Week 9

heart disease factors

heart disease factors

smoking, infections, alcohol, genetic predisposition, unhealthy food, obesity, sedentary lifestyle, age, stress

PQRST characteristics of pain

palliative/provocative factors, quality, radiation/region, severity, temporal factors

acute coronary syndrome

general term used for varying degree of blockage in a coronary artery

varying degrees of ACS

unstable angina, NSTEMI, STEMI, MI, sudden cardiac death

chronic stable angina

primarily caused by CAD/atherosclerosis, which results in a long-term but relatively stable level of obstruction in one or more coronary arteries; often triggered by increase in activity, emotional excitement, large meals, or cold exposure

vasospastic angina (prinzmetal’s/variant)

ischemia-induced myocardial chest pain caused by spasms of the coronary arteries

unstable angina

medical emergency; results from severe CAD complicated by vasospasm, platelet aggregation, and coronary thrombi or embolism

unstable angina symptoms

angina at rest, now-onset exertional angina, or intensification of existing angina

non-ST elevation MI (NSTEMI)

blockage of blood flow is only partial, no damage to cardiac muscle (+symptoms, + troponins, -ECG changes)

ST-elevation MI (STEMI)

blockage is complete, but hasn’t been long enough to cause myocardial wall damage (+symptoms, +troponins, +ECG changes in ST segment)

myocardial infarction

blockage is complete, causing necrosis of the myocardium

hemostasis

physiologic process by which bleeding is stopped

stage 1 of coagulation

formation of a platelet plug

formation of a platelet plug

platelets come in contact with collagen on the exposed surface of a damaged blood vessel & adhere to site of vessel injury. adhesion initiates platelet activation, which in turn leads to platelet aggregation

anti-platelet example

aspirin (ASA)

aspirin (ASA) mechanism

inhibits cyclooxyrgenase and prevents platelet aggregation

aspirin (ASA) uses

ischemic stroke, TIA, USA, coronary stenting MI, MI prevention

aspirin (ASA) routes

PO

aspirin (ASA) side effects

bleeding, especially GI bleed, dizziness, drowsiness, headache, flushing, visual changes, tinnitus, hearing loss, seizures, reye syndrome (children)

aspirin (ASA) nursing considerations

325 mg for MI/TIA/CVA, 81-160 mg for prevention; must be stopped 7-10 days before invasive procedures

anti-platelet (ADP inhibitor) example

clopidogrel (Plavix)

clopidogrel (Plavix) mechanism

alters platelet membrane so that it can no longer receive the signal to aggregate and form a clot

clopidogrel (Plavix) uses

prevent stenosis of coronary stent, secondary prevention of MI and ischemic stroke

clopidogrel (Plavix) routes

PO

clopidogrel (Plavix) side effects

bleeding, less than ASA for GI bleeding

clopidogrel (Plavix) nursing considerations

can be used in conjunction with ASA but increased risk for bleeding; cannot be used with another ADP receptor antagonist; must be stopped 7-10 days before any invasive procedure

ACS chest pain symptoms

crushing, constricting, or radiating pain, often substernal, radiating pain can be felt in arms or jaw, can be confused with angina, lasts longer than angina and not relieved by nitroglycerin

three groups who do not have typical ACS symptoms

women, diabetics, elderly

ACS diagnosis

chest pain, EKG changes, biochemical markers (blood lab test)

ACS EKG changes

conduction of electrical impulses through heart becomes altered in the region of injury; ST elevation

ACS blood lab test

when myocardial cells undergo necrosis, they release intracellular proteins called cardiac troponins; if serum blood levels of troponin are detected, it’s a sign of cardiac injury, as they are normally undetectable

immediate treatment of suspected MI

morphine IV, oxygen, nitroglycerin SL/IV, aspirin, beta blockers PO or IV (MONAB)

purpose of morphine in management of ACS

relieves pain, improves hemodynamics, promotes venodilation, reduces cardiac preload & some afterload

purpose of oxygen in management of ACS

can increase arterial oxygen saturation and thereby increase oxygen delivery to ischemic myocardium; goal is titrate to keep SpO2 between 95-99%

purpose of nitroglycerin in management of ACS

can reduce preload and therefore oxygen demand, increases collateral blood flow in the ischemic region of the heart, controls HTN

purpose of aspirin in management of ACS

suppresses platelet aggregation for immediate antithrombotic effect, should be chewed (4 baby ASA=325 mg)

purpose of beta blockers in management of ACS

reduce cardiac pain, infarct size, short-term and long-term mortality (by reducing HR and contractility, they reduce oxygen demand)

three families of pharmacological antianginal agents

1. organic nitrates

2. rapid-acting (NTG SL) during ACS

3. long-acting/XL (Isosorbide) after ACS when it is then called CAD

short-acting nitrates example

nitroglycerin (NTG)

long-acting nitrates example

isosorbide mononitrate (Imdur)

nitrates mechanism

vasodilation in veins and arteries but potent vasodilator in coronary arteries=decrease in preload

nitrates routes

SL, PO, IV drip, paste, transdermal

nitrates side effects

excessive effects of drug=decrease in BP, headache

nitrates nursing interventions

monitor BP closely=may need to put HOB flat and/or bolus with isotonic IV solution

nitrates patient education

-sit down before taking NTG

-get up & change positions slowly

-teach patients about symptoms of hypotension & advise them to sit or lie down if these occur

-cannot have within 24-48 hours of ED medications

-avoid saunas & hot tubs

-NTG x3, 5 min apart, between 1 & 2 if CP is present=call 911

-if pt has chronic stable angina, precipitate CP & take NTG SL prior to event

-do not eat or drink until 5-10 min after SL dose

-potency is felt by a burning or stinging under the tongue

-take acetaminophen for headache (no ASA or NSAIDs)

-keep NTG in brownish lightproof bottle, keep with at all times

-NTG SL pills only good 3-6 months (some say 6-12)

-sprays last 1-2 years

symptoms of hypotension

lightheadedness, dizziness

ED medications

sildenafil (Viagra), tadalafil (Cialis)

nitrates IV infusion/drips

-standard orders with parameters to adjust/titrate the rate up or down based on specific criteria; must be on a pump

interventions specific to IV NTG infusion

-glass bottle, must be vented

-evaluation/adjustment criteria: BP and CP

restoring perfusion

cardiac catheterization with percutaneous intervention, drug therapy (thrombolytic agents)

percutaneous coronary intervention

usually balloon angioplasty coupled with placement of a drug-eluting stent to reopen an occluded coronary artery; success rate higher than with fibrinolytic therapy

thrombolytic agents

-promote lysis of fibrin, causing dissolution of thrombi

-given to remove thrombi that have already formed

-used acutely and only for severe thrombolytic disease: ACS, PE, ischemic stroke

alteplase (tPA) use

used for ACS (STEMI, MI), ischemic stroke, massive PEs

alteplase (tPA) route

IV

alteplase (tPA) side effects

major bleeding

alteplase (tPA) contraindications

any previous or current bleeding risk

alteplase (tPA) antidote

aminocarpmroic acid (Amicar)

contraindications to fibrinolytic drugs

prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within the past 3 months, known intracranial neoplasm, active internal bleeding, suspected aortic dissection, severe uncontrolled hypertension

guideline for CAD & ACS prevention regimen upon discharge

ASA, NTG PRN for CP, BB prevents another episode, PRN clopidogrel dual therapy for one year if stent placement, PRN cholesterol-lowering medications for lipid management (usually statins), PRN HTN or HF management with ACEI or ARB or ARB with thiazide, PRN stool softeners

clot

insoluble solid elements of blood that have chemicaly separated from the liquid component of the blood

embolus

a blood clot that has been dislodged from the wall of a blood vessel and is traveling throughout the bloodstream

deep vein thrombosis

the formation of a thrombus in one of the deep veins of the body

ischemia

damaged cells/tissue as the result of inadequate oxygen supply

stage 2 of coagulation

production of fibrin that reinforces the platelet plug; produced by two convergent pathways: contact activation pathway and tissue factor pathway

arterial thrombosis

starts with adhesion of platelets to the arterial wall due to damage or rupture by an atherosclerotic plaque. aggregation continues until occlusion of the artery can occur. blood flow stops, coagulation cascade is initiated and the plug is reinforced with fibrin

venous thrombosis

develops at sites where blood flow is slow. stagnation of blood initiates the coagulation cascade. fibrin is produced, which enmeshes red blood cells and platelets to form the thrombus; has a long tail that can break off to produce an embolus. the emboli can traverse the vascular system and become lodged at other sites

antithrombotic drugs

1. antiplatelets: inhibit platelet aggregation

2. thrombolytics: promote lysis of fibrin, causing dissolution of thrombi

3. anticoagulants: disrupt the coagulation cascade thereby suppressing the production of fibrin

antithrombotics nursing considerations & pt ed

soft bristle toothbrushes, no contact sports, monitor for blood in urine/stool, no aspirin/NSAIDs, wear a med bracelet, blood in emesis looks like coffee grounds, use an electric razor, apply firm pressure, minimize physical manipulation of the patient, avoid subQ & IM injections, minimize invasive procedures, minimize concurrent use of antiplatelet drugs

anticoagulants

drugs that reduce the formation of fibrin by inhibiting the synthesis of clotting factors or inhibiting the activity of clotting factors

anticoagulant examples

warfarin, DOAC, heparin, LMWH

warfarin (Coumadin)

a vitamin K antagonist, oldest oral anticoagulant

warfarin (Coumadin) uses

prevent thrombosis, DVT, PE, AFib/flutter

warfarin (Coumadin) routes

PO

warfarin (Coumadin) nursing considerations

not to be given while pregnant, monitor serum blood levels of PT/INR (2-3), will needs to stop warfarin/monitor INR/give vitamin K if patient is to undergo any invasive procedure

warfarin (Coumadin) antidote

vitamin K (given sub Q, PO, or IV)

warfarin (Coumadin) side effects

bleeding/hemorrhage

warfarin (Coumadin) drug interactions

antibiotics, heparin, ASA, acetaminophen

warfarin (Coumadin) food interactions

anything with vitamin K (green leafy vegetables, prunes, mayonnaise, canola oil), alcohol

warfarin (Coumadin) nursing implications

include education on monitoring, diets, and risks of injury

advantage of warfarin (Coumadin)

it’s cheap

DOAC examples

rivaroxaban (Xarelto), apixaban (Eliquis), dabigatran (Pradaxa)

rivaroxaban (Xarelto) mechanism

direct factor Xa inhibitors; causes selective inhibition of factor Xa (activated factor X)

apixaban (Eliquis) mechanism

direct factor Xa inhibitors; causes selective inhibition of factor Xa (activated factor X)

dabigatran (Pradaxa) mechanism

direct inhibition of thrombin

anticoagulant uses

stroke prevention with nonvalvular AFib/flutter, DVT/PE prophylaxis after THA and TKA

anticoagulant route

PO

anticoagulant nursing implications

hold medication for 24-48 hours before any invasive procedures, unsafe while pregnant, educate on signs of bleeding, assist pt to see insurance coverage, don’t give to pts undergoing spinal puncture/anesthesia

anticoagulant side effects

bleeding (lower than warfarin), neurologic injury

anticoagulant reversal agent

rivaraxaban (Xarelto) & apixaban (Eliquis)=andexanet alfa (AndexXa), dabigatran (Pradaxa)=Praxbind

heparin (unfractionated)

work by activating antithrombin (a protein that inactivates two major clotting factors)

heparin (unfractionated) uses

PE, DVT, MI, low dose post-op, during dialysis, CABGs

IV heparin

given to maintain steady levels of heparin; initial dosing is a weight-based bolus followed by a weight-based infusion titrated to lab results

subq heparin

low dose is given for prophylaxis against thromboembolism while hospitalized; 5000 units Q 8-12 hours for duration of hospitalization; doesn’t require aPTT monitoring

heparin (unfractionated) nursing implications

serum blood levels must be monitored with aPTT levels when given IV, MM uses factor Xa for monitoring; CBC must be monitored for anemia and thrombocytopenia; hemorrhage can occur at any site and can be fatal; pt ed extremely important (avoid falls while hospitalized)

heparin side effects

hemorrhage, heparin-induced thrombocytopenia

heparin contraindications

thrombocytopenia, uncontrolled bleeding, hemophilia, dissecting AAA, PUD, hemorrhagic stroke

heparin antidote

protamine sulfate

heparin orders

heparin 5000 units IVP STAT, then follow standard heparin IV protocol with Xa monitoring

LMWH examples

enoxaparin (Lovenox), dalteparin (Fragmin)

LMWH mechanism

heparin preparations composed of molecules that are shorter than those found in heparin