W12 Ischemic Heart Disease Flashcards
Schematic for ischemic heart disease / CAD / coronary atherosclerosis
What falls under ischemic heart disease 2
What falls under those two categories?
Ischemia = supply < demand
How can you increase supply? 4
How can you decrease demand? 2
(In terms of medication)
Supply — increase blood flow
—prevent thrombosis
—prevent atherosclerosis
— ⬆️ diastolic time
—dilate coronaries
prevent plaque build up, prevent clots, get more blood out, make it easier for the blood to travel through the coronaries
Demand — make the heart need less O2
—lower HR and contractility (beat less)
—lower systolic wall tension via preload & afterload
Treatment of CAD
Chronic stable angina: “BASA”
Unstable angina
NSEMI
STEMI
What are the contraindications and cautions for fibrinolytic therapy in patients with STEMI?
Mainly brain/bleed related
—cerebral vascular lesion
—intracranial neoplasm
—aortic dissection
—active bleeding
—closed head/facial trauma <3mo
—intracranial or intraspinal surgery <2mo
Thrombotic: antiplatelets vs anticoagulants
Why is ASA so important, what does it prevent?
What is the rule of thumb for preventing arterial clots
Venous clots?
ASA — it is an antiplatelet (platelet aggregation precedes fibrin formation)
- Antiplatelets for arterial clots
- Anticoagulants to prevent venous clots
Nitroglycerin — what is it for?
—fast-acting nitroglycerin (sublingual tablet or spray) for:
—any patient at risk for recurrent angina (ie, medically managed UA)
RANolazine (Ranexa)
MOA
2 therapeutic effects
2 main drug interactions
inhibition of late sodium influx into myocytes ↓contractility
Therapeutic effects
● prevents angina, esp if taken in combination w/ other antianginal meds
● improves exercise tolerance in patients w/ stable IHD
● antiarrhythmic properties (off-label) role in therapy: chronic angina, if refractory or intolerant to standard antianginal meds
Many drug interactions (major CYP3A4 substrate)
● non-DHP CCBs inc ranolazine levels
● statins - ranolazine can inc concentrations (must cap dose of simvastatin at 20mg)
GPIIB/IIIa inhibitor — not important just FYI
glycoprotein (GP) receptor for fibrinogen
and vWf, promotes platelet activation
IV only, and typically used as an adjunct
to PCI in certain high-risk patients
can cause thrombocytopenia (incl ITP) and
of course bleeding
just know this class of antiplatelet agents
exist for use in certain patients getting PCI
dual antiplatelet therapy (DAPT) after ACS
Why? What is the goal? 2
Which agents?
Which agent post-PCI?
How long for?
ASA dose for acute?
Post acute daily dose?
goal:
● prevent stent thrombosis
● also helps prevent long-term restenosis
(Restenosis occurs when an artery that was opened with a stent or angioplasty becomes narrowed again)
🔑following stent, DAPT for at least 12 months
(though recent literature may support duration as short as 6 months)
if ischemia-guided treatment (ie, no stent), DAPT for up to 12 months
Some notes on aspirin
● 🔑for ACUTE management of ACS, must be 162 to 324/325mg, chewed, non-enteric-coated
SUBSEQUENTLY:
● once-daily dose ranges from 81 to 325mg, but most opt for the lower 81mg daily (and guidelines support this practice)
● must be <100mg/day if given w/ ticagrelor
MONA vs THROMBINS2
THROMBINS2
● 🔑Thienopyridines P2Y12 inhibit (clopidogrel,
prasugrel) or ticagrelor
● 🔑 Heparin/enoxaparin
● 🔑 RAAS inhibitor (ACEI, ARB) — w/i 24hrs
● Oxygen*
● Morphine*
● 🔑 Beta blocker
● 🔑 Intervention
● Nitroglycerin*
● 🔑 Statin
● 🔑 Salicylate (aspirin)
MONA
except for aspirin, these do not provide a mortality benefit. Utility is pre-hospital only
1. Morphine
2. Oxygen
3. Nitro
4. Aspirin — only one to improve mortality
Post ACS cardiac meds (after definitive treatment)
Which meds do you start? When? Duration?
ASA
P2Y12
UFH
ACE/ARB
BB
Statin
aspirin
—ASAP
—indefinitely
P2Y12 inhibitor/clopidogrel
—in or prior to cath lab.
—duration: ≥12mo DAPT if stent, less if medically managed or if high bleed risk
heparin or LMWH
—ASAP
—duration: until definitive tx (ie, stent, CABG)
ACEI or ARB
—within 24h
—duration: 4-6 weeks, at least 3 yr if LV dysfunction, to prevent early remodeling
beta blocker
—within 24h
—at least 3 yr, indefinitely if LV dysfunction
statin
—as soon as reasonable
—indefinitely?
nitroglycerin if +angina PRN
variant/Prinzmetal angina
Treatment —3 meds
If associated w/ cocaine, what do you not give?
Page 3
Vasospastic, not atherosclerotic, so focus on agents that dilate the coronaries
● nitrates (eg, isosorbide)
● calcium channel blockers (mostly DHP amolodapine, nifedipine, but non-DHP also have some effect)
● statins improve endothelium-dependent vasodilation, possible utility. Statins are pleotropic
Cocaine associated chest pain
● old rule: BBs are contraindicated if there’s “unopposed ɑ activity” (ie, no ɑ1 blockade) d/t potential for exacerbating coronary vasospasm and worsening cardiac insult. You slow the HR and BP and then you constrict and worsen Ischemia, that’s the theory.
● more recent evidence suggests this is not really a problem
What is shock
What is the patho
What are the signs
Definition:
—inability to maintain adequate tissue perfusion, which results in severe organ dysfunction
Pathophysiology:
—typically a result of decreased systemic vascular resistance (SVR) and/or cardiac output (CO)
Signs:
● altered mental status - agitation, confusion, unresponsiveness
● respiratory distress - increased respiratory rate or effort)
● renal failure
● hepatic dysfunction
● lactic acidosis
● GI death/ulcers
What are the shock states?
Pump or pipes — what are examples of these?
What is the patho?
Obstructive
Hypovolemic
Cardiogenic
Distributive
Obstructive
—tension pneumothorax
—pericardial tamponade
—PE
Hypovolemic
—haemorrhage
—dehydration
Cardiogenic
—valve dysfunction
—arrhythmias
—HF
—MI
Distributive
—sepsis
—anaphylaxis
—neurogenic
Treatment GOALS for shock
Main 3
How? 3
2 invasive measures
● MAP ≥65 mmHg to achieve organ perfusion
● ↓serum lactate - lactate is a surrogate for organ perfusion
● urine output ≥0.5 mL/kg/hr
HOW?
1. increase SVR and venous return WITH
—fluids
—+/- vasopressor (vasoconstriction)
2. increase cardiac output WITH
—inotropes
More invasive measures (only available in critical care settings)
● cardiac output, cardiac index
● SCvO2 and SvO2 ≥65-70% (venous measures of O2 extraction)
Summary of adrenergic receptors
Alpha 1
Beta 1
Beta 2
Which organ associated?
What happens when you agonise these receptors?
Alpha 1
—vasculature : vasoconstriction
—your main target if you want to↑SVR
Beta 1
—myocardium : ↑contractility
—your main target if you want to ↑CO
Beta 2:
beta receptors — SNS — dilate to increase blood for O2 diffusion to fight the bear
—vasculature: vasodilation
—bronchioles: bronchodilation
—myocardium: ↑contractility
Vasopressor pharmacology (clamp down on blood vessels to improve circulation)
What is the primary receptor?
What are the ADRs?
What is the antidote?
Primary receptor: α1
● agonism leads to smooth muscle vasoconstriction, esp in arteries
● additional effect: ↑venous vasoconstriction → ↑return and preload
Key adverse effects
● hypertension
● brady- or tachyarrhythmias
● bowel and digit ischemia
● extravasation injury
○ central line preferred
○ antidote: phentolamine (vasodilators)
Inotrope pharmacology
Which receptors 2
What do they do?
Key ADRs?
β1 receptors → ↑chronotropy, ↑inotropy
β2 receptors → vasodilation (and bronchodilation)
Key adverse effects
● hypertension
● hypotension (vasodilation from β2 agonism)
● tachyarrhythmias - in trying to achieve ↑inotropy, you usually also get↑chronotropy which can lead to increased myocardial O2 demand and ischemia
Vasopressors & inotropes
What is the spectrum from A1 to B1
To treat shock
Comparison of vasopressors and inotropes
Phenylephrine — type, good for?
Norepinephrine — 1st line for?
Epinephrine — uses 3
Dopamine — low, mod, high doses uses?
Dobutamine — 2 main uses?
A1, B1,B2
Phenylephrine
—can cause reflex bradycardia; a good option if pt is tachycardic
Norepinephrine
—1st-line for septic shock
Epinephrine
—typically used for vasopressor effect (ie, septic shock, cardiac arrest)
—or to increase chronotropy (ie, bradycardia)
Dopamine
—low doses: dopamine receptors → vasodilation of renal and other arteries
—mod dose (3-10 mcg/min): +β1 agonism, ↑endogenous NE release
—high dose (>10 mcg/min): +ɑ1 agonism, loses dopamine activity
know that dopamine has different affects based on the doses
Dobutamine
—increases myocardial O2 consumption
—utility for cardiac stress tests inotropic option for cardiogenic shock (ie, decompensated HF).
—Instead of making patient walk on the treadmill. Diagnostic
Vasopressin (ADH) — 2nd line for?
Angiotensin II — brand name? C/I for? ADR?
Milrinone — use?
Don’t memorise MOA here
Shock treatment for (drug classes):
Obstructive
Hypovolemic
Distributive
Cardiogenic
[know this]
Obstructive: either inotrope or vasopressor
Hypovolemic: vasopressor
Distributive: vasopressor
Cardiogenic: inotrope
