Kaplan guy - cardio Flashcards
chest pain on exertion relieved with rest or nitro
stable angina
what four things do you think of with sudden onset of chest/trunk pain?
MI
PE
pneumothorax
ectopic
What are causes of stable angina?
- CAD
- aortic stenosis
- hypertrophic obstructive cardiomyopathy
- aortic regurgitation
What is the only cause of stable angina without a murmur?
CAD
What stable angina pt should you not give nitro to?
Why?
hypertrophic obstructive cardiomyopathy
the heart is thickened below the level of the aortic valve, resulting in decreased cardiac output. if we give nitro, a vasodilator we could worsen the output
Both restrictive cardiomyopathy and constrictive pericarditis present with what major ssx?
Kussmaul sign: JVD on deep breath
What does S3 sound like?
rhythmic, melodious “I’m relaxed”
What does S4 gallop sound like?
abrupt “A stiff heart”
Chest pain radiating to the back, tearing pain
aortic dissection
What is the pathophysiology behind JVD and the Kussmaul sign specifically?
the heart muscle is not compliant upon filling; as the pt takes a deep breath, the entire chest is filled with a negative pressure, including the heart, but the heart can’t accomodate the blood trying to come in
Pt is having chest pain that gets worse with changing position, dx?
pericarditis
What are two different types of pericarditis and when would they occur?
- fibrinous pericarditis can happen almost immediately after MI
- autoimmune pericarditis/Dressler syndrome will be after 1 week s/p MI
What causes pleuritis?
fibrinous exudate from injury to the lung surface
What kind of things would increase afterload in a cardiac pt?
handgrip, HTN, squatting
What things would decrease the preload in cardiac pts?
valsalva, nitrates, standing, fluid depletion
How can we increase preload in cardiac pts?
fluid overload, squatting, leg raising, inspiration
How can we decrease afterload in cardiac pts?
vasodilators, ACE inhibitors
What type of cell starts acute inflammation process?
How does this work?
macrophages
- use toll-like receptors to find things that don’t belong
- sends message to nucleus with NF-kappaB
- to DNA to produce cytokines
- TNF
- IL-1
- IL-6
- IL-8
What do cytokines created s/p macrophage activation do?
- TNF
- increase temp and cause apoptosis by activating caspases causing cachexia
- IL-1
- increase temp and degranulate mast cells (doesn’t need IgE involved)
- IL-6
- stimulates hepcidin
- IL-8
- chemoattractant for neutrophils
What is hepcidin?
- hormone regulating iron absorption
- produced by the liver based on iron stored there
- increased Fe will cause increased hepcidin in order to keep iron in liver
What will too much IL-6 cause? Why?
anemia of chronic disease
stimualtes hepcidin which will sequester iron in the liver
In diastolic heart failure, what is the issue? What would my EF be?
poor filling capacity
normal EF >60%
If I have systolic heart failure, what is the issue and what will my EF be?
pump failure
low EF <45%
When are hemosiderin laden macrophages found? what else are they called? What stain is used to show these cells?
- blood gets into alveoli, macrophages break them down, and are filled with iron
- heart failure cells
- prussian blue stain
What is the clinical symptom of hemosiderin laden macrophages?
flecks of blood in sputum
What drugs have no direct affect on preload or afterload?
beta blockers
What are four classic ssx of CHF?
- hemosiderin laden macrophages
- Kerley B lines on CXR at the lung margins
- Interstitial and perivascular edema
- fluid in alveolar space with widening of alveolar septum
What is my first line drug for systolic CHF?
ACE inhibitor
When are S3 and S4 gallops best heard?
at the end of expiration
What is my first line drug for diastolic CHF?
beta blocker
When would I hear an S4 gallop?
“a stiff heart” with diastolic CHF, heart is still strong, but unable to fill well
What is the renin-angiotensin system?
- renal blood flow is reduced and stimulates renin release
- renin converts angiotensinogen to AT 1
- AT 1 is converted to AT II by ACE (angiotensin converting enzyme)
What is AT II and where does it work?
potent vasoconstrictor (efferent kidney) and stimulates aldosterone
What does aldosterone do once stimulated by AT II?
stimulates Na+ and water retention along with K+ excretion in order to raise BP and keep electrolytes even
What does an ACE-I do? What is an example of one?
What are some possible AEs?
- enalapril
- decreases peripheral resistance, decreasing afterload by inhibiting the conversion of AT I to AT II
- by decreasing the amount of AT II present, there is less vasoconstriction and aldosterone is inhibited as well
- with aldosterone inhibited, K+ may not be excreted as well causing hyperkalemia
- these also increase bradykinin by decreasing the degradation of it; bradykinin causes cough
Where does bradykinin come from and what does it do?
- phospholipids
- arachadonic acid
- PGs and bradykinin (inflammatory mediators)
- arachadonic acid
causes vasodilation at the afferent arterioles of the kidney
With classic CHF, what three drug classes should you give?
- ACE-I
- beta-blocker
- diuretic
Where would I find beta-1 adrenergic receptors and what do they do here?
- heart
- rate, contractility, conduction
- kidney
- stimulates renin production leading to vasoconstriction
What are three fairly common beta-1 selective blocking drugs?
What are they used for?
On the physiologic level, what is their MOA?
- metoprolol, acebutolol, atenolol
- control HR and force of contraction
- Beta-1 are Gs - so they get inhibited, reducing the production of cAMP by the heart, reducing contractility due to decreased amount of calcium
What are some indications for beta-blockers?
angina, MI, HTN, arrythmia (tachy), CHF (diastolic and systolic)
What is the small vessel pathology of DM?
Why would giving an ACE-I help?
hyaline arteriolosclerosis - narrowing of arterioles, compromising the blood supply to tissues
this drug would protect the kidney from microproteinuria because DM causes decreased GFR causing dilation of teh efferent arteriole; the drug would cause aff>eff and increase pressure in the kidneys, raising GFR
Where does furosemide work and what is its MOA?
thin ascending loop of henle
blocks Na/K/2Cl transporter
What numbers does the Na-K pump send back and forth?
How does this leave the cell, charge wise?
How does the lumen in the kidney respond?
for every 3 Na out, 2 K in,
leaving the cell with a slightly negative charge
K+ will still flow out of channels into the lumen, leaving Cl- in the cell; the lumen becomes positive because of Mg2+, Ca2+, and K+ being there. The positive ions then are mostly absorbed back into the body, leaving the lumen
All diuretics compete with what?
Therefore, what disease state contraindicates the use of diuretics, specifically HCTZ?
- excretion of uric acid
- gout
What electrolyte imbalances will you seen with use of furosemide?
- hypercalciuria
- hypocalcemia
- hypomagnecemia
- hypokalemia
- hyperuricemia
S4 gallop is caused by…
LVH
a non-occlusive thrombus over an atherosclerotic plaque will cause what?
unstable angina
spasm of a coronary artery
Prinzmetal angina
How would you calculate Mean Arterial Pressure?
= (SBP + 2(DBP))/3
what drug inhibits Na channels, blocking depolarization and can be used for angina?
ranolazine
What is the MOA of nitrates?
stimulate guanylate cyclase, increasing cGMP, dephosphorylating myosin, creating dilation of blood vessels
What converts phospholipids into arachidonic acid?
PL A2 (phospholipase A2)
If ASA is inhibiting the COX pathway, what happens?
arachidonic acid gets shunted to LOX side
Leukotrienes produced
- B4 - chemoattractant
- C4, D4, E4 - smooth muscle contraction
What can be used to prevent clot formation over rupture of atherosclerotic plaque?
acetyl-salicyclic acid
Pt has fluid overload, what three systems could be involved and how would you decide which was the one actually involved?
- cardiac
- S3 or S4 gallop
- renal failure
- protein in urine or elevated BUN or creatinine
- liver disease
- jaundice, caput medusa, ascites
What is the best way to hear S3/S4?
- bell of stethoscope
- laying on L side
- at end of exertion
What kind of murmur sounds like a sweeping broom?
Where is it best heard?
systolic murmur
best heard at base
Where is the murmur for HCM best heard? What is special about this murmur?
best heard in aortic area
murmur increases/gets worse with less blood (valsalva)
Both HCM and Aortic stenosis have what kind of murmur?
systolic murmur
What kind of murmur sounds like a washing machine?
diastolic murmur
If a murmur worsens with inspiration, where is it located?
R side
What are the three murmurs of aortic regurgitation?
- L sternal border hear aortic regurg
- Austin-Flint murmur hear anterior mitral valve with regurg
- Aortic flow murmur at base
Autosomal dominant mutation in cardiac sarcomeric protein gene; muscle fibers in disarray; prominent in septum; obstruction of outflow tract
dx?
hypertrophic obstructive cardiomyopathy
When do you always need to get an ABG?
why?
When RR >24
represents an acid-base disturbance
Quickest way to determine rate on EKG?
QRS complexes x 6
leads II, III, and aVF
inferior wall
V2, V3, V4
anterior wall
v5, V6
lateral
v1
septal
If both I and aVF are positive, what is the axis?
normal
I is negative on EKG
R axis
aVF is negative on EKG
L axis
1-4 hours s/p MI, what will you see on heart autopsy?
normal heart
4-12 hours s/p MI, what will you see on heart autopsy?
swelling of muscle fibers
When might rupture of structures occur after an MI?
3-10 days as macrophages are phagocytizing dead cells
2?-14 days s/p MI, what will you see on heart autopsy?
granulation tissue and neovascularization
When would you see contraction bands and karyolyis on heart autopsy s/p MI?
What is this from?
<1 day old MI
as heart is reperfused, calcium causes contraction bands
How long does it take neutrophils to show up?
How long will they be present, say after an MI?
about 24 hours
1-3 days s/p you will see coagulative necrosis and neutrophilic infiltration
What are three steps of ischemia and what parts are reversible?
- cell swells
- without O2, decrease ATP, Na-K pump stops, increasing Na, increasing water
- reversible
- decrease protein production from RER
- reversible
- Ca-ATP pump stops
- increase Ca2+ in cell, activating proteases and endonucleases, leaking into blood
- irreversible
What murmur acts similarly to HCM? Why is this unique?
mitral valve prolapse
murmur will decrease with more blood (ie handgrip)
After a pt suffers an MI, I will never give what medication?
anti-arrhythmia prophylactically
any rx you give has a greater risk of causing arrhythmia than the post MI pt alone
valve leaflets are too big for annulus causing…
what will I hear?
mitral prolapse
closing ‘click’ from valve leaflets
What is the MC cardiomyopathy?
What often occurs with it?
dilated cardiomyopathy
mitral regurgitation
What are common causes of dilated cardiomyopathy?
alcohol
doxorubicin
cocaine
coxsackie B, enterovirus
Chagas disease
pregnancy
What will exercise and chronic AV fistula do to CO and VR?
both CO and VR will increase in this scenario
If I am concerned for a possible reinfarct s/p MI, what should I do?
recheck enzymes
troponin lasts 10days while CPK-MB only lasts 3 days
Pt is having chest pain within 1 week of her MI and the pain is worse when laying down. What are we suspecting?
fibrinous pericarditis
About 3-4 days s/p MI of inferior lateral wall infarct and now the pt has a sudden onset of CHF, what am I concerned for?
papillary muscle rupture
What injury could occur 4-8 weeks s/p MI?
ventricular aneurysm
What type of hypersensitivity reaction is Dressler syndrome?
When does it occur?
type II HS rxn - autoimmune
1-8 weeks s/p MI
How do you tx dilated cardiomyopathy?
transplant
What four things can have liquefactive necrosis?
pancreas, brain, abscess, wet gangrene
Where would I be most likely to find fat necrosis?
breast tissue, calcium deposit
What arrhythmia might mitral regurgitation precipitate?
ventricular fibrillation
In what heart disease would I see myxomatous degeneration (mucous)?
Specifically what genetic disease might have this?
mitral valve prolapse
marfan syndrome
What heart defect might you see in Turner syndrome?
bicuspid aortic valve
age related wear and tear of the heart and cells in valves resemble osteoblasts - deposition of calcium salts
degenerative calcific aortic valve stenosis
What are the major Jones criteria for Rheumatic fever
- migratory polyarthritis - joint inflammation
- pancarditis
- nodules (subcutaneous)
- erythema marginatum
- sydenham chorea
Subacute infective endocarditis usually affects what side of the heart? What bacterial pathogen is usually associated?
L side of heart
Strep viridans
What are systemic symptoms of subacute infective endocarditis?
- roth spots in retina
- Janeway lesions (nonpainful)
- osler nodes (painful)
- splinter hemorrhages
defect in the arterial septum at the level of the tricuspid and mitral valves
What is this associated with?
ostium primum
Down Syndrome
People with a ventral septal defect are at higher risk for …
infective endocarditis
headache and nosebleed, weakness on exertion and leg pain, legs feel cool and under developed (claudication)
no cyanosis or clubbing
notching of the ribe
coarctation of the aorta
preductal coarctation of the aorta if it is preductal will be associated with what findings?
Turner syndrome
PDA
right ventricular hypertrophy
weak pulses and cyanosis
coarctation of the aorta postductal
HTN in UE
hypotension in LE
notching ribs
intracerebral hemorrhage
dissecting aortic aneurysm
overriding aorta, VSD, pulmonary stenosis, right ventricular hypertrophy in an infant
How can the cyanosis be relieved?
Tetralogy of Fallot
relieved by squatting
machine like murmur in an infant
cyanosis and clubbing of toes and not fingers
patent ductus arteriosis
To keep PDA open give…
To close PDA give…
Prostaglandin E2
indomethacin
What does vasoconstriction and increased platelet aggregation and is blocked by NSAIDs?
TXA2
What does vasodilation and decreased platelet aggregation?
PGI2, PGE2, PGD2
aortic regurgitation, s3 heart sound, eccentric sarcomere added in series
eccentric hypertrophy
aortic stenosis, S4 heart sound, concentric sarcomere added in parallel
concentric hypertrophy
