Pharmacology Pt. 1 Cardiac Drugs

What are the 2 categories of cardiac drugs?

1. antiarrhythmic + antihypertensives

2. only antihypertensives

What are the 2 types of antiarrhythmic and antihypertensive drugs?

What is the main function?

1. B blockers

2. Ca channel blockers

decrease the heart rate bc they affect the rhythm of the heart + also decrease blood pressure

What are the 3 types of only antihypertensive drugs?

What is the main function?

1. diuretics

2. ACE inhibitors

3. ARB blockers

only decreasing the blood pressure

What category are beta blockers and what is the suffix to remember?

What is the mechanism of action? (don’t necessarily need to know for NPTE but it will help us to connect the dots)

So what is the effect of beta blockers?

What patients would you NOT give beta blockers to?

• beta blockers = anti-arrhythmic + antihypertensive = “-olol”

  • “lol” = we block when someone is LOL at us

• mechanism

  • block the beta-adrenergic receptors, block the action of the sympathetic NS

    • SNS increases HR and BP, vasoconstriction, and bronchodilation = fight/flight response

• effects

  • decrease HR and BP, bronchoconstriction, vasodilation

• DO NOT give to patients with pulmonary conditions like COPD, asthma, because we don’t want the bronchioles to constrict

What are 3 indications for giving a patient beta blockers?

What are 6 adverse affects related to BP, head feeling, noises, HR

What ECG findings would you see?

• indications

  • to reduce HR: arrhythmias, coronary artery disease (CAD), HTN

• adverse effects

  • orthostatic hypotension, dizziness, lightheadedness, ringing of the ears, venous pooling (vascular system/veins are dilated and bloods are getting accumulated in the LEs and unable to pump back to the heart), bradycardia

• ECG findings

  • PR interval increases (time taken for impulse from atria to ventricle) because this prolongs when the HR is reduced

What are 3 considerations for patients using beta blockers?

1. use RPE for exercise prescription

2. do NOT use in asthma, COPD

3. no abrupt withdrawal

Preload is end diastolic volume which means what?

recall which mechanism that works at the end of diastole?

• end diastolic volume

• the amount of blood in the ventricles at the end of diastole

• frank sterling mechanism

  • when the ventricles are filled, the more stretch the ventricles have so the force of contraction is stronger

• if we have a good preload, the force of contraction is good —> good cardiac output

What does afterload mean?

• afterload

  • resistance the heart needs to overcome

• if there is atherosclerosis/plaque deposition, there will not be good cardiac output and there is more afterload/resistance

  • it is hard for the heart to pump

• we need a low afterload to have a good cardiac output

So what would we want for a good cardiac output?

And what happens to pre/after load with beta blockers?

• good CO

  • good/normal preload, reduced after load

• beta blockers slightly or do not reduce the preload, but they do reduce afterload, so it is good/beneficial for us

What category are calcium channel blockers for and what is the suffix(ces) to remember? Give three examples.

What is the mechanism?

What are the effects?

Compare it with beta blockers.

• calcium channel blockers = antiarrhythmic + antihypertensive = “-Pines and -Zems” - CA has pine trees and zem(n) people

  • amlodipine

  • verapamil

  • diltiazem

• mechanism

  • typically, Calcium is for Contraction; calcium deposits constrict in the arteries

  • so Ca blockers will block the entry of calcium in cardiac tissue, thereby reducing cardiac contractility and vasoconstriction

• effects

  • decrease HR, decrease BP

it is similar to beta blockers, but calcium channel blockers DO NOT cause bronchoconstriction, so we can give it to patients with pulmonary conditions

Like beta blockers, what are the indications and adverse effects for patients using calcium channel blockers?

Consideration?

But what is the ECG change?

• indications

  • CAD, HTN, arrhythmia

• adverse effects

  • orthostatic hypotension, dizziness, lightheadedness, venous pooling, bradycardia, ringing of the ears

• consideration

  • use RPE for exercise prescription

• ECG change

  • prolonged QT interval

    • ventricular depolarization = QRS complex + T wave

      • entire contraction; since contraction is reduced, QT is prolonged

CA has pine trees, zen people, and QTs

Practice Question 1

A patient is taking B blockers for three years post myocardial infarction. Which of the following is the MOST LIKELY response to exercise seen in this patient?

A. Rapid increase in HR

B. Decreased exercise tolerance

C. Blunted response of HR with exercise

D. Increased BP

C. Blunted response of HR with exercise

RATIONALE: B blockers reduces HR, BP and improves exercise tolerance. Patient will show a blunted response to exercise; blunted = slow response

Recall the 3 only antihypertensives

Main function?

What are shared common characteristics for the effects of antihypertensives?

1. diuretics

2. ACE inhibitors

3. ARB blockers

ONLY REDUCE BLOOD PRESSURE, NOT HEART RATE

• will be given for same function, HTN, CHF; reduce preload and after load

Which category are diuretics and what are 3 types of diuretics?

What is the mnemonic/suffix to remember?

• diuretics = only antihypertensives

• loop diuretics

• potassium sparing diuretics

• thiazides

di-uretics, -ides

Around the kidney tubule, recall there are small groups of nerve endings/blood vessels in capillaries.

It goes from the glomerulus, to proximal convoluted tubule, to loop of Henle, to distal convoluted tubule.

Where do loop diuretics act on?

What does this mean?

So, what are 4 indications to use loop diuretics?

• usually, some water and electrolytes are re-absorbed into the body at the loop of Henle, but loop diuretics act on the loop of Henle

• if loop diuretics act on the loop of Henle, this means they prohibit the reabsorption, then there is no water or electrolytes, they are flushed/excreted

LOOP diuretics = LOOP of HENLE

• use

  • HTN, CHF, edema, pulmonary edema

What are side effects for a patient using loop diuretics?

Which one is important when you take a lot of it?

Which side effect from B/Ca blockers would you not see in loop diuretics?

• hypokalemia

• hypocalcemia

• hyponatremia

• dehydration

• OH, dizziness, lethargy - due to decrease in blood pressure

• reflex tachycardia

  • although HR is not affected, when the BP decreases, the heart will response by reflexively increasing

• will NOT see venous pooling, because all of the fluid is able to be flushed out

If the fluid is being excreted, what happens to preload and after load for someone with diuretics?

Which patients would you want this in?

• both will decrease

• need this in patients with congestive heart failure (CHF) because the heart is failing and they do not have much strength to have a large preload

• we want to reduce the load on the heart

What is a type of potassium-sparing diuretic?

Think of how the mechanism is similar AND different from loop diuretics.

What are the side effects?

Used in which patients? (3) and do not have a lot of what?

• potassium-sparing diuretic

  • Spironolactone (Aldactone)

• mechanism

  • similar to loop diuretics, but acts on the distal convoluted renal tubule

  • does NOT collect potassium , so potassium stays in the body

• side effects

  • similar to others (OH, dizziness, etc.) but + hyperkalemia, gynecomastia (anti-androgen)

• use

  • CHF, HTN, combined with other drugs causing hypokalemia

    • use this specifically if the patient already has low potassium - should not take loop diuretics

  • do not give them bananas

What is a type of thiazide?

What mnemonic is important to memorize to know what 4 ions are spared?

Knowing this, in addition to regular antihypertensive side effects like dizziness, ringing of ears, OH, hypoKAlemia and hypoNAtremia, what are other side effects?

So who should this be avoided in?

• thiazide = antihypertensive - HTN, CHF, edema

  • hydrochlorothiazide (HCT)

• ions

  • CLUG - calcium, lipids, urea, glucose

• side effects

  • similar +

  • hypercalcemia, hyperuricemia, hyperlipidemia, hyperglycemia

• avoid use:

  • elderly, DM, renal dysfunction, hyperlipidemia, gout (uric acid), kidney

What category are ACE inhibitors and what is the suffix to remember?

Typically, what is the normal mechanism of the liver/angiotensin/aldosterone?

What is the normal function of aldosterone?

• ACE inhibitors = antihypertensives = “-Prils” - A-pril

• liver produces angiotensinogen —> angiotensin I —> lungs / angiotensin converting enzyme (ACE) —> angiotensin II —> adrenals —> aldosterone

• aldosterone

  • retains Na and water, kicks out K

If ACE in the lungs are responsible for converting angiotensin, what would happen if a person takes ACE inhibitors?

What would happen with aldosterone?

How does this affect the side effects?

• if ACE is prohibited, there cannot be conversion from I to II, there is no angiotensin II produced

• without angiotensin II, then aldosterone will not be produced

• if aldosterone is not produced, then there will be a lot of potassium and not enough sodium and water

  • hyponatremia, dehydration

  • hyperkalemia

What patients would you give ACE inhibitors to?

In addition to OH, dizziness/lightheadedness, ringing in the ear, blurred vision, what other side effects would there be?

What is the most important symptom?

• CHF, HTN, pulmonary edema, edema, taken orally

• side effects

  • hyperkalemia, hyponatremia

  • dry hacking cough

    • spring season —> allergies —> dry cough = april

  • decreased taste perception

  • angioedema

    • swelling/fluid in the mucous membranes (lips, under skin)

What is the category for ARB blockers and what is the suffix to remember?

What is the mechanism of ARB blockers?

Therefore, what are the side effects?

Why would you use this over ACE inhibitors?

• angiotensin RECEPTOR blocker = antihypertensive = SARTANS

  • Losartan, Telmisartan, Candesartan

• mechanism

  • blocks the binding of the angiotensin to the receptor, so aldosterone will NOT be produced

    • same thing will happen as ACE inhibitors - will throw out all of the fluid/water/sodium

• side effects

  • OH, dizziness, fatigue, hyperkalemia but there is NO dry hacking cough

• use

  • HTN, CHF

  • intolerance to ACE

Can you combine the use of ACE inhibitors and ARB blockers?

What is another drug you cannot combine with?

• NO, using ACE + ARB would cause too much dehydration and too much potassium

• cannot combine with potassium sparing diuretic

  • hyperkalemia

• ACE + ARB will NOT have reflex tachycardia, but both will reduce blood pressure and increase potassium

Practice Question 2

The physical therapist is educating a patient on the potential side effects from the medication Ramipril. Which of the following side effects will MOST LIKELY correlate with this drug?

A. Increased fluid retention

B. Causes hyperkalemia

C. Increases blood Pressure

D. Enhanced myocardial contractility

B. Causes hyperkalemia

RATIONALE: Ramipril is an ACE inhibitor. It reduces BP, does not affect the HR. It causes hyperkalemia and not Hypokalemia. It decreased fluid retention.

Practice Question 3

The physical therapist is educating a patient on the potential side effects from the medication Candesartan. Which of the following side effects will MOST LIKELY correlate with this drug?

A. Hypokalemia

B. Dry hacking cough

C. Hypotension

D. Prevents the recurrence of atrial fibrillation

C. Hypotension

RATIONALE: Candesartan is an ARB blocker. It reduces BP, reduces fluid retention, does not affect the HR. It causes hyperkalemia and not Hypokalemia. Dry hacking cough is a side effect of ACE inhibitors.

How could you remember cardiac glucosides? What’s an example?

What patients would you use this for? When exactly would this be implemented for the pt?

• cardiac glucosides = digs, oxin - Digitalis, Digitoxin, Digoxin (Lanoxin)

• used for CHF

  • systolic dysfunction = ventricles are not contracting forcefully, do not have the power to contract well

    • decreased ejection fraction <55%

  • used especially when patient demonstrates acute signs of decompensation

    • R side

      • fluid retention, edema, cyanosis, weight gain, JVD

    • L side

      • pulmonary edema, lung compensation

What is the function of cardiac glucosides/digoxin? (2)

ECG change?

End result?

Would a patient be using this drug long term?

• function

  • slows down the HR, allowing better filling of blood

  • increases the strength of the contraction —> increases CO

• ECG change

  • prolonged PR interval, shortened QT interval

    • reduced HR, increased contractility

• fewer + better contractions/beats

• only a SHORT TERM DRUG because the side effects are a lot more than the benefits of the drug

What are the side effects of cardiac glycosides/digitoxin/lanoxin?

How long would you use this for?

Understand those symptoms as if you think that something is wrong with the heart. (3) Think of toxic symptoms. (2) And cognitive (4).

And which common symptom we’ve seen?

• DIGOXIN TOXICITY

  • only a SHORT TERM DRUG because the side effects are a lot more than the benefits of the drug

    • JUST USE WHEN THEY SHOW S/S ACUTE DECOMPENSATION

    • not long term with compensated heart failure

      • compensated = no acute s/s, pt is taking regular medication, low CO

        • would give compensated heart failure patients diuretics, ACE, ARB

• arrhythmia, palpitations, fatigue

• GI disturbances - N/V

• visual disturbance, confusion, delirium, hallucinations

• hyperkalemia

Practice Question 4

A patient with congestive heart failure is taking Digoxin since the last few weeks. Which of the following is an EXCEPTION to common side effects of digoxin toxicity?

A. Disorientation and delirium

B. Ringing in the ears

C. Fatigue and palpitations

D. Gastrointestinal disturbances

B. Ringing in the ears

RATIONALE: Ringing in the ears is due to Hypotension. A,C and D are side effects of Digoxin.

The LAST cardiac drug is nitrates, what is an example?

When is this used for? Explain why the patient would be experiencing that symptom.

• nitrates = nitroglycerin (NTG) , nitrostat, nitroglyceride

• use

  • stable angina - chest pain (Levine sign, when they grab their chest)

  • experiencing angina due to more demand and less supply of blood

Differentiate stable and unstable angina and variant/prizmental angina.

• stable angina

  • occurs with exercise, works with nitroglyceride

  • heart’s demand is a lot more but not getting supply of demand

• unstable angina

  • occurs at rest, does NOT work with nitroglyceride

• variant/prizmental

  • vasospasm of arteries, works with nitroglyceride

Mechanism of nitrates: If you do not have enough blood supply to the heart, what is the purpose of nitroglycerides? What is the effect on HR and other side effects?

Since there is a drastic decrease in blood pressure, what other side effects would appear? (2)

How often would nitrates be used?

• vasodilation of all vessels - arterial and venous

  • to allow for supply to increase

  • causes a decrease in BP —> OH, dizziness, venous pooling because of vasodilation

• facial flushing - vasodilation

• reflex tachycardia - due to drop in BP/vasodilation for heart to compensate

• SHORT TERM when you have an acute episode

How are nitroglycerides taken?

How often?

What is the position the patient should be in when taking the drug?

When is it an emergency?

• sublingually - under the tongue bc it gets absorbed fast

• 1 dose every 5 mins x3

• patient must SIT/LAY when taking nitroglycerin because they can collapse with decrease in BP

• if there is no relief or you feel worse after taking the drug, CALL EMS BC PT MAY BE HAVING AN MI

FF TIPS for when to call 911 after patient is taking nitroglyceride:

• first, second, third dose

1. symptoms worsen after first dose

2. no improvement after second dose

3. pain persists 5 minutes after third dose

because if they are not getting better, the patient is experiencing UNstable angina and may go into MI

• if going through ischemia/MI, the ECG will appear as ST depression >2mm

Practice Question 5

A patient with angina pectoris has been advised to use sublingual nitroglycerin for stable angina. This drug will MOST LIKELY cause which of the following?

A. Lower preload and afterload

B. Increase myocardial oxygen demand

C. Increase preload and afterload

D. Hypertension and bradycardia

A. Lower preload and afterload

RATIONALE: Nitroglycerin (NTG) decreases Preload and afterload, decreases myocardial oxygen demand. The side effects are hypotension and tachycardia and not hypertension and bradycardia.

vasodilation = less blood coming back to heart, decreased preload + less pressure of the heart, decreased afterload

• that’s why we give it before exercise