Cardiac Conditions Flashcards
Tx for clotting
- Drug classes + MOAs
- Antiplatelet: decreases platelet aggregation
- Anticoagulant: inhibit the coagulation cascade (blood thinners)
- Thrombolytics: post-clot lysis
What drug class does ASA belong to?
- Antiplatelet DRUG OF CHOICE
- Blocks thromboxane A2 in degranulation - NSAID
- Blocks COX-1
Dipyridamole
Antiplatelet
- Blocks Thromboxane A2 in degranulation
Clopidogrel
What drug class? MOA? s/e?
Antiplatelet
- Blocks ADP in degranulation = decrease in platelet adhesion
s/e: easy bleeding, ulcerations
Heparin-induced thrombocytopenia (HIT)
An immune reaction to Heparin-Factor 4, resulting in disseminated coagulation.
Life-threatening:
- 50% in patients
- 30% in patients on Heparin X
Dabigatran (Pradaxa)
Anticoagulant (PRODRUG)
- Blocks thrombin receptors + factors
- *For stroke prevention
Warfarin (Coumadin)
Anticoagulant
- Inhibits hepatic formation of PF II, VII, IX, X (antagonizes Vit. K-dependent factors)
PK:
- Long t/12
- High PPB
- Narrow TI**
Alteplase, Reteplase
Describe PK.
Thrombolytics: clot lysis
- Based on Plasmin
- t1/2: 13-16 min (acute!)
- IV
Plasmin
A protein that degrades fibrin.
- Endogenously made
- Part of Thrombolytics drug class
Clinical manifestations of atherosclerosis
- Narrowing of vessel
- Vessel obstruction d/t plaque
- Thrombosis
- Weakening of vessel wall
What drug class do these belong to?
- Nitroglycerin (Nitro)
- Isosorbide
Organic nitrates
1ST LINE OF ACUTE CAD/ANGINA
1 SL q5min x 3 doses => CALL EMS IF IT DOESN’T WORK
What is angioplasty (PTCA) used for?
Tx for obstruction by CAD
- Opens blocked coronary arteries + cerebral vessels (STENTING)
What is CABG used for?
(Coronary artery bypass graft)
- Describe meds used, candidates
Tx for obstruction = re-routes/bypasses myocardial BF around blocked coronary arteries
- “Open heart surgery”
- INDUCES CARDIAC ARREST or beating heart
Meds: high CCB, beta-blockers, K+
Candidates: No high atherosclerosis
Pulmonary embolism
- S/S, Dx, Tx
Thrombus that has travelled to the lungs. Most commonly from DVT.
S/S: sob, low O2sat, chest pain, compensatory mechanisms (increase HR)
Dx: CT scan
Tx: prevention is key!
- Early mobilization
- Compression stocking
- Anticoagulation pre/during/post-Sx (Heparin, LMWH)
- ER: thrombolytics
Thrombus vs Thromboembolism
- List RFs
Thrombus: clot
Thromboembolism: migrating clot (usually to deep veins)
Coronary Artery Disease (CAD)
the narrowing of coronary arteries d/t atherosclerosis
(50-77% occlusion = Sx)
> > Angina - Stable, Variant, Unstable
Tx: Nitroglycerin
Stable Angina
Fixed plaque in coronary arteries that causes intermittent pain, exacerbated with exertion, but relieved with rest
Variant Agina
Chronic angina characterized by persistent contractions/spasms of coronary arteries that often occur at rest/sleep.
- Triggered by smoking
- ECG shows STE (but NOT MI, only temporary occlusion)
Ischemia
- Describe s/s, effect on body
When there is not enough blood flow for adequate oxygenation.
S&S (fast)
- sob, pain, hypoxemia, no contractility
Effect:
- Anaerobic metabolism
- Injury of myocardial cells (leaks intrinsic enzymes: troponin, CK, myoglobin)
- Cellular necrosis onset 20-40 min
Ischemia vs Hypoxemia vs Hypoxia vs Angina
Ischemia: not enough blood flow for adequate oxygenation
Hypoxemia: lower than average O2 in blood
Hypoxia: inadequate O2 in tissues
Angina: chest pain/discomfort d/t hypoxic tissues
Myocardial Infarction (MI)
Ischemia of the heart
(d/t blockage of BF = rupture of plaque or anything constricting)
- Duration of chest pain w/o precipitating event is >30 min
- STEMI = thrombus fully occludes
- NSTEMI (depresses) = partial occlusion
Prioritize RE-PERFUSION
Interventions
- Percutaneous Coronary Interventions (PCI) = to visualize artery
- CABG = to reroute BF
Unstable Angina
Acute rupture of plaque + blood clot in coronary arteries causing severe and prolonged pain at rest + exertion.
- Increases risk of MI
- Tx: Nitroglycerin q5min x3 max
Antioxidants
- Examples (2)
Neutralizes + eliminates ROS by giving up its electron.
- Supports normal cellular enzyme fx
- Proanthocyanidins (grape skin), Vit. C
Dyslipidemia
- Name drug classes + MOA
Elevated total or LDL cholesterol.
- Statins: lower LDL via HMG-CoA reductase inhibition + increasing hepatic metabolism
* FIRST LINE TX: POST-MI - Fibrates: lower vLDL via increasing lipolysis + metabolism
- Niacin: increases HDL via increasing clearance + lowering cholesterol synthesis (liver)
Where is cholesterol endogenously made?
Liver