All cardiovasc Flashcards
(284 cards)
1
Q
What three factors determine CO?
A
CO = SV x HR
where SV is a function of preload and contractility
1
Q
What kind of drug is clopidrogel? Use?
A
antiplatelet - adjunctive in pts w/ CAD, ischemic neuro syndromes, or stenting. PO.
1
Q
Discuss pathology of the following stages of cardiac ischemia
- 20 - 30 mins
- 24 h
- 1-3 d
- 3-7 (10) days
A
- 20 - 30 mins: reversible ischemia (angina)
- 24 h: cut surface pallor
- 1-3 d: mottling w/ yellow-tan infarct ctr
- 3-7 (10) days: sharply outlined w/ central pale, yellowish necrotic region
1
Q
Pattern of a Mobitz II 2nd degree AV block?
A
Same PR int. for each cycle w/ blocked P waves.
1
Q
Calcific aortic stenosis
A
- one of most common valvular probs
- congenital biscuspid valve –> aging degeneration of valve w/ calcification
1
Q
Major complications (3) of infective endocarditis?
A
- valve dest
- abscesses
- purulent pericarditis
1
Q
histologic findings of giant cell myocarditis
A
myocyte necrosis and numerous giant cells
1
Q
How do PDEi’s work (give rep. drug)
A
PDEs (milrinone) also increase contractility (similar to B1 agonists) but by inhibiting PDE thus keeping cAMP levels hi within myocytes.
1
Q
What hemydynamic finding correlates best w/ RH failure?
A
Prominent RA v waves
1
Q
Complete AV canal defect
- Describe (give 3 morphological features)
- Assoc. w/ what genotype
A
- Generally has complete mixing of ventricular contents due to defects in septation (endocardial cushions) – It is characterized by a primum atrial septal defect (ASD) that is contiguous with a posterior (or inlet) ventricular septal defect (VSD), and a common AV valve
- Assoc. w/ T-21.
1
Q
What is a major problem w/ Eisenmenger’s syndrome? What is the goal of corrective surg for shunts?
A
- Once Eisenmenger’s sets in, surg is contraindicated and outcomes much worse
- Corrective surg: goal is to avoid dev’t of Eisenmenger’s
1
Q
Temporal (Giant Cell) arteritis
- How common
- Symptoms
- Biopsy consideration
- Common complications
- Rx
A
- Most common vasculitis
- Headaches, scalp tender, jaw pain, visual loss
- A segmental dz so at least 2-3 cm of artery needed
- rapid response cort’s
1
Q
What are the ANCA+ dz’s we learned?
- pANCA+
- cANCA+
A
- pANCA = hypersens. vasculitis (in 70% of pts)
- cANCA = granulomatosis w/ polyangiitis
1
Q
What are 2 diff’s b/t PAN and hypersens. vasculitis?
A
- Hypersens = smaller vessels than PAN
- Lesions in hypersens at same stage of dev’t (as opposed 2 PAN)
2
Q
Primary use of Type II CCB’s? HOw does this differ from Type I?
A
These are vasodilators used more for HTN control, and generally don’t have electrophysiological (cardiac) effect. Type I used more for cardiac, and cause electrophys. changes.
2
Q
Infarction zones based on LAD, RCA or left circumflex?
A
- LAD: anterior wall LV
- RCA: post. wall LV + post septum
- Left Circ: lateral wall LV
2
Q
Typical pathology of bacterial myocarditis?
A
Infectious foci w/ PMNs and bacteria
2
Q
What are some causes of impaired DIA filling (leading to DIA heart failure)?
As these advance to HF, comment on the EF you might see.
A
Impaired DIA filling
- LV hypertrophy (Ao stenosis, HTN)
- Restrictive cardiomyopathy (amyloid, sarcoid, hemochromatosis, etc.)
- Pericardial constriction (constrictive pericarditis, cx, etc.) / tamponade
3
Q
Hallmark dz of restrictive cardiomyopathy? Other big players in this condition?
A
amyloid; hemocrhomatosis/siderosis, sarcoidosis
4
Q
Primary medical Rx of aortic regurg? Surg?
A
afterload reduction (nifedipine - CCB, ACEi)
surg: AVR
4
Q
What are some of the key S/S of HF?
A
Decreased CO leading to:
- fatigue
- increased pulmonary venous pressure (exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea)
- increased systemic venous pressure (lower extremity edema)
4
Q
Dichrotic notch
A
Brief uptick in aortic pressure after the AV valve closes (after S2) due to recoil pressure following vent. contraction.
5
Q
What are hallmark EKG signs in RBBB?
A
- wide QRS (>120ms)
- rSR’ in V1 (a tall “rabbit ear” secondary R wave in V1)
5
Q
Claudication
A
limb angina: Pain in calf, thigh or buttock after some excercise; generaly resolves w/ rest.
6
Findings in acute chagas
* physical exam
* gross path
* micro path
* chagoma (bump) + lymphadenopathy
* organ involvement (parasitemia)
* often myocardial involvement w/ **parasite-filled pseudocysts, INF**
6
Polyaerterisis nodosa (PAN)
* Arteries affected
* Lesion
* Popn most often affected
* IF
* Common co-infection
* Musc. a.s
* Nodular
* Young males
* pANCA+
* 30% have HepB
7
What is the significance of an AV block above, at, or below the AV node?
Very important - at level or above AV node = reliable escape rhythm.
Below = unreliable escaple rhythm. This is especially important b/c if pt. goes into complete AV block (3o), they won't have a reliable escape rhythm.
8
Histopath of **temporal (giant cell) arteritis (3)**
* Lc infiltration
* Intimal fibrosis
* Granuloma formation
9
Transposition of the Great A.s
Parallel circ. where RV outflows to Ao --\> systemic --\> back to RA
and
LV --\> pulm. a. --\> lungs --\> LA
10
rupture of fibrous cap =
progressive narrowing of vessel lumens (cor. a.s) =
weakening of vessel wall w/ dilatation =
* acute cor. syndrome
* chronic CAD
* aneurysm
11
What is the most common type of infarction in actue MI?
transmural... usually LV.
11
Granulomatosis w/ polyangiitis
* Key IF marker
* Vessels affected
* Lesions
* Other organ involvement
* Rx
* cANCA
* mostly small vessels (caps)
* Granulomas
* Kidney, lung
* Cyclophosphamide
12
Rx for variant angina?
nitro, CCB's (1st line)
12
top 3 RF's for CAD?
1. dyslipidemia
2. HTN
3. smoking
12
Etiology of renovascular HTN
Stenosis of one or both renal a.s --\> HTN.
13
What are two anti-arrhythmics to avoid in pts w/ renal dysfunction?
sotalol & dofetilide
13
Hallmark of cardiac sarcoidosis?
Micro path?
non-necrotizing granulomas w/ dilated & restrictive cardiomyopathy
* granulomas, giant cells
14
What are the major clinical manifestations (symptoms) of CAD?
1. chest pain (angina pect.)
2. SOB
14
Heart Dev't
* Origin tissue
* What key structure formed by day 22? How does it move to create chambers?
* What type of cells necessary for normal dev't?
* What structures contribue to normal septation?
* Mesoderm
* heart tube; rightward looping
* neural crest
* endocardial cushions
15
Effects of **aortic stenosis / incompetence?**
* Decreased output --\> angina, syncope
* Effects on LV --\> hypertrophy, failure
16
Explain how mital stenosis can lead to venous congestion of liver? What is a typical gross anatomical description of this condition?
Venous cong. of liver via advanced mitral stenosis that causes backup of pressure all the way to R side of heart and into the portal system thus congesting liver. Described as **nutmeg liver**
17
What is the standard way to quantify vasc. resistance? Give EQ.
**MAP** = Dia + 1/3 (Sys - Dia)
18
What does **mitral regurg** lead to?
LV overload --\> eccentric LV hypertrophy --\> symptoms/complications
19
Describe **hypertrophic cardiomyopathy** (PRIMARY/IDIOPATHIC)
* etiology of most cases
* clinical features & pop'n most often afflicted
* Hallmark gross path
* Hallmark micro path
* Uncommon condition w/ **genetic links**, _familial patterns_ (**B-myosin heavy chain**)
* Affects **young males**; commonly present w/ s**udden cardiac death, syncope, a fib, chest pain**, etc.
* Gross: hypertrophic LV, in particular a very **hypertrophic septum**
* Micro: **myofiber disarray,** esp. in septum
19
def Heart Failure
when heart is unable to pump blood florward at sufficient rate to meet metabolic demands of body (forward failure).
20
What drugs used in acute Rx of HF (types, not drug names)?
* diuretics
* O2
* nitrates
* inotropes
* vent. assist. devices
21
c wave
increase in atrial pressure as AV valves bulge out during ventricular SYS
22
S3
Normal until ~40 y/o. During filling (DIA) it's the sound of the mitral valve opening.
22
What does a wide QRS represent in AV block? Why signficiant?
Indicates block *below level of AV node* (generally a bundle branch block). Important b/c pt. may not have reliable escape rhythm.
22
*
* What types of drugs are Type II antiarrhythmics?
* What type preferred for cards pts?
* What is contraindicated in pts w/ CAD?
* What is the prototype drug?
* B blockers
* B1 selective preferred
* Contra: CAD pts should NOT use B blockers w/ ISA (**acebutolol**)
* **Metolprolol, atenolol** = B1 selective w/o ISA
22
Match the following genetic states to congenital heart defects
* Trisomy 21
* DiGeorge
* complete AV canal, VSD, ASD.
* Teratology of FAllot
23
Most common cause of dilated cardiomyopathy in UW/Europe?
* Etiology
Alcoholic DCM
etiology: direct tissue dmg from alcohol, metabolites
24
Although Pouseuille's law is nice, what is the important derivation in terms of pathophys/clinical medicine? Hint: resistance!
Q = dP x r4/8(Pi)(mu)L
Q = dP/R
therefore
**R = 8(pi)mu(L)/r4**
**This last derivation shows the very important fact that resistance increases by a factor of 4 for every decrease in the radius (r) of the vessel.**
24
What are three most common vessels in CAD, in order? What % obstruction do most pts have?
LAD \> RCA \> L circumflex
most have ~75%
25
* Receptor targets of _class III_ antiarrhythmics
* Drug names
* K channels
* **dofetilide**, **sotalol, amiodarone**
26
What characterizes RHF? What usually precedes it?
Generally preceded by LHF but not always (depends on etiology). If related to LHF, it shows advanced dz. Non-LH etiologies of RHF include Cor Pulmonale.
Characterized by:
* **SIgns of venous congestion:** Increased JVP, lower ext. edema due to _increased afterload_ on RV.
* Could have _RUQ pain_ if hepatomegaly.
26
An "anterolateral" infarct is due to occlusion of which cor. a.?
LAD
27
Draw out the **pressure-vol. loop** w/ proper lettering from a-d.
1. What does the slope reflect?
2. Discuss what's happening all along the loop, starting at **d** (lower left).
see notes
28
* Etiologies of RHF?
* Common manifestations?
* Etiologies: LHF, cardiomyop., valvular, lung dz, PE
* Manif: periph edema, ascites, lo card. output
29
Tetralogy of Fallot
* Genetic assoc.
* the 4 malformations
* 22q11 deletion
* VSD, sub-pulm. obstruction, overriding Ao, RV hypertrophy
30
Most common sympts of pericarditis
possible sign?
_symptoms_
* chest pain, sharp, well localized, relieved by leaning forward
* may get worse with inspiration (pleuritic component)
_sign_
* **friction rub** on auscultation.
31
What are the most common non-infx couses of myocarditis?
* Immune-related: Rheumatic, SLE, etc.
* Radiation
* Misc: Sarcoid
32
What is the major limitation to long-term success of cardiac transplantations?
Graft arteriopathy
33
what shown?
rhabdomyoma
33
Important secondary causes of hyperlipidemia (3)?
* Hypothyroidism
* DM
* Obstructive liver disease
33
SYS heart failure is primarily a problem of \_\_\_\_\_\_, whereas DIA heart failure is a problem of \_\_\_\_\_\_\_.
SYS: problem of contractility due to dilatation, remodeling, etc.
DIA: problem of filling due to stiffness or impaired relaxation.
35
What is the most common drug class that can lead to **drug-induced (dilated) cardiomyopathy?**
Anthracyclines (chemo agents) -- in some cases, S/E is that it leads to **necrosis** that results in dilated cardiomyopathy (non-reversible)
35
* What is the best diagnostic tool for assessing peripheral (including carotid) atherscler?
* How do you reduce risk of stroke in cases of confirmed carotid atherscler?
* Duplex US
* endarterectomy
36
What is the preferred class of AAA *w/o* the presence of structural heart dz?
**1C** (these are generally used for Rx of supraventricular arrythmias in pts w/o heart dz; in pts with heart dz [eg post MI], they are thought to *increase* mortality).
37
What is the hallmark EKG morphology of RBBB and LBBB? What is different clinically re: RBBBs vs LBBBs?
Wide QRS (\>120ms)
RBBB = probably normal heart
LBBB = probably CVD (HTN and/or CAD)
38
Key short - term and long-term cosequences of MI?
* short: cardiac arrest (v fib)
* long: CHF, sudden card. death (v tach/fib)
39
what does this show?
hemorrhagic pericarditis
40
* Most common type of cardiomyopathy?
* Etiology?
* Clinical progression
* Dilated (also called _congestive cardiomyopathy_)
* Viral (cocksackie B), alcoholic, pregnancy
* often asymptomatic then presenting w/ **exercise intol., CHF, arrythmia, death**
41
What is a way to quanitatively describe contractility?
Ejection fraction or left vent. ejection fraction (LVEF):
**LVEF = SV/EDV**
43
Where do the coronary arteries originate?
aortic valve
44
Pathology (micro) of viral myocarditits?
presence of chronic Lc's + myocyte necrosis.
45
A-fib: what is the common (and less common) way to return normal sinus rhythm?
* common: DC cardioversion (synchronized shock)
* less common: anti-arrhythmic agents
46
By definition in EKG, the left side is _____ and right side \_\_\_\_\_\_. A vector going toward the positive pole produces a ______ spike in the EKG reading.
Positive, negative, positive (up).
46
Buerger dz
* Etiology
* Leads to ?
* Histopath
* 1st line Rx
* Smoking-related
* dry gangrene ext's
* granulomatous actue & chronic INF
* smoking cess.
48
Describe the lesion in atherscler
Thickened **intima** w/ fibrous cap, necrotic core w/ chol clefts and calcification (intimal lesion = hi yield)
49
Rx for reversible DVT?
**Anticoag 6 mos** (if can't anticoag then _Greenfield IVC filter_)
50
What are some key signs that might point toward PVD?
* dec. periph. pulses
* bruits
* skin changes
* musc. atrophy
* ulceration/gangrene
51
What is key contraindication of nitrate therapy? How to Rx if taken together?
Sildenafil. Can lead to hypotensive shock/ hypotension. Rx w/ pressors, fluids, monitor.
52
What are type I (dihydropirine) CCBs used for? Type II? Give examples of each.
Major S/E of Type I CCB? Type II?
Type I (dihydropyridines): Rx HTN (**amlodipine**)
Type II: Cardiac drugs used an antiarrhythmics, and to reduce CO (**verapamil, diltiazem**)
S/Es:
type I: edema, headacne
type II: bradycardia, AV block
52
ECG sign of pericarditis
* diffuse ST elev (all leads)
54
Discuss the heart sounds S1 and S2; how do they correspond to SYS?
S1: vibration created when Pvent \> Patria, forcing the AV valve to close. So **this is the start of SYS**.
S2: This occurs when the Paorta \> PLV, at the **end of SYS**, forcing the aortic valve shut and producing a vibration.
55
What is a procedural cure for a-fib?
catheter ablation in LA (if fails to respond to 1st line Rx's)
55
* What type of drugs are _class IV_ antiarrhythmics?
* Prototype drugs to know
* Rx what condition?
* ***Non-dihidropyridine*** **CCB'**s (Fleckenstein Type I)
* **Diltiazem**, **verapamil**
* Rx superaventricular tachys
56
PSVT has a _____ QRS whereas ________ have widened QRS and usually occur in the setting of structural heart disease.
**PSVT**: narrow QRS (
**Ventricular tachyarhythmias**: *widened QRS* (\>120ms)
57
Differentiate b/t **monomorphic & polymorphic** ventricular tachyarhythmias
Monomorph: remote MI (scar formation)
Poly: ischemic/ACS
57
V-fib def & Rx
Vent. fibrillation not compatible w/ life. Rx w/ immediate defibrillation.
58
most common malignant neoplasm of heart?
Sarcoma
58
What characterizes hypersensitivity vasculitis? Mention what size vessels affected.
acute necrotizing inflammation of **small vessels,** especially _postcapillary venules of the skin._
60
v wave
gradual increase in Patria as they villed with "returning" venous blood (the AV valve is closed during v wave)
60
Def. **pericarditis**
INF of visc or parietal pericardium w/ formation of effusions
61
What are the 2 types of ASD? Which most common ASD?
* Primum and secundum ASDs
* **Secundum** most common, usually around fossa ovalis
62
Serious pericarditis
* Def
* Commonly caused by
* Gross appearance
* INF reaction w/ scant INF cells, slow accum. of fluid
* non-INFx (rheum fever)
* Yellowish (see below)
63
What is the mechanism by which ASA helps in angina?
Prevents platelet aggregation by inhibiting COX, reducing formation of **TxA2**.
64
Which classes of AAA's have elevated risk of TDP?
1a, 1c, 3
65
on EKG what does S wave represent?
Depol of ventricular bases/epicardium
67
P wave
atrial depolarization producing measured dipole. this is **atrial systole**
67
Rx 4 _granulomatosis w/ polyangiitis_?
cyclophosphamide
69
Major cardiac outcomes in chronic chagas
The infection causes tissue dmg lead**ing to Dilatation w/ fibrosis (LV)** + effacement --\>risk of aneurysm (LV/apex)
71
What is an acute indication for b blocker?
**acute MI**: reduces mortality, recurrence, etc.
72
Hallmark sign of acute STEMI? Weeks later what might you see?
elevated ST; weeks later = persistent Q.
72
Claudication may progress to **rest pain**.
* Describe
* Relieving factors
* Urgent?
* Complications/ sequellae
**Rest pain**:
* Dull, aching pain of foot or toes at rest.
* Releived by dependency (gravity, due to increased Q to area)
* **Needs prompt attention**
* can lead to tissue loss (ulcer, dry gangrene)
73
Sawtooth pattern on EKG indicates ?
Atrial flutter (atrial rate is between 250 and 350 bpm)
74
Eventual symptoms of **aortic regurg**?
* dyspnea on exertion
* fatigue
(Caused by decrease in SV and increased LV pressure)
76
What is most widely employed index of LV systolic function ? Normal range?
LVEF (normally 55-65%)
77
Statins
* Target
* Action
* Risk reduction
* S/E
* HMG CoA reductse (INH)
* Lowers LDL (66%), Lowers TG's
* Risk reduction in pts w/ CAD
* Myalgias most common, rare: rhabdo
78
How do you clinically diagnose an **acute MI**?
1. typical rise/fall of **cardiac enzymes** (CK-MB/troponin)
and
**_one_** of of the following four:
* ischemic symptoms
* ST changes
* persistent Q waves (old MI)
* Imaging/echo showing new loss or wall abnormality.
79
Most common infectious cause of myocarditis?
Coxsackie A/B viruses then range of viral, bact, fungal infxs (don't have to memorize those)
80
Clinical pres of rheum fever on heart?
**pancarditis:** pericarditis, myocarditis (aschoff), endocarditis (vegetations on mitral,aortic valves) --\> mitral (70%), mitral/aortic (25%) stenosis
80
How is **atrial septum** formed?
* **septum primum** forms first
* Cell death of *upper* septum primum
* **septum secundum** appears, growing sup--\>inf
* **for. ovale** remains b/t them
81
What is most common cong. heart dz in infants?
If large & persistent, what is one of the primary risks/complications?
VSDs
Eisenmenger's syndrome
83
SA node
dominant rate-setting pacemaker of the heart
84
Churg-Strauss Syndrome
* Common PMH
* Histo hallmark
* Rx
* asthma
* eosinophlic
* cort's
86
Common etiologies of LHF?
Clinical manifestations?
_Etiologies_
* MI (ischemic)
* valvular
* cardiomyopathy
* HTN
_Manifestations_
* pulm. congestion
* low CO
87
Primary sign of Eisenmenger's?
* **cyanosis**
88
Sick sinus syndrome (EKG, symptoms)
Rx:
* acute, symptomatic
* long-term
A type of **bradyarrhythmia** where P waves are absent.
- Often symptomatic (lightheadedness, presyncope, syncope, dyspnea on exertion, angina, and/or palpitations).
_Rx:_
* acute, symptomatic: B agonist (_atropine_)
* long-term: withdraw offending agent (eg _diltiazem_) +/or permanent pacemaker.
88
Key physical finding in **mitral regurg?** Rx? Which Rx preferred?
holoSYS murmur
_Rx:_ repair/replacement (**repair preferred if possible**)
90
How to Rx transposition of the great a.s (TGA)?
* Historical: atrial setpostomy
* Current: aterial switch
91
what does this show?
caseous pericarditis
93
What is 1st line for most pts in treating stable angina?
ASA (aspirin)
94
Most shunts are L--\>R in the beginning - why?
Why is it that the flow in shunts can become reversed in late dz? What is this called?
B/c left pressure \> R pressure so flow goes in that direction.
Can reverse to a R--\>L shunt as pulm pressures rise
(for example, a L--\>R shunt from ASD will eventually increase pulm. blood flow - and pressure - to such an extent that will result in eventual R--\>L shunting)
This reversal is called **Eisenmenger Syndrome**
95
Framingham Risk Score
* DEF
* Factors
* 10 yr risk of developing CAD
* Factpors: o LDL (or total cholesterol)
o HDL
o HTN
o Smoking
o Gender
o Age
96
Cardiac myxoma
* How common
* Common gross path
* most common primary tumor in heart
* tumor on stalk = "wrecking ball"
98
Def. of **cardiomyopathy**
heart dz resulting from _primary_ abnormality of myocardium excluding secondary causes (MI/ischemic, HTN, valvular, etc.)
99
Etiology of **mitral stenosis** in adults?
"always rheumatic"
100
SInus venosus ADS
ASD that causes inflow from pulm. v.s to be directed to RA (instead of LA) leading to vol. overload of RH
101
Histopath in dilated cardiomyopathy?
Same as other forms of hypertrophy w/ fibrosis; **abnormal, enlarged myocytes w/ interstitial fibrosis.**
103
_Tricuspid regurg_
* Etiology
* Popn often affected
* Signs
* EKG finding
* Rx
* Secondary to RV dilatation (or IVDA)
* IV drug users w/ endocarditis but also rheumatic pts.
* Pulsatile liver; SYS murmur LL sternal border.
* Large V waves in jugular veins.
* Repair (in severe cases)
104
Q = AV = CO= ~ Pi(r2)aorta x Vaorta
where V = velocity, CO = cardiac output
Given the above, how does doppler US measure CO?
Doppler approximates CO by measuring the area of the aorta and the velocity of flow.
Remember that CO = vol x HR. So if we can approximate CO, then we can calculate the volume which in this case would be the **ejection fraction** (the blood that is actively pumped out of LV during SYS).
104
How can the following help to diagnose/specify a PVD?
* Segmental pressures
* Duplex US
* Segmental P: shows diff's between diff't body parts, esp used in lower limb to assess stenosis.
* Duplex US: to asses Q in periph. arteries.
106
107
# Define **ejection fraction**. Why is it important?
What factors determine EF?
EF = SV/EDV
Key indicator of SYStolic performance
Determined by:
* Myocardial mass & architecture
* Contractility
* Preload
* Afterload
109
3 common etiologies of **mitral regurg?**
* prolapse (congenital)
* endocarditis
* rheumatic
110
Describe diff b/t primary and secondary dextrocardia.
* **Primary dextrocardia:** Heart is in right chest with rightward-pointing apex.
* **Secondary dextrocardia:** heart in right chest with *leftward-pointing apex*, due to starting out in the normal leftward-apex position but displaced into the right chest by extrinsic forces.
112
Common infectious cause of valvular dz? What is the common infectious agent?
**Rheumatic fever** (s/p **Group A beta hemolytic strep. pharyngitis**)
113
What is preferred drug for preventing VT/VF in pt w/ Class I-II heart failure? Class III-IV?
Sotalol; amiodarone.
114
Rx for pericarditis?
* Rx underlying condition
* NSAIDS
115
In terms of ion flux, discuss phases 0, 2 and 3 of the **myocyte** AP
* **Phase 0**: Na influx (depol)
* **Phase 2**: Slow Ca influx and K efflux (plateau phase)
* **Phase 3**: K efflux (rapid depol)
117
SE's/interactions of amiodarone?
amiodarone rarely causes **life threatening arrhythmias** (**TDP)**, it has **serious pulmonary, thyroid and hepatic toxicities that limit its long term use**
118
Anion XC resins
* Use
* MOA
* Examples
* S/E
* To lower LDL/chol
* Binds bile acids to drive increased chol--\>bile acid (liver)
* GI S/E's can be appreciable, limiting use to 3rd line
120
Fibrates
* use
* examples
* Effective TG-lowering drugs (for hyperTG \>200 mg/dL)
* Gemfibrozil, fenofibrate
122
What is the most common congenital heart defect found in adults?
What does it predispose pt. to?
Bicuspid Ao valve.
Predisposes pt. to aortic stenosis.
123
LV hypertrophy
* Symptoms
* Complication
* Rx's
* Can be asymptomatic for many years but then dyspnea, angina, syncope
* CHF
* If HTN-related, reduce afterload; Rx underlying condition.
124
Two primary causes of renovascular stenosis
atherslerosis & fibromusc. dysplasia
125
Abd. Ao. Aneurysm
* 2 RF's
* Complications
* Most common region
* **Smoking**, genetic (**Fam Hx very important!**)
* Rupture: related to diameter of affected site
* most common: infrarenal Ao
126
Constrictive pericarditis
* Def
* Etiology
* Most common causes
* Due to chronic pericarditis
* Cuased by repeated/chronic insults
* Post viral (50%), TB (15%), Rad Ther, PostSurg
127
Casesous pericarditis
* Assoc w/ what infx
TB
128
Major complication of a fib and a flutter? How to prevent?
**STROKE:** intra-atrial clots that can dislodge leading to devastating strokes.
**- Anticoagulation** is one of the cornerstones of managing both of these arrhythmias
129
What is the basic pathology of chronic ischemic heart dz?
myocard. atrophy & fibrosis
130
Discuss Ankle Brachial Index: how used, and values that show pathology?
* used to asses arterial obst. (stenosis) - quantifies it.
* Gives ratio of arm:leg BP's (leg at various segments); normal is \>0.92. The lower the ratio below normal, the higher the degree of stenosis.
131
Hallmark micro path of rheum fever?
**aschoff nodule**: fibrinoid necrosis and INF cells (LC's, histiocytes)
133
Describe pathophys of **mitral stenosis**
Primary increase in PLA --\> pulm. venous pressure --\> pulmonary congestion (and shortness of breath) --\> increased PA pressure --\> RV hypertrophy --(late stage)--\> liver congestion, etc. (signs of RH failure)
135
Renovasc. HTN
* Clinical picture
* What med should be avoided in pts w/ bilat dz?
* Hard to control HTN (often on \>2-3 antihypertensives)
* HI Diastolic BP \> 120 mmHg
* Flash pulmonary edema
* ACEi's should be avoided in pts with **bilateral** renal stenosis.
135
Constrictive pericarditis
* Sympts
* Exam
* CXR
* Hemodynamics
* Fatigue, dyspnea and leg swelling (edema)
* Exam: JVD, jugular venous pressure rises or fails to drop with inspiration (Kussmau), hepatomegaly, ascites, lower extremity edema
* CXR: pericardial calcification
* Hemodynamics: elevated JVP, **prominent y descent**, ventricular “square root sign, low cardiac output.
136
Chronic pericarditis, though rare, can lead to \_\_\_\_\_\_.
constrictive pericarditis
137
Rx for claudication?
* Cilastozol: PDEi - vasodilation.
* Endovasc. Rx: stents, for shorter stenoses
* Bypass grafts: for longer stenoses
137
Polyarteritis Nodosa (PAN) Rx
**Corts** or **cyclophosphamide** --\> 90% remission or cure
139
Metoprolol, atenolol (drug type and class)
B-1 selective blockers w/o ISA (B blockers are Type II anti-arrhtymics as well)
141
Fish Oil
* action
reduces VLDL & TG's
143
Why is a Mobitz II 2o block more ominous than a Mobitz I? What do these patients need?
Mobitz I is often asymptomatic whereas Mobitz II is usually at level *below* AV node and can progres to compolete heart block associated w/ slow/unreliable escape.
Pts need permanent pacemaker irrespective of symptoms.
143
Fibrinous pericarditis
* Def
* How common?
* Possible sign
* Causes
* INF rxn w/ exudate
* Most freq cause of pericarditis
* Friction rub
* MI, post MI, uremia.... (most of the general causes of any pericarditis!!)
144
What is the process by which restrictive cardiomyopathy results in decreased CO?
the restriction limits diastolic filling (due to dec. ventricular compliance) --\> dec. CO
145
What does PWCP approximate? Why important?
PCWP = filling pressure of LA; important b/c it characterizes **preload** and tells you the **pulm. *venous* pressure**
146
What would you see on a Wigger's in aortic stenosis?
gradient between LV pressure and aorta pressure - the LV has to generate additional pressure to overcome the increased resistance in the aorta.
148
What dz's put pt automatically in hi-risk category for developing CAD?
DM & vasc. dz
149
What 2 things needed to diagnose MI?
1. Rise/fall card. enzymes
2. EKG changes
150
What is the lipid goal for Framingham hi risk?
**LDL \< 100 mg./dL**
151
What are the 3 general etiologies of **myocarditis**?
* idiopathic
* infectious
* non-infx
152
What are the "5 P's" of **limb threatening ischemia?** Rx?
1. Pain, Pallor, Pulseless, Parasthesias, Paralysis.
2. An emergency that requires immediate **surgical intervention** to relieve irreversible limb ischemia that would likely lead to limb loss.
154
What is the normal PR interval?
What is the pattern in 1o AV block?
Where is the delay generally?
Normal PR = 200 ms = 1 large square = 0.2 s
1o AV block: represented by **prolonged (\> 200 ms) PR**, and **each P wave is followed by a QRS complex.**
- generally a delay at level of AV node.
154
What is the most important direct consequence of **aortic stenosis?** What does this lead to?
LV pressure overload --\> concentric LV hypertrophy
155
Sinus bradycardia
* Def
* Etiologies
* Rx
* HR \> 60bpm due to decreased SA node firing
* _Drugs_: B blockers, certain CCB's, **_Medica_**l: hypoThyr, aging, isch heart dz, cardiomyopathy.
* Generally, Rx underyling condition or remove offending agent.
156
What does this show?
purulent pericarditis
157
What is the difference between valvular vegetations in rheumatic vs. infective endocarditis?
Rheumatic: adherent lesions on valves
Infective: friable
158
Discuss SNS and PNS stimulation to heart, including where this happens.
**SNS**: E/NE stimulate B1 receptor --\> activation of adenylate cyclase --\> inc. cAMP --\> increased Ca influx --\> inhibition of Ca-sensitive K channels ---\> more rapid spontaneous **depol** = increased HR.
**PNS**: _mAChR_ stimulated via *vagus n.* --\> increase in K+ --\> hyperpol. --\> slower HR
159
What is the most common etiology of arrhythmias?
reentry (90%)
161
2 most common organisms contributing to **infective endocarditis?**
1. alpha hemolytic strep (60%)
2. S. aureus (20%)
162
Discuss epidem. of **chagas dz**
* Endemic Colombia, Brazil, Central Am, Mex
* **T. Cruzi** is transmitted by **reduviid bug** via feces
164
Drug classes/types used in long-term therapy for HF?
* ACEi or AT receptor blocker
* B blocker
* Aldo blocker
* Diuretic
165
Ezetemibe
* MOA
* Action
* Common co-drug
* Reduces intestinal abs. of chol (binds a receptor)
* Lowers LDL-chol
* Often w/ statins
167
ST segment depression - what does this signify?
unstable angia or acute cor. syndrome
169
Beck's Triad
* Def
* Sign of what condition?
* Hypotens, elev. JVP, muffled heart sounds
* Signs of **pericard. tamponade**
171
explain diff b/t a **junctional esape rhythm** and **ventricular escape**. where doe these come from? How do these differ on EKG?
* Junctional: 40-60 bpm, from AV node or *proximal* His bundle.
* Ventricular:
* EKG: Junctional = narrow QRS, ventricular = widened QRS (\>200ms).
172
What does this EKG show?
ST depression - NSTEMI.
173
Amaurosis fugax
* def
* what causes it?
complication of carotid atheroscler.: fleeting blindness from emboli.
174
**tricuspid stenosis**
* Etiology
* Signs on exam
* EKG changes
* Rx
* Generally **rheumatic**.
* **JVD** due to pressure overload/backup
* EKG: will see **large *a wave*** pushing against increased resistance.
* **Surgical valve replacement or valvuloplasty.**
176
Major effects of **mitral incompetence**
Mitral regurg (incompetence) leads to chronic vol overload of LV (normal DIA vol + regurgitant vol). This leads to dilatation + hypertrophy of LV. Can also lead to pulm. venous HTN if there is building up back pressure in system.
177
Hemochromatosis
* Etiology
* Type of dz?
abnormal Fe deposition in myocytes; leads to a _restrictive cardiomyopathy_
178
Patent Ductus Arteriosus
* Risk factor for ??
Ductus is abnormally open postnatally. A large PDA will cause clubbing, hypoxemia, and continuous murmur throughout card. cycle.
PDA is a L--\>R shunt that, if large enough, will increase pulmonary pressures. If the PDA is large enough, Pulm HTN ensues and could result in reversal of shunt (_Eisenmenger Syndrome_). This could cause **LV overload**.
180
Draw the various derangements on a pressure-volume loop, and explain them. Note the hallmark pathologies of each, in parens:
1. Decline in inotropy (post-MI)
2. Increase in afterload (aortic stenosis)
3. Decrease in preload (hemorrage or dehydration)
see notes
180
Henoch-Schonen Purpura
* Age affected
* Key skin finding
* Other organs affected
* IF findings
* Kids 3-8
* Purpurae (non blanching)
* Renal
* IgA deposition
181
* What is the action of Beta Blockers on myocardium?
* Key S/E or complication (2)
* reduce HR
* reduce BP (afterload)
* reduce contractility
S/E:
* increases wall tension acutely in pts w/ left vent. dysfunction.
* bradycardia if overshoot
183
What do the linear portions of the Frank-Starling curve tell us?
That as **preload** increases, **SV** increases.
185
What are two etiologies for complete heart block (aka ??)?
1. congenital
2. lyme dz
aka **3o AV block**
187
Mitral valve prolapse
* Def
* Etiology
* Gross pathology
* Common cause of mitral regurgitation
* Congenital, often assoc. w/ Marfans, Ehler-Danlos, etc.
* Floppy, enlarged leaflest --\> prolapse
188
What is the primary goal of anginal therapy? Via what mechanisms?
reduce the O2 demand of myocardium by decreasing:
* preload
* contractility
* afterload
* HR
189
Most common *cause* of periph. vasc dz? Most common sites for this form?
* Atheroscler.
* birfucation, branch points (eg carotid bifurc, aortoiliac, superficial fem., tibial)
191
Paroxysmal supreventricular tachycardia (PSVT)
* EKG signs
* Clinical picture
* EKG: narrow (QRS \< 120 ms) complex tachycardia w/ rapid rate.
* Clinical: sudden onset (paroxysmal) and sudden offset
192
What are the 2 causes of **renovasc. HTN?**
* Atherscler.
* Fibromusc. dysplasia
194
Physical findings (Exam findings!) of progressed **mitral stenosis (2)?**
* elevated JVP (if pulmonary HTN),
* decrescendo diastolic murmur ("rumble") from tubulent flow across valve during DIA.
* Opening snap following S2.
195
How would **mitral stenosis** appear on wigger's?
increase PLA due to impaired QLA-->LV.
196
What is **classic triad** of advanced, symptomatic calcific stenosis?
1. chest pain
2. heart failure
3. syncope
198
What is the primary systemic effect of nitrates?
Venodilation - decreases preload by increasing venous capacitance... but also dilates arterioles & arteries. Will decrease BP.
199
Hallmark restrictive HF cause?
chronic pericarditis (viral, TB, other)
200
By what mechanism does B1 stimulation affect myocytes, and how?
Agonist --\> B1R --\> +adenylate cyclase --\> +cAMP --\> +CaIC --\> **increased contractility** + HR
201
What does this show?
serous pericarditis
203
**a wave**
small increase in Patria as atrial pressure rises due to atrial SYS
204
Gross appearance of heart in dilated cardiomyopathy?
4-chamber dilatation --\> **enlarged globoid shape**
205
What class of AAA best if structural heart dz present?
Class III
206
Hallmarks of a-fib on EKG (2 criteria)?
* irregularly irregular, rapid QRS complex
* No P waves
207
Wolff-Parkinson-White syndrome
pts have an *accessory bypass tract* causing arrhythmias (mostly a-fib via reentry but can progress to Vfib)
208
Digoxin
* Uses (2) - first line?
* S/E's
* inotropic (HF), antiarrhytmic (SVT) - generally a 2nd line Rx to B-Blockers
* Narrow TM, small doses, **arrhythmias** + LOTS of others
209
Purulent pericarditis
* Etiology
* Signs
* Bact. infx
* fever, friction rub
210
3o AV block pattern; discuss high vs. low blocks
* All P waves blocked
* No visible relationship b/t P waves and QRS
* High block: OK escape w/ BPM = 40-60; Low block = unreliable
210
Rhabdomyoma
* Def
* Popn affected most
* Important assoc. w/ what condition
* Benign primary tumor of heart
* **Kids** (most common primary tumor in kids)
* **50% assoc. w/ tuberous sclerosis** (possibly same genotype leads to both tumors & tub. sclerosis)
211
**Virchow's Triad** (for what condition?)
* Stasis, hypercoag., epith. injury
* relates to **DVT**
212
Rx of hemodynamically stable v-tach? Unstable VT?
* *Stable:* IV procainamide or IV amiodarone (antiarrhytmics)
* *Unstable:* Immediate cardioversion
213
Aortic Dissection
* Diff b/t Type A & B
* How to Rx Type A vs B
* Major RF's
* Type A: asc. Ao, needs immed. surg.; Type B: desc. Ao could treat medically
* HTN, Ao stenosis, or connective tissue dz (Marfan's, Ehler-Danlos, etc.)
214
DEF vasculitis
leukocytes in vessel wall w/ reactive damage to tissues
215
Possible sign of Fallot on CXR
"**boot-shaped heart**" due to enlarged RV
216
Hypoplastic left heart synd
Often secondary to mitral or aortic stenosis/atresia causing lo Q to LV. **Inadequate Q = poor growth**.
217
What are symptoms and signs of Ao coarctation?
* Symptom: leg fatigue
* Signs: HTN, lower ext BP\>upper ext. BP
219
What is the char histopath of acute cardiac rejection?
Interstitial lymphocytic infiltrate with focal myocyte degeneration.
220
x descent
following c wave, relaxed venous pressure/ low return.
222
Pericard. tamponade
* Def
* Common causes
* Symptoms
* Exam
* Fluid accumulation pericardial space ---\> **poor diastolic filling**
* idiopathic, malignancy, hemorrhage and uremia
* Fatigue, shortness of breath
* Exam; **hypotension\***, tachycardia, pulsus paradoxus (\> 10 mmHg drop in systolic BP with inspiration) **jugular venous distension (with blunted y descent)\***, clear lungs, **muffled heart sounds\***
223
What are the major causes of SYS dysfunction (impaired contractility)?
What might you see on gross inspection of heart?
_Causes_
* CAD --\> MI
* Chronic vol overload (mitral or Ao regurg)
* Dilated cardiomyopathies (familial/genetic, viral, EtOH, secondary, pregnancy)
_Gross dissection_
* Large globoid heart.
225
* Which vessels most affected in diabetic vasc. dz?
* distal \> proximal
226
what are 2 factors that can increase ejection fraction?
1. increase preload (the reason this happens is indirect; due to the Frank-Starling "law", when ventricular stretch increases, so does the ability of the ventricle to strongly contract; so as preload increases, stretch increases, and EF increases).
EDV and preload are more directly related; in physiolgical terms they are equivalent except in dz states.
2. increase inotropy (contractility): could be done vis SNS stim, reduced PNS tone, inotropic drugs.
227
What is characteristic of "systolic dysfunction"(3) ?
Some dz processes leading to it?
* chronic **volume overload**
* **_dilated_** & **hypertropic** LV
* **Reduced EF at rest** (reduced contractility)
* **Vol overload in LV**: think _aortic stenosis_, _aortic regurg_, _mitral regurg_.
228
dP = QR. Why is this important? What is the actual physiological dP?
Just says that the diff in pressure is the driving force for the flow.
Derivation of Q = dP/R (Ohm's law)
dP = Paorta - Pvena cava/central venous pressure
For entire system:
**Paorta - Pvena cava/central venous pressure = CO x R**
230
Hemorrhagic pericarditis
* Def
* Usual etiology
* Bloody, fibriounus exudate
* secondary to malignancy
231
What are the most common etiologies for **aortic stenosis** for the following age groups?
* 50-60
* 60-70
* \>70
* Bicuspid (congenital)
* Rheumatic
* Senile degenerative
233
By what mechanism do nitrates reduce myocardial O2 demand? What is best way to avoid tolerance?
By decreasing preload through venodilation. At least 8 hours free of dosage / 24h period.
234
What does chronic LV vol. overload lead to? What is a possible complication?
**eccentric hypertrophy**; as wall stress increases, leads to **CHF**
235
General effects of mitral stenosis?
Buildup of "back pressure" into LA --\> Pulmonary system, resulging in **pulmonary edema** (assoc. w/ dypsnea, caough, exertional dyspnea, etc.)
236
# Define **preload**; what is relationship b/t preload and CO? How would you clinically approximate preload (technique & theory)?
def: amount of blood the heart receives to distribute to body.
increasing preload --\> increase in CO; this has a limit - when vent. wall compliance exceeded, CO decreases dramatically (CHF)
**Preload = pressure in LA = PCWP** (via Swan-Ganz cath)
237
Class I Anti-arrhythmic agents
* Channel action
* 1A prototype, used for what?
* 1B used for ? What are the 2 types and how administered?
* Indications & contraindications of 1C? What are the prototype drugs?
* act on Na and K channels
* _1A:_ **Quinidine**, used for a-fib.
* _1B_: used for vent. tachyarrhythmias; **lidocaine** (IV), **mexiletine** (PO)
* _1C_: For prevention of a-fib *only* in pts w/o structural heart dz; _contra:_ BBB w/o pacemaker, structural heart dz. prototypes: **propafenone** and **flecainide**
238
Junctional rhythm
Rhythm coming from atria or AV node, producing a reliable rhythm. Infranodal rhythms (below AV node) = unreliable escape rhythm.
240
EKG time:
large square =
small square =
large = 5 mm = 0.2 s (200 ms)
small = 1mm = 0.04s (40 ms)
241
When do the *coronary a.s* receive most of their flow?
DIA
242
Rx for pericardial tamp?
Pericardiocentesis
243
Microscopic changes in ischemic heart dz
1. 1st 24 hrs
2. 1-2 days
3. 5-10 days
1. **wavy fibers**, eosinophilic w/ **contraction band necrosis** (banding across width of myocytes)
2. Polymorphonuclear monocytes (**PMNs** = neutrophils) attracted to necrosis; edema, hmg, obviously necrotic myocytes.
3. **Few** PMNs; **granulation tissue: fibroblasts, LCs + pigment-laden MP's**, w/ abundant neocaps.
244
Most common etiologies of pericarditis?
* Infectious (viral)
* Immuno (eg rheum fever)
* Misc (rad, uremia, trauma etc)
245
What does this picture show?
myocard. hypertrophy
246
General approach to dyslipidemia Rx
* exclude secondary causes
* lifestyle mod (diet, exc)
* adherence (meds, etc)
248
What are the two types of inotropic drugs most often used? Give prototype of each.
* _B-agonist_ (**dolbutamine**)
* _PDEi:_ **milrinone**
249
Small VSD's have a ____ murmur; large ones have a _____ murmur
large; small
250
Torsade de Pointes
Wide complex Vtach w/ hi risk mortality; caused by some AAA's including Class Ia (quinidine, procainamide), Ic (flecainide, propafenone), III (amiodarone, dofetilide, sotalol)
251
What are two types of non-infective valvular vegetations?
* Non-bacterial thrombotic endocarditis (NBTE)
* Libman-Sacks endocard (SLE)
252
EKG signs of a LBBB?
1. Lead I: widened R (quite prominent)
2. V6: often a notched R
253
Primary effect of Type I CCBs?
_myocardial vasodilation_ w/ **electrophysiological effect of slowing HR**
254
What is area affected in **secundum ASD?**
fossa ovalis
255
What two primary factors determine BP? Break those down into their respective contributions.
1. Now, explain how **hypovol. shock** affects those.
2. **Cardiogenic shock** takes place often post-MI. How does this derange above? Why do you see cold, clammy skin?
3. **Hypotension 2ndary to anaphylaxis or sepsis**
BP = CO x PVR
CO = HR x SV
SV is a function of preload, contractility, and afterload.
1. **Hypovol. shock:** decrease in *preload* --\> decreased in SV --\> decreased CO --\> decreased BP.
2. **cardiogenic shock** results in *reduced contractility* which in turn reduces SV --\> CO --\> BP. See cold, clammy skin b/c the body's compensatory mechanism is to vasoconstrict (to raise BP/perfusion). This has skin effects.
3. **anaphylaxis** or **sepsis:** these are somewhat unique in that they lead to systemic vasoDILATION resulting in decreased in PVR --\> dec. in BP.
256
What is characterized by valvular dz w/ bulky friable vegetations anywhere on valve?
infective endocarditis
257
What is the more common location of a cardiac fibroma?
LV \> RV
NB: fibromas are 2nd most common pediatric card. tumor (primary).
259
What is the hallmark EKG sign of an acute MI? Do all acute MI's have it?
How to Rx STEMI?
ST segment elevation (STEMI). NO - there are also non-ST elevation MI's (non-STEMI).
Rx: angioplasty if avail. otherwise lytic (latter is not standard of care but more like best option if cath lab not avail.)
260
Useful/common lab tests/diag. tests for vasculites?
* cANCA
* pANCA
* SED rate (INF marker)
* ANA (SLE)
261
Ostium primum ASD
* Malformation
* Association w/ what genotype
* An ASD due to endocard. cushion defect, one variation is a large, malformed AV valve.
* assoc. w/ T-21
262
What kind of murmur is heard w/ VSD?
holoSYS
263
QRS complex
vent. depolarization dipole
264
What is the most common heart defect in children? What is the most common subtype?
ASD; secundum most common.
265
What is the most common combination therapy for Rx'ing angina?
ASA, nitro, b blocker.
267
def. Ductus arteriosus
fetal circ. shunt (R--\>L) from Pulm a. --\> Ao, thus shunting flow from the **_hi resistance_** _pulm. circulation_ of the fetus.
268
What is the primary mechanism by which **aortic regurg** causes dz? Discuss early and late stages of regurgitant dz.
regurg --\> chronic LV vol. overload; this causes dilatation of the LV w/ some hypertrophy.
As remodeling continues, the heart progresses to SYS dysfunction. Back pressure also builds up, creating high pressures in the LA and pulmonary vasculature. All of these can lead to LHF.
269
End dias vol. (EDV)
This is also termed the **preload**; this is the volume of the 'comletely filled' ventricle at the end of DIA. Remember that the ejection fraction = EDV - ESV.
270
Subclavian Steal Synd
* Which side more common?
* Symptoms
* Signs
* What is the "steal" part about?
* L \> R
* Usually asympt.
* Higher BP in unaffected vs. affected arm
* activity of affected side arm --\> "stealing" (shunting) of arterial Q from verterbral a.
271
What is considered a high risk Framigham score and what should you do?
** \> 20%** = **aggressive risk modification**
272
Possible consequences (2) of carotid athersclerosis?
TIA (from carotid emboli) or stroke
273
What are the three most important determinants of myocard. O2 consumption in order of importance?
How does this affect Rx of CAD?
HR \> load \> contractility
This is also the Rx priority - **first line is beta blockers** whose primary action is to reduce HR.
274
Def. **afterload**; what is the hallmark pathology assoc. w/ increased afterload?
Afterload: pressure the LV needs to overcome during SYS = SYS BP; this is essentially the impedance or R.
_Hallmark pathology of increased afterload_ = **aortic stenosis**
275
What is the pattern of a **Mobitz I 2o AV block (Wenckenbach)**?
Normal PR --\> prolonged PR --\> blocked P wave
**NB:** a 'blocked P wave' means P wave that is not followed by QRS.
276
What EKG anomaly found in **acute** chagas dz?
LBBB
277
Niacin
* aka
* Action
* Evidence
* Vit B3
* Inc. HDL, lower LDL
* Lack of clinical evidence that it works
278
Supraventricular Tachy
* Def
* Rx's
* A narrow complex (
* Rx: Type I CCB's (Type IV AAA) - diltiazem, verapamil.
279
What does this show?
Fibrinous pericarditis
280
When reading EKG, remember that the first negative deflection = ?, the first positive = ? and the 2nd neg = ?
Q, R, S
281
"Diastolic HF" characterized by ?
Chronic **pressure overload**: results in _hypertrophy w/o dilatation_. Association w/ **normal or "preserved" EF** w/ poor relaxation & compliance.
282
Def'n of a 2o AV block. What is an *advanced* AV block?
Non-consecutive blocked P waves. *advanced AV block* is similar but w/ consecutive blocked P waves.
283
What are some common clinical manif's of vasculitis?
* Multisys dz
* Skin lesions
* Ischemic vasc. changes
* Weight loss
284
What combo of drugs (classes, not names) has statistically led to greatest decrease on HF mortality?
ACEi/ARB + B blocker + Aldo blocker
