1
Q
HFrEF
HFpEF
A
LVEF < 40
LVEF > 50
2
Q
NYHA HF classification
A
1 - no limitations
2 - slight limitations, ordinary activity ok
3 - Limitations, less than ordinary activity causes issues
4 - can’t do physical activity without symptoms
3
Q
HFpEF
A
Diuretics, BP control
Definitely: SGLT2 inhibitors, loop diuretic if needed.
Can consider ARB/ARNi/spirinolactone, no benefit of BB or nitrate
4
Q
If at one point HFrEF but now improved > HFimpEF
A
Continue GDMT and device therapy indefinitely
5
Q
BP thresholds
A
Normal <120/80
Elevated 120-129/<80
Stage 1 - 130-139/80-89
Stage 2 - >140/>90
CRISIS - Higher than 180 and/or > 120
6
Q
Decreasing BP by 10 mmHg
A
Decrease risk of CAD and Stroke
7
Q
Lab testing for new diagnosis HTN
A
CBC, electrolytes, Cr, Lipids, A1c, TSH, urinalysis, urine albumin:creatinine ratio and protein:creatinine ratio
8
Q
First line Anti HTN
A
Goal HTN <130/80
CCB, ACEi/ARB, Thiazide
9
Q
Lifestyle modification of BP if
A
Low 1-year CVD risk (prevent < 7.5%)
AND
Average BP 130-139/80-89
After 3-6 months if no change > medications
10
Q
HTN plus BMI > 27
HTN plus BMI > 35
A
GLP1s, bariatric surgery, in addition to HTN medications
11
Q
CCB
A
Amlodipine - block L type voltage gated calcium channels
12
Q
ACE
A
Lisinopril
Enalapril
Inhibit ACE activity and Angiotensin II formation
Ideal for CKD with proteinuria, HF, diabetes
13
Q
ARB
A
Losartan
Inhibits angiotensin II from binding
CKD with proteinuria, HF diabetes
14
Q
Thiazide diuretic
A
Hydrochlorathiazide
Chlorthalidone
Blocks renal distal tubule sodium reabsorption
15
Q
Other options for HTN
A
Spinolactone (block MRA activity) - good for HF and primary hyperaldosteronism
Beta blocker (carvedilol, labetalol), good for heart failure or prior MI
Direct vasodilator (hydralazine) - dilates peripheral arteries
Central alpha 2 agonist (clonidine) - stimulates CNS alpha 2 receptors
Loop (furosemide) - inhibits sodium reabsoprtion in thick ascending tubule - good for CKD, HF with fluid overload
16
Q
BP treatment
A
Initiate Anti HTN with 2 first line agents of DIFFERENT class in stage 2 HTN >140/90
17
Q
Resistant HTN
A
> 3 anti HTN, with one being a diuretic and no BP control
18
Q
Refractory HTN
A
Greater > 3 anti HTN meds, 1 which is thiazide diuretic and 1 spironolactone without BP control
19
Q
Secondary HTN
A
OSA, CKD, primary hyperaldosteronism, drug/alcohol, renovascular HTN
20
Q
Renovascular HTN
A
Atherosclerosis, or young people (fibromuscular dysplasia)
21
Q
Unilateral renal artery stenosis > leads to decrease in perfusion > increase in renin»_space;> increase in Aldosterone > high BP
A
secondary hyperaldosteronism
vs primary HA which is does not lead to increase in renin
22
Q
Clue for renovascular HTN
A
Worsening kidney function after ACEi/ARB use
Severe HTN in patients with diffuse atherosclerosis, onset after 55, unexplained kidney atrophy, unilateral abdominal bruit, recurrent flash pulmonary edema
23
Q
Imaging for renovascular HTN
A
MR Angiogram, Spiral CT, kidney US with doppler
24
Q
Renovascular HTN treatment
A
Treat with ACEi/ARB - block the effect of increased RAAS
Revascularization
25
Screen for Primary hyperaldosteronism +/- hypokalemia
Resistant HTN, OSA, adrenal nodule on image, FH of early HTN or stroke (<40)
26
High Renin, High Aldo
Renal artery stenosis or renin secreting tumor
27
LOW renin, High aldo
Primary hyperaldosteronism
28
Low renin, low aldo
Cushing, 11 beta hydroxylase, 17 alpha hydroxylase deficiency
29
Primary hyperaldosteronism
Screning: plasma aldo/renin ratio. Prove non suppressible aldo production with saline infusion test, oral sodium test, adrenal CT/MRI
Tx: spironolactone or surgical tx
30
Cushing syndrome
Excess glucocorticoids
24 hr free cortisol, 1 mg dexamethasone suppression test
Adrenal CT/MRI and brain MRI
for dexamethasone test - Normal test is that cortisol is SUPPRESSED. If cortisol is NOT suppressed > cushings
high dose dexamethasone test tells you difference between central and peripheral. High dose will partially suppress cortisol if coming centrally, will not suppress peripheral cortisol production.
31
Pheochromocytoma
Chromaffin cells in adrenal medulla > excess catecholamines
- Severe HTN, headaches, sweating, palpitations
- plasma metanephrines concentration or 24 hour urine catecholamines
- Adrenal CT/MRI
32
HTN algorithm
ACEi/ARB + CCB/diuretic
ACEi/ARB + CCB + Diuretic
Resistant HTN: ACEi/ARB + CCB + Diuretic + spironolactone/other diuretic/beta blocker/alpha blocker
33
RF for ASCVD
primary hypercholesterolemia, metabolic syndrome, CKD, inflammatory conditions like psoriasis, RA, lupus, HIV, South asian ethnicity
Lipids:
Primary HC: LDL 160-1898, nonHDL 190-219
Elevated ApoB > 130, tested when TF > 200
elevated TGs > 175 non fasting
Elevated CRP> 2
Elevated lipoprotein > 50
ABI < 0.9
34
Daily low dose aspirin primary prevention
40-7o years old with higher ASCVD risk but no increased bleed risk
NOT routinely for:
> 70 years
Increased risk of bleeding
other sources say not use for > 60
35
Daily low dose aspirin secondary prevention
Hx of prior heart attack, stroke, bypass surgery or stent
unclear for elevated lipoprotein or atherosclerosis
36
Coronary calcium scoring and CT coronary angiogram
Calcium score - usually intermediate risk screen - risk bucket
Coronary CT angiogram - patients with angina symptoms
37
Carotid bifurcation disease
Carotid duplex, CT/MR angiography
Medical therapy: antiplatelet, lipid lowering, blood pressure lowering.
Revascularization: CEA, CAS, TCAR
38
Symptomatic carotid bifurcation stenosis > 50%
Revascularization promptly
39
TCAR stenting
Avoids catheter manipulation of the aortic arch in patients that are at high risk for traditional CEA
40
Asymptomatic patients
degree of stenosis is a surrogate for embolic risk
41
Symptomatic carotid patients
Revascularization
42
Asymptomatic patients
CREST2 trial evaluating. Medical therapy or revascularization depending on scenario
43
TCAR best for
Patients with prior neck surgery/radiation, contralateral laryngeal nerve palsy, contralateral carotid occlusion, high-risk surgical profile
CEA = first-line for most patients, especially >70 years old or with favorable anatomy.
TCAR (or transfemoral stenting) = considered if CEA carries high surgical risk (prior neck surgery/radiation, contralateral laryngeal nerve palsy, contralateral carotid occlusion, severe cardiopulmonary disease).
44
Aortic aneurysm
Fusiform - uniform dilation
saccular - only one part
penetrating aortic ulcer/pseudo-aneurysm - does not include all the layers of the vessel (sometimes from the vasa venorum)
45
Intramural aortic hematoma
No tear in the intima
46
Aortic aneurysm
Dilation (4-4.4)
Aneurysm (>4.5)
Ectasia
thoracic - 1.5x diameter
47
Sporadic aneurysm ascending aortic root
younger, FH
48
Sporadic aneurysm descending aorta
Older
Atherosclerosis risk factors
Aortic calcifications
49
Sporadic aneurysm
TTE at diagnosis, CT or MRI also ok
TTE, CT, MRI after 6-12 months and then if stable every 6-24 months
Treat BP and other risk factors
50
Marfan syndrome
Single mutant gene FBN1 (Fibrillin)
AD, equal sex
3/4 inherited, 1/4 sporadic
Diagnosis:
- Aortic root dilation AND ectopia lentis
- AR dilation and FBN1 mutation
- AR dilation and systemic score >.7
- Ectopia lentis and FBN1
Managmenet:
- 1. Echo follow up
- 2. BP control, Beta blocker or ARB
- Aortic root intervention
51
Loeys Dietz syndrome
AD CT
Aortic aneurysms, dissections, arterial tortuosity, high arched palate, abnormal ubula, hypertelorism
Craniosynostosis and cleft palate with TGFBR1 and TGFBR2
Osteoarthritis with SMAD3
Peripheral neuropathy with SMAD3
1. Head to pelvis imaging
2. Beta blocker/ARB
3. Surgery depends on mutation
(TGFBR1/2)
52
Vascular EDS
COL3A1
AD
- protruding eyes
- thin nose
- sunken cheeks
- small chin
-head to pelvis imaging
53
Bicuspid aortic valve
Male predominance
AD
associated with congenital heart defects and other syndromes like LD syndrome
- evaluate with echo or CT/MRI
- genetics to see if LD
- BAV and dilated aorta - screen first degree relatives
- Surgery
54
Turner's syndrome
XO
- CV defects like bicuspid aortic valve and coarcation of aorta, ASD, VSD, aortic aneurysm and increased risk of aortic dissection.
55
Aortic Dissection
Type A - ascending aorta
Type B - descending aorta
- ICU, beta blocker, BP monitoring
- Keep SBP < 120, heart rate 60-80
- Pain control
Type A - Immediate servical intervention, valve sparing
Type B - medical therapy, endovascular intervention if complicated
56
Abdominal aortic aneurysm
Age > 65, M>F, smoking, FH, atherosclerosis, HTN< dyslipidemia.
US screening in M>65 ever smoked, reasonable women > 65 ever smoked, or M/F>65 with first degree relative with AAA.
- Statin therapy (atherosclersois)
- Consider aspirin
- Surveillance
- Recommended if M > 5.5 and F > 5
57
PAD spectrum
Asymptomatic > Claudication (angina of leg) > chronic limb threatening ischemia > acute limb ischemia (STEMI of leg)
58
PAD affects
Women and men equally but worse in diabetic women. Higher in AA
59
Highest risk of PAD
older, smoker (present or former), diabetes
60
PAD risk factor
think smoking > significantly higher risk for PAD with smoking than other cardiovascular disease
61
Other PAD risk factors
Diabetes > higher chance of amputation
Dyslipidemia
Systolic HTN
62
Normal ABI
1-1.4
>1.4 - noncompressible arteries
<0.9 - abnormal ABI
0.9 - 0.99 borderline
63
Resting ABI
Divide higher of PT/DP pulse / higher of RUE or LUE
for UE, even if you calculate Left ABI and use left leg, use the highest of the upper extremity (either arm).
If resting is normal but high pretest probability > exercise ABI
64
PVR
change in limb volume with each pulse - represents pulse pressure x vascular wall compliance
Healthy - rapid upstroke, dicrotic notch > downstroke
PAD - loss of notch, upstroke delayed, decreased amplitude, decreased upstroke.
65
PVR phasic
Triphasic → normal arterial flow
Biphasic → mild–moderate arterial disease
Monophasic → advanced PAD with poor distal perfusion
66
PAD management
- exercise, lifestyle and risk modification, flu vaccine
- Antiplatelet therapy (ASA/Plavix)
- Statin (LDL < 55)
- ACE/ARB
- Smoking cessation
- Cilostazol - helps improve symptoms and walking distance (PDE3-i, increases cAMP and prevents platelet aggregation/direct arterial vasodilator). DO NOT USE IN HF patients
- if previous endovascular/revascularization > low dose rivaroxaban
67
Chronic limb threatening ischemia
Chronic (>2 weeks) ischemic rest pain, nonhealing wound or ulcer, gangrene. Low ABI does not mean CLTI.
68
Revascularization in claudication
Reasonable for lifestyle limiting claudication and inadequate response to GDMT
- do not perform to prevent progression to CLI
69
Endovascular strategy
more prevalent, used in high risk population
70
After endovascular revascularization
ASA or clopidogrel daily lifelong
low dose rivaroxaban 2.5 mg BID
High intensity statin goal LDL < 70
ACE inhbitor if possible
71
Acute limb ischemia of leg
Pain, pulselessness, pallor, parasthesias, paralysis
Thromboembolic process
Revascularization
72
ASCVD score > 7.5%
Start statin
73
LDL goals
LDL-C targets by risk category
Very high risk (e.g., established ASCVD, diabetes with target organ damage, severe CKD, recurrent events):
Target: <55 mg/dL (<1.4 mmol/L)
Aim for at least 50% reduction from baseline
High risk (e.g., markedly elevated single risk factors, diabetes >10 years, moderate CKD, SCORE ≥5%):
Target: <70 mg/dL (<1.8 mmol/L)
Aim for at least 50% reduction from baseline
Moderate risk:
Target: <100 mg/dL (<2.6 mmol/L)
Low risk:
Target: <116 mg/dL (<3.0 mmol/L)
🔹 Key points
The higher the baseline risk, the lower the LDL-C goal.
For patients at very high or high risk, absolute target AND ≥50% reduction are both emphasized.
In secondary prevention (established ASCVD), intensive lipid-lowering is recommended, often requiring statins plus ezetimibe or PCSK9 inhibitors.
✅ Summary:
LDL targets are tiered by cardiovascular risk:
<55 mg/dL (very high risk)
<70 mg/dL (high risk)
<100 mg/dL (moderate risk)
<116 mg/dL (low risk)
74
Statins
- stabilize plaque, reduce inflammation, reduce endothelial dysfunction, plaque regression.
- Better LDL lowering than ezetimibe
- better cost than PCSK9
- works at HMGcoA reductase
- myalgias, liver enzyme elevation, glucose intolerance side effects
75
High intensity statins
Atorvastatin 40-80
Rosuvastatin 20-40
76
Statins algorithm
Clinical ASCVD (<75 yrs) → High-intensity statin
LDL ≥ 190 mg/dL (age 20–75) → High-intensity statin
Diabetes (age 40–75) + multiple ASCVD risk factors → High-intensity statin
10-yr ASCVD risk ≥ 20% (age 40–75) → High-intensity statin
77
Statins algorithm decision tree
78
Ezetimibe
- cholesterol absorption inhibitor
- inhibits NPC1L1 protein
- impairs dietary and biliary cholesterol absorption at brush border
- net decrease in cholesterol absorption
- 20 % LDL lowering (vs 50% statin)
79
PCSK9 0 evoluvumab/repatha
removes LDL
80
Statin intolerant
Bempedoic acid (ATP-citrate lyase inhibitor) – last line after tried everything else above
81
Doses of statins
High intensity statins = atorva 40-80, rosuva 20-40
Low intensity statins = simva 10, prava 10-20, lova 20, fluva 20-40
(all the other combos are mod intensity)
82
Triglycerides
<150 normal
moderate is 150-499
400-999 mod/severe
severe > 1000
83
Moderate 150 - 85 TG
Lifestyle intervention, LDL, ACSVD risk assessment
- high dose omega 3 fatty acid
- fibrate therapy
Net lipid changes with a fibrate:
↓↓↓ Triglycerides
↓ LDL
↑ HDL
84
Severe TG > 885
Strict diet, avoid alcohol, limited drug effectiveness until levels decrease
85
Familial chylomicronemia syndrome
- severe hyper TG, biallelic loss of function in lipoprotein lipase genes (LPL)
- treatment: olezarsen 80 mg SQ once per month
Reduce TG by 40% at 5 weeks
very strict diet
AVOID omega 3 fatty acids
86
Statins goal
Reduce ASCVD risk
reduce VLDL and TGs
Pancreatitis risk reduction
can be beneficial in hyper TG
87
Fibrates
Downregulate APOC3 (inhibitor of Lipoprotein Lipase) and upregulate apolipoprotein A1
Reduce TG
Elevate HDL
Reduce LDL
Preferred fenofibrate 145 mg daily
can cause liver enzyme elevation, muscle pain, increase serum cr
88
Omega 3 fatty acids
Reduce hepatic secretion of TG rich lipoproteins
Lower serum TG
89
Summary of lipid treatments
90
Cold and wet management
91
92
Why did the cold and wet patient decompensate so fast after being given CCB for Afib with RVR
93
Cold/Wet/Dry/Warm with RHC values
“Cold” → low output → cool extremities, weak pulses, low SvO₂.
“Wet” → high PCWP → pulmonary edema, elevated JVP, crackles.
“Dry” → no pulmonary congestion → normal lungs, flat neck veins.
“Warm” → preserved output → warm extremities, good perfusion.
94
Defibrillation
non synchronized shock
used for Vfib, pulseless Vtach
95
Synchronized cardioversion
Shock is synchronized to QRS complex
not usually used in cardiac arrest
96
STEMI
Emergent coronary angiography
97
Without STEMI
safe to delay and stabilize
consider delayed coronary angiography if suspected cardiac cause of arrest, LV dysfunction, recurrent ventricular arrhythmias.
98
TTM
Brain injury main cause of death from cardiac arrest
- Cool within 1-2 hours and maintain for 24 hours
99
Shockable rhythms
100
PEA, check for H and T's
Hs
Hypovolemia – severe blood/fluid loss
Hypoxia – inadequate oxygenation
Hydrogen ion (acidosis) – metabolic/respiratory acidosis
Hypo-/hyperkalemia – electrolyte derangements (especially potassium)
Hypothermia – low body temperature
Ts
Tension pneumothorax – obstructed venous return, impaired filling
Tamponade (cardiac) – fluid in pericardium compresses heart
Toxins – drug overdose, poisoning (e.g., TCAs, digoxin, beta-blockers, calcium-channel blockers)
Thrombosis (pulmonary) – massive pulmonary embolism
Thrombosis (coronary) – acute myocardial infarction
101
WHO Group 1 PAH
Idiopathic PAH, heritable, drug/toxin induced, PAH with CTD, HIV, Portal HTN
- Who group 1 (precapillary)
102
Who Group 2 PH
due to left heart disease
- systolic dysfunction
- diastolic dysfunction
- valvular disease
- Post capillary PVH
103
Who group 3
PH due to lung disease/hypoxia
- COPD
- ILD
- Sleep disordered breathing
- chronic exposure to high altitude
- capillary bed, lung disease
104
Who Group 4
Chronic PE
- Precapillary in the artery
105
Who Group 5
PH due to multifactorial reasons
- hematologic disorders (anemia)
- systemic disorders like sarcoid
- metabolic disorders
106
Workup for PH
CT chest, PFTs, Echo
107
Echo of PAH
Normal LA, LV, no LVH
Septal bowing
pericardial effusion
108
Echo of PVH
Dilated LA, dilated LV, variable EF, MR, diastolic dysfunction
109
PAH
mPAP > 20
PCWP < 15
PVR > 3 wood units
110
PVR can be variable
mPAP > 20
PCWP > 15
111
PH with lung disease
mPAP > 20
chronic lung disease
112
PH due to Chronic PE
mPAP > 20
PCWP < 15
chronic perfusion defects
Similar to group 1 stats
113
Prognosis of PH
Prognosis: determined by clinical signs of right HF, progression of sxs, syncope, WHO class, exercise testing, BNP, imaging (RA area big is bad), hemodyanmics (RAP high is bad)
114
PAH Treatment (group 1)
Pulmonary vasodilator therapy
sildenafil, tadalafil, sotatercept (increase Hgb, bleeding/epistaxis, HIIT like illness)
115
Group 2 PVH
Optimize heart failure medications and diuresis
- pulmonary vasodilators may cause pulmonary edema
- PDE5 inhibitors
116
Who group 3 PH lung disease
Optimize lung disease medications
reverse hypoxia
- PDE5 inhibitors
- Transplant evaluation
- prostacyclin in ILD?
117
Who group 4 Chronic PE
Anticoagulate
pulmonary vasodilators
thrombo-enarterectomy
Get echo and VQ scan, confirm with right heart cath/ pulmonary angiography MRA, assess risk
118
Chronic PE what scan
VQ scan more sensitive than CTPA
- Look for web defect on pulmonary angiogram
119
sGCS agent is riociguat
for PH?
study in inoperable or persistent CTEPH > improved outcomes and exercise capacity
120
Surgical options for PH
Lung transplant
PTE
Atrial Septostomy
RVAD - right ventricular assist devices
121
PVH images
122
Right heart cath PH
123
Who Group 1
124
Who Group 2
125
Who group 3
126
Who group 4
127
Procedures for PH
Pulmonary endarectomy - Chronic PE
lung transplant - PAH (group 1)
128
HTN emergency
BP > 120 and/or 120 plus organ damage
129
HTN urgency or severe htn
severe htn without organ damage
130
End organ damage
HF, pulmonary edema, ACS, Acute renal failure, hematuria, proteinuria, enceleopathy, stroke, aortic dissection, papilledema, Micrioangiopathic hemolytic anemia
131
HTN Emergency
- continuous BP monitoring, IV rapid acting infusion, avoid large swing in BP
- reduce NO MORE than 25% in first hour, if stable reduce to <160/100 in next 2-6 hours.
- then SLOWLY to 130-140 over next 24-48 hours.
SLOW to avoid organ injury
132
Exceptions to HTN emergency rules for lowering
Acute aortic dissection - reduce systolic to <120 in first hour
Acute intracranial hemorrhage - 130-140 systolic target, DO NOT GO LOWER
Pheochromocytoma crisis < 140 in the first hour
133
Meds Acute HTN
Med options: CCB (Nicardipine), NO vasodilators (nitro, sodium nitroprusside), direct vasodilators (hydralazine), B1 antagonist (esmolol), a1 and BB (labetalol), nonselective a and B blockers (phentolamine), D1 agonist (fenolodopam), ACE (enalapril)
134
BP meds
135
HTN meds for conditions
136
Asymptomatic severe HTN
- Avoid short acting IV or parenteral agents as can cause AKI, hospital stay, higher mortality
137
HTN emergency and severe HTN
138
Aortic dissection severe HTN
< 120 systolic at 1 hour
Esmolol or labetolol - decrease BP and HR to minimize shearing forces across dissection
139
Acute hypotension
BP < 90 and/or 60
140
Shock
Distributive (dec SVR) - septic vs nonseptic (anaphylaxis, transfusion reaction, liver failure
Hypovolemic (dec preload) - bleeding/volume depletion
Obstructive (dec CO) - PE, tamponade, tension pneumothorax
Cardiogenic (dec CO) - MI, HF
141
Assessment for hypotension
Preload - fluid bolus/type and screen
SVR - vasopressors (phenylephrine (alpha 1), epinephrine (alpha 1 and beta 1), NE (alpha 1 > beta 1), dopamine (Alpha 1, beta 1, dopamine 1), vasopressin (V1). if rash > epinephrine
CO - For dec CO positive inotropy with vasoconstriction (NE, Epi, dopamine) Other inotropry drugs like dobutamine and milrinone also vasodilate, NOT good for acute hypotension.
Overdose - reversal agents like flumazenil for benzos, naloxone opiates, glucagon beta blocker)
Acute vagal episode - atropine, fluid bolus
142
Acute HTN
Preferred agents include IV nitroprusside, labetalol, or nicardipine. Nitroprusside, in particular, is widely used because of its quick onset (< 1 min) and broad applicability to various hypertensive emergency syndromes. It is important to reduce blood pressure slowly, i.e., by a maximum of 25% within the first hour, to prevent coronary insufficiency and to ensure adequate cerebral perfusion.
Nitroprusside reduces renal perfusion and should be avoided in patients with acute renal failure.
143
Cerebral performance categories scale
CPC1 - conscious, able to work, alert, might have some deficits
CPC2 - concious, can be independent, able to work in sheltered environment
CPC 3 - conscious, dependent for support - can be ambulatory or severe dementia or paralysis
CPC4 - coma
144
Delayed awakening > 48 h frequent
many have no pupillary reflex or motor response 48 hours after sedation discontinued.
RF: > 59, post resuscitation shock, renal insufficiency, shock liver, post anoxic status epilepticus
145
Neuroprognostication
Exam - 72 hours or more from arrest or reworming
- general exam, focus on coma evaluation
- absent pupillary/corneal reflex > increase poor outcome prediction
- early motor withdrawal may suggest a decreased ischemic injury burden
- image at 72 hours
146
Four score for neuroprognostication
147
EEG in neuroprognostication
- Absent reactivity, burst suppresion, voltage attenuation, epileptiform discharge > poor outcomes
- early findings of reactivity > increase likelihood of good outcome
- later > 36 hours, study with normal reactivity > also reassuring
148
Somatosensory evoked potenials SSEPs
N20 peaks > if absent > increase likelihood of poor outcome. Amplitude of N20 also might predict good outcome
149
Neuron specific enolase
can suggest ongoing brain injury
150
Tests for neuroprognostication
Neurophysiology EEG - initial, every 1h at first 12h
Clinical exam with pupillary and corneal reflexes - 72 h after rewarming
MRI - 3-5 days after arrest
151
Adenosine
Only if regular, monomorphic
🔎 Why adenosine can be given
In confirmed regular monomorphic VT, adenosine can be tried as a diagnostic and sometimes therapeutic tool.
Rationale:
Some arrhythmias that appear as monomorphic VT are actually SVTs with aberrant conduction (e.g., AV reentrant tachycardia with bundle branch block).
Adenosine blocks AV nodal conduction, which may:
Terminate reentrant SVTs that depend on the AV node.
Fail to terminate true VT, but this helps confirm the diagnosis.
Therefore, adenosine may be useful when the rhythm is stable and regular, and when the diagnosis is uncertain.
It is contraindicated in:
Polymorphic VT (e.g., torsades de pointes) → risk of ventricular fibrillation
Irregular wide-complex tachycardias (e.g., pre-excited AF) → risk of VF
152
Monomorphic Vtach
Synchronized cardioversion
Adenosine IV Dose
Infusion - Amio, Lidocaine, procainamide
Maybe IV beta blockers EXCEPT for if risk of HF decompensation
153
Procainamide
Prolongs the action potential and refractory period, especially in ventricular myocardial cells.
Slows the conduction
154
WPW
Cardioversion
Procainamide
NO BB, CCB, Adenosine >> can precipitate Vtach
155
Vfib
Pulseless VT/VF protocol > defibrillate
Epinephrine, amio, lidocaine after unsuccessful shock
156
Lidocaine
Good for ischemic VT/VF
157
Complete heart block
Can administer atropine/dopamine/epi but don't usually work (function at AV node).
PACE
Causes:
RCA infarction (supply AV node artery)
electrolyte abnormality (hypokalemia)
Medication toxicity - bb, ccb, amio
158
Torsades des pointes (QT prolongation)
Magnesium infusion
Increase sinus rate (dopamine, isoproterenol, pacing)
Meds that cause QT prolongation:
1. Class III AADs
2. Macrolide antibiotics
3. antiemetics
4. Antidepressants
Electrolyte disturbances: HypoK, HypoMg
Bradycardia
Ischemia, polymorphic VT
159
Type 1 MI
Acute plaque rupture
STEMI, NSTEMI, unstable angina
160
Type 2 MI
supply demand ischemia
161
Troponin elevation without MI - NIMI
Myocardial necrosis, but not due to myocardial oxygen supply
- toxin mediated, myocarditis, blunt trauma
162
Acute MI
Troponin 15 for females or 20 for males
Rise and fall delta 20%
Symptoms: ischemic ecg changes, ischemic imaging change like new wall motion abnormality or perfusion defect
Need both of trop and one symptom/imaging finding
163
STEMI
ST elevation
T wave inversion
164
Coronary distribution
165
STEMI
Narcotic (fentanyl > morphine)
O2 (only to 90%)
Nitrates
Aspirin ****
Beta blockers (not in shock, or bradycardia)
Antiplatelet therapy: aspirin and clopidogrel (p2y12 platelet inhibitor)
Heparin (binds to antithrombin, blocks thrombin and factor Xa activation).
Statin therapy -- acutely stabilizes vulnerable plaque
ACE/ARB/Spironolactone
REPURFSION
166
Cardiogenic shock
complication of anterior stemi
- hypotension, narrow pulse pressure -- hypoperfusion
elevated JVP
pulmonary edema (rales)
cool extremeties
renal failure
167
Delayed complications of MI
LV thrombus - higher risk of CVA in post MI period
Ischemic ventricular septal defect
ventricular free wall rupture
168
Unstable angina
Typical ischemic CP at rest
crescendo angina in patient with previously stable symptoms
New onset chest pain
169
ASC Midterm
flashcards
Decks in class (5)
# Cards
