Angina, A-Fib, Direct VD, MI, HF

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29 Terms

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what is angina pectoris + list drugs?

-Pain due to insufficient oxygenation of myocardial cells

•exercise, stress, blood clot or spasm, VC

-Drugs

•Beta-blockers

•Calcium channel blockers

•Nitrates

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Beta-blockers

*talked previously

-decrease HR and contractility

-Use: stable anhinga

<p>*talked previously</p><p>-decrease HR and contractility</p><p>-Use: stable anhinga</p>
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Calcium Channel Blockers (CCB)

*talked previously

-diaretic

<p>*talked previously</p><p>-diaretic</p>
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Organic Nitrates: Nitroglycerian

-Fast acting

-How they work: Vasodilation of large veins and coronary arteries; Decreased cardiac work/decrease O2 demand

-Adverse effects: HA, hypotension, flushing, reflex tachycardia, dizziness, nausea, falls risk*

-Route of administration: Sublingual/under tonuge (skips first pass/right into blood), patches

Important things to remember/therapy implications

-should have on self when exercising

-1 minute onset; Immediate relief for exercise, stress induced angina

-Sublingual 

  • Cause vasodilation therefore should be sitting when taking to prevent falling 

  • Heat will also cause vasodilation and may lead to excessive vasodilation [ie hot tub]

*take couple times before call 911

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Organic Nitrates: Isosorbide minonitrate + dinitrate

-How they work: Vasodilation of large veins and coronary arteries; Decreased cardiac work/ decrease O2 demand

-Adverse effects: HA, hypotension, flushing, reflex tachycardia, dizziness, nausea; Falls Risk*

-Route of administration: Oral (prevention)

-long acting with 30 minute onset

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Nitrates APTA vital signs

*closely monitor BP

*avoid skin contact

<p>*closely monitor BP</p><p>*avoid skin contact</p>
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Knwoledge check

-Patient in clinic has diagnosis of stable angina. What medication should they always have during therapy? Why?

-Patient in SNF reports being dizzy when standing…what medication could cause dizziness and why?

-Patient will history of angina, develops chest pain while using stationary bike during PT session. Next steps?

-Nitroglycerian. Increased activity during therapy can be overtaxing to the heart causing increased oxygen demand

-Any medication affecting BP – causes orthostatic hypotension increasing patient’s risk for falls

-Have patient end session, take their nitro per directions if not resolved may need to active EMS and inform the provider

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A-Fib: management and goal of therapy

-Goal of Therapy: multimodal approach for symptom control & thromboembolism prevention

<p>-<span><strong>Goal of Therapy</strong>: multimodal approach for symptom control &amp; thromboembolism prevention</span></p>
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Heart Rate Control

-Used in acute & chronic settings

-Promotes hemodynamic function

  • ↓ ventricular response

  • ↓ myocardial oxygen demand

  • Improved coronary perfusion & mechanical function

-Beta Blockers [previously discussed]: Atenolol, Carvedilol, Esmolol, Metoprolol

-Calcium Channel Blockers [previously discussed]; Diltiazem, Verapamil

-K+ channel blockers: Amiodarone

-Cardiac Glycosides: Digoxin

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Amiodarone

-K+ Channel Blocker

-Most widely used

-Rate and rhythmic control

-Adverse Effects: Ventricular tachycardia, pulmonary toxicity, thyroid issues & liver damage

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Cardiac glycosides/Digitalis

“Diagoxin is a toxin”;older med w/ a lot of SE

-Example: digoxin (Lanoxin)

-Physiological effect:

•negative chronotropic effect - slows the heart rate

•positive inotropic effect- increase strength of contraction

-Used to treat heart failure and atrial arrhythmias, including atrial fibrillation and atrial flutter

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Digitalis Toxicity

Serious and frequent adverse effect

-Low therapeutic index

•narrow margin between therapeutic dose and toxic dose

-Long half-life (~30 hours)

•consider the elderly patient with decreased kidney function

-Symptoms

•pulse rate <60bpm

•confusion

•restlessness

•N/V

•diarrhea

•yellow-green halos around lights

•hallucinations

-Blood tests to ensure drug level is therapeutic

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rhythm control 4 classifications + AE

Adverse Effects

Class 1(Na+ channel blocker): Increase rhythm disturbances 

Class 2(Beta-blocker): Bronchoconstriction

Class 3 (K+ channel blocker): Increase arrhythmias, ventricular tachycardia

Class 4 (Ca2+ channel blocker): bradycardia, dizziness, HA

<p><span><strong>Adverse Effects</strong></span></p><p style="text-align: left;"><span><strong>Class 1</strong>(Na+ channel blocker): Increase rhythm disturbances&nbsp;</span></p><p style="text-align: left;"><span><strong>Class 2</strong>(Beta-blocker): Bronchoconstriction</span></p><p style="text-align: left;"><span><strong>Class 3</strong> (K+ channel blocker): Increase arrhythmias, ventricular tachycardia</span></p><p style="text-align: left;"><span><strong>Class 4</strong> (Ca2+ channel blocker): bradycardia, dizziness, HA</span></p>
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timing of rate control vs rhythm control

Rate control is done before rhythm control drugs

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Anti-Arrytmias APTA acute care vital signs

-increased fall risk

-increase risk heart block

-assess BP

<p>-increased fall risk</p><p>-increase risk heart block</p><p>-assess BP</p>
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Direct Vasodilators

*not for normal world, in ER; take them off once BP lowers

Drugs: Hydralazine (Apresoline), Minoxidil

-Clinical Use: HTN, hypertensive crisis, severe preeclampsia, malignant HTN, heart failure

-Side effects: reflex tachycardia, ↑ blood volume

-Adverse effects: systemic lupus erythematosus

Drug: Sodium Nitroprusside (Nipride, Nitropress):

-Clinical Use: Hypertensive Crisis, ARDS, severe HF

-Adverse effects: dizziness, orthostatic hypotension, weakness, nausea, fluid retention

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MI: what is it, effect ACE inhibitors, drugs effects on secondary MI

-Myocardial ischemia progresses to myocardial infarction, i.e. cell death

-Certain ACE inhibitors can increase survival rate if given within 24 hours of an MI

•example: quinapril (Accupril)

-Long-term studies have shown that some drugs prevent occurrence of a second MI

•Aspirin

•Beta-blockers: atenolol (Tenormin), metoprolol (Lopressor, Toprol-XL), propranolol (Inderal), timolol (Blocadren)

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acture treatment of MI: ST-segment elevation vs non-ST segment elevation

*do while getting preped and ready for surgery

<p>*do while getting preped and ready for surgery</p>
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long-term management of STEMI

•Goal is to promote survival and prevent a 2nd MI

•Aspirin

•Clopidogrel

•Beta-blocker

•Statin

•ACE inhibitor/ARB

•Revascularization (stent, bypass) or ICD

•Risk factor reduction

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SSRI’s and MI

-Certain antidepressants have been found to reduce the risk of a 2nd MI

-Depression is a risk factor for heart disease but these drugs work by preventing platelet aggregation and blood clot formation

-Examples: Prozac, Paxil, Luvox, Zoloft

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what is heart failure?

Heart muscle is weakened and is unable to adequately fill with or pump blood

-Right versus left sided heart failure

-Systolic heart failure

•Heart failure with reduced EF (HFrEF)

•LVEF ≤ 40%

-Diastolic heart failure

•Heart failure with preserved EF (HFpEF)

•LVEF > 40%

*heart only pumps 30% blood so “saggy and baggy” bad

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pharmacologic management for HF

-HFrEF

•Loop diuretics

•ACE inhibitor/ARB

•Beta-blocker

•Digoxin

-HFpEF

•Mineralocorticoid receptor antagonist

•Diuretic (*K+ sparing diaretic)

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heart failure 4 pillars medications

-Betablocker “lol”

-Angiotensin Receptor Neprilysin Inhibitor (ARNI). RAAS Medications

•OR: ACE Inhibitors "prils"; ARB "sartans"

-MRA - potassium sparing diuretic

-SGLT-2 Inhibitors "flozin"

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what med use for acute heart failure?

-direct vasodilators

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last resort medications (chart)

*if acute crisis adminsiter via IV; cause dysrhtmias

<p>*if acute crisis adminsiter via IV; cause dysrhtmias</p>
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summary special concerns PT

Know signs and symptoms of

-Acute HF

•Cough, SOB, dyspnea, abnormal lung sounds, sputum

-BB SE

•Bradycardia – RPE/MBORG

-Digitalis Toxicity  [digoxin]

•Dizziness, confusion, nausea, arrythmias, visual disturbance

-Diuretic SE

•Hypotension, electrolyte imbalance [*hypokalemia/*hyperkalemia], excessive fatigue/weakness

-Vasodilators

•Hypotension

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Knowledge check

-Patient with heart failure complains of SOB and reports difficulty fastening her pants today.  Which medication(s) may NOT be at an effective dose? (4 answer choices=Lasix (diuretic), Atenolol (BB), Hydrochlorothiazide (diuretic), Lisinopril (ACEi))


-Patient has HF and is taking Metoprolol, Lasix, Lisinopril, Jardiance. During your PT session, the patient c/o muscle cramping

•Which medication could be the issue and why?

•How do you determine if it is from the medication or MS issue?


-Patient has HF and is taking Metoprolol, Lasix, Lisinopril, Jardiance. During your PT session, you take their vitals [HR, BP, RR]

•Which sign would be inaccurate and why?

•What can you use to assess the patient instead?


-Patient has HF and is taking Metoprolol, Lasix, Lisinopril, Jardiance. During your PT session, the patient has on a mask and tells you they have a dry cough.

•Which medication could be the issue?

•How can you tell if it is a potential illness or the medication?

•What is your next step?

•What would the provider potential change the medication to?


-Patient has HF and has been taking Digoxin for a long time. During your PT session, the patient tells you the lights look funny and they feel nauseated and weak.

•What is your next step?


-The patient reports they haven’t gotten the blood test for digoxin in months

•Why does this medication need a blood test?

-Diuretic: Lasix or Hydrocholorthiazide

-(cramping=electrolytes off) Lasiz. Ask questions, all over body or just specific muscle

-HR. Bc beta-blocker blunts HR. RPE, MBorg, Talk Test

-ACE inhibitor. Ask questions when start, type of cough. Notify provider. Off ACE → onto ABB (angiotension blocker)

-911 (if HR 50 and irregular= call the provider)

-narrow theraputic window

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Summary therapy implications CV medications

-Potential side effects: Hypotension

-Vasodilation should be avoided: Heat, whirlpool

-Betablockers blunt HR: Use RPE, Mborg, or talk test

-Being active can lower BP

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CV picture summary

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