Ch 12: Heart Flashcards
what is the leading cause of mortality in the world
cardiovascular disease (1 in 4 deaths in US)
what is heart type 1
-supply
right preponderance (dominant)
80% of people - most common
right coronary artery supplies the right ventricle, posterior half of septum, and the left posterior ventricle
what is heart type 2
-supply
balanced
8% of people - least common
each ventricle is supplied by the corresponding coronary artery
what is heart type 3
-supply
left preponderance (dominant)
12% of people - second most common
two types:
two posterior descending branches, one from each coronary artery
or
single posterior descending branch coming from the left circumflex branch
what are the three layers of the heart
epicardium (outer layer)
myocardium (muscle layer)
endocardium (inner layer)
what are the three layers of the pericardium
serious pericardium (visceral layer/epicardium)
serious pericardium (parietal layer)
fibrous pericardium (outermost layer)
what are the three layers of the aortic valve
ventricularis layer (outermost) - ventricularis because it abuts ventricle
spongiosa layer (middle)
fibrosa layer (innermost)
what are the three layers of the mitral valve
atrialis layer (outermost) - atrialis because it abuts atria
spongiosa layer (middle)
fibrosa layer (innermost)
what does the fibrosa layer of the aortic/mitral valves do
made of dense collagen
connected to the valve’s supporting structures
provides mechanical integrity
what does the the ventricularis/atrialis layer of the aortic/mitral valve do
made of elastin
provides leaflet recoil
what are the 6 main mechanisms that lead to heart failure
failure of the pump
obstruction to flow
regurgitant flow
shunted flow
disorders of cardiac conduction
rupture of the heart or major vessel
what is the end stage of heart failure
congestive heart failure
what are the three major conditions of heart failure
insufficient output to meet metabolic demands
can only meet demands when there is higher filling pressures
marked increased in tissue demand
what is the frank-sterling mechanism
compensatory mechanism
increased venous return leads to increased diastolic filling volumes
extra amount of blood causes dialation of heart
dilation is a result of cardiac myofibril stretching (more cross bridge formation)
leads to increase stroke volume and contractility
what is the equation for stroke volume
end diastolic volume (EDV) - end systolic volume (ESV)
amount of blood ventricle filled with - amount of blood left in ventricle after contraction
what is the activation of neurohumoral systems
compensatory mechanism
release of substances (norepinephrine, renin, and atrial natriuretic peptide)
affects heart function and regulates filling volumes and pressures
where does norepinephrine come from and how does it affect the heart
neurotransmitter released from ANS
elevates HR and contractility to compensate for vascular resistance
how does the renin-angiotensin-aldosterone system affect the heart
regulates blood pressure and volume
promotes water and salt retention to increases vascular tone and circulatory volume
how does atrial natriuretic peptide affect the heart
counters the renin-angiotensin-aldosterone system
causes diuresis (peeing) and vascular smooth muscle relaxation
what is systolic dysfunction
left ventricle can’t contract normally
decreases amount of blood circulating in the body
what are two causes of systolic dysfunction
hypertension
ischemic heart disease
what is diastolic dysfunction
inability of the heart to relax and fill enough
what are the four main causes of diastolic dysfunction
left ventricular hypertrophy
myocardial fibrosis
amyloid deposition
constrictive pericarditis
cardiac dysfunction is characterized by which three things
heart failure
arrhythmias
neurohumoral stimulation
what is the most common cause of right sided heart failure
left sided heart failure
what is the most common cause of isolated right sided heart failure
pulmonary disease
what are the four most common causes of left sided heart failure
ischemic heart disease
systemic hypertension
mitral or aortic valve disease
amyloidosis
what happens during chronic heart failure
RBCs leak out of capillaries, breakdown, and release their hemoglobin
alveolar macrophages engulf hemoglobin and become known as heart failure cells
what are the microscopic features of acute left-sided heart failure
accumulation of edema/blood in alveolar macrophages
what are heart failure cells
alveolar macrophages that have engulfed hemoglobin from broken down RBCs
“hemosiderin laden macrophages”
alveolar macrophages that have engulfed hemoglobin from broken down RBCs
“hemosiderin laden macrophages”
heart failure cells
what are three ways to treat left sided heart failure
restrict salt diet
drugs
cardiac pacemakers
what are the top two most common congenital heart abnormalities (with percentages)
ventricular septal defect (42%)
atrial septal defect (10%)
congenital heart disease makes up what percentage (range) of all birth defects
20-30%
when is an embryo most susceptible to a congenital heart disease (week range)
development during weeks 3-8
what are the three main types of congenital heart diseases
septal defects
stenotic lesions
outflow tract abnormalities
which congenital factors can lead to congenital heart disease
specific loci
chromosome abnormalities (trisomies 13, 15, 18, and 21; monosomy X; turner syndrome )
what is a shunt
abnormal connection between chambers or blood vessels which allows blood to move between the two sides of the heart
what are the two major consequences of a right-to-left shunt
cyanosis + clubbed fingers/toes
deoxygenated blood is entering systemic circuit
what are the consequences of a left-to-right shunt
increased pressure and volume to pulmonary circulation
right sided heart failure
what is the most common congenital cardiac malformation
left to right shunt
what are the three main causes of a left to right shunt
atrial septal defect
ventricular septal defect
patent ductus arteriosus
what are the two main causes of right to left shunts
tetralogy of fallot
transposition of the great vessels
where do 90% of ventricular septal defects occur
membranous region of interventricular septum
what is the most common type of atrial septal defect
type 1 - secundum defect (old side of foramen ovale)
what is a systolic thrill and in which cardiac malformation is it mostly seen
a heart palpitation most commonly seen in those with a patent ductus arteriosus
a heart palpitation most commonly seen in those with a patent ductus arteriosus
systolic thrill
what is a common characteristic of pulmonary stenosis
right ventricular hypertrophy
what are the four components of tetralogy of fallot
ventricular septal defect
pulmonary stenosis
overriding aorta
right ventricular hypertrophy
what is coarctation of the aorta and what does it cause
narrowing of the aorta
causes left ventricular hypertrophy
pressure of everything above coarctation is increased and decreased below it
what is an atrioventricular septal defect
incomplete atrial and septal walls, usually with no tricuspid or mitral valves
causes mixing of arterial and venous blood
what congenital heart defect is most common in Down’s Syndrome
atrioventricular septal defect
what is congenital aortic stenosis and who is most at risk
stiffening of aortic valve that you’re born with
valve can be uni or bicuspid
maybe be asymptomatic for years
3x more common in males
what is transposition of the great vessels
reversal of the pulmonary and aortic arteries
deoxygenated blood goes to the body, oxygenated to the lungs
must be surgically repaired after birth
what is ischemic heart disease (IHD)
imbalance between perfusion and oxygen requirements of the heart
what causes 90% of ischemic heart disease cases
coronary artery disease obstruction (plaque)
what is the most common clinical manifestation of ischemic heart disease
angina due to 70% stenosis
what is angina pectoris
chest pain caused by sudden and recurrent attacks of chest pain (15 seconds to 15 minutes)
does not cause myocyte necrosis
what is angina pectoris (chest pain) specifically caused by
release of molecules that stimulate sympathetic and vagal afferent nerves
what is the most common form of angina
stable (typical)
what is unstable (crescendo) angina
prolonged (over 20 minutes) severe angina
usually caused by plaque disruption
how does disruption of a plaque cause a myocardial infarction
plaque is disrupted by some kind of force
platelets adhere and aggregate to newly exposed collagen and plaque contents
coagulation is activated
thrombus occludes the lumen
how long does it take for a myocardial infarction to achieve its full extent
3 to 6 hours
what are the three factors that impact a myocardial infarction
rate of development and duration of occlusion
metabolic demands of myocardium
extent of collateral supply
when do myocytes lose their contractility during an MI
before two mintues after the event began
what is the timeframe of irreversible cell injury during a myocardial infarction
20-40 mins
myocytes are damaged beyond repair
what is a transmural infarct
death of myocytes due to prolonged total occlusion of an artery (MI)
includes the entire thickness of wall
what are multiple diffuse infarcts
small, intramural vessel occlusions that cause myocyte death
do not include entire thickness of wall
what is the most common occluded artery to cause an MI (40-50% of cases)
left anterior descending (interventricular)
which parts of the heart are most affected by an MI involving the left anterior descending (interventricular) artery
anterior wall of ventricle
2/3rds interventricular septum
apex
which parts of the heart are most affect by an MI involving the left circumflex artery
lateral left ventricle
which parts of the heart are most affected by an MI involving the right coronary artery
most of the right ventricle
which parts of the heart are most affected by an MI involving the posterior descending artery
posterior 1/3rd of septum and posterior left ventricle
what is the second most common occluded artery to cause an MI (30-40% of cases)
right coronary artery
global hypotension leads to a non-transmural infarct that can be seen where on the heart
causes a circumfrential subendocardial infarct
what are the three results of reperfusion during an MI
vascular injury (leakiness)
no ATP - sarcomeres get stuck in tetanic state
saves injured cells but changes morphology
when is troponin at its highest after an MI
3 to 12 hours after MI
stays elevated for 14 days
when is creatine kinase myocardial band fraction highest after an MI
increases within 3 to 4 hours
peaks at 24 hours
returns to normal within 36 hours
what are the three treatments for an MI
thrombolytic drugs
angioplasty with stent
bypass surgery
what are the three criteria used to diagnose an MI
clinical history of chest pain
elevation of cardiac markers (troponin-1, CK-MB, myoglobin)
changes on an electrocardiographic
must have 2/3 to consider it an MI
what is the weight of a male heart
270-360g (300 g)
what is the average weight of a female heart
200-280g (250 g)
what is the thickness of the left ventricle
1.0-1.5 cm
what is the thickness of the right ventricle
0.2-0.4 cm
what is the average circumference of the aortic valve (males and females)
males: 6.7 cm
females: 6.3 cm
what is the average circumference of the pulmonary valve (males and females)
males: 6.6 cm
females: 6.2 cm
what is the average circumference of the mitral valve (males and females)
males: 9.6 cm
females: 8.6 cm
what is the average circumference of the tricuspid valve (males and females)
males: 11.4
females: 10.6
what are the three predictors of how damaging a MI will be
size, site, and type of infarct
what are three things that large transmural infarcts increase your risk for
cardiogenic shock
arrhythmias
late congestive heart failure
what are three things that anterior transmural infarcts increase your risk for
free wall rupture or expansion
aneurysm formation
mural thrombi formation
what are two things posterior transmural infarcts are more complicated by
conduction blocks
right ventricular involvement
what is the main thing that a subendocardial infarct increases your risk for
thrombi
rarely pericarditis, rupture, or aneurysms
what is the first piece of macro/microscopic evidence of an MI and when is it first seen
variable waviness of fibers at border
seen 30 mins to 4 hours after
what macroscopic/microscopic changes from an MI do you see 4-12 hours in
macroscopic changes: dark mottling
microscopic changes: early coagulative necrosis, edema, hemorrhage
what macroscopic/microscopic changes from an MI do you see 12-24 hours in
macroscopic: dark mottling
microscopic: pyknosis (shrinking of nucleus), early neutrophilic infiltrate, contraction band necrosis
what macroscopic/microscopic changes from an MI do you see 1-3 days in
macroscopic: mottling with yellow-tan infarct center
microscopic: loss of nuclei and striations more infiltrate of neutrophils
what macroscopic/microscopic changes from an MI do you see 3-7 days in
macroscopic: blood boarder with central yellow-tan softening
microscopic: dead myofibers start to break down, dying neutrophils, phagocytosis by macrophages at boarder
what macroscopic/microscopic changes from an MI do you see 7-10 days in
macroscopic: yellow-tan with depressed red-tan margins
microscopic: phagocytosis and granulation at margins
what macroscopic/microscopic changes from an MI do you see 10-14 days in
macroscopic: red-grey depressed borders
microscopic: new blood vessels and collagen deposition
what macroscopic/microscopic changes from an MI do you see 2-8 weeks in
macroscopic: grey-white scar staring at infarct border; gelatenous appearance
microscopic: more collagen, less cells
what macroscopic/microscopic changes from an MI do you see after 2 months in
macroscopic: fully formed scar
microscopic: dense collagenous scar
where is the most common spot to get a myocardial rupture
free ventricular wall
what is a cardiac tamponade and when is it most commonly seen after an MI
collection of blood in the pericardial sac due to a myocardial rupture
usually seen around 7 days after an MI
what are the two most common consequences of myocardial ischemia
arrhythmia and conduction defects which can cause sudden death
what percentage of patients experience one or more complications of myocardial ischemia
75%
what is ventricular remodeling
consequence after an MI
scarring and thinning of the infarcted zones
hypertrophy
dilation
what is the mortality rate (%) of an MI in the first year
90% mortality rate
what does the Bundle of His (AV) bundle do
part of the heart’s conduction system that connects the right atrium to the ventricular septum
what is atrial fibrillation
atria become irritable and depolarize independently and sporatically
leads to upper and lower chambers being uncoordinating
cause all different types of rythyms (tachy, brady, sytole, etc)
what are the two duration types of arrhythmias
sustained
sporadic (paroxysmal)
what are the three treatments of atrial fibrillation
anticoagulants
electrical conversion
ablation
what is atrial fibrillation a major risk factor for
stroke (15%)
what are the four contributing factors to atrial fibrillation
alcohol
smoking tobacco
diabetes mellitus
thyrotoxicosis (high levels of T3/T4)
what is the most common location of a heart block
interventricular septum
what is a bundle branch block
complete or partial interruption of the electrical pathways inside the wall of the heart
what are primary electrical disorders
inherited disorders that cause sudden death in the absence of structural caridac pathology
diagnosed through genetic testing
most are channelopathies
ex. long QT syndrome
what is the most common cause of sudden cardiac death
coronary artery disease leading to ischemia
what is the drug used to help more easily identify an early MI
nitro blue tetrazolium - regular tissue appears dark maroon, MI is much paler in color
what does pulmonary hypertensive heart disease (cor pulmonale) cause
right ventricular hypertrophy and dilation
what is valvular insufficiency
valve is unable to open or close all the way which leads to regurgitation of blood
what is a mitral valve prolapse and what does it cause
mitral valve bulges into the atrium and may not close properly, leading to a leak or regurgitation
what is a thrill
palpation of a severe lesion that can be felt on the skin over area of turbulence
what are heart murmurs caused by
turbulent flow through diseased valves
what is a prolapsed ventricle
leaflets of valve balloon upwards as the ventricle contracts
what is regurgitation
valve leaflets do not properly close, forcing blood back into the atrium
what is the most common congenital valvular lesion
bicuspid aortic valve
what is myxomatous degeneration
ballooning of the mitral valve leaflets
due to deposition of myxomatous mucoid material in the spongiosa layer of the valve
what is rheumatic valvular disease
caused by A B-hemolytic strep infections
clinical manifestation of rhematic fever
can cause vegetations and stenosis of mitral or aortic valves
who is most affected by acute rhematoid fever
80% of cases affect children
what are aschoff bodies
myocardial inflammatory lesions that are only seen in rheumatic fever
made of T lymphocytes, plasma cells, and macrophages
what is infective endocarditis and what does it look like
microbial infection of the heart valves or endocarium
causes formation of bright red, friable vegetations mostly on valves
can be acute or subacute
which organism causes 50-60% of infective endocarditis cases with exsisting damaged valves
streptococcus viridans
95% cure rate
which organism causes 10-20% of infective endocarditis cases seen in damaged or non-damaged valves
staph. auerus
seen mostly in acute cases and has a 60-90% cure rate
what are the three characteristic signs of endocarditis
roth spots
osler nodes
janeway lesions
what are roth spots
white centered retinal hemorrhages in acute endocarditis
what are janeway lesions
irregular, nontender hemorrhagic macules located on palms and soles seen in acute endocarditis cases
what are osler nodes
tender, purple pink nodules with a place center found on fingers and toes in cases of subacute endocarditis
what are four adverse reactions of endocarditis
glomerulonephritis
septicemia
arrhythmias
systemic embolization
what is the treatment of endocarditis
6+ weeks of antibiotic therapy or valve replacement
what is nonbacterial thrombotic endocarditis
deposition of sterile thrombi on cardiac valves
ususally nondestructive and can occur in healthy individuals
what are three precursor conditions of nonbacterial thrombotic endocarditis
malignancy
DIC
endocardial trauma
what is libman-sacks endocarditis
sterile vegetations on valves associated with SLE (10%)
vegetations on both sides of valve surrounded by fibrinoid necrosis
what are the two most common valves affected by libman-sacs endocarditis
aortic and mitral valves
what is the most common type of cardiomyopathy
dilated cardiomyopathy (dilation of atria/ventricles) which has a high mortality rate
what is hypertrophic cardiomyopathy and what causes it
myocardial hypertrophy
genetic causes manifesting during a post puberty growth spurt
what is restrictive cardiomyopathy and which special stain helps to diagnose it
extracellular deposition of amyloid leading to loss of normal tissue architecture
diagnosed through congo red stain
caused by: fibrosis, amyloidosis, or sarcosis
what is dilated cardiomyopathy
hypertrophy of myocytes with enlarged nucleis and fibrosis
most commonly caused by myocarditis or it’s hereditary
what is arrhythmogenic right ventricular cardiomyopathy and how does it present under the microscope
type of dilated cardiomyopathy
usually caused by right-sided heart failure and rhythm disturbances
fat replacement seen microscopically
causes 10% of sudden death in atheletes
what are the two most common viral infections to cause myocarditis
enteroviruses
coxsackieviruses A and B
what percentage of cardiac tumors are benign
80-90%
what are the four types of cardiac tumors
myxomas (most common)
fibromas
papillary fibroelastomas
rhabdomyosarcomas
what do myxomas of the heart look like
lobulated and polypoid with soft gelatinous appearence (look like a brocolli floret made of jelly)
usually found in left atrium
what is a papillary fibroelastoma
benign tumor on aortic or mitra valves
surfaces have fronds
can have a stalk
what is the most frequent primary tumor of pediatric heart
rhabdomyoma
what are the four most frequent tumors that metastasize to the heart
lung and breast carcinomas
melanomas
leukemias
lymphomas
what is carcinoid heart disease
carcinoid tumors release bioreactive components and cause valvular plaque thickening
what is allograft arteriopathy
most important long term limitation for cardiac transplantation
intimal proliferation of coronary arteries leads to stenosing and ischemia
