Hemodynamic Disorder Word Documents 1, 2, and 3 Flashcards
What is the pressure of the right atrium?
Lest atrium?
Right ventricle (systolic)?
Left ventricle (systolic)
right atrium: 3 mmHg
Lest atrium: 8 mmHg
Right ventricle (systolic): 25 mmHg
Left ventricle (systolic): 130 mmHg
What 2 things represent preload
end diastolic pressure and volume
the resitance the ventricle must overcome to pump out all of its contents is…
afterload
systolic ventricular wall tension is _____ and diastolic ventricular wall tension is _____
afterload
preload
What is the laplace relationship?
ventricular wall stress is proportional to the pressure and radius of the camber and inversely proportional to the thickness of the wall
S = Pv x R / 2t
If the thickness of the ventricular wall increases (while pressure and radius of ventricular chamber stays constant), will the stress on the ventricular wall increase or decrease?
stress will decrease
during diastole
What are examples of endogenous “inotrophic” substances and exmaples of drugs that are “inotrophic”
epi and nor epi
dobutamine and milrinone
What condition is being describe below?
What can cause this condition?
When ventricular compliance decreases below the ability of the atrium to fill normally
restrictive cardiomyopathy
caused by fibrosis, amyloidosis, interstitial infiltration by anything that is more rigid
Impaired cardiac filling is called ____ and impaired cardiac pumping is ____
diastolic dysfunction and systolic dysfunction
Will diastolic dysfunction typically reduce the ejection fraction?
no
EF = SV / EDV (they decrease proportionally)
What are the 5 major categories of the factors that determine the CO?
Imp concept
preload afterload contractility compliance heart rhythm
Are there more pts with chonic or acute HF?
chronic
CAD as a causes of HF by _____
dec contractility
Uncontrolled/severe HTN causes HF by _____
increasing afterload
Aortic stenosis causes HF by _____
increasing afterload
What can cause HF without changing ejection fraction?
What can causes HF by decreasing ejection fraction?
Why is there a difference?
No change to EF:
- left ventricular hypertrophy
- restrictive cardiomyopathy
- pericardial disease
Decreasing EF:
- aortic stenosis
- severe HTN
- CAD
those that decrease EF all increase the afterload (dec SV with Inc EDV), while those that have no change in EF decrease both the SV and the EDV!
EF = SV/EDV
What are the 2 most common symptoms of HF?
What are the 2 most specific symptoms of HF?
What 7 signs of HF?
common: dyspnea and fatigue
specific: paroxysmal nocturnal dyspnea and orthopnea
signs: tachycardia, tachypnea, hypotension, pulmonary crackles, wheezing, diaphoresis, and gallops
How does HF cause dyspnea? (what is the mechanism)
congestion of blood causes inc pulmonary pressure which increases filtration of fluid into interstitium. this inc in ISF compresses the alveoli and increases their resistance to airflow
How does HF cause paroxysmal nocturnal dyspnea? (what is the mechanism)
lying down causes a redistribution of the blood volume such that venous return is increased. the heart in failure cannot pump out this inc venous BV so there is a back up of it into the lungs –> pulmonary HTN and edema
How does HF cause tachycardia? (what is the mechanism)
CO = SV x HR
to compensate for the dec in SV, the HR will increase to try to maintain CO/Ejection fraction
What happens when pulmonary venous pressure goes over 25 mmHg?
tansudate passes not only into interstitium but also into the airspaces
How does HF cause diaphoresis? (what is the mechanism)
dec in CO causes a stimulation of SNS = sweating increased
When is an S3 gallop heard (what part of cardiac cycle)?
What is it attributed to?
low or high pitched?
early diastole
rapid filling of ventricle
low pitched
______ is a biomarker of HF and the level correlates with _____
BNP correlates with severity of HF
What are the effects of BNP? (3)
How is this counter-regulatory?
Why is that important?
it causes (1) an excretion of Na and water, vasodialtion
(2) inhibition of renin secretion (therefore also dec angio II and aldo),
(3) inhibits ADH
BNP compensates for/opposes the actions that low BP has on the kidney
helps to maintain homeostasis
What is the most common cause of HF with preserved ejection fraction?
HTN
What is an S4 gallop assc with?
What causes this sound?
What state name does this sound like (imp concept
HF due to HTN
the sound of left atrial contraction as it works to inject blood into a stiffened left ventricle
Tennessee
What are the profiles of acute HF?
A: Warm and dry: perfused extremities (normal or due to vasodialtion) and no edema, no JVD, no crackles
B: Warm and Wet: perfused extremities, edema, JVD, crackles
C: Cold and dry: poor perfusion of extremities (due to dec CO or abn vasoconstriction), no edema JVD, or crackles
D: Cold and wet: poor perfusion of extremities, edema JVD, or crackles
What commonly causes warm and dry HF profile?
transient myocardial ischemia
HF due to lung disease (RT heart failure)
Cold and dry is most commonly caused by
hypovolemia
Mitral regurg + left ventricular dilation + exercise would produce what acute HF profile?
cold and dry
Describe the action of the “respiratory pump”
rapid breathing promotes negative intrathorasic pressure during inspiration which promotes the movement of blood into the heart
What CN does info from the carotid body travel on to get tot he CNS?
9 and 10
What effect does the presence of epi have on the liver?
induced glycogenolysis and raises the blood glc level = causes a shift of of water into the plasma/intravasular space
What 2 process result in “autotransfusion”
epi inc glycogenolysis in liver to inc blood glc to inc OPc = fluid into PV
vasopressin (arteriole contriction dec HPc and fluid moves into PV)
How can cardiogenic shock be distinguished from hypovolemic shock?
the central venous pressure will be elevated in CS and low in HS
What is the most common cause out aortic stenosis in pts younger than 65? older than 65?
congenital anomalous bicuspid valve
senile degeneration
crecendo-decrecendo systolic murmur + weak or delayed pulse + atrial (S4) gallup
aortic stenosis
What are the pathophysiologic consequences of mitral regurgitation?
- decreased forward SV
- inc left atrial volume and pressure –> dilation (if chronic)
- volume related stress on left ventricle
“Flash pulmonary edema” is assc with …
What is the mechanism of developing it?
sudden mitral regurgitation
inc left atrial pressure which is transmitted back to the lungs = rapud pulmonary congestion and edema
**medical emergency
What is the most common symptom of acute mitral regurg? chronic mitral regurg?
acute: dyspnea
chronic: fatigue + paroxysmal nocturnal dyspnea
apical holosytoic (pan systolic) murmur
mitral regurgitation
In terms of SV, how is actue and chronic mitral regurgitation different?
in chronic there is more blood going backwards than acute bc the left atrium dilates and pressure falls (favoring the movement of blood backwards to the left atrium)
What drug can be given to decompensated mitral regurgitation pts?
ACEi
assc with Marfan syndrome
mitral valve prolapse
mitral valve prolapse heart sound
mid systolic click and late systolic murmur
RHF follows what kind of infection
group A beta-hemolytic streptocoocal pharyngitis
What are Aschoff bodies and what disease are they assc with?
foci of fibrinoid necrosis with histiocyes and anitschkow cells
sign of RHD
systolic and diastolic murmur + pericardial friction rub
When do symptoms of RHD appear? I.e what age group does it affect?!
20 years after childhood infection ~ 30s
Complications of RHD
mitral stenosis (fused and shortened chordae)
and/or
aortic regurgitation which lead to…
left atrial HTN
left atrial dilation
atrial fibrillation
left atrial thrombus formation
pulmonary HTN
right ventricular hypertrophy and right heart failure
***basically the compications are anything that will result from not being able to get blood into the left ventricle/overloading the left atrium
WHat are MacCallum patches?
What are they assc with
RHD
maplike areas of atrial endocardial thickening and fibrosis
gross pathology of RHD
shortened, thickened, fused chordae
MacCallum patches
What are the 4 etiologies of aortic regurgitation?
- insufficiency due to anomalous bicuspid valve
- endocarditis
- chronic rheumatic valve deformation
- dilation of aortic ring by aortic aneurysm or dissection
consequences of acute aortic regurg on heart chambers
inf left ventricular diastolic pressure and volume –> pulmonary congestion and edema
consequences of chronic aortic regurg on heart chambers
left ventricle increases muscle mass –> inc compliance and less elevated ventricular diastolic pressure
(lancelace relationship stress = 1/2thickness)
How does aortic regurg affect diastolic blood pressure?
drops bc blood is leaking back into the heart
How does aortic regurgitation affect the blood supply of the heart itself?
since it causes a dec in diastolic pressure it will decrease the blood supply to the heart
** remember, the blood flows thru the coronary ostia during diastole (when diastolic BP drops, less blood is available for the CA)
What is the heart sounds assc with decompensated aortic regurg?
daistolic decrescendo + hyperdyanmic bounding + rapidly collapsing pulse (corrigan pulse) + head bobbing with each pulse (de Musset sign
What is de Musset sign? What is it assc with?
head bobing with each pulse
assc with aortic regurg
Why is the pulse pressure widedned with aoritc regurg?
inc ventricular systolic pressure and volumes –> inc ejection fraction (inc systolic pressure)
then more blood falls backwards decreased diastolic pressure)
Tx for aortic regurgitation
valve replacement
Mecanical valves require life long treatment with _____
anti-coagulants
What are the common complications of surgical valve replacement?
structural failure leak thrombosis embolism bleeding endocarditis
autoimmune inflammation of heart valves
libman-sacks endocarditis
where do the vegetations form in libman sacks endocarditis?
mitral and tricuspid on either or both sides
condensed naked nuclei of dead, degenerate, cells that were ingested by phagocytes
hematoxylin bodies
chronic adhesive pericarditis
complication of libman sacks endocarditis
In what conditions do marantic endocarditis form secondary to?
adenocarcinomas DIC chronic sepsis Swan-Ganz right heart cateterization **anything that will make pt hyper coagulable
Marantic endocarditis is the deposition of ____ on valves and is important bc they ….
blood clots
frequently embolize and is the precursor to infective endocarditis
friabile masses of blood clot and infecting organisms
vegetation
What is the pathogenesis of infective endocarditis?
- vascular injury
- platelet and fibrin deposition
- microbial seeding
- microbial multiplication
what is the difference between acute and subacute bacterial endocarditis?
ABE = sudden and due to virulent orgs (S. aureus) SBE = insidious and due to less virulent orgs (strep viridans)
What organism typically causes PVE (prosthetic)?
Staph epidermis
where does the endocarditis typically form in IV drug users?
tricuspid valve
On what sided valves does 75% of infective endocarditis occur?
left
70% of pts with infective endocadritis also have ______
a predisposing heart disease
MVP, prosthetic valve, RHD, previous occurrence, etc
Adherence of some _____(name species) to valves is facilitated by _____
strep (esp strep mutans)
dextran
elevated ESR
non-specific infective endocarditis lab finding but is present in 95% of cases)
What test has >90% specificity for picking up infective endocarditis
transesophageal ECG
T or F Abcensce of vegetation of transesophageal ECG rules out endocarditis.
F
Duke criteria
infective endocarditis
What is the most common cause of right heart failure?
left heart failure
What is the most common cause of isolated right heart failure?
pulmonary disease (vascular or parenchymal)
What is cor pulmonale? What causes it
RHF due to pulmonary disease (HTNive diseases)
- emphysema
- embolism
- interstitial lung disease
How is actue and chronic cor pulmonale distinguished?
acute: dilation of right heart chanmbers
chronic: hypertrophy of right heart chambers
Acute on chronic cor pulmonale is characterized by
dilation superimposed on hypertrophy
What do all the lung disease that cause cor pulmonale have in common?
pulmonary HTN
What are the 4 common manifestations of RHF?
- leg edema
- hepatomegaly
- asciteis
- JVD
Sildenafil (viagra)
drug that will work on the pulmonary arterial vessels to decrease pulmonary HTN
What is the term for toal lack of cardiac puping
asystole
What frequently causes sudden death?
80% attributed to CAD
cardiac electrical signaling malfunction
–> ventricuakr tachyarrythmia
How are electrical signals to contract spread rapidly from cell to cell?
low resistance gap-junctions
mutations in genes for cell adhesion
RT ventricular cardiomyopathy
L-type ion channel
calcium channel open in phase 2
L type ion channels are in close proximity to ____
ryanodine receptors on SR
mutation in ryanodine receptor is assc with what condition?
familial catecholeminergic ryanodine receptors
What is the term for a cells abilty to depolarize itself?
automaticiy
How do injured myocytes develop automaticity? (healthy ones do not have this property)
injured myocytes have leaky membrane that causes their resting membrane potential to become less negative. this allows them to be closer to threshold for depolarization to initiate an arrhythmia
What is the term for abnormal ion fluxes that interrupt repolarizations
afterdepolarizations
afterdeoplarizations that occur in phase 2 or 3 are called _____
Afterdepolarizations that occur in phase 4 are called ____
early
delayed
early afterdepolarizations that occur during the long, plateau of phase 2 are due to defective _____
Ca ion channels
early afterdepolarizations that occur during phase 3 are due to defective _____
Na channels (Na sodium inflow)
delyaed afterdepolarizations that occur during phase 4 are due to _____
high intracell Ca from chatecholamine stimulation
During what phase does re-entry tachycardia NOT occur? WHy?
2
bc they myocytes are refractory to another AP until they are repolarized
What typically causes re-entry tachycardias?
patchy myocardial ischemia (necrosis) or scarring
What is a heart block?
What cuases it?
What usually causes it in young AA females?
electrical impulse cannot travel through bundles of purkinjie fibers
caused by myocardial scarring and amyloidosis
AA young women = cardiac sarcoidosis
the time it takes for a signal to SA node to AV node is represented by the ___ on an EKG. and the normal time is _____
PR interval: 120-200 milliseconds
What is it called when the PR interval is prolonged (>200 milliseconds)?
first degree AV block or first degree heart block
The QRS interval is normally less than or = to ____
100 milliseconds
wider (long) QRS intervals usually indicate …
impulses from an abnormal place or ones that were abnormally conducted
prolonged QT interval usually indicates …
myocardial ischemia
low K, Ca, Mg
channelopathy
What part of the heart do the following leads correspond to and is the blood supply?
V1-4
V5 and 67
II, III, aVF
anterior left ventricle (LAD coronary a)
lateral left ventricle (left circumflex artery)
inferior left ventricle (right CA)
What EKG change corresponds to a major epicardial CA blockage?
elevated ST segment
inverted T wave
What is sinus tachycardia?
How is is differentiated from a tachyarrythmia?
when person with a normal heart exercises and get their heart rate over 100 bpm with normal SA node conduction
a sinus tachycardia will not go over 220 - age bpm
irregular rhythm
high to normal rate (60 to 220)
no p waves
atrial fibrillation
2 p waves for every QRS complex with HR ~ 150 bpm
atrial flutter
responds to valsalva maneuvers, carotid sinus massage and immersion of the face in a pan of ice water
supraventricular tachycardia
widened QRS > 220 msec with HR less than 200 bpm
ventricular tachycardia
chaotic EKG with no clear QRS complexes
ventricular fibrillation
punch or baseball to sternum that precipitates a fata arrhythmia
commotio cordis
A prolonged QTc over ____ miliseconds is a signal of dangerous heart disease
440
mutations in I-Ks
Name?
EKG?
LQT1
prolonged QT allowing –> early afterdepolarizations
Mutations in cardiac Na channel
Name?
EKG?
brugada syndrome
elevated ST with ventricular fibrillation @rest
–> phase 2 reentry
mutations in cardiac ryanodine R
name?
EKG?
familial catecholeminergic polymorphic VT
VT or VF during emotional stress –> delayed afterpolarizations
Which channelopathy is assc with the following:
Phase 2 renetry
early afterdepolarizations
delayed afterpolarizations
brugada (Na channel)
LTQ1 (I-Ks)
familial catecholeminergic polymorphic VT (ryanodine)
Viral myocaditis is assc with what 2 virsues?
Parovirus B
human herpes virus 6
What are the 2 phases of viral myocarditis?
direct viral infection of myocytes –> autoimmune attack on myocytes
higher incidence in northern italy
RT ventricular cardiomyopathy
mutations in (with a 2nd hit) desmoplakin plakoglobin plakophillin 2 desmocollin 2 desmophillin 2
RT ventricular cadriomyopathy
fatty replacement of myocytes with lymphocytic infiltration and later fibrous scarring
RT ventricular cardiomyopathy
