Angina, ACS, Hypertension, Heart failure Flashcards
1
Q
Most hypertention cases in adults are what type?
A
Primary (essential)
No specific cause
2
Q
What is cushing’s triad and what does it indicate?
A
Hypertension + bradycardia + irregular respirations (Cheyne-Stokes)
= high ICP
3
Q
Estrogen and hypertension?
A
Endogenous is protective against Ht/coronary heart disease
Oral increases BP, coagulopathy
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
5
Q
Almost any ___ can trigger hypertension. Disorders that ______ lead to mechanisms that increase systemic BP
A
Renal disease
Decrease renal perfusion
6
Q
Nonspecific symptoms of hypertension
A
Headaches (esp morning) Dizziness, tinnitus, blurry vision Flushing Epistaxis Chest discomfort, palpitations, bounding pulse Nervousness/sleep issues
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
8
Q
Isolated systolic hypertension: 2 main mechanisms
A
1) Age –> reduced arterial compliance
2) High CO (aortic regurg, hyperthyroidism, etc)
9
Q
BP much higher in upper limbs than lower limbs may indicate
A
Coarctation of aorta distal to the L subclavian
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)
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)
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+
13
Q
Don’t combine ____ with ACEi/ARBs
A
Direct renin inhibitors
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)
15
Q
What might you heart on heart auscultation in chronic htn?
A
S4
16
Q
Hypertensive nephropathy leads to what type of nephrotic syndrome?
A
FSGS
17
Q
Cutoffs for hypertensive urgency/emergency?
A
180+ and/or 120+
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)
19
Q
Feature of renal artery stenosis on clinical exam
A
Abdominal bruit over flank or epigastrium (syst-diast)
20
Q
Renal artery stenosis might have what electrolyte imbalance?
A
Hypokalemia (RAAS!)
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
22
Q
Imaging to diagnose RAS?
A
Duplex US (doppler) CT or MR angiography
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)
24
Q
Triple whammy of kidney meds
A
Diuretics + NSAIDS + ACEi
25
Pathophys of NSAIDs causing AKI
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)
26
"Viability imaging" (e.g. PET, dobutamine echo) can differentiate between what?
```
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
27
What is the clinically relevant difference between hibernating & infarcted myocardium?
Infarcted will not regain contractile function even if revascularized
Hibernating needs revascularization in order to start working again
28
Is variable threshold angina always unstable angina?
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
29
Causes of unstable angina
Plaque rupture
Platelet aggregation
Thrombus formation
Unopposed vasoconstriction
30
What is variant angina? AKA? 3 causes?
AKA Prinzmetal angina
Focal artery spasm w/out over atherosclerotic lesions
Cocaine, alcohol, triptans
31
What extra heart sound might you hear during myocardial ischemia and why?
S4 (stiff ventricle) because ischemia reduces diastolic compliance
32
Ischemia is common in what layer of heart tissue?
Subendocardium (farther from large vessels, pressure from ventricular chamber, few collaterals)
33
Most common changes on EKG during cardiac ischemia?
Transient ST-segment depressions and T-wave flattening/inversion
34
EKG change during Prinzmetal's angina?
ST elevation
| Diff than STEMI because transient & reversible w/ vasodilators
35
Signs of a positive exercise stress test (5)
```
Drop in BP
Replicated chest pain
Ischemic EKG changes
High-grade ventricular arrhythmia
Exercise intolerance <2min for cardiopulmonary reason
```
36
What do you do in a stress test if patient has a baseline EKG abnormality (e.g. LBBB)
Nuclear imaging (inject IV radionuclide @ peak exercise --> accumulates proportionally to viable myocardial cells)
37
Explain "cold spots" on nuclear imaging during stress test
Ischemic or infarcted
| Repeat at rest to tell, if temp ischemia will fill in
38
When is exercise echocardiography stress test done?
Same as nuclear (i.e. when results don't make sense or baseline EKG abnormalities)
39
How do you perform a stress test if the pt can't exercise? (2 methods + indications)
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
40
What is the gold standard for CAD diagnosis? What is a less-invasive alternative
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)
41
Cardiac catheterization: inserted via what arteries?
Femoral or radial
42
Nitroglycerin is a ___dilator
VENOdilator
43
3 main ADEs of nitrates + solution for one of them
Headache
Hypotension
Reflex tachycardia due to venodilation reducing CO (coadmin w/ BB or CaB)
44
What are the 2 modes of delivery of organic nitrates for myocardial ischemia, and indication for each?
Sublingual: during acute attacks of prophylaxis before provoking activity
Oral/transdermal: chronic daily use (SYMPTOM relief only, doens't prolong survival)
45
How does nitro work for ischemia
Reduces O2 demand (reduces preload through venodilation)
| Increases O2 supply (more perfusion, less vasospasm)
46
How do beta blockers work for ischemia
Reduces O2 demand (lowers contractility/HR)
| Increases O2 supply (longer diastole --> more perfusion)
47
5 main ADEs of beta blockers
```
Excessive bradycardia
Reduced LV contractile function
Fatigue
Hypoglycemic unawareness
Bronchoconstriction
```
48
What is the difference between dihydropyridine and nondihydropyridine Ca-channel blockers in terms of mechanism? Examples?
Dihydros: Nifedipine - vasodilation
| Non-dihydros: Verapamil = cardiac depression (reduce contractility/HR)
49
Name 3 drugs that help SYMPTOMS of coronary ischemia and 4 drugs that reduce RISK OF MI/DEATH
Symptoms: nitrates, BBs, CaBs
| MI/death: Aspirin and/or P2Y12 antagonists, Statins, ACE-inhibitors
50
____ should be continued indefinitely in all CAD patients unless contraindicated (allergy, gastric bleeding).
Aspirin
51
High-intensity ____ regiment to achieve 50% ___ reduction recommended in all coronary ischemia patients (even if baseline below threshold)
Statin
52
Do PCIs reduces MIs/death in stable CAD?
No
53
2 types of PCI
```
Balloon angioplasty (percutaneous transluminal coronary angioplasty)
Stents
```
54
CABG stands for
Coronary Artery Bypass Graft Surgery (using patient's native BVs)
55
Critical narrowing of what artery threatens most of the L ventricle? Branches off what?
Left anterior descending artery (AKA anterior interventricular artery) which branches off the L coronary artery
56
What are the 4 classes of ischemia according to the Canadian Cardiovascular Society? Which warrant hospitalization?
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
57
Usually coronary pathology & myocyte necrosis?
Unstable angina =
NSTEMI =
STEMI =
```
UA = partially occlusive thrombus, No
NSTEMI = partially occlusive thrombus, Yes
STEMI = fully occlusive thrombus, Yes
```
58
90% of ACS results from...
Rupture of atherosclerotic plaque (e.g. SNS activation, high BP) --> platelet aggregation --> thrombus formation
Superficial plaque erosion can also cause it (more rare)
59
Exposure of what substance (e.g. during atherosclerotic plaque rupture) results in white thrombus formation
Collagen!
| vWF in blood binds collagen which then binds vWF on platelets
60
What substance is synthesized by COX1 and released during platelet hemostasis? Role? Clinical relevance?
TXA2 (thromboxane A2) --> vasoconstriction + more platelet activation
NSAIDS/aspirin!
61
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?
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
62
What part of platelet hemostasis does clopidogrel impact?
P2Y12 inhibitors = ADP receptor inhibitors, prevent platelet activation irreversibly
Duration of action ~7 days (like aspirin), platele lifespan
63
Mechanism of GPIIb/IIIA inhibitors
| Administered how?
Prevent aggregation of platelets + fibrinogen binding & cross-linking
Administered inpatient IV (e.g. during ACS)
64
A partially occlusive thrombus will show what on EKG? How to differentiate between UA & NSTEMI (diff test)?
```
ST depression and/or T-wave inversion
Check troponins (+ in NSTEMI only)
```
65
Mechanism by which cocaine can cause MI?
Severe coronary artery spasm
66
In gradual atherosclerosis w/ brief preceding ischemias you're more likely to get a (STEMI/NSTEMI)? more or less likely to survive?
NSTEMI because gradual process allows angiogenesis of collateral ("ischemic preconditioning"); also more release of mediators like adenosine, bradykinin. More likely to survive
67
___ % of MIs are asymptomatic, esp in ___ patients
```
25%
Diabetic patients (neuropathy)
```
68
What reflex causes dyspnea in MI?
J reflex
Ventricular dysfunction --> pulmonary/alveolar congestion --> stimulates juxtacapillary ("J") receptors --> rapid/shallow breathing + dyspnea
69
Does MI cause systolic or diastolic dysfunction?
Both! Relaxation is also ATP-dependent
70
What can happen to noninfarcted parts of heart during ventricular remodelling post-MI
Possible treatment for prevention?
Dilation because overworked --> HF, arrhythmias
| Combat w/ RAAS inhibitors
71
What structually happens to infarcted area a few days following MI?
"Yellow softening" (macrophages removing dead myocardium, before scar tissue generated) - weaker, dilates; risk of aneurysms
72
Name 3 cardiac signs during MI (not EKG)
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
Pathological S3 = ___gallop
| S4 = ___ gallop
```
S3 = Ventricular gallop (dilated ventricle, or increased flow e.g. regurg)
S4 = atrial gallop (stiff ventricle)
```
74
EKG difference between STEMI and pericarditis?
Both have ST elevation
STEMI: only in leads overlying infarction
Pericarditis: DIFFUSE ST-elevation (all leads except aVR + V1)
75
Does an NSTEMI feel more like a STEM or UA?
more like a STEMI (prolonged "crushing" pain etc)
76
2 cardiac troponins
| Indicate what?
cTnI & cTnT
| Injury to cardiomyocytes
77
Name 4 conditions other than MI where troponins may be detectable
PE
Myocarditis
Pulmonary embolism
Heart failure
78
Troponins rise___after discomfort starts, peak @___, decline slowly (detectable for __ days after large MI!)
Troponins rise 3-4h after discomfort starts, peak @18-36 hours, decline slowly (detectable for 10 days after large MI!)
79
How is treatment for STEMI decided?
Emergent PCI available within 90 min (or 120 min if transferring)? Yes --> PCI
No --> fibrinolytics (if not contraindicated)
80
4 categories of concurrent treatment for ACS
1) Anti-ischemics
2) Anti-thrombotics
3) Adjunctives (Statins, ACEi)
4) Supportive (O2 for hypoxemia, morphine for pain/anxiety)
81
2 main treatment approaches for UA/NSTEMI and how you choose
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
What are the 3 anti-ischemic therapies used in AU/NSTEMI? Which has some mortality benefit?
B-blockers (target = 60bpm, initiate within first 24 hours) - some mortality benefit!
Nitrates (symptoms)
Ca channel blockers (no mortality benefit)
83
Antiplatelet therapy in UA/NSTEMI
| indicate types, how many, mortality benefit
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
Anticoagulant therapy in UA/NSTEMI
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
When are fibrinolytics appropriate for UA/NSTEMI?
NEVER, only for STEMI
86
What is the main cause of sudden cardiac death during acute MI?
Ventricular fibrillation
87
Beck's triad cardiac tamponade
Hypotension
Muffled heart sounds
Distended neck veins
88
Treatment of acute tamponade
Pericardiocentesis
89
Sign of tamponade on EKG
Electrical Alternans (QRS complexes have diff heights due to swinging of heart)
90
Name 5 main complications of ACS
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
Cardiac tamponade after MI could be caused by what 2 things?
Ventricular rupture due to tissue necrosis
| Pericarditis
92
2 med categories for cardiogenic shock
Inotropes
| arterial vasodilators
93
Name 5 predictors of poor post-MI outcomes
1) Extent of LV dysfunction (most important)
2) Early recurrence
3) Severe CAD
4) High-grade ventricular arrhythmia
5) Very abnormal stress test
94
Standard post-discharge therapy after MI (7)
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
What is a pseudoaneurysm
Incomplete rupture with thrombus "plugging" the hole - ticking time bomb, must detect & repair surgically asap!! (rupture --> tamponade)
96
Describe pericarditis after MI (pathophys + timeline)
Inflammation spreads from myocardium --> pericardium
| Usually in-hospital (early); rarely can occur weeks later = Dressler syndrome
97
CO =
SV x HR
98
Afterload is approximated by
Systolic ventricular/arterial pressure
99
Preload is approximated by what? What does it represent?
Ventricular end-diastolic volume or end-diastolic pressure
| =stretch on ventricular fibers just before contraction
100
What 3 factors influence stroke volume
Preload
Afterload
Myocardial contractility
101
SV = ___ - ____
EDV - ESV
102
EF = ?
| Normal range?
```
EF = SV / EDV
Normal = 55-75%
```
103
Compliance =
change in volume /change in pressure
104
What is diastasis?
Lull when initial passive filling of ventricle has slowed, before atrial contraction
105
EDV depends on ___ and represents ___; ESV depends on ___ & ____
EDV: compliance, preload
ESV: afterload, contractility
106
Is LHF or RHF most commonly seen clinically?
Actually, BIventricular is most commonly seen!
107
Describe HF with reduced EF
Mostly systolic issue; reduced contractility or increased afterload (resistance to flow)
108
Describe HF with sustained EF
Mostly diastolic issue;
| Impaired early diastolic relaxation (active process) or increased stiffness of V wall (passive), or external restriction
109
name 2 things that can cause chronically high afterload
1) Aortic stenosis
| 2) Severe hypertension
110
Name 3 things that can cause impaired contractility leading to HF-REF
1) CAD (--> ischemia/MI)
2) Chronic volume overload (regurg)
3) Dilated cardiomyopathy
111
Restrictive cardiomyopathy would cause what type of HR?
HF-PEF
112
L ventricular hypertrophy would cause what type of HF?
HF-PEF
113
R heart is susceptible to failure due to what mechanism?
High afterload (rather than high filling V)
114
R heart failure caused by primary pulmonary disease =
Cor pulmonale
115
BP = ___ x ___
CO x TPR
116
What are natriuretic peptides and what is their clinical significant?
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
Does heart failure manifest as orthopnea or platypnea?
Orthopnea! Difficulty breathing when flat (sleep with more pillows, PND)
118
S3 gallop = ___ dysfunction
S4 gallop = ____ dysfunction
[systolic/diastolic]
```
S3 = systolic
S4 = diastolic
```
119
Stages of HF (A - D)
```
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
What abnormal pulse might be observed in pt w/ HF & advanced ventricular dysfunction
Pulsus alternans (strong-weak alternating contractions)
121
What type of abnormal breathing pattern may be present in a pt w/ advanced HF?
Cheyne-Stokes breathing (inadequate perfusion of resp centre in brain)
122
What is cardiac asthma? Possible cause?
wheezing due to compression of airways by pulmonary edema
| e.g. during L-HF
123
Kussmaul sign could indicate __ HF
Right
| increased JVP during inspiration
124
Do pleural effusions happen in LHF or RHF?
Either! because pleural veins drain into both systemic + pulmonary venous beds
125
Radiographic findings when PCWP (~L atrial pressure) > 15 mmHg
BVs in upper lung larger than lower
| ="upper zone vascular redistribution" (because edema compresses @ base)
126
Radiographic findings when PCWP (~L atrial pressure) >20
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
Radiographic findings when PCWP (~L atrial pressure) >25
Opacification of air spaces;
Perihilar "batwing" appearance
= alveolar pulmonary edema (lymph failing to drain interstitium enough)
128
Cardiomegaly on radiograph =
Cardiothoracic ratio > 0.5
129
What on transverse CT is the correlate of Kerley-B lines on radiograph?
Thickening of septal lines
130
Gold standard test for diagnosing HF
Echo
131
Do diuretics target preload or afterload in HF?
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
Example of standard HF therapy sequence for REDUCED EF (4 steps)
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
If on ACEi + aldosterone antagonist, pt must be monitored for
Hyperkalemia
134
How do B-blockers work in HF-REF? What is the caution?
Increase cardiac output, anti-ischemic properties, blunt SNS
| Caution: negative inotropes, can induce acute deterioration
135
What drugs can be used to address the contractility aspect of HF? Which type of HF?
```
Positive inotropes (increase intracellular Ca) - for SYSTOLIC dysfunction (HF-REF)
e.g. digoxin
```
136
What positive inotropes can be used in acute HF? (via IV)
B-adrenergic agonists (dobutamine, dopamine)
| PDE-3 inhibitors (milrinone)
137
First line chronic therapy for LV systolic dysfunction =
ACE inhibitors (e.g. ramipril)
138
What is a mechanistic advantage of ACEi > ARBs?
ACEi increase bradykinin --> vasodilation
139
Role of nitrates in heart failure
Venous vasodilators --> reduce venous return/preload
140
What is an arteriolar vasodilator that can be prescribed to reduce afterload in HF-REF?
Hydralazine
141
What is indicated in many pts w/ HF-REF & LVEF <35%? Purpose?
ICD implantation (treat arrhythmias & prevent sudden cardiac death even if no preexisting arrhythmia)
142
2 fundamental principles of treating HF-PEF?
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
How is a pt w/ acute HF exacerbation classified?
```
Fluid overload (wet/dry) - LV filling pressure/congestion
Tissue perfusion (cold/warm) - CO, SNS vasoconstriction
```
144
What are the 2 main goals during an acute HF exacerbation?
1) Normalize ventricular filling
| 2) Restore tissue perfusion
145
Frothy sputum is a sign of...
pulmonary edema (fluid in alveoli)
146
Acute management of pulmonary edema mnemonic + overall aim?
```
LMNOP + identify underling cause
Lasix
Morphine (anxiety + vasodilation)
Nitrates
Oxygen
Position (upright)
**aimed at reducing LV preload + pulmonary capillary hydrostatic pressure
```
147
Why is afib so detrimental in restrictive heart disease?
Pressure gradient isn't as large b/w atrium + ventricle; diastasis is reached faster and for longer, the atrial kick is V important
148
3 main types of cardiomyopathy
Dilated, hypertrophic, restrictive
149
Dilated cariomyopathy involves impaired...
Systolic contraction
150
Arrhythmia treatment in dilated cardiomyopathy?
Antiarrhythmic drugs actually tend to WORSEN the arrhythmias in DCM
ICD is recommended
151
Best option in many very symptomatic patients w/ dilated cariomyopathy?
Heart transplant, but often not possible :(
152
Key component of DCM treatment other than treating HF & arrhythmia?
Systemic anticoagulation to prevent thromboembolism!
153
What causes hypertrophic cardiomyopathy?
Autosomal dominant GENETIC impairment of contraction (not due to pressure overload)
154
In hypertrophic cardiomyopathy, what is impaired? What is the hypertrophy like?
CHAOTIC fibres, asymmetric, esp ventricular septum (diff than pressure overload which is uniform)
Impaired diastolic relaxation
155
When a pt is diagnosed with hypertrophic cardiomyopathy, should asymptomatic family be screened
Yes! Autosomal dominant, risk of complications/death even if asymptomatic
156
Gold standard for refractory hypertrophic cardiomyopathy
Myomectomy (excision)
157
How does HCM w/ outflow tract obstruction (Hocum) work?
Ventricles contracts, blood flows through narrowed outflow tract, mitral leaflet pulled twd septum, obstructs aorta --> mitral regurg + outflow obstruction!
158
What INCREASED obstruction in Hocum? DECREASE? (generally)
Anything that increases leaflet proximity to septum (e.g. positive inotropes, reducing LV size, exercise) & vv (LV enlargement/beta-blockers decrease it)
159
Sudden death in HCM
VFib
160
Orthostatic syncope in Hocum due to
Reduced venous return --> smaller LV, greater obstruction
| *also syncope due to arrhythmias due to chaotic miofibers
161
Angina in HCM is due to
Increased myocardiocyte O2 demand (higher pressure etc) and reduced supply (BV compression etc)
162
What abnormal pulse do you get with hocum?
(Pulsus Bisferiens (outflow obstruction temporarily reduces flow)
163
Maneuvers that increase and decrease outflow obstruction & murmur in hocum?
Valsalva + standing --> increase HCM murmur
| Squatting --> decrease
164
Maneuvers that increase/decrease murmur in AS?
Valsalva/standing --> decrease
| Squatting --> increase
165
Medication for Hocum?
Beta-blockers (reduce O2 demand/OO (V size can increase more), fewer ectopic beats
**doesn't slow disease progression or reduce sudden death
166
Avoid what drugs with hocum?
Diuretics/vasodilators because reduce diastolic volume
Positive inotropes since increase contractile force
^both of above increase outflow obstruction
167
Restrictive cardiomyopathy has pretty much the same signs/symptoms as ____, but distinguishing is important, why?
Constrictive pericarditis
| Distinguishing important because pericarditis much more treatable
168
MONABASH mnemonic for ACS acute management (NSTEMI)
```
Morphine sulphate
Oxygen
Nitroglycerin
Aspirin
Beta blocker (metoprolol)
ACEi (watch BP)
Statin (high-intensity)
Heparin
```
169
What is the mnemonic for don't-miss diagnoses for chest pain?
```
PETMAC
Pulmonary embolism
Esophageal rupture
Tension pneumothorax
Myocardial infarction
Aortic dissection
Cardiac tamponade
```
170
What is MINS (definition + relevance)?
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
What are Type 1 and Type 2 MIs?
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
Characteristics of aortic stenosis murmur
Crescendo-decrees endo
Systolic (b/w S1 and S2)
URSB
Pulsus parvis et tardis
173
Differentiate typical, atypical, and non-cardiac designations of chest pain
```
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!)
```
