Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
191 Cards in this Set
- Front
- Back
What are the 3 structures inside the carotid sheath?
|
L - internal jugular vein
M - common carotid artery P - vagus nerve |
|
In most people, the SA & AV nodes are fed by which coronary artery?
|
RCA
|
|
In most cases, which artery supplies the inferior part of the LV?
|
RCA - specifically the Posterior Descending. When the PD is off the RCA, this is a right dominant heart.
|
|
Coronary occlusion most often occurs in which artery? What territory does that artery supply?
|
LAD, which feeds anterior interventricular septum.
|
|
Which chamber lies most posteriorly?
|
LA - enlargement can cause dysphagia
|
|
Mean Arterial Pressure =
|
CO x Total Peripheral R
|
|
Pulse Pressure =
|
systolic - diastolic
(~ stroke volume) |
|
Cardiac Output =
|
SV x HR
|
|
SV = (___) - (___)
|
EDV - ESV
|
|
Mean Arterial Pressure = 1/3 (?) + 2/3 (?)
|
1/3 systolic + 2/3 diastolic
|
|
When you first start running, your CO increases as a result of increased ___.
|
Stroke Volume
|
|
After you've been running for 2 hours, your CO is increased because of an increase in ___.
|
Heart Rate
|
|
What happens if your HR is too high?
|
Diastolic filling will be incomplete and CO will decrease. (like in v-tach)
|
|
What are 3 variables that affect SV?
|
contractility, preload, afterload
|
|
How do catecholamines increase contractility (and SV)?
|
increase activity of Ca pump in sarcoplasmic reticulum
|
|
How does digitalis increase contractility?
|
blocks action of Na/K pump, intracellular Na rises, ruins inward Na gradient for Ca/N exchanger --> intracellular Ca rises
|
|
What 3 conditions have increased SV?
|
1) anxiety
2) exercise 3) pregnancy |
|
What 5 things reduce contractility (and SV)?
|
1) beta 1 blockers
2) heart failure 3) acidosis 4) hypoxia/hypercapnea 5) Ca channel blockers |
|
What 4 things increase myocardial O2 demand?
|
1) inc. afterload
2) inc. contractility 3) inc. HR 4) bigger heart size |
|
What is preload equivalent to?
|
ventricular EDV
|
|
What is afterload equivalent to?
|
systolic arterial pressure, which is proportional to peripheral R
|
|
Things that dilate your veins will lower ___.
|
preload (nitroglycerin)
|
|
Things that dilate your arterioles will lower ___.
|
afterload (hydralazine)
|
|
What 3 things will cause your preload to increase?
|
1) exercise
2) overtransfusion of blood 3) excitement (sympathetics) |
|
Force of contraction is proportional to:
|
initial length of cardiac muscle fiber (preload)
|
|
Ejection Fraction =
|
SV / EDV
|
|
What is a normal EF?
|
> or = 55%
|
|
What is EF a measure of?
|
ventricular contractility
|
|
What 3 things can increase blood viscosity?
|
1) polycythemia
2) hyperproteinemic states (multiple myeloma) 3) hereditary spherocytosis |
|
Resistance is inversely proportional to:
|
blood vessel radius to the 4th power
|
|
Which phase of the cardiac cycle consumes the most O2?
|
isovolumetric contraction - when developing the LV pressure needed to open AO valve
|
|
What are the 5 phases of the cardiac cycle?
|
1) isovolumetric contraction
2) ejection 3) isovolumetric filling 4) rapid filling 5) slow filling |
|
S1 =
|
mitral and tricuspid valves close
|
|
S2 =
|
AO and pulmonary valves close
|
|
S3 =
|
end of rapid ventricular filling, heard just after S2, associated with dilated CHF (ventricle walls vibrating)
|
|
S4 =
|
stiff ventricle or high atrial pressure ("atrial kick"), associated with hypertrophic ventricle
|
|
a wave =
|
atrial contraction
|
|
c wave =
|
RV contraction
|
|
v wave =
|
inc. atrial P due to filling against closed tricuspid valve
|
|
Under what pathologic circumstance do you see Jugular Venous Distention?
|
right heart failure
|
|
What is normal S2 splitting?
|
S2 is when AO and Pulm valves close, but 2 split sounds are heard because the AO valve closes slightly earlier than the Pulm
|
|
What is paradoxical splitting?
|
when Pulm valve closes before AO valve during S2 - associated with AO stenosis (because stenotic valves close slower?)
|
|
What stimulates Ca release from cardiac myocyte SR?
|
extracellular Ca, which enters myocyte during axn potention plateau (K eflux balanced by Ca influx)
|
|
What connects cardiac myocytes to each other so that electricity can pass quickly from one to the next?
|
gap junctions
|
|
What are the phases of the myocardial axn potential for atria/ventricle/Purkinje?
|
Phase 0 - rapid depolarize
Phase 1 - initial repolarize Phase 2 - plateau Phase 3 - rapid repolarize Phase 4 - resting potential |
|
What is the normal resting potential for a atria/ventricle/Purkinje fiber?
|
- 85 mV
|
|
What is the duration of the axn potential in atria/ventricle/Purkinje fibers?
|
~300 msec
|
|
The slope of Phase ___ in the SA node determines the heart rate.
|
Phase 4 - slow diastolic depolarization via funny current (Na+)
|
|
ACh ___ the rate of SA node depolarization, thereby ___ the heart rate.
|
decreases, decreases
|
|
How do catecholamines affect the slope of Phase 4 depolarization in the SA node?
|
increase the slope, increase heart rate
|
|
P wave =
|
atrial depolarization
|
|
PR segment =
|
conduction delay thru AV Node (<200 msec)
|
|
QRS complex =
|
ventricle depolarization (<120 msec)
|
|
QT interval =
|
mechanical contraction of ventricles
|
|
T wave =
|
ventricular repolarization
|
|
U wave =
|
hypokalemia!
|
|
ST segment =
|
isoelectric, ventricles still depolarized
|
|
If you see a gradual slope preceding the QRS complex, what does that mean?
|
That is a delta wave, indicating the ventricles begin to partially depolarize earlier because there is an extra bundle of conduction fibers (Kent) between the atria and ventricles that bypasses AV Node. May cause supraventricular tachycardia. Wolff-Parkinson-White syndrome.
|
|
A patient's EKG shows erratic baseline with no discrete P waves and irregularly spaced QRS complexes. This is called:
|
atrial fibrillation
|
|
A patient's EKG shows rapid identical looking atrial depolarization waves. This is called:
|
atrial flutter
|
|
An asymptomatic patient's EKG shows a prolonged PR interval but is otherwise normal. This indicates:
|
1st degree AV block
|
|
What is happening in an EKG that shows progressive lengthening of the PR interval until there is a QRS spike not preceded by P wave (dropped beat)?
|
2nd degree AV block - usually asymptomatic
|
|
What is it called when an EKG shows random drops in P waves not preceded by lengthening PR intervals?
|
Mobitz type II, 2nd degree AV block
|
|
What is it called when an EKG shows P waves and QRS spikes that occur independently to each other?
|
3rd degree AV block - Tx with pacemaker
|
|
What is it called when an EKG shows completely erratic rhythm w/no identifiable waves?
|
ventricular fibrillation - fatal arrhythmia without immediate CPR and defibrillation!!
|
|
How does your brain sense low MAP?
|
medullary vasomotor center - senses less baroreceptor firing
|
|
How do your kidneys sense low MAP?
|
JGA - senses lower effective circulating volume
|
|
Stimulating Beta-1 receptors on your heart will:
|
inc. HR & contractility --> inc. CO
|
|
Stimulating Alpha-1 receptors on your heart will cause:
|
venoconstriction --> inc. venous return and inc. CO
arteriole constriction --> inc. TPR |
|
What 2 substances do your kidneys release to raise MAP?
|
- A II (vasoconstriction --> TPR)
- aldosterone (raise blood volume and CO) |
|
AO arch baroreceptors send signals to the medulla by cranial nerve ___.
|
X - vagus
|
|
Carotid sinus receptors send signals to the medulla via cranial nerve ___.
|
IX - glossopharyngeal
|
|
Why does a carotid massage lower BP?
|
inc. P on carotid artery --> inc. stretch on baroreceptor
|
|
Carotid and AO bodies respond to which peripheral changes in the body?
|
- low PO2
- high PCO2 - low blood pH |
|
Central chemoreceptors respond to which changes in brain interstitial fluid?
|
- pH
- PCO2 ** do not directly respond to PO2! |
|
What is the Cushing reaction?
|
response to cerebral ischemia, inc. intracranial P --> HTN and bradycardia
|
|
What is pulmonary capillary wedge pressure an approximation of?
|
LA pressure (< 12 mmHg)
|
|
What is the normal P inside the RA?
|
< 5 mmHg
|
|
What is the normal P inside the LA?
|
< 12 mmHg
|
|
What is the normal P inside the LV?
|
systolic - < 130
diastolic - 10 |
|
What is the normal P inside the RV?
|
systolic - < 25
diastolic - < 5 |
|
What is the normal P in the AO?
|
systolic - < 130
diastolic - 90 |
|
What is the normal P in the pulmonary artery?
|
systolic - < 25
diastolic - 10 |
|
The pulmonary vasculature is unique because hypoxia -->
|
vasoconstriction!
|
|
What are 4 changes in net fluid flow that can lead to edema?
|
1) inc. capillary P
2) dec. plasma proteins 3) inc. capillary permeability 4) inc. interstitial osm. P |
|
Which 3 congenital heart diseases produce early cyanosis?
|
all right-to-left shunts:
1) Tetralogy of Fallot 2) Transposition 3) Truncus Arteriosis |
|
What is the most common congenital cardiac anomaly?
|
VSD
|
|
What does an ASD sound like?
|
loud S1
wide fixed split S2 |
|
What do you give to close a PDA?
|
indomethacin (NSAID)
|
|
Left-to-right shunts eventually cause what to thicken?
|
pulmonary arterioles --> inc. pulmonary R
|
|
What is Eisenmenger's syndrome?
|
Uncorrected VSD/ASD/PDA leads to pulmonary HTN which causes RVH --> reversal of shunting and late cyanosis (clubbing, polycythemia)
|
|
What are the components of a Tetralogy of Fallot?
|
1) pulmonary stenosis
2) RVH 3) overriding Aorta 4) VSD |
|
What causes Tetralogy of Fallot?
|
anterosuperior displacement of infundibular septum (huh?)
|
|
What does Tetralogy of Fallot look like on x-ray?
|
boot-shaped heart due to RVH
|
|
What is the congenital heart defect where the AO is connected to the RV and the pulmonary trunk leaves from the LV?
|
Transposition of Great Vessels
|
|
A new patient presents with HTN when BP taken in the arms, but has bilateral weak femoral pulses. What do you suspect?
|
Postductal coarctation of Aorta - also associated w/notching of ribs
|
|
Under what circumstance would you want to maintain a PDA?
|
Transposition of Great Vessels to allow mixing of blood (VSD or ASD would work too)
|
|
22q11 syndromes are associated with which cardiac defects? (2)
|
- Tetralogy of Fallot
- Truncus Arteriosis |
|
Down's syndrome is associated wtih which cardiac defects? (2)
|
ASD, VSD
|
|
Congenital rubella is associated with which cardiac defects? (2)
|
- septal defects
- PDA |
|
Turner's syndrome (45, XO) is associated with which cardiac defect?
|
coarctation of Aorta
|
|
Marfan's syndrome is associated with which cardiac defect?
|
Aortic insufficiency
|
|
Children of diabetic mothers often have which cardiac defect?
|
Transposition of Great Vessels (recall: this one needs mixing of blood)
|
|
What is considered high blood pressure?
|
BP > or = 140/90
|
|
What are some risk factors for HTN?
|
- older age
- obesity - diabetes - smoking - genetics - black > white > Asian |
|
90% of HTN is primary and related to increased ___ and ___.
|
CO, TPR
|
|
10% of HTN is secondary to:
|
renal disease
|
|
What does Malignant HTN look like?
|
- marked inc. in diastolic BP
- focal retinal hemorrhage, papilledema - LVH and LV failure - rapid early death!! - mostly young AA males |
|
Having HTN predisposes one to what other pathologic conditions?
|
- athersclerosis
- stroke - CHF - renal failure - retinopathy - aortic dissection |
|
Atheromata =
|
plaques in blood vessel walls
|
|
Xanthoma =
|
nodules of lipid-laden mac's in the skin
|
|
Tendinous xanthoma =
|
lipid deposit in tendon (Achilles)
|
|
Corneal arcus =
|
lipid deposit in cornea, nonspecific (acrus senilis)
|
|
Monckeberg arteriosclerosis =
|
calcification of the arteries, esp. radial or ulnar; usually benign
|
|
Arteriolosclerosis =
|
hyaline thickening of small arteries in essential HTN; "onion skinning" in malignant HTN
|
|
Atherosclerosis =
|
fibrous plaques and atheromas in intima of arteries
|
|
What are 5 risk factors for atherosclerosis?
|
- smoking
- HTN - family Hx - diabetes mellitus - hyperlipidemia |
|
Progression of athersclerosis: (3 steps)
|
fatty streaks --> proliferative plaque --> complex atheromas
|
|
Complications of atherosclerosis: (6)
|
- infarct
- ischemia - aneurysms (weakened wall) - peripheral vascular disease - thrombus - emboli |
|
Where does atherosclerosis usually occur?
|
abdominal AO > coronary artery > popliteal artery > carotid artery
|
|
Sxs of atherosclerosis:
|
angina, claudication, or asymptomatic
|
|
How stenosed does a vessel have to be for a person to develop angina?
|
> 75%
|
|
Stable angina =
|
retrosternal pain with exertion; mostly due to atherosclerosis
|
|
Prinzmetal's angina =
|
occurs at rest due to coronary vasospasm (recall: do not give Sumatriptan!)
|
|
Unstable angina =
|
worsening chest pain, thrombosis but no necrosis
|
|
MI most often is acute thrombosis due to _____. Results in myocyte _____.
|
coronary artery atherosclerosis; necrosis
|
|
What is sudden cardiac death usually due to?
|
lethal arrhythmia - death within 1 hr of sxs onset!!!
|
|
Hemorrhagic infarcts occur in which organs?
|
"loose" tissues with collaterals, like lung, intestine; or can occur following reperfusion
|
|
Where do pale infarcts occur?
|
solid tissues with single blood supply, like brain, heart, kidney, spleen
|
|
A man presents to the ER sweating profusely, vomiting, severe retrosternal pain, pain in left arm and jaw, and SOB. What is going on?
|
acute MI (most likely coronary occlusion of LAD)
|
|
On the 1st day of an MI, what would the heart look like grossly?
|
dark mottling in the area of occluded vessel; pale if stain with tetrazolium
|
|
Microscopically, what changes can you see after 2 hours of an MI?
|
contraction band necrosis
|
|
How many days after an MI is cardiac muscle most weak?
|
4-7 days (watch out for free wall rupture, interventricular septum, papillary muscle, and cardiac tamponade)
|
|
What kind of necrosis occurs after an MI?
|
coagulative necrosis
|
|
How many days after an MI would the infiltrating neutrophils be replaced by macrophages?
|
3-7 days
|
|
On autopsy, grossly, what does an old MI scar look like?
|
gray-white area of scarring
|
|
How do you Dx an acute MI?
|
EKG in the first 6 hrs - gold standard! See ST elevation (transmural infarct), ST depression (subendocardial infarct), pathological Q waves (transmural infarct)
|
|
Cardiac troponin I is elevated how soon after an MI, and stays elevated for how long?
|
4 hours, 7-10 days
|
|
CK-MB is found in heart muscle but also in:
|
skeletal muscle
|
|
CK-MB peaks at:
|
24 hours after MI
|
|
AST is nonspecific and can be found in:
|
- liver
- heart - skeletal muscle |
|
AST peaks:
|
between 1-2 days after MI
|
|
LDH peaks:
|
~2 days after MI
|
|
Which complication of an MI is an important cause of death within the first few days?
|
arrhythmia
|
|
What is cardiogenic shock?
|
A huge MI could weaken the pumping function of the heart and lead to shock (hypotension).
|
|
Fibrinous pericarditis is often seen ___ days after MI.
|
3-5 days
|
|
Dressler's syndrome =
|
autoimmune phenomenon resulting in fibrinous pericarditis weeks after MI
|
|
What is the most common cardiomyopathy?
|
dilated (90% of cases) - systolic dysfunction
|
|
What can cause dilated cardiomyopathy?
|
- chronic alcohol abuse
- wet beriberi (B1 deficiency) - Coxsackie B virus - chronic cocaine abuse - Chaga's disease - doxorubicin (Adriamycin) - peripartum - hemochromatosis |
|
Hypertrophic cardiomyopathy impairs:
|
diastole
|
|
Hypertrophic cardiomyopathy often involves which part of the heart?
|
interventricular septum (HOCM)
|
|
A patient's heart looks like a balloon on chest x-ray. Which cardiomyopathy does he have?
|
dilated
|
|
___% of cases of hypertrophic cardiomyopathy are autosomal ___.
|
50%, dominant
|
|
What would you auscultate in someone with hypertrophic cardiomyopathy?
|
loud S4 (stiff wall), apical impulses, systolic murmur
|
|
What drug would you give for hypertrophic cardiomyopathy?
|
beta blocker
|
|
What are major causes of restrictive/obliterative cardiomyopathy?
|
- sarcoidosis
- amyloidosis - post-radiation fibrosis - endocardial fibroelastosis - endomyocardial fibrosis |
|
You hear a holosystolic, high-pitched "blowing" murmur that is loudest at the apex of the heart. What is the murmur?
|
Mitral regurgitation
|
|
You hear a crescendo-descrescendo, systolic ejection murmur with an ejection "click" radiating to the carotids. The patient's pulses are also weak compared to his heart sounds. What is his murmur?
|
Aortic stenosis
|
|
What would a VSD sound like?
|
holosystolic murmur
|
|
You hear a late systolic murmur with a mid-systolic "click." What is the murmur?
|
Mitral valve prolapse
|
|
What is the most frequent valvular lesion?
|
Mitral valve prolapse
|
|
What is the murmur heard during diastole that sounds like a decrescendo and is associated with a wide pulse pressure?
|
Aortic regurgitation
|
|
What does mitral stenosis sound like?
|
Late diastolic murmur that follows "opening snap." LA > LV pressure during diastole.
|
|
How can you tell a tricuspid stenosis from a mitral stenosis?
|
Tricuspid stenosis gets louder with inspiration.
|
|
You hear a continuous murmur in an infant that's loudest during S2. What does the baby have?
|
PDA
|
|
Overall, what is the most common heart tumor?
|
METASTASES!
|
|
What is the most common primary heart tumor in children? What is it associated with?
|
Rhabdomyoma; tuberous sclerosis (also astrocytoma, ash leaf spots, renal cysts, seizures...)
|
|
What is the most common primary heart tumor in adults? Where is it most often located? What does it make?
|
Myxoma, "ball-valve" obstruction in LA, known to produced VEGF
|
|
Presence of hemosiderin-laden macrophages =
|
heart failure
|
|
What are 6 types of emboli?
|
Fat, Air, Tumor, Bacteria, Amnion fluid, Thrombus
|
|
How does a pulmonary embolus present?
|
chest pain, tachypnea, dyspnea
|
|
Amnion fluid emboli can lead to ___ postpartum.
|
DIC
|
|
What 3 things predispose one to deep vein thrombosis?
|
1) stasis
2) hypercoagulability 3) endothelial damage |
|
What is cardiac tamponade?
|
compression of the heart by fluid in the pericardium, leading to decreased CO
|
|
What do you find in someone with cardiac tamponade?
|
decreased heart sounds, jugular venous distension, hypotension
|
|
What does cardiac tamponade look like on EKG?
|
"Pulsus paradoxus" - beat-to-beat alterations of QRS complex height
|
|
Acute bacterial endocarditis caused by:
|
Staph aureus, large vegetations on previously normal valves
|
|
Subacute bacterial endocarditis caused by:
|
Strep viridans, small vegetations on congenitally abnormal, or diseased, valves; often following dental procedures
|
|
A patient presents with a new murmur, anemia, fever, tender raised lesions on his finger pads, erythematous lesions on his palms, splinter hemorrhages, and round white spots on his retina surrounded by hemorrhage. You want to do a blood culture to confirm:
|
bacterial endocarditis
|
|
What is the most frequently involved valve in bacterial endocarditis? For IVDU's?
|
Mitral, tricuspid
|
|
What is marantic endocarditis?
|
Associated with metastatic cancer and other wasting conditions; small sterile deposits randomly arraned along line of closure of leaflets; can embolize as well
|
|
On autopsy, you find vegetations on both sides of the mitral valve. This person had what disease?
|
SLE
|
|
Children with pharyngitis caused by Group A beta-hemolytic streptococci can sometimes go on to have:
|
rheumatic fever - multisystem inflammatory disorder with major cardiac manifestations and sequelae
|
|
What is rheumatic heart disease?
|
Strep antigens cause autoimmune cross-reaction to own heart valves (mitral > aortic > tricuspid), eventually thickening and calcifying.
|
|
What are the manifestations of Rheumatic Fever?
|
fever, erythemia marginatum, valve damage, inc. ESR, polyarthritis, subQ nodules, Sydenham's chorea, inc. ASO titers, Aschoff bodies
|
|
What is an Aschoff body?
|
classic lesion of Rheumatic Fever, focal interstitial myocardial inflammation characterized by large cells (Anitschkow myocytes) and multinucleated giant cells (Aschoff cells)
|
|
Serous pericarditis is caused by: (4)
|
SLE, rheumatoid arthritis, uremia, infection
|
|
Fibrinous pericarditis is caused by: (3)
|
uremia, MI, rheumatic fever
|
|
Hemorrhagic pericarditis is caused by: (2)
|
TB, malignancy (melanoma)
|
|
What do you find in someone with pericarditis?
|
friction rub, EKG changes, pericardial pain, pulsus paradoxus, distant heart sounds
|
|
What kind of cardiac manifestations can be seen in tertiary syphilis?
|
dilation of ascending Aorta and valve ring --> aneurysm and valve incompetence
|