ACS 2 - Quiz 3 Flashcards
goals of ACS therapy
- restore epicardial coronary blood flow
- limit myocardial damage
- minimize risk for complications
general therapies
- bed rest
- supplemental oxygen
- analgesia
- anti-ischemic therapies
- Anti-platelet and Antithrombotic therapies
purpose of bed rest
- minimize oxygen demand
purpose of supplemental oxygen
- improves oxygen supply
purpose of analgesia
- reduce anxiety and chest pain
- minimize oxygen demand
treatment for ST segment elevation
- open artery emergently
treatment for no ST segment elevation
- antiplatelet therapy
- anti-ischemic therapy
- anticoagulant therapy
- invasive versus conservative
goals of anti-ischemic medications
- restore balance between oxygen demand versus supply
goals of anti-thrombotic therapy
- prevent further growth of thrombus
- enhance resolution
drugs for anti-ischemic therapy
- beta blockers
- nitrates
- non dihydropyridine calcium channel blockers
sympathetic effect of beta blockers
- decrease sympathetic drive
- reduce O2 demand
electrical stability effect of beta blockers
- enhance electrical stability
mortality effect of beta blockers
- reduce mortality
contraindications of beta blockers
- marked bradycardia
- severe bronchospasm
- hypotension
- acute heart failure
when do you start beta blockers
- orally within first 24 hours
target HR on beta blockers
- below 60
do you continue beta blockers?
- yes, indefinitely
nitrates purpose
- venodilation
- coronary vasodilation
result of venodilation
- decreases preload
- less wall stress
- lower O2 demand
what is pre-load
- venous return to the heart
coronary vasodilation result
- improve blood flow
- reduce vasospasm
- improved O2 supply
nitrates given how
- sublingual (underneath the tongue)
nitrates contraindications
- patients with RV infarction
why we don’t use nitrates in patients with RV infarction
- these patients are preload dependent
- nitrates cause hypotension
non-dihydropyridine calcium channel blockers result
- vasodilation
- decreased myocardial O2 demand
- increased supply
non-dihydropyridine calcium channel blockers - mortality effect
- no mortality benefit
non-dihydropyridine calcium channel blockers - when to use
- refractory ischemic symptoms
- contraindication to beta blocker
non-dihydropyridine calcium channel blockers - contraindications
- patients with LV systolic dysfunction
- increases their mortality
Anti-platelet therapies
- aspirin
- clopidogrel
- IV glycoprotein IIB/IIIA inhibitor
aspirin effect
- inhibits platelet synthesis of TxA2
- inhibits platelet activation
aspirin mortality effect
- reduces mortality
when to give aspirin
- give immediately
clopidogrel effect
- P2Y12 inhibitor
- give to aspirin-allergic patients
best way to reduce mortality in patients with NSTEMI-ACS
- give aspirin and plavix
which is the most potent Anti-platelet agent
- IV glycoprotein IIB/IIIA inhibitor
result of IV glycoprotein IIB/IIIA inhibitor
- block final common pathway of platelet activation
use of IV glycoprotein IIB/IIIA inhibitor
- adjunctive therapy with PCI
anticoagulant therapies
- unfractionated heparin
- low molecular weight heparin
- fondaparinux
- bivalirudin
result of unfractionated heparin
- enhance antithrombin effects
- impedes thrombus development
- improves cardiovascular outcomes
UFH versus LMWH
- reduced death and ischemic rates with LMWH
problem with LMWH
- hard to monitor during procedures
fondaparinux inhibits
- factor Xa
fondaparinux result
- reduces CV events
- less bleeding risk
fondaparinux used for
- when no PCI is planned
bivalirudin inhibits
- thrombin
bivalirudin result
- reduced clinical events
- less bleeding risks
bivalirudin used for
- in Cath lab for PCI
what do we use now for PCI
- drug eluting stent
how does a drug eluting stent work?
- anti proliferative agent elutes from Bare metal stent platform
approach for unstable angina
- conservative
approach for NSTEMI
- early invasive
process for early invasive therapy
- urgent coronary angiography
- followed by coronary revascularization
process for conservative therapy
- medical management
when do you do a cardiac Cath in conservative therapy
- only with recurrent ischemia
- positive stress test
most important factors from TIMI score
- ST change
- elevated cardiac markers
reperfusion strategies with STEMI
- fibrinolysis
- PCI
result of fibrinolysis
- accelerates clot lysis
- restore blood flow
- salvage myocardium
MOA of fibrinolysis
- transforms plasminogen to plasmin
- lysis fibrin clot
major complication of fibrinolysis
- bleeding
when do we give fibrinolysis
- within 120 minutes of onset of symptoms
contraindications for fibrinolysis
- active ulcer disease
- bleeding disorder
- recent CVA or surgery
- uncontrolled HTN
- elderly
what do we usually give with fibrinolysis
- aspirin
- heparin
- clopidogrel
when does PCI need to be performed
- within 90 minutes of hospital presentation
adjunctive therapies with PCI
- aspirin
- P2y12 inhibitor
- bivalirudin or heparin
- IV GP IIB/IIIA inhibitor
when do we give fibrinolytics over PCI
- if time taken to PCI is longer than one hour
complications of MI
- recurrent ischemia
- arrhythmias
- heart failure
- right ventricular infarction
- ventricular aneurysm
- pericarditis
- thromboembolism
recurrent ischemia may represent problem with
- malplacement of stent
- acute thrombosis
- repeat cardiac cath
mechanisms of why you get arrhythmias after MI
- impaired perfusion to conduction system
- accumulation of toxic metabolic products
- autonomic stimulation
- arrhythmic drugs
what is the most common cause of death within first 48 hours after an MI
- Vtach or Vfib
early Vtach or Vfib after MI due to
- electrical instability
late Vtach or Vfib after MI due to
- structural disease
AV node supplied by
- RCA
bundle of His supplied by
- LAD
right bundle branch supplied by
- proximal portion by LAD
- distal portion by RCA
left bundle branch anterior fascicle supplied by
- LAD
- most susceptible to ischemia
left bundle branch posterior fascicle supplied by
- LAD
- PDA
conduction block arrhythmias development from
- ischemia
- necrosis of conduction tracts
post MI heart failure caused by
- impaired contractility from ischemia
- increased myocardial stiffness
signs/symptoms of post MI heart failure
- dyspnea
- rales
- S3
- peripheral edema
- SOB when lying flat
how to treat HF
- revascularization
- ace inhibitors, beta blockers, diuretics
cardiogenic shock due to
- severely decreased cardiac output
- hypotension
physiologic effects of intra-aortic balloon pump
- enhanced coronary blood flow
- left ventricular unloading
- improved cardiac output
EKG for right heart fialure
- ST elevation in lead II, III, and aVF
- more III than II
- also check V4R
signs of right heart failure
- elevated JVP
- hypotension
- clear lungs
treatment of right heart failure
- volume and reperfusion
mechanical complications of MI
- papillary muscle rupture
- ventricular septal rupture
- ventricular free wall rupture
when does papillary muscle rupture occur
- 3-5 days post MI
papillary muscle rupture results in
- acute, severe mitral regurgitation
- holosystolic murmor
when does ventricular septal rupture occur?
- 3-7 days post MI
ventricular septal rupture results in
- form in inter ventricular septum
- shunt from LV to RV
- holosystolic murmor
diagnosis of ventricular septal rupture
- EKG
ventricular septal rupture leads to
- heart failure
ventricular free wall rupture occurs when
- 14 days post MI
ventricular free wall rupture result
- blood fills pericardial space
- causes cariogenic shock
when would a ventricular aneurysm occur
- weeks to months after an MI
when does a ventricular aneurysm develop
- as well weakens with phagocytic process used to clear necrotic tissue
how to check for ventricular aneurysm
- persistent ST segment elevation weeks after STEMI
acute pericarditis symptoms
- sharp, pleuritic pain
- fever
- pericardial friction rub on auscultation
how to treat acute pericarditis
- aspirin
- avoid anticoagulants
Dressler syndrome
- immune process directed against necrotic myocardium
Dressler syndrome treatment
- aspirin
- NSAIDS
thromboembolism due to
- stasis of blood in regions of impaired LV wall contractility
thromboembolism can be seen with
- LV aneurysm
thromboembolism requires
- anticoagulation
other therapies for ACS
- ACE inhibitors
- statins
purpose of ACE inhibitors
- reduce incidence of heart failure
- reduce recurrent ischemia
- reduce mortality
ace inhibitors greatest benefit with which patients
- those with LV dysfunction
- high risk patients
statins effects
stabilize endothelium
standard post discharge therapy following MI
- aspirin
- P2Y12 inhibitor
- beta blocker
- statins
- ACE inhibitors
- aldosterone antagonists
- risk factor modification
why do we give aldosterone antagonists
- for patients with LV dysfunction
