with COPD
-Failure of right ventricle to empty causes blood to backup into right atrium, causing increased pressure in the systemic venous circulation
-Increased volume and pressure are transmitted to distensible organs such as the liver and spleen
-Results in transudation of fluid into abdominal cavity (ascites) and systemic peripheral edema
-What is the mechanism for peripheral edema?
-Hepatomegaly, splenomegaly, gravity dependent edema results

Signs and Symptoms:
-Pitting edema noted on sternum or sacrum as well as feet and legs depending on position
-Respiratory impingement and organ dysfunction
-Deactivation of aldosterone by the liver may lead to additional fluid retention
-Jaundice and coagulation problems may result if effects on liver are severe
-Jugular venous distension in the neck can be measured at the bedside
Right Heart Failure