Cardio Patho Flashcards
How much blood does the heart pump per day
6000L
How thick is the Right and left ventricle
R=0.3cm-0.5cm
L=1.3-1.5cm
how is cardiomegaly defined
inc in cardiac weight(hypertrophy) or size(dilation) or both
what is the concentration of mitochondria in the cardiac myocytes compared to skeletal muscle
cardiac=23% (heart needs more O2)
skeletal= 2%
how are myocytes arranged
cirumferentially in a spiral orientation to allow for maximal ejection fraction
what are cytoplasmic electron dense granules
found in the atria and contain ANP
what is the significance of intercalated discs with gap junctions
allow atria or ventricles to function as a unit and contract together
what are the 3 types of pathologic changes that can occur in heart valves and what is their effect
collagen damage=prolapse
nodular calcification=stenosis
fibrotic thickening= stenosis
how does Rheumatic heart dz affect the heart
The body forms antibodies to group A strep. These antibodies then attack the heart valves causing fibrotic thickening
what is the likely effect from a bicuspid aortic valve
causes early stenosis(40-60yo) bc one valve takes the brunt of the pressure
what is the blood supply to the 1)SA node 2)AV node 3) Bundle of His
1)55%RCA 45% circumflex
2)70% RCA(Right dom)
20% circumflex (Left dom)
10% Codominant
3) RCA
Can a heart convert from R dominant to L dominant
a heart can convert to codominant only with chronic ischemia
A occlusion to which cardiac wall is the most concerning in regards to rate control
Inf wall MI bc a R dom heart will have infarct to the SA and AV node
how much necrosis is considered not viable to life in the L ventricle
40% or more
how much necrosis is considered not viable to life in the R ventricle
90% or more
what are the branches of the circumflex
obtuse marginals
what are the branches of the L ant descending artery
diagonals and septal perforators
with a infarct, where are the myocytes located that typically die 1st?
the endocardial surface
how long does it take for irreversible damage(necrosis) to occure from ischemia
20-30min
where are common locations of stenosing plaques?
First several cm of LAD
First several cm of circum flex
Entire length of RCA
are most cases of ischemic heart Dz single or multivessel
90% are multivessel
what % of a coronary artery must be obstructed for Sx to occur on exertion
> 75%
what % of a coronary artery must be obstructed for Sx to occur at rest
> 90%
what % of obstruction to a coronary artery would indicate PCI and what percent would indicate medical treatment?
PCI at >70% occlusion but still medically treat those with >50% occlusion
what % of acute ischemia is caused from vessels with <70% occlusion
2/3 of events happen in <70%
what type of patients are likely to have silent angina pectoris
DM, Alcoholics
what are the 3 biochemical components of IHD
1) Hypoxia=dec contractility
2) insufficient metabolic substrates(glucose)
3) accumulation of metabolic waste (lactic acid
how does lactic acid affect cardiac myocytes
it blocks the actin/myosin crossbridge= dec contractility
what is done prior to surgery to negate the hypotensive effect of anesthesia
IV bolus to inc fluids
How does volume overload affect those with IHD
inc ventricular volume= inc actin/myosin crossbridge overlap= inc O2 demand
what is ashen
grey appearance from severe cyanosis and vasoconstriction
What is the mechanism for IHD causing pallor
vasoconstriction from
1) dec CO= shunting of blood to central organs
2) Pain activates sympathetics
what is the mechanism for IHD causing diaphoresis
pain activates sympathetics= activation of diaphoresis
Ischemia to which part of the heart will dec CO the most and how does the heart respond
blocking the free wall(anterior) of the LV will dec CO the most bc it is unable to expand= dec CO= inc HR= tachy arrhythmias
What is a important consideration when CP is accompanied with N/V
This type of discomfort is typically from the phrenic nerve which indicates inf infarct= RCA blockage= possible arrhythmias.
how do nitrates relieve CP
Vasodilate the periphery= dec afterload and dec preload= heart works less
what three terms is unstable angina AKA
preinfarction, crescendo, impending MI
what is prinzmetal angina
spasm of epicardial artery causing transmural ischemia(ST elevation)
when does prinzmetal angina occur
its unpredictable and can occur at rest
what causes prinzmetal angina
may be due to inc SNS, inc Ca++, TXA2/PGI2 imbalance
how do you diagnose prinzmetal angina
ergonovine maleate is used to induce a spasm to confirm diagnosis
how is Thallium 201 used in radioisotope imaging
only enters cells by Na/K pump so it indicates cells that are alive making it a hot isotope
what do the different grades IHD indicate
grade1=up to 25% occlusion
grade2= 25-50
grade3= 50-75
grade 4= 75-100
how do you dec O2 demand in the heart
Bed rest
Preload reduction
Afterload reduction
(Beta/Ca++ blockers, nitrates)
how do you inc O2 supply to the heart
MONA, rate reduction(Beta/Ca++ blockers)
when is morphine typically used in IHD
only for MI (rarely for stable angina)
what is paclitaxel (taxol)
Chemo agent combined with stents which disrupts tubular dynamics necessary for endothelial cell division
what is sirolimus(rapamycin)
immunosupressant combined with stents to dec inflammation= dec endothelialization
what meds are typically given after stents are put in
ASA and plavix are usually given for 6-9m to prevent clots
when is CABG typically performed
if more than 2 vessels occluded
what is the definition of a MI
persistent occlusion resulting in death of the heart muscle
what are key features of necrosis
membrane disruption, cardiac enzymes are released
what is the WHO criteria for MI
2 or more of the following
- prolonged ischemic type chest discomfort
- serial ECG changes
- Rise and fall of serum cardiac markers
what typically causes global hypotension and what type of MI does it cause
caused from anesthesia causing dec blood flow in all coronary arteries=circumferential subendocardial infarct
what type of MI would DIC cause
small intramural vessel obstructions=microinfarcts= subendocardial infarct
what is stunned myocardium
located in periphery of infarcted area-edematous and dysfunctional that is not yet dead and may be recovered
what factors determine the extent of structural or functional changes after infarction
Location, severity and rate of development
Size of vascular bed perfused by obstructed vessel
Duration of occlusion
Metabolic/oxygen needs of myocardium at risk
Extent of collateral blood vessels
Presence, site, and severity of vessel spasm
Other factors: HR, rhythm, and blood oxygenation
what information do collateral coronary blood vessels give you
most hearts have collaterals but they are only noticeable if there is a chronic obstruction
what determines how beneficial reperfusion therapy will be
Rapidity of alleviating obstruction
Extent of correction
what causes reperfusion injury
oxidative stress
calcium overload
inflammation and lactic acid build up distal to clot
how does reperfusion injury cause arrhythmias
inc necrotic tissue= inc extracellular K+=raise resting membrane potential= inc excitability= arrhythmias
what is the most common type of reperfusion injury
hemorrhage d/t inflammation
what causes a Q wave
necrotic tissue becoming fibrotic. (Typically from transmural infarct)
how specific and sensitive is ST elevation
- specificity of 91%
- sensitivity of 46%
In regards to ST elevation, how do you determine the severity of a infartion
the higher the elevation and the more leads involved, the larger the infarction and greater mortality
when does troponin I begin to rise, peak, and disappear after MI
rises 2-4 hrs, peaks 48hrs, and lasts up to to weeks
what is acute organic brain syndrome
Confusion/ disorientation usually caused by dec perfusion to brain
when is greatest risk for ventricular wall rupture post MI
usually 4-7 days post transmural MI
what has dec risk for cardiogenic shock post MI
intra aortic balloon pump perfusing the coronary and brain arteries
what are common complications of transmural anterior wall MI
thrombi or rupture(tamponade)
what are common complications of transmural post wall MI
conduction block d/t AV node involvement
poor prognosis post MI are associated with what
female
DM
age
hx of prev MI
what is sudden cardiac death
Unexpected death from cardiac causes in individuals without symptomatic heart disease. Usually from lethal arrhythmias
what is often the first clinical manifestation of IHD
sudden cardiac death
what are heritable conditions associated with SCD
channelopathies (long QT syndrome) causing overlap of depolarization and repolarization= inc risk for arrhythmias
what is the effect of chronic ischemic heart dz with heart failure
Left vent hypertrophy and dilation
what is the hearts adaptive mechanism to heart failure
Frank-Starling mechanism
Myocardial hypertrophy with or without dilation (ventricular remodeling)
how are catecholamines related to heart failure
dec CO= inc SNS= inc HR and TPR= heart working harder
Deleterious effects: apoptosis of myocytes, down regulation of adrenergic receptors, arrhythmias
how is Angiotension II related to heart failure
dec kidney perfusion= inc Ang II release
Deleterious effects: inc fluid retention
fibroblast remodeling stimulation
-hypertrophy from mitogen activated protein kinase
how is arginine vasopressin(ADH) related to heart failure
inc ADH= peripheral vasoconstriction(to inc kidney perfusion) and fluid retention
Deleterious effect= exacerbation of hyponatremia and edema
how is natriuretic(ANP, BNP) peptides related to heart failure
inc natriuretic= dec preload/afterload
how are endothelial hormones related to heart failure
Endothelin is a potent vasoconstrictor and associated with a poor prognosis in individuals with CHF. It is also a growth factor for myocytes.
how are endotoxins related to heart failure
Linked to myocyte apoptosis and release of tumor necrosis factor and interleukins.
Endotoxins are from gram neg bacteria so typically only problematic in sepsis pts.
how is TNF-alpha related to heart failure
Elevated in CHF and contributes to myocardial remodeling
Down-regulates the synthesis of nitric oxide=vasoconstriction
Induces myocyte apoptosis
Contributes to weight loss and weakness
how do ACE/ARB affect heart failure
diuretic= dec preload, dec afterload
prevent remodeling
what is meant when the heart is in fetal production mode
BNP usually not produced on a daily basis except in fetuses. Fetal mode indicates the ventricles are producing BNP on daily basis. This occurs during heart failure
what is characteristic of hypertrophic myocytes
contain increased mitochondria and have enlarged nuclei (Increase DNA ploidy-DNA replication in absence of cell division))
what is concentric hypertrophy
inc in thickness more than dilation
what is essentric hypertrophy
inc in diameter of ventricle
how are sarcomeres assembled in pressure overload hypertrophy
assembled in parallel to long axis of cells forming concentric inc in wall thickness
how are sarcomeres assembled in volume overload hypertrophy
assembled in series with existing sarcomeres forming essentric hypertrophy
how does myocardial hypertrophy affect the vascular bed
decreased capillary density
increased intercapillary distance
deposition of fibrous tissue
what is the effect of diastolic failure
CO preserved at rest
During exertion: “flash pulmonary edema”
