Cardiovascular Exam 3

angina pectoris

chest pain or discomfort due to myocardial ischemia

weight or pressure on chest

numbness/tingling in arms

pain

shortness of breath

What are symptoms of angina pectoris

demand angina

chronic stable angina (class or effort as well)

Supply angina

unstable angina and vasospastic angina

women

Are men or women more likely to get vasospastic angina?

stable angina therapeutic objectives

The following therapeutic objectives are for what type of angina?

• increase myocardial blood flow by dilating coronary arteries and arterioles (increase oxygen supply)

• decrease cardiac load (preload and afterload; decreasing oxygen demand)

• decrease heart rate (decrease oxygen demand)

• decrease fatty acid metabolism (decrease oxygen demand)

unstable angina therapeutic objectives

The following therapeutic objectives are for what type of angina?

• inhibit platelet aggregation and thrombus formation (increase oxygen supply)

• decrease cardiac load (preload and afterload; decrease oxygen demand)

• vasodilate coronary arteries (increase oxygen supply)

Variant Angina therapeutic objectives

The following therapeutic objectives are for what type of angina?

• decrease vasospasm of coronary vessels (CCBs are efficacious in >70% of patients; increase oxygen delivery)

Stable angina - decrease oxygen demand

Variant angina - increase oxygen supply

How does this drug class effect stable and variant angina? nitrates

stable angina - decreases oxygen demand

variant angina - not used

How does this drug class effect stable and variant angina? beta blockers

stable angina - decrease oxygen demand

variant angina - increases oxygen demand

Drugs - verapamil, diltiazem

How does this drug class effect stable and variant angina? Calcium channel blockers. Specifically what drugs?

stable angina - decrease oxygen demand by switching heart from FA metabolism to glucose

variant angina - not used

How does this drug class effect stable and variant angina? partial fatty acid oxidation (pFOx) inhibitors

stable angina - decrease oxygen demand by lowering heart rate

variant angina - not used

How does this drug class effect stable and variant angina? ivabradine

amyl nitrite

This is the only nitrite that can be inhaled

nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate

these are nitrate compounds that are administered via oral, sublingual, topical, transdermal and IV

Decreases preload → decreases oxygen demand

Dilation of veins » arteries

Decrease venous return → decrease in LVEDV and LVEDP

Less strain on the heart

What is the primary effect of nitrites and nitrates?

reduced wall stress (due to decreased preload) → increase in coronary blood flow → increase in oxygen supply

What is the secondary effect of nitrites and nitrates?

Low at 10-20%

High first pass metabolism

The oral availability of Nitroglycerin (NTG) and isosorbide dinitrate (ISDN) is _____. Because of…

mononitrate; 100%

Isosorbate ______nitrate is ____% available after oral administration.

tolerance of nitrites and nitrates

The inactivation of aldehyde dehydrogenase causes…

orthostatic hypotension

reflex tachycardia - due to baroreceptor

severe throbbing headache

What are the major adverse effects of nitro vasodilators (nitrites and nitrates)?

PDE-5 inhibitors for erectile dysfunction

Elevated intracranial pressure
Separate by at least 6 hours.

Nitrites and nitrates are contraindicated in patients that use _______, and patients that have elevated ________ ________.

PDE-5 inhibitors

• sildenafil

• Vardinafil

MOA: potentiate actions of nitro vasodilators b/c they inhibit breakdown of cGMP

What are specific drugs that interact with nitro vasodilators? What is the MOA that causes the interaction?

pFOX *acts like it only at higher doses

Ranolazine is in what class?

MOA: switches fuel preference of the heart from fatty acids to glucose

Importance: glucose oxidation makes ATP while using LESS oxygen → decreasing Oxygen demand

w/ no hemodynamic changes

What is the MOA of pFOX drugs?

inhibits late Na+ current → limiting Ca²⁺ entry (Phase 2 of AP) → decreased inotropic effect

What is the primary mechanism of Ranolazine?

positively inotropic drugs

These drugs counteract decreased cardiac output in heart failure.

vasodilators

These drugs counteract increased venous volume and pressure in heart failure

diuretics

These drugs counteract congestion and edema in heart failure.

ACE inhibitors

These drugs counteract renin-angiotension aldosterone system activation in heart failure.

diuretics

these drugs counteract sodium and water retention in heart failure

vasodilators

these drugs counterat increased afterload in heart failure

Beta blockers and ACE inhibitors

These drugs both (two classes) counteract cardiac remodeling in heart failure.

60-65

A normal ejection fraction is…

Beta blockers

What drug class would you use when your therapeutic objective is decreasing heart rate → decreasing oxygen demand? This drug class unfortunately decreases inotropy as well.

ivabradine

What is the drug can decrease heart rate with not cost to contractility?

visual disturbances

avoid if using: verapamil, diltiazem, or Beta blockers

What are some adverse affects of Ivabradine? If already on WHAT DRUGS you need to avoid.

1. sympathetic tone declines

2. urine production increases

3. renin release declines

What are the 3 major secondary responses from cardiac glycosides?

decrease

decrease

increase

increase

In ischemia:

the decreased oxygen supply causes,

____ ATP availability

____ Na/K ATPase

____ membrane potential

____ arrythmias

positive inotropic effect due to increase in Ca during systole

What is the total net effect in the heart (caused by cardiac glycosides)

Slows AV node conduction velocity = increased PR interval

With cardiac glycosides an increase in vagal tone does what to the AV node conduction velocity?

0.5-2 ng/ml

Ideal is under 1 to decrease mortality

Toxic above 2 ng/ml

What is the ideal therapeutic plasma concentration for digoxin? What is the toxic level?

overloading of intracellular calcium creating oscillations in free calcium

What is the likely cause of spontaneous delayed after polarizations during digoxin use?

decreases - helpful to decrease toxicity

increases

Hyperkalemia ____ digoxin effect (helpful how?)

Hypokalemia ____ digoxin effect

arrhythmia

hypercalemia increase risk of ______ due to calcium overload while using digoxin

Mg DEFICIENCY increases digoxin risk

Mg decreases risk of arrhythmias on digoxin

MONITOR

magnesium interacts with digoxin how?

bolus IV followed by continuous influsion

Half life = 18 minutes

How is nesiritide dosed and what is it’s half life?

Entresto (Sacubitril/Valsartan)

This drug allows the body to use BNP longer, and is a key drug for HFrEF

ventricle and atrium

what are the two types of muscle tissue?

conduct

myococytes _____

calcium current channel

conduction velocity in SA and AV nodes depend on…

sodium channel current

conduction velocity everywhere else (AV bundle, His-Purkinje, and fascicles) depend on…

Fast potentials

Myocytes in atrium and ventricle, bundle of His, and purkinje fibers have _____ (fast/slow) potentials

Slow potentials

the SA and AV nodes have _____ (fast/slow) potentials

Na/K ATPase pump

What is digoxin’s site of action?

Symp/Parasymp tone

What causes arrhythmias?

vagal maneuvers and beta blockers

What can be done to mitigate arrhythmias?

increase in intracellular Ca

Digoxin

late (delayed) afterdepolarizations (DADs) are caused by…

Which drug can cause these?

Ventricular Tachycardia

What type of arrhythmia is this?

Ventricular tachycardia and torsades de pointes

What type of arrhythmia is this?

Supraventricular Tachycardia

What type of arrhythmia is this?

Atrial flutter

Rapid firing out of sink

What type of arrhythmia is this?

Atrial fibrillation

No effective beating

What type of arrhythmia is this?

antibiotics and antidepressants

What kinds of drugs commonly cause Long QT syndrome?

Class: IA antiarrhymic sodium channel blocker

MOA: local anesthetics acting on nerve and mycardial membranes → slows conduction

Quinidine, Procainamide, Disopyramide: Class and MOA?

Indication: supraventricular arrhythmias, supraventricular tachycardia

Adverse effects: nausea, vomiting, diarrhea, headache, dizziness, anti-cholinergic effects

Quinidine

Indication

Adverse effects

Indication: similar to quinidine, good for patients that are unresponsive to quinidine

Adverse effects: lupus syndrome

Administration: Oral

Procainamide

Indication

Adverse effects

Administration

Indication: certain ventricular and atrial arrhythmias

Adverse effects: anti-cholinergic effects

Administration: oral

Disopyramide

Indication

Adverse Effects

Administration

Class: IB antiarrhythmic sodium channel blockers

Lidocaine, Tocainide, Mexiletine, Phenytoin

Class?

Indication: DOC emergency treatment of ventricular arrhythmias, prevention of ventricular arrhythmias

Adverse effects: CNS, heart, dizziness, paresthesia, seizures

Admin: IV injection

Lidocaine

Indication

Adverse effects

Administration

Indication - treatment and prevention of ventricular arrhythmias

Adverse effects - GI, CNS effects

Admin - oral

Tocainide

Indication

Adverse effects

Administration

Indication - ventricular arrhythmias

Adverse - GI, CNS, dizziness

Admin - oral

Mexiletine

indication - atrial and ventricular arrhythmias DUE TO DIGITALIS TOX

Adverse/Contra - agents that liberate phenytoin can cause toxicity

Admin - Oral and IV

Phenytoin

1C Antiarrhythmic Sodium channel blockers

Flecainide and encainide what class?

Indication - ventricular arrhythmias

Adverse - aggrevate existing arrhythmias, blurred vision, headache, nausea, abdominal pain

Admin - oral

Flecanide

Indication

Adverse

Admin

Encainide has a less negative inotropic effect

What is the difference between Flecainide and encainide?

Quinidine

What is the prototype drug for class 1 sodium channel blockers?

Class II antiarrhythmic drugs, beta-adrenergic receptor blockers

Propranolol, what class?

MOA - decrease sympathetic activity in heart → reduce cAMP levels → reduces Ca influx → decrease conduction through AV node

Prototype - propranolol

What is the MOA and prototype drug of Class II antiarrhythmics?

Indication - supraventricular arrhythmias, digitalis induced ventricular arrhythmias

What is the indication of class II antiarrhythmics

Too much positive inotropic effect

What does it mean when an arrhythmia is digitalis-induced?

Potassium channel blockers

Class III antiarrhythmic drugs are also called ____ channel blockers.

Class II antiarrhythmic drugs, potassium channel blockers

Class?

Bretylium Tosylate, Amiodarone

Indication - management of ventricular tachycardia and fibrilation due to other first line treatments (defibrillation or lidocaine)

Adverse - hypotension (orthostatic hypotension)

Admin - injection used in hospital settings

Bretylium Tosylate

Indication

Adverse effects

Administration

Indication - only ventricular arrhythmias

Adverse - nausea, constipation, liver problems, heart arrhythmias, vision, death, NOT FOR PREGNANCY

Admin - idk

Amiodarone

Indication

Adverse effects

Calcium channel blockers

Class IV antiarrhythmics are also called ____ channel blockers.

Verapamil

What is the prototype drug for Class IV antiarrhythmic drugs?

Indication - treatment of supraventricular arrhythmias

Adverse - (IV) hypotension, bradycardia, asystole w/ atrioventricular blocks

Admin - oral and IV

Verapamil

Indication

Adverse effects

Admin

Hypertension

Ischemia (loss of muscle)

valvular regurgitation (volume overload)

What are some factors that indicate development of heart failure?

<40%

HFrEF LVEF?

>50%

Evidence of LV filling pressures

HFpEF LVEF? Other indications?

Fatigue

Orthopnea

Dyspnea

cough

edema

Symptoms of CHF

Echocardiogram

What is the gold standard test for diagnostic tests?

More severe the disease = increase in BNP

What does the BNP tell you?

Stage A

What stage of HF:

no symptoms

At risk - heart disease, cardiac biomarkers, family history

Stage B

What stage of HF:

no symptoms

reduced function, elevating filling pressures suggested

Stage C - Symptomatic HF

What stage of HF:

symptoms

structural heart disease

Stage D - Advanced HF

What stage of HF:

symptoms that interfere with daily life

1. ARNI, ACEi or ARB

2. Beta blocker

3. MRA

4. SGLT2i

5. Diuretics as needed

What are the pillars of treating HFrEF?

Diuretics and SGLT2i

What are the go to drug(s) for HFpEF?