Pharmacology Exam 3

Hypertension is the

#1 cause of cardiovascular disease

Hypertension can be

• Primary: essential, unknown cause (>95% of patients)

• Secondary: result of other diseases

  • pheochromocytoma: tumor of the medulla of the adrenal gland (increased epinephrine)

  • Renovascular disease (renal artery stenosis)

  • Aldosteronism (secreted by adrenal cortex→ increased Na+ and H2O retention)

  • Coarctation of the aorta

Normal blood pressure

<120/<80

Menopause increases the risk of heart disease in women due to

decreased estrogen level in the patient

• estrogen is cardio protective

New guidelines for hypertension

• <120/<80 mmHg (normal)

• 120-129/<80 mmHg (elevated)

• >130/80 mmHg (Hypertension)

  • Stage 1: Systolic between 130-139 or diastolic between 80-89

  • Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg

  • Hypertensive crisis: Systolic over 180 and/or diastolic over 120

As providers we should promote

patients to regularly check blood pressures at home

Medications in HTN

• Stage I if pt has had a CV event (MI, CVA)

• High risk of MI/stroke based on age

• Presence of DM, CKD, atherosclerosis risk

  • Pts may need 2+ meds

  • Pt compliance is important (can use combo meds)

  • Identify socioeconomic status and psychosocial stresses that may put pt at risk for HTN

HTN is a

silent killer

Secondary HTN clues on exam

• Pallor, edema, (pedal or periorbital) signs of renal disease

• Abdominal bruit

• Tunnel obesity, purple striae, buffalo hump (hypercortisolism)- Cushing syndrome

  • Increased creatinine, abnormal urinalysis

  • unexplained hypokalemia (hyperaldosteronism)

  • impaired blood glucose (jhypercortisolism)

  • Impaired TFT (Hypo/hyperthyroidism)

HTN can lead to

Target organ damage

• Heart

• Left ventricular hypertrophy

• MI

• Prior CABG

• Heart failure

• Brain (stroke or TIA)

• Chronic kidney disease

• PAD

• Retinopathy

Hypertensive crisis

Acute elevation of BP associated with end organ damage that is potentially fatal

• >180/120 mmHG for 2+ readings

• Damage is done to nervous tissue, renal end arteries and renal arteries as well as ischemia to the mural cardiac musculature

  • Hypertensive encephalopathy

  • Acute aortic dissection

  • Acute MI

  • Acute CVA

Common causes of a hypertensive crisis

• Antihypertensive drug withdrawal (clonidine)

• Sympathetic hyperactivity

• Collagen vascular disease- SLE

• Renal Disease- ARF/CRF

• Trauma to the head- contusion/concussion

• Neoplasia- pheochromocytoma

• Pre-eclampsia leading to eclampsia

• Recreational drugs- cocaine, magic mushrooms, meth

Identifiable causes of HTN

• Sleep apnea

• Drug-induced

• CKD

• Primary aldosteronism

• Renovascular dz

• Chronic steroid therapy and Cushing’s syndrome

• Pheochromocytoma

• Coarctation of the aorta

• Thyroid or parathyroid dz

• Dietary/lifestyle causes

Hypertension acts as

internal pressure on the arterial walls that damages cells and causes inflammatory changes within the body

• macrophages and foam cells start working away at arterial damage and can aggregate enough to cause atherosclerosis within the vessels

Blood pressure can be quantified by

Cardiac output x peripheral vascular resistance= blood pressure

• Blood flow and pressure is determined by vessel resistance and pressure difference between two ends

Anti-HTN drugs

• Diuretics

• Angiotensin Converting enzyme (ACE) Inhibitor

• Angiotensin Receptor blockers

• Calcium channel blockers (CCB)

• Beta (b) blockers

• Alpha (a) blockers

• Centrally acting antihypertensives

• Vasodilators

Baroreceptor reflexes modulate

sympathetic stimulation of CO and PR and adjust BP in response to postural changes and altered physical activity (orthostatic control)

• short term BP control

Kidney regulates the

plasma volume and the RAS system (renin-angiotensin-aldosterone axis)

• long term control of blood pressure

Diuretic MOA

Act at various sited in the nephron to increase urine production and inhibit sodium reabsorption from the nephron that causes an increase in excretion of sodium in the urine (renal tubular secretion)

Classification of Diuretic drugs

• High ceiling (loop) diuretics (Furosemide)

• Thiazide diuretics (hydrocholorathiazide)

• Potassium sparing diuretics (spirnolactone (aldosterone), triamterene (non-aldosterone)

• Others: Carbonic anhydrase inhibitors, Osmotic diuretics

Loop Diuretics

MOA: acts at the ascending limb of henle and inhibits sodium, potassium and chloride reabsorption

• MOST EFFECTIVE Diuretics

• Drugs: Furosemide (lasix), bumetanide, ethacrynic acid

Furosemide (Lasix)- loop diuretic

• MOA: Acts at the ascending loop of Henle and results in the retention of Na+, Cl- and water in the tubule

  • These drugs are the most efficacious of the diuretics, potent natriuretic effect highly efficient

  • Produce kaliuresis by increasing sodium-potassium exchange in the late distal tubule & collecting ducts

  • Increase magnesium & calcium excretion.

Adverse effects of loop diuretics

• Hypokalemia: Loss of potassium via increased secretion in the distal nephron (Dysrhythmias)

• Ototoxicity (reversible) Tinnitus, ear pain, vertigo & hearing impairment

• Dehydration Dry mouth; unusual thirst and scanty urine output

• Hypotension: dizziness, lightheadedness

Furosemide (Lasix) Drug interactions- loop diuretics

• Digoxin induced ventricular dysrhythmias

  • Only when serum potassium level is low

  • Furosemide causes Hypokalemia!!

• Lithium excretion reduced

  • Increase serum lithium levels

• Ototoxic drugs

  • Aminoglycosides (increased ototoxicity)

• Potassium sparing diuretics (spironolactone, triamterene)

Thiazide Diuretics

• Very commonly used diuretics.

• MOA: Block reabsorption of sodium and chloride in the distal convoluted tubule, Increase renal excretion of sodium, chloride, potassium and water

  • Orally efficacious (effective), have moderate natriuretic effect, Low ceiling diuretics

• Contraindications: Not effective when immediate Diuresis required, use cautiously in Sulfa-drug allergy, do not use in pregnancy

Hydrochlorothiazide- thiazide diuretics used to tx

• Essential hypertension

  • Reduce blood volume: Decrease load, immediate anti-hypertensive effect.

  • Reduce arterial resistance: This effect develops over time, mechanism unknown

• Edema

  • Patients with heart failure (mild to moderate) or with renal or hepatic disease

• Diabetes insipidus -excessive urine production

  • A paradoxical effect; Mechanism unknown

Hydrocholorathiazide (HCTZ) adverse effects

• Hypokalemia (Excessive loss of K+)

• Elevated Uric acid (hyperuricemia)

  • Inhibit uric acid secretion from the proximal tubule (DO NOT USE IN GOUT)

• Elevated lipid levels (hyperlipidemia)

  • Altered serum lipids: HDL, LDL

• Elevated blood glucose (Hyperglycemia)

  • In part due to hypokalemia, which reduces insulin secretion by pancreatic beta cells

• Sulfa allergies

Cannot use this drug in DM, Gout, hyperlipidemia

Potassium sparing diuretics

Act in the distal tubule where sodium is normally reabsorbed in exchange for Potassium, they decrease sodium reabsorption and thus decrease Potassium excretion

• Useful to counteract potassium loss induced by Thiazide and Loop diuretics

• They produce a modest increase in urine production

• Not potent as a stand-alone drug to promote diuresis

2 Types of Potassium sparing diuretics

• Epithelial sodium channel blockers (Amiloride; Triamterene)

• Aldosterone receptor antagonists (Spironolactone): blocks action of Aldosterone ( Adrenal cortex hormone)

  • Aldosterone promotes Sodium retention and Potassium excretion

  • Decrease Na+ reuptake (more in lumen)

  • Increase retention of K+

Adverse effects of potassium-sparing diuretics

• Hyperkalemia

• Endocrine effects

  • Male: Gynecomastia; Impotence

  • Female: Menstrual irregularities, Breast tenderness and enlargement

• Spironolactone (Aldactone)

  • blocks action of aldosterone

    • decreased Na+ reuptake (more in lumen)

    • Increased retention of K+ (more recovered)

Clinical uses of Potassium Sparing drugs

• Prevention & treatment of hypokalemia

• Primary hyperaldosteronism

• Polycystic ovary disease (antiandrogen effect)

• Hirsutism

Hyperkalemia presentation

N/V, dizziness, blood dyscrasia

Osmotic Diuretics

• They are freely filtered at the glomerulus and undergo minimal reabsorption

• They do not have a molecular target (no receptors).

• They act via their physiochemical properties

  • Increase osmotic pressure of tubular fluid, reducing water reabsorption

• Meds: Mannitol, Isosorbide, Urea, Glycerol

Carbonic Anhydrase Inhibitors

• Carbonic anhydrase: Enzyme

  • Present in many nephron sites -luminal, basolateral membranes and cytoplasm of the epithelial cells and RBC.• Critical step in bicarbonate reabsorption

• Carbonic Anhydrase Inhibitor

  • Block sodium bicarbonate reabsorption, causing sodium bicarbonate diuresis and a reduction in body bicarbonate stores

Uses for a diuretic

• Cardiovascular diseases

• Hypertension

• Renal diseases

• Endocrine abnormalities

• Treatment of glaucoma

• Managing increased intracranial pressure

• Altitude sickness (Acetazolamide- Diamox)- carbonic anhydrase inhibitors

Angiotensin Converting Enzyme Inhibitors (ACE-I) Method of action

• MOA: Renin is released from its storage in afferent and efferent vessels with adrenergic stimulation

  • Renin (kidney) combines with angiotensinogen (liver) = Angiotensin I,

  • Angiotensin I goes to the lung and is acted upon by Angiotensin Converting Enzyme (ACE) to convert to Angiotensin II

    • Blocking the ACE means that no vasoconstriction occurs

  • Angiotensin II is a potent Vasoconstrictor, It also stimulates release of Aldosterone from adrenal cortex

  • Aldosterone results in sodium reabsorption

• Used in Hypertension (first line), Heart Failure and post Myocardial Infarction (MI)

ACE-Inhibitors recognize (prils)

Widely used, important class of antihypertensive drugs

• All generic names of this drug class end in ‘- pril

  • Enalapril (Vasotec), Ramipril (Altace), Lisinopril (Prinivil)

  • Used alone or in combination with other Antihypertensives

ACE-Inhibitor Overview

Captopril; Enalapril; Fosinopril; Lisinopril; Ramipril

• Clinical Uses: Hypertension; cardiac failure; diabetic nephropathy; MI

• Mechanism: Inhibition of ACE, inhibits production of angiotensin II

• Pharmacological Effects

• Vasodilation: Mainly arterioles, less on veins. Decrease PR

• Loop & Thiazide Diuretics

  • Augmented hypotension and renal insufficiency

  • Caution when used in combinations

  • Anti-hypertensives, Combined hypotension

• Drugs that increases Potassium levels

  • K supplements/ Potassium-sparing diuretics.

• Lithium increases

Side effects of ACE-Inhibitors

• Rash: maculopapular erythematous

• Dry cough (lisinopril- bradykinin)

• Contrainidcated in pregnancy and renal failure

Angiotensin II Receptor blocker (Sartan)

• MOA: Angiotensin II has a strong vasoconstrictor effect due to activation of Angiotensin II receptors present on Blood vessels, ARBs compete for these receptors and Block them

  • block activation of angiotensin receptors which makes vascular smooth muscle dilate

• Losartan, Olmesartan, Telmisartan, Valsartan

• No cough

• Adverse effects: dizziness, not given in pregnancy or renal dz

• Pros: DO NOT increase serum glucose, uric acid, alter serum lipid levels

Beta blockers (olol)

Propranolol, Metoprolol, Atenolol

• MOA: Sympathetic Antagonists at the Beta receptors in Heart and Blood vessels

  • Inexpensive agents used with diuretics for hypertension.

  • Decrease pulse rate and Oxygen demand of heart muscle

    • Block Beta 1 and beta 2 receptors or only Beta 1

      • Beta 2- make sure pt doesn’t have asthma (problem with breathing)- bronchoconstriction lifethreatening

    • Block the positive inotropic (force) and chronotropic (frequency) effect

    • Decrease rate of spontaneous depolarization, slow AV conduction (dromotropic effect)

Uses of beta blockers

Management of hypertension: Acute and chronic

• Atenolol is cardio-selective: Mx of Angina pectoris

• Timolol blocks beta receptors on Ciliary blood vessels: Decreases production of aqueous humor (IOP) in Glaucoma

• Propranolol: Mx of Hypertension, Angina, SVTs, Migraine prophylaxis, tremors, social phobia, GAD (anxiety)

• Esmolol (Ultra short acting): critically ill patients

Propranolol- B-Blockers

• Mild to moderate hypertension

• Severe hypertension - combine with vasodilators

• Blocks B1 and B2 adrenoceptors (non-selective)

  • Decreases BP by decreasing Cardiac Output

• Inhibit the stimulation of renin production• (which is via B1 stimulation by catecholamines)

  • Depress (partly) the renin-angiotensin-aldosterone system

  • Propranolol is contraindicated in First degree heart block, Congestive heart failure, Cardiogenic shock COPD and bronchial asthma

• Given orally for hypertension/ IV for arrhythmias

Metoprolol (Lopressor/Toprol XL)

• Cardioselective (block B1, B2 sparing), given IV

• Used for: HTN, Angina, MI, CHF

• Cons: Enhances effects of benzodiazepines (CNS depression), masks signs of hypoglycemia and hyperthyroidism

• Advantage: HTN with history of asthma, diabetes, PVD

Labetolol

• Normodyne/ Trandate

• Alpha 1 + Beta 1 and 2 Blocker

• Alpha: Vasodilation, decreased PR, orthostatic hypotension• Beta: SA node, AV node, Ventricular muscle: Bradycardia

• Used IV intra-op

• Attenuates hypertension and tachycardia post surgery

• Used for Pheochromocytoma and Clonidine withdrawal

• Specifically used for Cardiac, Vascular, General and intracranial surgical procedures

Calcium Channel Blockers (CCB)

• MOA: blocking calcium channels inhibits smooth muscle contraction that leads to vasodilation of arterioles and negative ionotropic and chronotropic effects on the heart

  • Nifedipine: peri-op HTN

  • Verapamil: slows SA and AV conduction transmurally

Types of CCB

• Dihydropyridines: Amlodipine, Nifedipine- good for HTN

  • Nifedipine is used in ACUTE episodes

• Non-dihydropyridines: Diltiazem, Verapamil- act on SA and AV

  • DOC for cardiac arrhythmia

  • Decrease contractility (dromotropic), ionotropic, and chronotropic

Clinical considerations of CCB

Dizziness, headache, syncope, tachycardia, drug induced hypertrophy

• increased CV depression with general anesthesia

• Diltiazem increases sedative effects of benzos

• Increased chances of HoTN and bradyarrhythmia with concomitant use of Diltiazem and BBlockers

Anti-Anginal Drugs

• Angina: pain in chest syndrome

  • occurs d/t ischemia in heart muscle

• Risks: hypercholesterolemia, famhx of MI, HTN, age/race/gender, co-existing cardiac dz, smoking, alcohol, substance abuse, vasospasm (Prinzmetal’s angina)

Symptoms of angina

Substernal pain (squeeze/constriction/burning)

• radiation to jaw, neck, shoulder, left arm

• associated with N/V, dizzy, fear of doom

6 classes of drugs used for management of Anginan

1. Organic nitrates- Nitroglycerin

2. CCB- Nifedipine, Verapamil

3. Beta-Blockers- Propranolol, Atenolol

4. Antiplatelets and Anticoagulants- Aspirin

5. Ranolazine- Chronic angina pts who fail traditional therapy

6. Trimetazidine- Decrease oxidation of free fatty acids

Nitrates

Nitroglycerin (Nitrostat, Nitro-dur patch)

• EDRF: Endothelial derived relaxing factor→ Nitric oxide

  • Prodrug that converts in the smooth muscle

• Dilates coronary and pulmonary vasculature

• Used sublingually in acute angina attacks

  • HA are common (use Tylenol)

  • Use up to 3 doses, onset of 1-3 mins

  • STORE IN GLASS BOTTLES

Nitro patches

• Used prophylactically for angina

• Applied for 12 hours, off for 12 hours

  • Risk of tachyphylaxis (NEED off period)

• SE: HA, dizzy, lightheaded, HoTN, alcohol risk)

Angina types

• Angina pectoris- atherosclerosis, blockage beyond a certain time

  • Stable: atherosclerosis

  • Unstable: atherosclerosis with blood clot

• Prinzmetal’s (variant)- coronary vasospasm often with transient ST-segment elevation, often occurs at rest

  • Responds to CCB and nitrates

• Ludwig’s angina- bacterial cellulitis of the floor of the mouth and neck d/t bacterial infection

Angina s/s

• manifests as a tightening or pressure sensation in the chest (elephant on my chest)

• imbalance between myocardial oxygen supply and the oxygen demand

Angina Pectoris

Chest pain or discomfort that arises when the myocardial oxygen supply (dependent on coronary blood flow) is insufficient to meet the heart’s metabolic demands

• cardinal manifestation of CAD

Chronic stable vs unstable angina

• Chronic: presents as discomfort precipitated by exertion or stress, relieved by rest or nitroglycerin

• Unstable: more dangerous form of ischemia heart disease that demands urgent medical attention (acute coronary syndrome) and often occurs at rest

• Medication therapy focuses on

  • reducing O2 demands

  • improving coronary blood flow

  • minimizing atherosclerotic progression

  • lifestyle modification

Goals of pharmacotherapy in angina

1. Improvement of myocardial O2 balance

2. Symptom relief- minimizing severity and frequency

3. Prevention of cardiac events

4. Enhancement of quality of life

5. Decrease hear rate, contractility, and other contributors to myocardial workload

6. Dilate coronary vascular to improve blood flow in ischemic regions

7. Prevent platelet aggregation and thrombosis

8. Slow progression of atherosclerosis by modifying lipid profiles (statins are foundational)

Beta-Blockers in angina (olol)

First line therapies of choice for chronic stable angina (use B1 for more selective heart)

• MOA: Prevent catecholamines from binding to B1 receptors

• decrease heart rate (negative chronotropic), contractility (negative ionotropic), and conduction velocity (negative dromotropic) that causes a reduction of oxygen requirements for the cardiac muscles

  • B1 selective: Metoprolol, Bisoprolol, Atenolol

  • Non-selective: Propranolol, Carvedilol

    • Block B1/B2/A1: Carvedilol and Labetelol

Clinical uses of beta blockers

• Stable Angina: standard for rate control, symptom alleviation and limiting ischemic episodes

• Post-MI Management: lowers mortality post MI

• HTN pts: esp those with angina too

• SE: bradycardia and potential heart block, fatigue and exercise intolerance, bronchospasm (COPD or asthma), exacerbation of PAD (modulates SA-AV conduction), abrupt withdrawal can cause rebound tachycardia or ischemia

Calcium Channel blockers (CCBs)

• Dihydropyridines- (dipine: Amlodipine, Nifedipine): target vascular smooth muscles leading to arterial dilation and a drop in systemic vascular resistance (after load)

• non-Dihydropyridines (Verapamil, Diltiazem): reduce heart rate and contractility by inhibiting calcium enters in the sinoartial (SA) and atrioventricular (AV) nodes

  • Class 4 anti-arrhythmia meds

• Clinical use

  • Prinzmetal’s Angina: CCB of both subtypes for vasospastic angina

  • Stable Angina: Symptomatic relief or alt when B-Blockers contraindicated

  • HTN+Angina: Amlodipine

SE of CCB

• Dihydropyridines: peripheral edema, HA, flushing, reflex tachycardia (immediate release)

• Non-dihydropyridines; bradycardia, AV nodal blockade, constipation (verapamil), additive negative ionotopy (decreased contractility)

  • With a Beta-blocker: potential for excessive bradycardia and AV block

Nitrates

Nitroglycerin- release nitric oxide (NO), vasodilator of veins and arteries

• MOA: NO activates guanylyl cyclase that raises cGMP levels that promotes dephosphorylation of myosin light chains and leads to smooth muscle relaxation

  • reduce venous return (preload) and thereby lowering myocardial wall stress and O2 consumption

  • High dose can dilate after load as well

• Forms:

  • Sublingual Nitroglycerin tablets/spray (bypasses hepatic first pass effect): rapid onset for acute angina relief

  • Transdermal patch or ointment: provides longer-duration prophylaxis

  • Oral isosorbide mononitrate/Isosorbide dinitrate: prophylactic of chronic angina

SE of Nitrates

• TACHYPHYLAXIS

  • Nitrate free interval with the patches to maximize effectiveness during the day when needed

    • 12 hrs on, 12 hrs off

• HA

• Orthostatic HoTN

• Flushing

• Interaction with PDE5 Inhibitors (Tadalafil or Vardenafil, Sildenafil) used in ED: potentially life threatening HTN

Ranolazine

• MOA: inhibits late inward sodium current in cardiac myocytes that reduces intracellular calcium→ reduces diastolic wall tension and oxygen demand

• Indications (adjuvant)

  • Chronic stable angina: Added to standard therapy (B-blocker, CCB, nitrates) to reduce angina freq. and increase exercise tolerance

  • Preserved BP and HR: use in pts that develop bradycardia or HoTN on other agents

  • Good with pts with refractory angina

• SE

  • QT prolongation: esp with the addition of “azole” antifungal drugs and macrolide abx (azithromycin, clarythromycin, erythromycin)

  • Dizziness, HA, constipation

  • Drug interactions (metabolized by CYP3A4): antifungals, macrolide antibiotics

CYP2D6

Metabolize opioids

ASA Therapy

Integral for preventing ACS events (esp in unstable angina)

• ASA (Asprin)

  • MOA: irreversible inhibition COX-1 curtails A2 synthesis reducing platelet aggregation

  • Low dose aspirin (75-100 mg) is recommended for most pts with CAD

  • SE: GI irritation (reduced PGE1/2- good prostaglandins in the stomach), bleeding risk, rare hypersensitivity reaction (Samter’s Triad)

Clopidogrel (Plavix), Prasugrel (Effient)

• MOA: Block ADP-mediated platelet aggregation

  • Often combined with Aspirin (dual antiplatelet therapy) for high-risk patients or after stent placement.

  • Antiplatelet agents prevent progression from stable angina to unstable presentations or myocardial infarction.

Statins

Do not provide anginal relief, prevent atherosclerotic progression and improve endothelial fxn and stabilize plaques

• Atorvastatin, Rosuvastatin

• MOA: inhibit HMG-CoA reductase which lowers LDL cholesterol

  • Low levels or LDL slow plaque accumulation and helps regress existing atherosclerotic lesions

  • Low levels of LDL/High levels of HDL (need a balance)

• Evidence for use

  • reduce CV events and mortality

  • Statin is recommended in angina unless contraindicated

• Ezetimibe and bile acid sequesterants can be used if statins are not effective alone

• SE:

  • Myalgia/Myopathy: muscle aches potentially leading to rhabodomyolisis (myopathy: d/t release of myoglobin, acute renal failure)

  • LFT abnormalities: monitor periodically

  • New-onset diabetes risk

Evidence based combo

• Beta blockers and nitrates: no reflex tachycardia and reduce preload

• Beta blockers and Dihydropyridine CCBs: balance each other out no reflex tachycardia

• Ranolazine as an Add-On: Unresponsive or intolerant of high dose antianginal

• Antiplatelet agents and statins

Intervention of Unstable angina

Heightened risk of MI

1. Hospitalization and cont. ECg monitoring

2. High intensity statins: plaque stabilization

3. DAPT: thrombosis prevention (Aspirin+Plavix)

4. Anticoagulant (IV heparin)

5. Possible revascularization (CABG)

Future direction of anti-ischemic treatment

• Ivabradine: lower heart rate without reducing contractility (HF)

• Gene and cell therapies

• PCSK9 Inhibitors: lower LDL cholesterol

• Novel antiplatelet/antithrombotic agents

• Ongoing trials: IL-1 inhibitors

Arrhythmias can present as

• MI

• Syncopal episode

Arrhythmia- abnormal heart beat

• Fast: tachycardia

• Slow: bradycardia

• Irregularly (Flutter- too fast but regular rhythm/Fibrillation)

  • Life threatening (V-fib)

  • Incidental ectopic (skipped or too early-premature contraction)

The electrical impulse originates (pacemaker) from which of the following area in the heart?

SA node

Normal HR

72 bpm

• In the absence of extrinsic neural or hormonal influences (parasympathetic) the SA node would be around 100 bpm

What is responsible for the contraction of the ventricles?

Purkinje fibers

In what part of the heart’s conducting system is impulse delayed?

AV node

• Purpose: Give time for the ventricles to fill

Parasympathetic control of the heart

Medulla and vagus nerve

• Ach controls rate of SA and AV node

• Ganglia close to the organ

• Decrease chronotropy

Sympathetic control of the heart

• Ganglia far from the heart

• Nerve ending in heart produces NE

• Ach at the end of the sympathetic ganglia chain

• Increase chronotropy, ionotropy, dromotropy

ANS is comprised of

Both sympathetic and parasympathetic

• Which of the above systems controls the heart rate at a resting rate of 60-75 bpm during rest, sleep, or emotional tranquility?

  • Parasympathetic- Ach

Which of the following is the NT at the neuromuscular jxn (skeletal muscle)?

Acetylcholine

Both sympathetic and parasympathetic pathways are composed of how many number of neuron chains?

Two

Which of the following NT is secreted at preganglionic neurons of both the sympathetic and parasympathetic system?

Acetylcholine

Which of the following NT is secreted at majority of the postganglionic endings of the sympathetic nervous system?

Noradrenaline

Norepinephrine (sympathetic) receptors and their functions in the heart and vessels

• a1: postive ionotropy, chronotropy, dromotropy→ vasoconstriction

• B1: postive ionotropy, chronotropy, dromotropy→ vasoconstriction

• B2: postive ionotropy, chronotropy, dromotropy→ vasodilation

  • Sympathetic agonist acting on the blood vessels: Ephedrine

Ach (parasympathetic) receptors and their functions in the heart and vessels

• M2: negative ionotropy, chronotropy, dromotropy→ vasodilation

  • Parasympathetic antagonist: atropine

Symptoms of arrhythmia

Can be none

• Fluttering in the chest, chest pain, SOB, lightheaded/dizzy, sweating, fainting (syncope) or near syncopal episode, cardiac arrest

Risk factors for arrhythmia

• HTN

• DM

• Thyroid disorders

• Smoking

• Alcohol

• Caffeine

• MI

• Stroke/pulmonary embolism

• Cardiomyopathy

• HF

• Orth HoTN

• Lyte imbalance

• Hypothermia

• Drugs: Digoxin, narcotics, antianginals, inotropes, anesthetics, antibacterials, bronchodilators, antiarrhythmics, Illegal drugs

Dx arrhythmia

• PE: pulse and auscultation

• Definitive tests

  • ECG

  • Blood and urine

  • Holter monitor

  • ECHO

  • Chest X-ray

  • EP studies

  • Cardiac catheter (CABG) or percutaneous intervention (PCI)

• Tests that are contraindicated

  • Exercise stress tests

T- wave

ventricular repolarization

P-wave

Atrial depolarization

QRS complexes

ventricular depolarization (and atrial repolarization)

CHF has

isolated ectopic beats

• a sudden abnormal atrial beat

Digitalis toxicity has

Scooped T-wave/curved ST segment

• premature AV beats

• requires therapeutic drug monitoring

Hypokalemia

premature ventricular beats “U waves”

Hyperkalemia

Tall T-waves (spiked T-waves)

Paroxysmal super ventricular tachycardia (PSVT)

• Suddenly come and go

• P waves are buried

• QRS may be wide or normal

• PE: dizzy, lightheadedness, anxiety, 150-250 bpm

Sinus bradycardia is caused by

• Normal in young, healthy athletic people

• Medication causes: Digoxin (HF), phenothiazines (anti-psychotics), opioids

AV Heart Block is caused by

• Coronary artery disease

• Medication causes: B-blockers, CCB

• Electrolyte imbalance (hyperkalemia)