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389 Cards in this Set

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  • Back
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pregnant woman in 3rd trimester has normal BP when standing and sitting. When supine BP drops to 90/50. what is the dx?
compression of the IVC
35 y/o man has high BP in arms and lowBP in his legs. what is the dx
coarction of teh aorta
5 y/o boy presents with a systolic murmur and a wide fixed split S2. what is the dx
ASD
None
During a game a young football player collapses and dies immediately. What is the most likely type of cardiac dz
hypoertrophic cardiomyopathy
pt has a stroke after incurring multiple long bone fractures in trauma stemming from a MVA. What caused the infarct
fat emboli
elderly woman presents with a headache and jaw pain. labs show elevated ESR. what is teh dx
temporal arteritis
80 y/o man presents w/ systolic crescendo-decrescendo murmur. What is the most likely cause?
aortic stenosis
Man starts a medication for hyperlipidemia. He then develops a rash, pruritis, and GI upset. What drug was it
Niacin
Pt developes a cough and must discontinue captopril. What is a good replacement drug and why doesn't it have the same side effects?
losartan, an angiotensin II receptor antagonist, does not increase bradykinin as captopril does.
What are the 3 struct inside the carotid sheath
1) Internal jugular Vein (lateral) 2) Common carotid Artery (medial) 3) Vagus Nerve (posterior) mneu: VAN
In the majority of cases, the SA and AV nodes are supplied by this coronary artery?
Right coronary artery
80% of the time the ____ coronary artery is "dominant", suppplying the inferior left ventricle via the _________ branch
RCA, Posterior descending artery
Which coronary is most commonly occuluded? What does it supply?
LAD, antierior interventricular septum
Enlargement of this chamber may cause dysphagia?
Left atrium (most posterior chamber)
cardiac output =
SVxHR
During exercise, CO ↑ as a result of an ↑ in _____. After prolonged exercise, CO ↑ as a result of an ↑ in ____
SV HR
Mean arterial Pressure (MAP)= give 2 equasions: 1) CO, TPR 2) systolic, diastolic
1) CO x TPR
2) 1/3Systolic + 2/3Diastolic
None
2)1/3 systolic +2/3 diastolic
(Fick’s Equation)
rate of O2 consumption / ( aa O2 content-vv O2 content)
Pulse pressure =
systolic-diastolic
None
SV= (2 equasions) 1) CO, HR 2)EDV,ESV
1)=CO/HR 2)=EDV-ESV
Stroke volume is affected by what 3 things
Contractility, Afterload, and Preload

mneu: SV CAP
None
↑Preload →__SV
↑Afterload→ __SV
↑contractility→ __SV
SV ___ in anxiety, exercise, & pregnancy
a failing heart has a ___ SV
Contractality (and SV), ____ with catecholemines
Contractality (and SV), ____ with ↑ intracellular Ca++
Contractality (and SV), ____ with ↑ extracellular sodium
↓ (think of how digoxin increases SV by retaining Na in cells)
None
Contractality (and SV), ____ with digitalis
Contractality (and SV), ____ with β1 blockade
Contractality (and SV), ____ with heart failure
Contractality (and SV), ____ with acidosis
Contractality (and SV), ____ with hypoxia/hypercapnea
Contractality (and SV), ____ with Ca++ channel blockers
Myocardial demand is ___ by ↑ afterload (diastolic BP)
Myocardial demand is ___ by ↑ contractility
Myocardial demand is ___ by ↑ heart rate
Myocardial demand is ___ by ↑ heart size
ventricular EDV is equivalent to (preload or afterload?)
Preload
Systolic arterial pressure is equivalent to (preload or after?)
afterload
proportional to peripheral resistance (preload or afterload?)
afterload
venous dialators (example drug?) ↓ _______ (preload or afterload)
preload : VENous dialator (nitroglycerine)
vaso dialators (example drug?) ↓ _______ (preload or afterload)
Afterload (hydralazine)
______ ↑ w/ exercise, ↑ blood volume, exitement (sympathetics) (preload or afterload)
Preload
Starling Hypoth:
Force of contraction is proportional to initial length of cardiac mm fiber (preload)
contraction state of the myocardium is ____ by circulating catecholamines (+,-)
+
contraction state of the myocardium is ____ by digitalis (+,-)
+
contraction state of the myocardium is ____ by sympathetic stimulation (+,-)
+
contraction state of the myocardium is ____ by pharmacologic depressants (+,-)
-
contraction state of the myocardium is ____ by loss of myocardium (MI) (+,-)
-
EF= (give 2 equasions)
1) SV/EDV 2) EDV-ESV/EDV
this is an measurable index of ventricular contractility
Ejection fraction
EF is normally > ___%
55
Place condition on the Starling curve [pic p.219]
1)exercise 2)CHF + digitalis 3)CHF
(driving Pressure)ΔP= Q (flow) ,R (resistance)
ΔP = Q x R (V=IR)
Resisitance (R) = Give 2 equasions: 1)ΔP(driving pressure),flow(Q) 2)Poiselle's Eqn
1)=ΔP/Q 2)8nxl/Πr(^4) (poiselles’s)
None
viscosity depends mostly on _______
hematocrit
increased viscosity in 3 conditions:
1) Polycythemia 2) Hyperproteinemic states (e.g., multiple myeloma (IgG)) 3) hereditary spherocytosis
resistance is ________ to viscosity (proportional or inversely proportional)
proportional
resistance is ________ to the radius to the 4th power (proportional or inversely proportional)
inversely proportional
cardiac and vascular fx curves [pic p.219]
1) (+) inotropy 2) (-) inotropy 3) (↑) blood volume 4) (↓) blood volume
cardiac cycle image [p. 220]
1)isovolumetric contraction 2) aortic valve opens 3) ejection 4) aortic valve closes 5) isovolumetric relaxation 6) mitral valve opens 7)ventricular filling 8) mitral valve closes
Name the phase of the cardiac cycle: period between mitral valve closure and aortic valve opening.
isovolumetric contraction
Name the phase of the cardiac cycle: period of highest O2 consumption
isovolumetric contraction
Name the phase of the cardiac cycle: period between aortic valve opening and closing
systolic ejection
Name the phase of the cardiac cycle: period between aortic valve closing and mitral valve opening
isovolumetric relaxation
Name the phase of the cardiac cycle: period just after mitral valve opening
rapid filling
Name the phase of the cardiac cycle: period just before mitral valve closure
slow filling
name the event at: S1
mitral and tricuspid valve closure
name the heart sound: aortic and pulmonary valve closure
S2
name the event causing the sound: S3
at the end of rapid ventricular filling
What causes S4 sound?
high atrial pressure/stiff ventricle
this heart sound is associated w/ dilated CHF
S3
this heart sound is associated with a hypertrophic ventricle
S4
Jugular venous pulse waves: a wave
Atrial contraction
Jugular venous pulse waves: c wave
RV Contraction (tricuspid valve bulging into atrium)

* Remeber jugular venous pressure is based on RIGHT HEART since that is where the vena cava drains!
None
Jugular venous pulse waves: v wave
increaseed atrial pressure due to filling against closed tricuspid Valve
jugular venous distention is seen in ___________
right heart failure
What happens when S2 splitting occurs? (which valve is closing first)
the aortic valve closes before the pulmonic this heart sound abnormality results
None
S2 splitting is increased upon ________
inspiration
Paradoxical splitting (S2 split increasd upon expiration is associated with what?
aortic stenosis
pressure volume relationship [pic p. 221]
--
cardiac mm contraction is dependent on extracellular ________, which enters the cells during plateau of action potential and stimulates ______ release from the cardiac mm sarcoplasm reticulum.
calcium calcium calcium induced calcium release
In contrast to skeletal mm, cardiac mm action potential has a plateau, which is due to ____ influx.
Ca+
In contrast to skeletal mm, cardiac nodal cells ________ depolarize, resulting in automaticity
spontaneously
In contrast to skeletal mm, cardiac myocytes are electrically coupled to each other by ________
gap junctions
myocardial action potential occurs in what cells?
atrial, ventricular, and perkinje fibers
None
In a myocardial action potential, this phase is the rapid upstroke, when voltage gated ______ open
phase 0, Na+ channels
None
In a myocardial action potential, this phase is the initial repolarization-inactivation of voltage0gated Na+ channels. Voltage gated K+ channels begin to open
Phase 1
In a myocardial action potential, this phase is the plateu--Ca++ influx through voltage-gated Ca++ channels balances K+ efflux. Ca++ influx triggers another Ca++ release from sarcoplasmic reticulum and myocyte contraction.
phase 2
In a myocardial action potential, this phase is the rapid repolarization--massive K+ efflux due to opening of voltage-gated slow K_ channels and closure of voltage gated Ca++ channels.
Phase 3
In a myocardial action potential, this phase is the resting potential--high K+ permeability through K+ channels.
phase 4
Pacemaker action potentials occur where
SA & AV nodes
In a pacemaker action potential this phase is the upstroke phase--it involves opening of voltage-gated Ca++ channels. These cells lack fast voltage-gated Na+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
phase 0
In a pacemaker action potential this phase, the plateau is absent.
phase 2 (both 1 and 2 are absent in pacemaker cells)
None
In a pacemaker action potential this phase, the slow diastolic depololarization results in membrane potential spontaneously depolarizing as Na+ conductance increases. This accounts for automaticity of SA and AV nodes. The slope of this phase in the SA node determines the heart rate. ACh decreases and catecholamines increasee the rate of diastolic depolarization decreasing or increasing heart rate respectively.
phase 4
myocardial action potential [pic p. 221]
--
Pacemaker action potential [pic p 222]
--
electrocardiogram: atrial depolarization
P wave
electrocardiogram: conduction delay through AV node (normally < ____ msec)
PR INTERVAL. Less than 200 ms
None
electrocardiogram: vetricular depolarization (normally < ____ msec)
QRS complex. Less than 120 ms
None
electrocardiogram: mechanical contraction of the ventricles
QT interval
electrocardiogram: ventricular repolarization
T wave
electrocardiogram: atrial repolarization is masked by _______
QRS complex
electrocardiogram: isoelectric, ventricles depolarized
ST segment
electrocardiogram: These waves caused by hypokalemia
U wave
image ECG p. 223
--
Wolff-Parkinson-White syndrome
- what causes it
- how does it appear on EKG
- complication
this syndrome is caused by an accessory conduction pathway from atria to vetricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic DELTA wave on ECG!! May result in reentry current leading to supraventricular tachycardia [image p.223]
None
This ECG tracing has a chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes (pic. p 224)
Atrial fibrillation
This ECG tracing has a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves. (pic. p 224)
Atrial flutter
In this condition PR interval is prolonged (>200 msec). Asymptomatic. (pic. p 224)
1st degree AV block.
Progressive lenthening of the PR interval until a beat is "dropped" (a P wave not followed by a QRS complex). Usually asymptomatic. (pic. p 224)
2nd degree AV block Mobitz type I (Wenckebach)
On ECG shows dropped beats that are not preceded by a change in the length of the PR interval. These abrupt, nonconducted P waves result in a pathologic condition. It is often found as a 2:1 block, where there are 2 P waves to 1 QRS response. May progress to 3rd degree block.(pic. p 225)
Mobitz type II AV block
In this condition, the atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treat with pacemaker.
3rd degree AV block (complete)
completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation. (pic. p 225)
Ventricular Fibrillation
control of mean arterial pressure [pic. p 226]
--
What do aortic arch baroreceptors respond to? Through what nn. and to where is this relayed?
transmits via vagus nn to medulla (responds only to increase blood pressure)
None
How does the carotid sinus function in baroreception?
1. Decreases firing with decrease in BP.
2. Signals via CN 9 (glossopharyngeal nn.)
3. Transmits to medulla. (Medulla then increases SNS and decreases PNS)
None
decreased firing by aroreceptors during hypotension results in an increase in efferent ________ firing
sympathetic
In a carotid massage, the increased pressure on carotid aa results in increased stretch and ____ in heart rate
decrease
Peripheral chemoreceptors in the carotid and aortic bodies respond to (3 things)
decreased PO2 (<60mmHg), increased PCO2 and decreased pH of blood
Central chemoreceptors respond to what changes (2)
changes in pH and Pco2 (not Po2)
This chemoreceptor is responsible for Cushing reaction?

What is the cushing response?
Central chemoreceptor

response to cerebral ischemia, response to increase intracranial pressure leads to hypertension (sympathetic response) and bradycardia (parasympathetic response)
None
Baroreceptors & Chemoreceptors image p. 226
--
This orgen gets the largest share of systemic cardiac output
liver
this organ gets the highest blood flow per gram of tissue
kidney
this orgen has a large arteriovenous O2 differnece. Increased O2 demand is met by increased blood flow, not by increased extraction of O2.
heart
None
Normal pressure of the heart chambesr (image p.227)
--
this is a good approximation of L atrial pressure and measured with a Swan-Ganz catheter
Pulmonary capillary wedge pressure
blood flow is altered to meet demands of tissue
autoregulation
Name the organ regulated by the local metabolites: O2 adenosine, NO
heart
Name the organ regulated by the local metabolites: CO2 (pH)
brain
Name the organ regulated by the local metabolites: Myogenic and tubuloglomerular feedback
kidneys
Name the organ regulated by the local metabolites: hypoxia causes vasoconstriction
lungs
_______ vasculature is unique in that hypoxia causes vasoconstriction (in other organs hypoxia causes vasodilation)
pulmonary
Name the organ regulated by the local metabolites: lactate, adenosine, K+
skeletal mm
Name the organ regulated by the local metabolites: sympathetic stimulation most important mechanism--temp control
skin
______ forces determine fluid movement by osmosis throug capillary membranes
starling
moves fluid out of capillary
P(c) capillary pressure
moves fluid into capillary
P(i) interstitial fluid pressue
moves fluid into capillary
π(c) plasma colloid osmotic pressure
moves fluid out of capillary
π(i) interstitial fluid colloid osmotic pressure
net filtration pressure=Pnet=
[Pc-Pi)-(πc-πi)] capillary pressure -interstitial pressure - plasma colloid osmotic presure - interstitual fluid colloid osmotic pressures
Kf=
filtration constant (capillary permeability)
excess fluid outflow into interstitium
edema
edema is commonly caued by ___ capillary pressure (give example)
↑ P(c) Heart failure
edema is commonly caued by ___ plasma protiens(give example)
↓π(c) plasma proteins (nephrotic syndrome, liver failure)
edema is commonly caused by ___ capillary permeability (give example)
↑Kf infections, burns
edema is commonly caued by ___ interstitial fluid colloid osmotic pressure (give example)
↑ πi lymphatic blockage
capillary fluid exchange [pic p. 227]
--
right-to-left shunts (early cyanoisis) "blue babies"
3 Ts Tetrology Transposition Truncus
Children with this type of shunt may squat to increase venous return
right to left shunts
capillary fluid exchange [pic p. 227]
--
Right-to Left shunts (early cyanosis) - "blue babies"
1) Tetrology of fallot 2) Transposition of great vessels 3) Truncus arteriosis The 3 Ts
children with this type of shunt may squat to increase venous return.
right to left shunt
Left to right shunts (late cyanosis) - "blue kids"
1) VSD 2) ASD 3) PDA
this is the most common cause of early cyanosis
tetralogy of fallot
this is the most common congenital cardiac anomaly
VSD
this congenital heart dz manifests itself with a loud S1 and a wide, fixed split S2
ASD
this congenital heart defect is closed with indomethacin
PDA
give the frequency of occurance with PDA VSD ASD
VSD>ASD>PDA
eisenmenger's syndrome
- what is it caused by
- what happens
eisenmenger's syndrome

Uncorrected VSD, ASD or PDA leads to progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from L to R to R to L, which causes late cyanosis (clubbing & polycythemia). [pic p. 228]
None
Tetrology of Fallot [pic. p 228]
1) Pulmonary stenosis 2)RVH 3) Overiding aorta (overides VSD) 4) VSD mneu: PROVe
most important determinant for prognosis of tetrology of fallot
pulmonary stenosis
ON x-ray Tetrology of Fallot looks ________
boot shaped
None
give the frequency of occurance with PDA VSD ASD
VSD>ASD>PDA
Transposition of great vessels
- What is the physiology?
- How does it present?
- When can a patient survive?
One of the 3T's (R->L shunts!) Blue baby.

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)leading to separation of systemic and pulmonary circulations.

Must have an ASD, VSD, or PDA for this to be compatible with life.
None
Transposition is not compatable with life unless a _____is present to allow adequate mixing of blood [pic p. 229]
shunt (e.g. VSD, PDA or patent foramen ovale)
transposition of great vessels is due to failure of the _________ septum to spiral
aorticopulmonary
this type of coarction of aorta is aortic stenosis proximal to insertion of ductus arteriosus (preductal)
infantile INfantile: IN close to the heart
What occurs in "Adult" form of Coarctation of the Aorta?
- findings
- location of coarctation
- imaging
this type of coarction of aorta is aortic stenosis is distal to ductus arteriosus (postductal) it is associated with notching of the ribs, hypertension in upper extremities, weak pulses in lower extremities.
None
Coarction of aorta has a male: female ratio of ____
3:01
what is best way to diagnose coartation of aorta
femoral pulses on pysical exam
In fetal period, shunt is right to left. In neonatal period, lung resistance decreases and shunt becomes L to R w/ subsequent RVH and failure. [pic p. 229]
patent ductus arteriosis
______ is used to closed a PDA
indomethacin
______ is used to keep a PDA open, which may be necessary to sustain life in conditions such as transposition of the great vessels
PGE
Congenital cardiac defect associations: 22q11
truncus arteriosus, tetralogy of Fallot
Congenital cardiac defect associations: Down syndrome
ASD, VSD
Congenital cardiac defect associations: Congenital rubella
septal defects, PDA
Congenital cardiac defect associations: Turners syndrome
coarctation of aorta
Congenital cardiac defect associations: Marfan's syndrome
aortic insufficiency
Congenital cardiac defect associations: Offspring of diabetic mother
transposition of great vessels
Hypertension
BP >140/90
HTN risk factors
increase age, obesity, diabetes, smoing, genetics, blck>white>asians
90% of hypertension is this kind
essential
essentail hypertention is related to either one of these two factors
increased CO or TPR
10% of HTN is mostly secondary to ______ dz
renal
this type of HTN is severe and rapidly progressing
malignant
HTN predisposes pts to (give 3)
athrosclerosis, stroke, CHF, renal failure, retinopathy, & aortic dissection
Hyperlipidemia signs: Plaques in blood vessel walls
Atheromata
Hyperlipidemia signs: plaques or nodules composed of lipid-laden histocytes in the skin, especially the eyelids
Xanthoma
Hyperlipidemia signs: lipid deposits in the tendon, esp. the achilles
Tendinous xanthoma
Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)
corneal arcus
This type of arteriosclerosis is in the media of the arteries, esp radial or ulnar. Usually benign.
Monckeberg
This type of arteriosclerosis is hyalin thickening of small arteries in essential hypertension. Hyperplastic "onion skinning" in malignant hypertension.
Arteriolosclerosis
This type of arteriosclerosis is when fibrous plaques and atheromas form in intima of arteries
atherosclerosis
this is a disease of elastic arteries and large and medium sized mm arteries (image 79)
atherosclerosis
risk factors for atherosclerosis
smoking, hypertension, dbts, hyperlipidemia, family hx
progression of atherosclerosis complex atheromas, fatty streaks, proliferative plaque
fatty streaks to proliferative plaque to complex atheromas
complications of atherosclerosis (give 3)
aneurisms, ischemia, infarcts, peripheral vascular dz, thrombus, emboli
most common location of atherosclerosis
abdominal aorta> coronary artery>popliteal artery>carotid artery
symptoms of atherosclerosis
angina, claudication, but can be asymptomatic
CAD narrowing >75%
angina
retrosternal chest pain with exertion , mostly secondary to atherosclerosis
stable angina
chest pain occurring at rest secondary to corony artery spasm
prinzmetal's variant (unstable angina)
worsening of chest paiin due to thrombosis but no necrosis
unstable/crescendo angina
most often acute thrombosis due to coronary artery atherosclerosis. Results in myocyte necrosis
myocardial infarction
death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrythmia
sudden cardiac death
progressive onset of CHF over many years due to chronic ischemic myocardial damage
chronic ischemic heart dz
infarcts occuring in loose tissues with collaterals, such as lungs, intestine, or follwing reperfusion
red (hemorrhagic) infarcts REd=REperfusion
infarcts occur in solid tissues with single blood supply, such as brain, heart, kidney and spleen.
pale infacts
give order of highest frequency of coronary artery occlusion CFX, LAD, RCA
LAD>RCA>CFX
symptoms of MI (give 4)
diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm or jaw, shortness of breath, fatigue, adrenergic symptoms.
color image 80.
--
How long ago did the MI occur? Occluded artery but no visable change by light microscopy
2-4 hours
How long ago did the MI occur? Gross: dark mottling; pale with tetrazolium stain. Micro: coagulative nocrosis. coagulation bands visable. release of contents of necrotic cells into bloodstream and the begining of neutrophil emigration.
after 4 hrs. 1st day
How long ago did the MI occur? Gross: hyperemic border; central yellow-brown softening. Micro: outer zone (ingrowth of granulation tissue), macrophages, & neutrophils
5-10 D
How long ago did the MI occur? Gross: grey-white Micro: scar complete
7 weeks
dx of MI what is gold standard in the 1st 6 hrs
ECG
This lab test rises after 4 hours and is elevated for 7-10D.
troponin I
this lab test is more specific than other protein markers
troponin I
This is predominantly found in myocardium but can also be relased from skeletal mm
CK-MB
This is nonspecific and can be found in cardiac, liver and skeletal mm cells
AST
lab image p.233
1)troponin 2) CK-MB 3)AST 4)LDH
ECG changes include ST elevation which indicates
transmural infarct
ECG changes include ST depression which indicates
subendocardial infarct
ECG changes include pathological Q waves
transmural infact
This MI complication is the most important cause of death before reaching hosptial; it is common in the 1st few days
cardiac arrhythmia
This MI complication results in pulmonary edema
LV failure
This MI complication has a high risk of mortanilty and occurs when there is a large infarct
cardiogenic shock
Rupture of ventricular free wall, interventricular septum, or paillary mm, usually occurs _____ post MI
4-10D
This MI complication of an MI results in decreased CO, a risk of arrythmia, and embolus from mural thrombus
aneurism formation
this MI complication is also known as a friction rub and occurs 3-5 D post MI
fibrinous pericarditis
This MI complication is an autoimmune phenomenon resulting in fibrinous pericarditis, several weeks post-MI
dresslers syndrome
This is the most common cardiomyopathy (90%)
dialated (congestive) cardiomyopathy
In dialated (congestive) cardiomyopathy ________ dysfunction ensues
systolic
In this type of cardiomyopathy, the heart looks like a baloon on chest x-ray
dialated (congestive) cardiomyopathy
etiology of dialated (congestive) cardiomyopathy
Alcohol Beriberi Coxsackie B Cocaine Chagas dz Doxorubicin peripartum hemochromatosis
this type of cardiomyopathy often involves an asymetric enlargement of the intraventricular septum
hypertrophic cardiomyopathy
In hypertrophic cardiomyopathy ______ diastolic disfunction occurs
diastolic
hypertrophic cardiomyopathy is a __________ trait, and 50% are familial
autosomal dominant
This is a very common cause of sudden death in young athletes.
hypertrophic cardiomyopathy
What are the heart sound findings with hypertrophic cardiomyopathy
loud S4, apical impulses, systolic murmur
How do you tx hypertrophic cardiomyopathy
Beta blocker
major causes of this type of cardiomyopathy include sarcoidosis, amyloidoss, postratdiation fibrosis, endocarrdial fibroelastosis, and endomyocardial fibrosis (Loffler's)
restrictive/obliterative cardiomyopathy
Heart Murmurs: holostolic, high piched "blowing murmur" loudest at apex[pic. p 234]
mitral regurgitation
Heart Murmurs: crecendo-decrescendo systolic ejection murmur following ejection click. radiates to carotids/apesx. "pulsus parvus et tardus" pulses weak compared to heart sounds [pic. p 234]
aortic stenosis
Heart Murmurs: holosystolic murmur [pic. p 234]
VSD
Heart Murmurs: Late systolic murmur with midsystolic click. Most frequent valvular lesion [pic. p 234]
mitral prolapse
Heart Murmurs: immediate high-pitched "blowing" diastolic murmur. Wide puse pressure [pic. p 234]
aortic regurgitation
Heart Murmurs: follows opening snap. delayed rumbling late diastolic murmur. [pic. p 234]
mitral stenosis
Heart Murmurs: Continuous machine like murmur. Loudest at time of S2 [pic. p 234]
PDA
most common primary cardiac tumor in adults. Usually described as a "ball-valve" obstruction in the LA
myxomas.
90% of myxomas occur in the _____
atria (mostly LA)
Most frequent primary cardiac tumor in children, associated with tuberous sclerosis
rhabdomyomas
Most common heat tumor (see color image 88)
metasteses
Given the pathophysiology tell me the symptom of CHF: failure of LV output to increase during exercise
dyspnea on exertion
Given the pathophysiology tell me the symptom of CHF: greater ventricular end-diastolic volume
cardiac dilation
Given the pathophysiology tell me the symptom of CHF: Lv ventrical failure leads to increased pulmonary venous pressure which leads to pulmonary venous distention and transudation of fluid.
pulmonary edema (paroxysmal nocturnal dyspnea)
this CHF abnormality is associated with presence of hemosiderin-laden macrophages
pulmonary edema
Given the pathophysiology tell me the symptom of CHF: increase venous return in supine position exacerbates pulmonary vascular congestion
orthopnea (shortness of breath when supine)
Given the pathophysiology tell me the symptom of CHF: increased central venous pressure leading to increased resistance to portal flow.
hepatomegaly (nutmeg liver)
Given the pathophysiology tell me the symptom of CHF: RV failure leads to increased venous pressure which leads to fluid transudation
ankle , sacral edema
embolus types
Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor mneu: an embolus moves like a a FAT BAT
CHF [pic p. 235]
--
this type of emboli are associated with long bone fractures and liposuction.
fat
approximately 95% of pulmonary emboli arise from where?
deep leg veins
this type of emboli can lead to DIC, especially postpartum
amniotic fluid
this type of embolus is associated with chest pain, tachypnea, and dyspnea
pulmoary embolus
compression of heart by fluid (i.e.,blood) in pericardium, leading to decreased cardiac output and equilibration of pressures in all four chambers.
cardiac tamponade
youre pt presents with hypotension, JVD, and distant heart sounds. He shows pulsus paradoxus and ECG shows electrical alternans
cardiac tampanad
pulsus paradoxus
(exaggeration of nml variation in the systemic arterial pulse volume with respiration-- becoming weaker with inspiration and stronger with expiration)
electrical alternans
(beat to beat alterations in QRS complex height)
Symptoms of bacterial endocarditis
Fever Roth spots osler nodes Murmur (new) Janeway lesions Anemia Nail-bed hemorrhage Emboli mneu: bacteria FROM JANE
osler nodes
tender raised lesions on finger or toe pads
Roth's spots
round white spotss on retina surrounded by hemorrhage
Janeway lesions
small erythematous lesions on palm or sole
What is the most frequently involved valve in bacterial endocarditis
mitral valve
What valve is associated with endocarditis associated with IV drug abuse
tricuspid valce
what are some of the complications associated with bacterial endocartitis (give 2)
chordae rupture glomerulonephritis supportive pericarditis emboli
acute endocarditis has a rapid onset. It results from large vegetations on previously normal valves. It is most often caused by this bug.
S. aureus (high virulence)
Subacute bacterial endocarditis has a more insidious onset. It consists of smaller vegetations on congentitally abnormal or diseased valves. It can be a sequela of dental procedures. Often caused by this bug
viridans streptococcus (low virulence)
endocarditis may also be nonbacterial and secondary to these 2 conditions
metastasis or renal failure (marantic/ thrombotic endocarditis)
In this condition, associated with lupus, vegetations develop on both sides of valve leading to mitral valve stenosis but do not embolize
libman-sacks endocarditis mneu: SLE causes LSE
Rhematic heart dz is a late consequence of pharyngeal infection with this organism
a beta hemolytic streptococci
rhematic heart dz affects heart valves in this order
mitral>aortic>>tricuspid mneu: high pressure valves associated most.
Give the symptoms of rheumatic heart dz
Fever Erythema marginatum Valvular damage ESR (high) Red-hot joints (polyartheritis) Subcutaneous nodules St. Vitus' dance (chorea) mneu: FEVERSS
This is associated with Aschoff bodies, migratory polyarthritis, erythema marginatum, elevated ASO titers.
Rheumatic heart dz
is rheumatic heart dz immune mediated or the direct effect of bacteria
immune mediated
Associated ith Aschoff bodies and Anitschkow's cells
rheumatic heart dz mneu: think of 2 RHussians with RHeumatic heart dz (Aschoff & Anischkow)
Aschoff bodies
granuloma with giant cell
Anitschkow's cells
activated histiocytes
This condition presents with pericardial pain, friction rub, ECG changes (diffuse ST elevation in all leads) pulsus paradoxus, distant heart sounds
pericarditis
pericarditis can resolve without scarring however, scarring can lead to this
chronic adhesive or chronic constrictive pericarditis
this type of pericarditis is caused by SLE, rheumatoid arthritis, infection, or uremia
serous pericarditis
this type of pericarditis is caused by uremia, MI, rheumatic fever
fibrinous pericarditis
this type of pericarditis is caused by TB or malignancy (e.g., melanoma)
hemorrhagic
this dz disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring. It often effects the aortic root and results in calcification of ascending arch of the aorta
syphalitic heart dz (tertiary syphalis)
This dz can result in aneurism of the ascending aorta or aortic arch and aortic valve incompetence.
syphalitic heart dz (tertiary syphalis)
pic p. 238
1) + ionotropic drugs 2) B blockers 3) ACE-inhibitors 4) ATN II antagonists 5) diuretics 6)Vasodialtors
This Rx used for HTN has the adverse effect of HYPOKALEMIA, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
hydrochlorothiazide (diuretic)
This Rx used for HTN has the adverse effect of potassium wasting, metabolic alkalosis, hypotension, ototoxicity
loop diuretics
This sympathoplegic used in the tx of HTN has the adverse effect of dry mouth, sedation, severe rebound HTN
clonidine
This sympathoplegic used in the tx of HTN has the adverse effect of sedation, positive Coomb's test
methyldopa
This sympathoplegic used in the tx of HTN has the adverse effect of severe orthostatic hypotension, blurred vision, constipation, sexual disfunction
hexamethonium
This sympathoplegic used in the tx of HTN has the adverse effect of sedation, depression, nasal stuffiness, diarrhea
reserpine
This sympathoplegic used in the tx of HTN has the adverse effect of orthostatic and exercise hypotension, sexual dysfunction, diarrhea
Guanethidie
This sympathoplegic used in the tx of HTN has the adverse effect of 1st dose orthostatic hypotension, dizziness, headache
Prazosin
This sympathoplegic used in the tx of HTN has the adverse effect of impotence, asthma, bradycardia, CHF, AV block, sedation & sleep alterations
B blockers
This vasodialator used in the tx of HTN has the adverse effect of nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retension
hydralazine
This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension
minoxidil
This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea
nifidipine, veripamil (constipation)
This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)
nitroprusside
This ACE inhibitor used in the tx of HTN has the adverse effect of Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II
Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II
This angiotensin II receptor inhibitor has theadverse effect of fetal renal toxicity, hyperkalemia
Losartan
This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension
minoxidil
This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea
nifidipine, veripamil (constipation)
This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)
nitroprusside
This ACE inhibitor used in the tx of HTN has the adverse effect of Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II
Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II
The MOA of this drug used for severe HTN & CHF is that it increases cGMP leading to smooth mm relaxation. It vasodilates arterioles > veins resulting in a reduction of afterload
hydralazine
Toxicity of this drug for severe HTN & CHF include compensitory tachycardia, fluid retension, & lupus like syndrome
hydralazine
The druges Nifedipine, verapamil & diltiazem belong to this category
calcium channel blockers
The MOA of these drugs is that they block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce mm contractilty
calcium channel blockers
give the order of potency of the 3 CCBs (nifedipine, verapamil, diltiazem) in 1) the heart 2)vascular smooth mm
heart-verapamil>diltiazem>nifedipine vascular sm mm-- nifedipine>diltiazem>verapamil
CCBs are used in hypertension but also in these 2 conditions
angina, arrhytias (not nifedipine)
These drugs produce a toxicity of cardiac depression, peripheral edema, flushing, dizziness, & constipation
CCBs
These 2 drugs used for angina, pulmonary edema, and as an erection enhancer have a MOA of vasodilating by releasing NO in smooth mm, causing an increase in cGMP and smooth mm relaxation. They dialate vv>>arteries resulting in a decrease in preload
nitroglycerine, isosorbide dinitrate
toxicity of these drugs include tachycardia, hypotension, headache, "Monday dz" in industrial exposure, development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting intahycardia, dizziness, and headache.
nitroglycerin, isosorbide dinitrate
What are the 2 major Rxs used in the tx of antianginal therapy
nitrates & B blockers
In antianginal therapy the goal is to due what?
reduce myocardial O2 consumption.
In order to reduce myocardial O2 consumption you need to decrease 1 or more of the determinants of MVO2 which are give 2(5)
1)EDV 2)BP 3)HR 4) contractility 5) ejection time
Used for antianginal therapy Nitrates reduce _______ (preload or afterload)
preload
Used for antianginal therapy B-blockers reduce _______ (preload or afterload)
afterload
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. EDV
N (preload):↓ BB (afternoad):↑ C: no effect or ↓
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. BP
N (preload):↓ BB (afternoad):↓ C:↓
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Contractility
N (preload):↑ (reflex response) BB (afternoad):↓ C:little or no effect
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. HR
N (preload):↑ reflex response BB (afternoad):↓ C:↓
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Ejection time
N (preload):↓ BB (afternoad):↑ C:little or no effect
For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. MVO2
N (preload): ↓ BB (afternoad): ↓ C: ↓↓
CCBs: Nifedipine is similar to ________ (nitrates or B blockers); Verapamil is similar to ________nitrates or B blockers)
Nitrates B blockers
Cardiac drugs: sites of action
1) Digitalis (-) 2) CCB (-) 3) B blockers 4) Ryanodine (+) 5) Ca++ sensitizers
This cardiac drug inhibits Na+/K+ ATP ase
digitalis
These 2 cardiac drugs inhibit on voltage gated Ca++ channels
CCBs B blockers
This cardiac drug sensitizes Ca++ release channel in the SR
Ryanodine
These cardiac drug is a site of Ca+ interaction with troponin-tropomyosin system
Ca++ sensitizers
This cardiac glycoside has 75% bioavalibility, is 20-40% protein bound, has a half life of 40 hours and is excreted in the urine
digoxin
the MOA of this drug is that it inhibits the Na+/K+ ATPase of the cardiac sarcomere, causing an increase in intracellular Na+. Na+-Ca++antiport does not function as efficiently, casing an increase in intracellular Ca++, leading to positive inotropy.
digoxin
this drug may cause an elevated PR, a depressed QT, a scooping of ST segment, and a T-wave inversion on ECG
digoxin
The clinical uses for this drug include 1) ________ due to increased contractility 2) _______ due to decreased conduction at AV node
1) CHF 3) atrial fibrillation
toxicity of this drug includes N/V/D. Blurry yellow vision. Arrhythmia.
digoxin
Digoxins toxicities are increased by _________(decreased excretion), _______(potentiates drug's effects) , and _________ (decreases digoxin clearance and displaces dignoxin from tissue binding sites
renal failure hypokalemia quinidine
What is the treatment for digoxin toxicity
slowly normalize K+ lidocaine cardiac pacer anti-dig Fab fragments
antiarrythmics (Class I) are _____ channel blockers
Na+
antiarrythmics (Class II) are _____ blockers
Beta
antiarrythmics (Class III) are _____ channel blockers
K+
Thhs class of antiarrhthmics are local anesthetics. They act by slow or decreasd conduction. They decrese the slope of phase 4 ddepolarization and increase threshhold for firing in abnormal pacemaker cells.
antiarrhythmics-Na+ channel blockers (class I)
antiarrhythmics-Na+ channel blockers (class I) are state dependent meaning what
they selectively depress tissue that is frequently depolarized (e.g., tachycardia
this class of antiarrhythmics has 3 subcategories A, B, & C
antiarrhythmics-Na+channel blockers (class I)
this class of antiarrythmics includes Quinidine, Amiodarone, Procainamide, Disopyramide.
Class IA mneu: Queen Amy Proclaims Diso's PYRAMID
This class of antiarrhytmics has an ↑ AP duration, ↑ effective refractory period (EERP, ↑ QT interval. It can affect both atrial and ventricular arrhythmias
IA
This member of class IA antiarrhytmics has toxicities that include (cinchonism-headache, tinnitis, thrombocytopenia, torsades de pointes due to prolonged QT interva)
quinidine
This member of class IA antiarrhytmics has toxicities that include reverible SLE-like syndrome
procainamide
This class of antiarrythmics include lidocaine mexiletine, tocainide
IB (Na+ channel blockers)
this class of antiarrythmics acts to decrease AP duration. It effects ischemic or depolarized purkinje and ventricular tussue. It is useful in acute ventricular arrhytmias (especially post-MI) and i digitalis-induced arrhythmias.
IB (Na+ channel blockers)
This class of antiarrhytmics has toxicities that include local anesthetic effects, CNS stimulation/depression, cardiovascular depression
IB (Na+ channel blockers)
This class of antiarrhythmics includes flecainide, encainide, propafenone.
class IC (Na+ channel blockers.
This class of antiarrhythmics has no effect on AP duration. It is useful in V-tachs that progress to VF and intractable SVT. Usually used only as last result in refractory tachyarrythmias.
class IC (Na+ channel blockers.
Toxicities of this class of antiarrhythmics includes arrythmias, especially post MI (CONTRAINDICATED)
class IC (Na+ channel blockers.
picture p. 242 Class I antiarrythmics (Na+ channel blockers)
1) IA 2) IB 3) IC
This clas of antiarrythmics includes propanolol, esmolol, metroprolol, atenolol, timool.
Beta Blockers (Class II)
This class of antiarrythmics acts by ↓ cAMP, ↓ Ca+ currents, and by supressing abnormal pacemakers by ↓ slope of phase 4. The AV node is particularly sensitive resulting in increaed PR interval
B-blockers (Class II antiarrythmics)
this is the shortest acting B blocker
esmolol
Toxicities of this class of antiarrythmics include impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). It may mask signs of hypoglycemia.
B-blockers (Class II antiarrythmics)
This class of antiarrythmics includes Sotalol, ibutilide, bretylium, & amiodarone
K+ channel blockers (class III)
This class of antiarrythmics acts by ↑ AP duration, ↑ERP. It thends to ↑ QT interval. It is used when other antiarrhythmics fail.
K+ channel blockers (class III)
This class III antiarrythmic has toxicities which include torsades de pointes and excessive beta block
sotalol
This class III antiarrythmic has toxicities which include new arrhytmias& hypotension
bretylium
This class III antiarrythmic has toxicities which include PULMONARY FIBROSIS, HEPATOTOXICITY, HYPOTHYROIDSIM/HYPERTHYROIDISM, corneal deposits, skin depsits resulting in photodermatiitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF
amiodarone mneu: remember to check PFTs, LFTs, and TFTs when using amiodarone.
class III antiarrythmics [pic.p.243]
--
This class of antiarrythmics include the drugs verapamil, and diltiazem.
Ca++ channel blockers (class IV)
The MOA of this class of antiarrythmics is primarily on AV nodal cells. They ↓ conduction velocity, ↑ ERP, ↑ PR interval.
Ca++ channel blockers (class IV)
this class of antiarrythmics is used in prevention of nodal arrhythmias (e.g., SVT)
Ca++ channel blockers (class IV)
Toxicity of this class of antiarrythmics can include constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression, & torsades de pointes.
Ca++ channel blockers (class IV)
Ca++ channel blockers (class IV) [pic.p244]
--
Other antiarrythmics: this antiarrhythmic is the drug of choice in diagnosing/abolishing AV nodal arrhythmias
adenosine
Other antiarrythmics: this antiarrhythmic depresses ectopic pacemakers, especially in digoxin doxicity
K+
Other antiarrythmics: this antiarrhythmic is effective in torsades de pointes and digoxin toxiciity
Mg+