Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Preclerkship > Angina, ACS, Hypertension, Heart failure > Flashcards

Angina, ACS, Hypertension, Heart failure Flashcards

1
Q

Most hypertention cases in adults are what type?

A

Primary (essential)

No specific cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is cushing’s triad and what does it indicate?

A

Hypertension + bradycardia + irregular respirations (Cheyne-Stokes)
= high ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Estrogen and hypertension?

A

Endogenous is protective against Ht/coronary heart disease

Oral increases BP, coagulopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 5 endocrine causes of secondary hypertension?

A

Conn syndrome (1o hyperaldosteronism, low renin)
Cushing syndrome (hypercortisolism, increases E/NE sensitivity)
Hyperthyroidism: high T3/T4 —> high HR, E/NE sensitivity
Hypothyroid: low T3/T4 –> Na retention
HyperPTD –> high Ca –> vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Almost any ___ can trigger hypertension. Disorders that ______ lead to mechanisms that increase systemic BP

A

Renal disease

Decrease renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Nonspecific symptoms of hypertension

A 
Headaches (esp morning)
Dizziness, tinnitus, blurry vision
Flushing
Epistaxis
Chest discomfort, palpitations, bounding pulse
Nervousness/sleep issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What other abnormalities may be present in a patient who has hypertension secondary to Conn syndrome?

A

Hypokalemia + metabolic alkalosis

High aldosterone:renin ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Isolated systolic hypertension: 2 main mechanisms

A

1) Age –> reduced arterial compliance

2) High CO (aortic regurg, hyperthyroidism, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

BP much higher in upper limbs than lower limbs may indicate

A

Coarctation of aorta distal to the L subclavian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is pharmacologic treatment for hypertension indicated?

A

> 140/90 or >130 w/ other RFs (DM, kidney disease, HF, ischemic heart disease, stroke hx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

First line drugs for Htn & specific pt populations?

A

ACEi & ARBs (esp in pts w/ DM, renal disease, HF, ischemic heart disease)
Thiazide diuretics and/or Ca-channel blockers (usually dihydropyridines) (esp Black pts, isolated systolic Htn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can loop & thiazide diuretics potentially cause hypokalemia & metabolic alkalosis?

A

Both inhibit channels that absorb Na –> more Na in distal tubules –> aldosterone-sensitive Na pump increases Na reabsorption in exchange for K/H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Don’t combine ____ with ACEi/ARBs

A

Direct renin inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hypertension drugs menmonia

A

A - ACEi, ARBs, Alpha-1 receptor blockers, Aldosterone antagonists, Arteriolar vasodilators (hydralazine)
B - beta-blockers
C - Ca-channel blockers
D- Diuretics, direct renin inhibitors
E - endothelin receptor antagonists (pulmonary arterial htn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What might you heart on heart auscultation in chronic htn?

A

S4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hypertensive nephropathy leads to what type of nephrotic syndrome?

A

FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cutoffs for hypertensive urgency/emergency?

A

180+ and/or 120+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Renal artery stenosis is caused by ___ in 90% of cases, but may be caused by ____ in ___ population

A

Atherosclerosis (90%)

Fibromuscular dysplasia in younger women (“string-of-beads” appearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Feature of renal artery stenosis on clinical exam

A

Abdominal bruit over flank or epigastrium (syst-diast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Renal artery stenosis might have what electrolyte imbalance?

A

Hypokalemia (RAAS!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When someone with Htn is treated with ACEi/ARBs, what change on bloodwork might indicate that they have renal artery stenosis?

A

Increased serum Cr because RAAS is maintaining GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Imaging to diagnose RAS?

A 
Duplex US (doppler)
CT or MR angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List 6 main adverse effects of ACEi/ARBs

A

Hyperkalemia
Teratogenic effects
Cough (kinins not metabolized by ACE; mostly ACEi)
Angioedema (also kinin-mediated, mostly ACEi)
Hypotension (worse with ARBs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Triple whammy of kidney meds

A

Diuretics + NSAIDS + ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pathophys of NSAIDs causing AKI

A

Inhibit prostaglandin production, and PGs have vasodilatory role where they decrease preglomerular resistance to preserve renal blood flow

Note: can also cause AKI via acute interstitial nephritis (inflammatory cell infiltrate in the interstitium of the kidney, usually after about a week)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

“Viability imaging” (e.g. PET, dobutamine echo) can differentiate between what?

A 
Hibernating myocardium (chronically low blood supply & ventricular contractile dysfunction) 
Infarcted (necrotized)

Stunned myocardium = transient ischemia w/out necrosis –> prolonged systolic dysfunciton after bloodflow returns due to ionic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the clinically relevant difference between hibernating & infarcted myocardium?

A

Infarcted will not regain contractile function even if revascularized
Hibernating needs revascularization in order to start working again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Is variable threshold angina always unstable angina?

A

NO, it’s a subset of stable angina where vasoconstriction plays more of a role (in addition to stenosis)
Unstable is a sudden increase w/ less exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of unstable angina

A

Plaque rupture
Platelet aggregation
Thrombus formation
Unopposed vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is variant angina? AKA? 3 causes?

A

AKA Prinzmetal angina
Focal artery spasm w/out over atherosclerotic lesions
Cocaine, alcohol, triptans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What extra heart sound might you hear during myocardial ischemia and why?

A

S4 (stiff ventricle) because ischemia reduces diastolic compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ischemia is common in what layer of heart tissue?

A

Subendocardium (farther from large vessels, pressure from ventricular chamber, few collaterals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Most common changes on EKG during cardiac ischemia?

A

Transient ST-segment depressions and T-wave flattening/inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

EKG change during Prinzmetal’s angina?

A

ST elevation

Diff than STEMI because transient & reversible w/ vasodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Signs of a positive exercise stress test (5)

A 
Drop in BP
Replicated chest pain
Ischemic EKG changes
High-grade ventricular arrhythmia
Exercise intolerance <2min for cardiopulmonary reason
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What do you do in a stress test if patient has a baseline EKG abnormality (e.g. LBBB)

A

Nuclear imaging (inject IV radionuclide @ peak exercise –> accumulates proportionally to viable myocardial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Explain “cold spots” on nuclear imaging during stress test

A

Ischemic or infarcted

Repeat at rest to tell, if temp ischemia will fill in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When is exercise echocardiography stress test done?

A

Same as nuclear (i.e. when results don’t make sense or baseline EKG abnormalities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do you perform a stress test if the pt can’t exercise? (2 methods + indications)

A

Pharmacologic: coronary vasodilator (e.g. adenosine)
Ischemic regions are already maximally dilated so will shunt blood away
OR
Give inotrope (dobutamine) if pt has reactive airway disease where adenosine could cause bronchospasm or if they took adenosine antagonist (e.g. caffeine)

Couple w/ nuclear imaging or echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the gold standard for CAD diagnosis? What is a less-invasive alternative

A

Coronary angiography (contrast injected into artery via catheterization)
(invasive though so only in unstable pts that haven’t responded to treatment)
Coronary CT angiography is less invasive (IV contrast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Cardiac catheterization: inserted via what arteries?

A

Femoral or radial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Nitroglycerin is a ___dilator

A

VENOdilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

3 main ADEs of nitrates + solution for one of them

A

Headache
Hypotension
Reflex tachycardia due to venodilation reducing CO (coadmin w/ BB or CaB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the 2 modes of delivery of organic nitrates for myocardial ischemia, and indication for each?

A

Sublingual: during acute attacks of prophylaxis before provoking activity
Oral/transdermal: chronic daily use (SYMPTOM relief only, doens’t prolong survival)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does nitro work for ischemia

A

Reduces O2 demand (reduces preload through venodilation)

Increases O2 supply (more perfusion, less vasospasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How do beta blockers work for ischemia

A

Reduces O2 demand (lowers contractility/HR)

Increases O2 supply (longer diastole –> more perfusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

5 main ADEs of beta blockers

A 
Excessive bradycardia
Reduced LV contractile function
Fatigue
Hypoglycemic unawareness
Bronchoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the difference between dihydropyridine and nondihydropyridine Ca-channel blockers in terms of mechanism? Examples?

A

Dihydros: Nifedipine - vasodilation

Non-dihydros: Verapamil = cardiac depression (reduce contractility/HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name 3 drugs that help SYMPTOMS of coronary ischemia and 4 drugs that reduce RISK OF MI/DEATH

A

Symptoms: nitrates, BBs, CaBs

MI/death: Aspirin and/or P2Y12 antagonists, Statins, ACE-inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

____ should be continued indefinitely in all CAD patients unless contraindicated (allergy, gastric bleeding).

A

Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

High-intensity ____ regiment to achieve 50% ___ reduction recommended in all coronary ischemia patients (even if baseline below threshold)

A

Statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Do PCIs reduces MIs/death in stable CAD?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

2 types of PCI

A 
Balloon angioplasty (percutaneous transluminal coronary angioplasty)
Stents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

CABG stands for

A

Coronary Artery Bypass Graft Surgery (using patient’s native BVs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Critical narrowing of what artery threatens most of the L ventricle? Branches off what?

A

Left anterior descending artery (AKA anterior interventricular artery) which branches off the L coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the 4 classes of ischemia according to the Canadian Cardiovascular Society? Which warrant hospitalization?

A

Class I = only w/ strenuous/prolonged exertion
Class II = Slight limitation in ordinary activities
Class III = marked limitation of ordinary activity
Class IV = unable to perform any activity w/out angina (incld rest)

New-onset III/IV –> admission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Usually coronary pathology & myocyte necrosis?
Unstable angina =
NSTEMI =
STEMI =

A 
UA = partially occlusive thrombus, No
NSTEMI = partially occlusive thrombus, Yes
STEMI = fully occlusive thrombus, Yes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

90% of ACS results from…

A

Rupture of atherosclerotic plaque (e.g. SNS activation, high BP) –> platelet aggregation –> thrombus formation

Superficial plaque erosion can also cause it (more rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Exposure of what substance (e.g. during atherosclerotic plaque rupture) results in white thrombus formation

A

Collagen!

vWF in blood binds collagen which then binds vWF on platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What substance is synthesized by COX1 and released during platelet hemostasis? Role? Clinical relevance?

A

TXA2 (thromboxane A2) –> vasoconstriction + more platelet activation
NSAIDS/aspirin!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the difference between how aspirin and other NSAIDS affect platelet function? What interaction do they have and what does this mean for taking them?

A

Aspirin IRREVERSIBLY inhibits COX-1 (why you need to stop aspirin 5-7 days preop)
NSAIDS interfere reversibly

If you take both the ibuprofen will wear off and those platelets will be back in action. Need to take aspirin 30 min before or 8 hrs after ibuprofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What part of platelet hemostasis does clopidogrel impact?

A

P2Y12 inhibitors = ADP receptor inhibitors, prevent platelet activation irreversibly
Duration of action ~7 days (like aspirin), platele lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Mechanism of GPIIb/IIIA inhibitors

Administered how?

A

Prevent aggregation of platelets + fibrinogen binding & cross-linking
Administered inpatient IV (e.g. during ACS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

A partially occlusive thrombus will show what on EKG? How to differentiate between UA & NSTEMI (diff test)?

A 
ST depression and/or T-wave inversion
Check troponins (+ in NSTEMI only)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Mechanism by which cocaine can cause MI?

A

Severe coronary artery spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

In gradual atherosclerosis w/ brief preceding ischemias you’re more likely to get a (STEMI/NSTEMI)? more or less likely to survive?

A

NSTEMI because gradual process allows angiogenesis of collateral (“ischemic preconditioning”); also more release of mediators like adenosine, bradykinin. More likely to survive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

___ % of MIs are asymptomatic, esp in ___ patients

A 
25%
Diabetic patients (neuropathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What reflex causes dyspnea in MI?

A

J reflex
Ventricular dysfunction –> pulmonary/alveolar congestion –> stimulates juxtacapillary (“J”) receptors –> rapid/shallow breathing + dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Does MI cause systolic or diastolic dysfunction?

A

Both! Relaxation is also ATP-dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What can happen to noninfarcted parts of heart during ventricular remodelling post-MI
Possible treatment for prevention?

A

Dilation because overworked –> HF, arrhythmias

Combat w/ RAAS inhibitors

71
Q

What structually happens to infarcted area a few days following MI?

A

“Yellow softening” (macrophages removing dead myocardium, before scar tissue generated) - weaker, dilates; risk of aneurysms

72
Q

Name 3 cardiac signs during MI (not EKG)

A

1) Extra heart sounds - S4, S3 if systolic dysfunction –> V overload
2) Systolic murmur (pap muscle dysfunction –> mitral regurg; OR infarct ruptures septum –> VSD)
3) Dyskinetic bulge

73
Q

Pathological S3 = ___gallop

S4 = ___ gallop

A 
S3 = Ventricular gallop (dilated ventricle, or increased flow e.g. regurg)
S4 = atrial gallop (stiff ventricle)
74
Q

EKG difference between STEMI and pericarditis?

A

Both have ST elevation
STEMI: only in leads overlying infarction
Pericarditis: DIFFUSE ST-elevation (all leads except aVR + V1)

75
Q

Does an NSTEMI feel more like a STEM or UA?

A

more like a STEMI (prolonged “crushing” pain etc)

76
Q

2 cardiac troponins

Indicate what?

A

cTnI & cTnT

Injury to cardiomyocytes

77
Q

Name 4 conditions other than MI where troponins may be detectable

A

PE
Myocarditis
Pulmonary embolism
Heart failure

78
Q

Troponins rise___after discomfort starts, peak @___, decline slowly (detectable for __ days after large MI!)

A

Troponins rise 3-4h after discomfort starts, peak @18-36 hours, decline slowly (detectable for 10 days after large MI!)

79
Q

How is treatment for STEMI decided?

A

Emergent PCI available within 90 min (or 120 min if transferring)? Yes –> PCI
No –> fibrinolytics (if not contraindicated)

80
Q

4 categories of concurrent treatment for ACS

A

1) Anti-ischemics
2) Anti-thrombotics
3) Adjunctives (Statins, ACEi)
4) Supportive (O2 for hypoxemia, morphine for pain/anxiety)

81
Q

2 main treatment approaches for UA/NSTEMI and how you choose

A

1) Early invasive approach: cardiac cath + coronary revascularization within 72 hours
2) Conservative (meds)
Choose based on TIMI (thrombolysis in myocardial infarction) risk score

82
Q

What are the 3 anti-ischemic therapies used in AU/NSTEMI? Which has some mortality benefit?

A

B-blockers (target = 60bpm, initiate within first 24 hours) - some mortality benefit!
Nitrates (symptoms)
Ca channel blockers (no mortality benefit)

83
Q

Antiplatelet therapy in UA/NSTEMI

indicate types, how many, mortality benefit

A

Give at least 2:

1) Aspirin (mortality benefit! give immediately and continue indefinitely)
2) P2Y12 receptor antagonists (mortality benefit when added to aspirin)
3) GCP IIb/IIIa receptor antagonists (for high-risk patients, usually started in cath lab during PCI

84
Q

Anticoagulant therapy in UA/NSTEMI

A

Use 1:

a) UFH (must monitor)
b) LMWH (better, don’t need to always monitor)
c) Bilvalirudin (bivalent direct thrombin inhib)
d) Fondaparinux (inhibits factor Xa via antithrombin activation)

85
Q

When are fibrinolytics appropriate for UA/NSTEMI?

A

NEVER, only for STEMI

86
Q

What is the main cause of sudden cardiac death during acute MI?

A

Ventricular fibrillation

87
Q

Beck’s triad cardiac tamponade

A

Hypotension
Muffled heart sounds
Distended neck veins

88
Q

Treatment of acute tamponade

A

Pericardiocentesis

89
Q

Sign of tamponade on EKG

A

Electrical Alternans (QRS complexes have diff heights due to swinging of heart)

90
Q

Name 5 main complications of ACS

A

1) Embolism (ventricular thrombus)
2) Cardiogenic shock (reduced contractility –> more ischemia, viscious cycle)
3) Congestive HF
4) Arrhythmias
5) Pericarditis
6) Pericardial effusion/cardiac tamponade

91
Q

Cardiac tamponade after MI could be caused by what 2 things?

A

Ventricular rupture due to tissue necrosis

Pericarditis

92
Q

2 med categories for cardiogenic shock

A

Inotropes

arterial vasodilators

93
Q

Name 5 predictors of poor post-MI outcomes

A

1) Extent of LV dysfunction (most important)
2) Early recurrence
3) Severe CAD
4) High-grade ventricular arrhythmia
5) Very abnormal stress test

94
Q

Standard post-discharge therapy after MI (7)

A

1) Aspirin
2) Beta-blocker
3) P2Y12 platelet inhibitor
4) Statin
5) ACE inhibitor and/or aldosterone antagonist
6) ICD (if ejection fraction <30%)
7) Risk factor management plan

95
Q

What is a pseudoaneurysm

A

Incomplete rupture with thrombus “plugging” the hole - ticking time bomb, must detect & repair surgically asap!! (rupture –> tamponade)

96
Q

Describe pericarditis after MI (pathophys + timeline)

A

Inflammation spreads from myocardium –> pericardium

Usually in-hospital (early); rarely can occur weeks later = Dressler syndrome

97
Q

CO =

A

SV x HR

98
Q

Afterload is approximated by

A

Systolic ventricular/arterial pressure

99
Q

Preload is approximated by what? What does it represent?

A

Ventricular end-diastolic volume or end-diastolic pressure

=stretch on ventricular fibers just before contraction

100
Q

What 3 factors influence stroke volume

A

Preload
Afterload
Myocardial contractility

101
Q

SV = ___ - ____

A

EDV - ESV

102
Q

EF = ?

Normal range?

A 
EF = SV / EDV
Normal = 55-75%
103
Q

Compliance =

A

change in volume /change in pressure

104
Q

What is diastasis?

A

Lull when initial passive filling of ventricle has slowed, before atrial contraction

105
Q

EDV depends on ___ and represents ___; ESV depends on ___ & ____

A

EDV: compliance, preload
ESV: afterload, contractility

106
Q

Is LHF or RHF most commonly seen clinically?

A

Actually, BIventricular is most commonly seen!

107
Q

Describe HF with reduced EF

A

Mostly systolic issue; reduced contractility or increased afterload (resistance to flow)

108
Q

Describe HF with sustained EF

A

Mostly diastolic issue;

Impaired early diastolic relaxation (active process) or increased stiffness of V wall (passive), or external restriction

109
Q

name 2 things that can cause chronically high afterload

A

1) Aortic stenosis

2) Severe hypertension

110
Q

Name 3 things that can cause impaired contractility leading to HF-REF

A

1) CAD (–> ischemia/MI)
2) Chronic volume overload (regurg)
3) Dilated cardiomyopathy

111
Q

Restrictive cardiomyopathy would cause what type of HR?

A

HF-PEF

112
Q

L ventricular hypertrophy would cause what type of HF?

A

HF-PEF

113
Q

R heart is susceptible to failure due to what mechanism?

A

High afterload (rather than high filling V)

114
Q

R heart failure caused by primary pulmonary disease =

A

Cor pulmonale

115
Q

BP = ___ x ___

A

CO x TPR

116
Q

What are natriuretic peptides and what is their clinical significant?

A

Atrial natriuretic peptide released when atrial cells distended
B-type natriuretic peptide during hemodynamic stress on ventricle
Both ANTAGONIZE volume-retaining effects (protective)

Can order BNP or NT pro BNP, higher levels indicate worse HF

117
Q

Does heart failure manifest as orthopnea or platypnea?

A

Orthopnea! Difficulty breathing when flat (sleep with more pillows, PND)

118
Q

S3 gallop = ___ dysfunction
S4 gallop = ____ dysfunction
[systolic/diastolic]

A 
S3 = systolic
S4 = diastolic
119
Q

Stages of HF (A - D)

A 
A = risk of HF but no structural dysfunction (e.g. CAD, Ht, FmHx)
B = structural heart disease/HF but no Sx
C = structural HF + Sx
D = refractory Sx despite therapy, advanced intervention required
120
Q

What abnormal pulse might be observed in pt w/ HF & advanced ventricular dysfunction

A

Pulsus alternans (strong-weak alternating contractions)

121
Q

What type of abnormal breathing pattern may be present in a pt w/ advanced HF?

A

Cheyne-Stokes breathing (inadequate perfusion of resp centre in brain)

122
Q

What is cardiac asthma? Possible cause?

A

wheezing due to compression of airways by pulmonary edema

e.g. during L-HF

123
Q

Kussmaul sign could indicate __ HF

A

Right

increased JVP during inspiration

124
Q

Do pleural effusions happen in LHF or RHF?

A

Either! because pleural veins drain into both systemic + pulmonary venous beds

125
Q

Radiographic findings when PCWP (~L atrial pressure) > 15 mmHg

A

BVs in upper lung larger than lower

=”upper zone vascular redistribution” (because edema compresses @ base)

126
Q

Radiographic findings when PCWP (~L atrial pressure) >20

A

Kerley B lines = short lines at periphery of lower lungs near the CVAs
= perpendicular to the pleural surface and extend out to it. They represent thickened subpleural interlobular septa and are usually seen at the lung bases.
(interstitial edema)
Blood vessels also appear indistinct due to peribronchovascular IS edema

127
Q

Radiographic findings when PCWP (~L atrial pressure) >25

A

Opacification of air spaces;
Perihilar “batwing” appearance

= alveolar pulmonary edema (lymph failing to drain interstitium enough)

128
Q

Cardiomegaly on radiograph =

A

Cardiothoracic ratio > 0.5

129
Q

What on transverse CT is the correlate of Kerley-B lines on radiograph?

A

Thickening of septal lines

130
Q

Gold standard test for diagnosing HF

A

Echo

131
Q

Do diuretics target preload or afterload in HF?

A

PRELOAD
Volume overload doesn’t actually increase afterload much
If in “flat” part of F-S curve won’t reduce SV & CO, but if you overuse could reduce CO

132
Q

Example of standard HF therapy sequence for REDUCED EF (4 steps)

A

1) ACEi + diuretic (if congestive); substitute ARB or H-ISDN if ACEi not tolerated
2) If recent deterioration/V overload –> B-blocker
3) Persistent –> Add aldosterone antagonist
4) Refractory –> digoxin

133
Q

If on ACEi + aldosterone antagonist, pt must be monitored for

A

Hyperkalemia

134
Q

How do B-blockers work in HF-REF? What is the caution?

A

Increase cardiac output, anti-ischemic properties, blunt SNS

Caution: negative inotropes, can induce acute deterioration

135
Q

What drugs can be used to address the contractility aspect of HF? Which type of HF?

A 
Positive inotropes (increase intracellular Ca) - for SYSTOLIC dysfunction (HF-REF)
e.g. digoxin
136
Q

What positive inotropes can be used in acute HF? (via IV)

A

B-adrenergic agonists (dobutamine, dopamine)

PDE-3 inhibitors (milrinone)

137
Q

First line chronic therapy for LV systolic dysfunction =

A

ACE inhibitors (e.g. ramipril)

138
Q

What is a mechanistic advantage of ACEi > ARBs?

A

ACEi increase bradykinin –> vasodilation

139
Q

Role of nitrates in heart failure

A

Venous vasodilators –> reduce venous return/preload

140
Q

What is an arteriolar vasodilator that can be prescribed to reduce afterload in HF-REF?

A

Hydralazine

141
Q

What is indicated in many pts w/ HF-REF & LVEF <35%? Purpose?

A

ICD implantation (treat arrhythmias & prevent sudden cardiac death even if no preexisting arrhythmia)

142
Q

2 fundamental principles of treating HF-PEF?

A

1) Relieve pulmonary/systemic congestion (WITHOUT underfilling L ventricle)
2) Address correctable causes (hypertension, CAD)
Overall not very treatable - B-blockers, ACEi/ARBs, inotropes don’t help :(

143
Q

How is a pt w/ acute HF exacerbation classified?

A 
Fluid overload (wet/dry) - LV filling pressure/congestion
Tissue perfusion (cold/warm) - CO, SNS vasoconstriction
144
Q

What are the 2 main goals during an acute HF exacerbation?

A

1) Normalize ventricular filling

2) Restore tissue perfusion

145
Q

Frothy sputum is a sign of…

A

pulmonary edema (fluid in alveoli)

146
Q

Acute management of pulmonary edema mnemonic + overall aim?

A 
LMNOP + identify underling cause
Lasix
Morphine (anxiety + vasodilation)
Nitrates
Oxygen 
Position (upright)
**aimed at reducing LV preload + pulmonary capillary hydrostatic pressure
147
Q

Why is afib so detrimental in restrictive heart disease?

A

Pressure gradient isn’t as large b/w atrium + ventricle; diastasis is reached faster and for longer, the atrial kick is V important

148
Q

3 main types of cardiomyopathy

A

Dilated, hypertrophic, restrictive

149
Q

Dilated cariomyopathy involves impaired…

A

Systolic contraction

150
Q

Arrhythmia treatment in dilated cardiomyopathy?

A

Antiarrhythmic drugs actually tend to WORSEN the arrhythmias in DCM
ICD is recommended

151
Q

Best option in many very symptomatic patients w/ dilated cariomyopathy?

A

Heart transplant, but often not possible :(

152
Q

Key component of DCM treatment other than treating HF & arrhythmia?

A

Systemic anticoagulation to prevent thromboembolism!

153
Q

What causes hypertrophic cardiomyopathy?

A

Autosomal dominant GENETIC impairment of contraction (not due to pressure overload)

154
Q

In hypertrophic cardiomyopathy, what is impaired? What is the hypertrophy like?

A

CHAOTIC fibres, asymmetric, esp ventricular septum (diff than pressure overload which is uniform)
Impaired diastolic relaxation

155
Q

When a pt is diagnosed with hypertrophic cardiomyopathy, should asymptomatic family be screened

A

Yes! Autosomal dominant, risk of complications/death even if asymptomatic

156
Q

Gold standard for refractory hypertrophic cardiomyopathy

A

Myomectomy (excision)

157
Q

How does HCM w/ outflow tract obstruction (Hocum) work?

A

Ventricles contracts, blood flows through narrowed outflow tract, mitral leaflet pulled twd septum, obstructs aorta –> mitral regurg + outflow obstruction!

158
Q

What INCREASED obstruction in Hocum? DECREASE? (generally)

A

Anything that increases leaflet proximity to septum (e.g. positive inotropes, reducing LV size, exercise) & vv (LV enlargement/beta-blockers decrease it)

159
Q

Sudden death in HCM

A

VFib

160
Q

Orthostatic syncope in Hocum due to

A

Reduced venous return –> smaller LV, greater obstruction

*also syncope due to arrhythmias due to chaotic miofibers

161
Q

Angina in HCM is due to

A

Increased myocardiocyte O2 demand (higher pressure etc) and reduced supply (BV compression etc)

162
Q

What abnormal pulse do you get with hocum?

A

(Pulsus Bisferiens (outflow obstruction temporarily reduces flow)

163
Q

Maneuvers that increase and decrease outflow obstruction & murmur in hocum?

A

Valsalva + standing –> increase HCM murmur

Squatting –> decrease

164
Q

Maneuvers that increase/decrease murmur in AS?

A

Valsalva/standing –> decrease

Squatting –> increase

165
Q

Medication for Hocum?

A

Beta-blockers (reduce O2 demand/OO (V size can increase more), fewer ectopic beats
**doesn’t slow disease progression or reduce sudden death

166
Q

Avoid what drugs with hocum?

A

Diuretics/vasodilators because reduce diastolic volume
Positive inotropes since increase contractile force
^both of above increase outflow obstruction

167
Q

Restrictive cardiomyopathy has pretty much the same signs/symptoms as ____, but distinguishing is important, why?

A

Constrictive pericarditis

Distinguishing important because pericarditis much more treatable

168
Q

MONABASH mnemonic for ACS acute management (NSTEMI)

A 
Morphine sulphate
Oxygen
Nitroglycerin
Aspirin
Beta blocker (metoprolol)
ACEi (watch BP)
Statin (high-intensity)
Heparin
169
Q

What is the mnemonic for don’t-miss diagnoses for chest pain?

A 
PETMAC
Pulmonary embolism
Esophageal rupture
Tension pneumothorax
Myocardial infarction
Aortic dissection
Cardiac tamponade
170
Q

What is MINS (definition + relevance)?

A

Myocardial injury after non-cardiac surgery
Asymptomatic
Prognostic!! Higher post-op mortality
Manage w/ anticoagulants/aspirin/statins
*Test trops after surg if >65, RFs, RCRI (Revised Cardiac Risk Index)

171
Q

What are Type 1 and Type 2 MIs?

A

Type 1 = Acute coronary obstruction (1A = plaque rupture/erosion w/ thrombus)
Type 2 = Oxygen supply-demand imbalance (atherosclerosis w/out rupture, vasospasm, coronary micro vascular dysfunction, excessive demand, etc.); 2A = fixed obstructive CAD, 2B = w/out fixed obstructive CAD

172
Q

Characteristics of aortic stenosis murmur

A

Crescendo-decrees endo
Systolic (b/w S1 and S2)
URSB
Pulsus parvis et tardis

173
Q

Differentiate typical, atypical, and non-cardiac designations of chest pain

A 
Typical = retrosternal, exceptional, relieved by rest/nitro
Atypical = 2/3 of above
Noncardiac = 0 or 1/3 of above (note: may still actually have cardiac cause!)

Preclerkship (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions