Cardiovascular

Front 1

How many L a day does the heart pump

Back 1

7000L/day

Front 2

What contributes to cardiac output?

Back 2

CO = HR x SV (stroke volume)

Front 3

Afterload =

Back 3

The pressure that must be overcome by the left ventricle that is set by the aorta.

Front 4

Laplace's Law =

Back 4

T = PR/W (tension in the wall of a cylinder, pressure, radius, wall thickness). The more it stretches, the more energy required to contract. If the heart is very full of blood, more energy required to pump.

Front 5

Frank-Starling mechanism

Back 5

The Frank–Starling law of the heart states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.

Front 6

Ejection fraction =

Back 6

= left ventricle stroke volume / end diastolic ventricular volume

Front 7

NO, PGI2 (prostacyclin), endothelium-derived relaxing factor, C-type natriuretic peptide

Back 7

Vasodilation

Front 8

TXA2, endothelins, endothelium-derived contracting factor. What do they do?

Back 8

vascular contraction

Front 9

What does renin (kidney) do?

Back 9

Converts angiotensinogen (liver) into Angiotensin I (inactive)

Front 10

What does ACE (angiotensin converting enzyme, in the lungs) do?

Back 10

Converts angiotensin I into angiotensin II

Front 11

What does angiotensin II do?

Back 11

stimulates adrenals to release aldosterone

Front 12

What does aldosterone do?

Back 12

Stimulates heart function, vasoconstriction, and sodium and water retention in kidneys (raises BP)

Front 13

What contributes to the resting potential of cardiac muscle?

Back 13

K+ channels open at rest (Nernst potential), Na+/K+ pumps maintaining gradients (3Na+ out / 2K+ in)

Front 14

When do L-type calcium channels open?

Back 14

contraction of myocyte. Ca2+ flows in, interacts with troponin C, actin-myosin cross-linking, contraction.

Front 15

Two mechanisms to relax myocytes after Ca2+ influx

Back 15

Ca2+ sequestered by Ca2+-ATPase into stores; Ca2+ pumped out of cell by Na+/Ca2+ exchanger

Front 16

How does digitalis glycoside work?

Back 16

Normally, Na/K ATPase pump pumps 3Na+ out of the cell in exchange for 2K+ into the cell, causing polarization. Digitalis blocks the pump, resulting in myocyte depolarization and heart pumping

Front 17

What is the difference in action potential initiation in ventricular cell vs. sinoatrial cell?

Back 17

Na+ initiates the ventricular depolarization, but Ca2+ initiates SA action potential.

Front 18

What are the contributing factors to blood pressure?

Back 18

BP = CO x PVR x BV

(Blood pressure, cardiac output, peripheral resistance, blood volume)

Front 19

Autonomic receptors for blood pressure/CO2 concentration

Back 19

Carotid sinus nerve and aortic arch receptors

Front 20

Which populations are more worrisome with hypertension?

Back 20

Pregnant women, children, diabetics

Front 21

How do NSAIDs affect blood volume and anti-hypertensive drugs?

Back 21

Increase blood volume, and COX1/COX2 (nonspecific) interact with antihypertensive meds.

Front 22

Thiazides target what? What are the relevent AE's?

Back 22

Na/Cl cotransporter, distal convoluted tubule, block Na reabsorption. Also mildly vasodilate by opening of ATP-sensitive K+ channels.

AEs: Increase Ca2+ reabsorption (can cause hypercalcemia). Also eliminates K+, can result in hypokalemia. Can also cause volume depletion and xerostomia.

Front 23

Furosemide class and mechanism. AE's of hydrochlorothiazide and furosemide

Back 23

Loop diuretic. Xerostomia, sialadenitis, thrombocytopenia (increased bleeding)

Front 24

Propanolol

Back 24

Non-selective beta blocker (antagonist). Both beta-1 and beta-2 blockers

Front 25

Metaprolol, atenolol

Back 25

Beta blocker.Selective beta-1 antagonist. Cardioselective, metaprolol is the drug of choice for patient with history of CAD and HF. Better than propanolol for asthmatics.

Front 26

Acebutol

Back 26

Beta blocker.Partial beta-1 agonist. Cardioselective

Front 27

Carvedilol, labetolol

Back 27

Beta blocker. Mixed beta/alpha1 blockers (decreases inotropy and chronotropy, and prevents vasoconstriction). Carvedilol can cause periodontitis and thrombocytopenia

Front 28

Prazosin- minipress

Back 28

alpha1 antagonist, blocks vasoconstriction. Also increases good cholesterol and decreases bad. AE: dizziness, drowsiness, orthostatic hypotension

Front 29

alpha-methyldopa

Back 29

antihypertensive drug with many mechanisms. Metabolite acts as alpha2 agonist, DOPA decarboxylase inhibitor

Front 30

Clonidine

Back 30

CNS alpha-2 agonist, stimulates vasodilation, decreased HR and BP.

Front 31

Reserpine

Back 31

Sympatholytic (indirect acting antihypertensive). Inhibits the NE pump, prevents NE transport into vesicles. AE: depression.

Front 32

Guanethidine

Back 32

Sympatholytic (indirect acting antihypertensive). Compteition for the NE/E pump. Blocks exocytosis and release of NE/E

Front 33

Beta blockers dental AE's

Back 33

Xerostomia, thrombocytopenia (increased bleeding), orthostatic hypotension.

DI with non-selective beta-antagonists and epi in local anesthesia (increases BP)

Front 34

Nifedipine, Amlodipine

Back 34

Dihydropiridine. Calcium channel blocker in heart. Vasodilation, decreased cardiac output. Does not affect AV conduction or contractility. More effective on smooth muscle cells- blood vessels- than myocytes).

AEs: dizziness, palpitations, edema, peripheral venodilation

Front 35

Verapamil, diltiazem

Back 35

Non-dihydropiridine. More effective on myocytes (L-type Ca2+ channels) than smooth muscles (bv's). Decreased myocardial O2 consumptions by decreased chronotropy and inotropy.

AEs: reduces conduction of AV node at high doses. Constipation.

Front 36

Dihydropiridines (nefidipine and amlodipine), and non-dihydropiridines (diltiazem and verapamil), have what dental AE?

Back 36

Gingival hyperplasia. Much higher in nifedipine and diltiazem (older meds). Can replace these with amlodipine and verapamil.

Front 37

Calcium channel blockers used to treat hypertension can also be used to treat what?

Back 37

Cardiac arrhythmias and angina. (Dihydropiridines- nifedipine, amlodipine. Non-dihydropiridines- verapamil and diltiazem)

Front 38

Sodium nitroprusside

Back 38

Direct-acting vasodilator. cGMP-induced NO secretion. Only emergency situation, very short half life. Affects both veins and arteries

Front 39

Minoxidil

Back 39

Direct acting vasodilator (opening of ATP-sensitive K+ channels). Does not affect veins .Very effective but water retention AE!

Front 40

Hydralazine

Back 40

Direct acting vasodilator. Decreases pre-capillary resistance. Tx of mild to moderate hypertension.

Front 41

Captopril, enalapril, benazepril

Back 41

ACE inhibitor. Prevents angiotensin I -> angiotensin II (by the lungs).

Preferred drug in HT/diabetes, HT/syst or diastolic HF.

More effective in young and white patients.

AE: Dry, hacking non-productive COUGH when supine. Sensitivity in COPD/asthma pts. Do not administer in 1st trimester pregnancy- renal development abnormalities/abortion.

Front 42

Losartan, Candesartan

Back 42

Angiotensin receptor blocker (in adrenal glands). -tan = antagonist.

Same AE's as ACE inhibitors- don't administer in 1st trimester pregnancy. Dry hacking cough when supine, but less than in ACE-inhibitors.

Front 43

Spironolactone, eplerenone

Back 43

Aldosterone receptor blocker. Targets kidney.

Front 44

What constitutes a hypertensive emergency? What are the drugs to treat?

Back 44

diastolic > 120mmHg. IV nitroprusside, nitroglycerine, fenoldopam, nicardipine

Front 45

What do myoglobin, CK-MB, and troponin measure?

Back 45

Acute coronary syndrome and MI

Front 46

What markers assess coronary risk?

Back 46

hsCRp (c-reactive protein), homocysteine

Front 47

What markers signal cogestive heart failure?

Back 47

B-type natriuretic peptide (BNP) and ProBNP

Front 48

Stable angina causes what electrical changes?

Back 48

ST depression (NSTEMI). No detectable damage, induced by stress.

Front 49

Unstable angina causes what electrical changes?

Back 49

Elevation or depression of ST, inversion of T waves. May lead to permanent damage, occurs during rest or stress.

Front 50

Variant angina (Prinzmetal's)

Back 50

hypoxia and ischemia caused by vasospasm, ST elevation only at time of angina. Not due to atherosclerosis, but random vasospasm.

Front 51

Subendocardial ischemia vs transmural or epicardial injury

Back 51

Subendocardial is directed toward inner layer of ventricle, so overlying leads record ST depression (NSTEMI) or T wave inversion.

Transmural involves the outer ventricular layer, so leads will record STEMI.

Front 52

Order of marker presentation after acute MI

Back 52

Myoglobin (1-4h until 24h),

CK-MB (3-12h until 1.5-2 days),

Troponin (3-12h until 1-2 weeks)

LDH and CK

Front 53

Dipyridamole

Back 53

stress agent for myocardial perfusion imaging. Also a platelet aggregation inhibitor. Coronary vasodilator (increases adenosine availability?).

AE: dyspnea in 45% patients with COPD

Front 54

Adenosine

Back 54

stress agent for perfusion imagining. Decreases AV conduction (antiarrhythmic), potent vasodilator, decreases BP

Front 55

Which drugs interact with dipyridamole and adenosine?

Back 55

Theophylline, caffeine, Ca2+ blockers and nitrates, beta blockers

Front 56

Dobutamine

Back 56

Sympathomimetic, stress agent for perfusion imaging. Vasodilator, increased BP (chornotropy and inotropy). Drug of choice in patients unable to exercise or tolerate vasodilator.

DI: beta blockers

Front 57

How can you decrease cardiac work load?

Back 57

Decrease preload by venodilation. Decrease afterload- lower BP and peripheral resistance through vasodilation. Decrease myocardial work.

Front 58

What does heparin do?

Back 58

Antithrombotic but not fibrinolytic. Does not dissolve existing clot.

Front 59

recombinant tissue plasminogen activator (rt-PA)

Back 59

Fibrinolytic- decrease and reverse ischemia.

Front 60

How does ASA work?

Back 60

Decreases platelet aggregation initiated by endothelial injury (thus decreasing vasoconstrictors- TXA2, serotonin, ADP, thrombin, platelet activation factor). Irreversibly inhibits COX, leading to reduction in thromboxane and prostaglandins (prostacyclin)

Front 61

Clopidogrel (Plavix)

Back 61

Antiplatelet aggregation. Prodrug, activated by CYP2C19, which is inhibited by PPIs and fluconazole! Antifungal drugs (azoles) which treat oral candidiasis can inhibit clopidogrel!

Front 62

Folic acid

Back 62

prevention of nitrate tolerance. Still must remove NO patch overnight

Front 63

Mechanism of NO

Back 63

increased GMP, phosphorylated PKG, decreased Ca2+, vasodilation.

Front 64

How soon after ischemia must rt-PA and other fibrinolytics be used?

Back 64

Preferably before 6 hours for heart cells, 3 hours for cerebral occlusion, and longer for peripheral. Pulmonary embolism- minutes.

Front 65

How do Ca channel blockers work for decrease/reverse ischemia?

Back 65

Block L-type Ca2+ channels. Decreased intracellular Ca2+ and contractility of heart and vascular muscle.

The pathway: Ca2+ + calmodulin join MLCK which phosphorylate MLC. It joins actin to cause contraction.

Note that NO increases cGMP which blocks MLC phosphorylation.

Front 66

Acebutolol, atenolol, propranolol (what are the differences)

Back 66

Acebutolol- beta1 selective, partial agonist

Atenolol- beta1 selective, antagonist

Propranolol- beta1,2 (nonselective), antagonist

Front 67

Emergency protocol for CAD

Back 67

POACH- phone EMS, oxygen, ASA, clopidogrel (Plavix), heparin

Front 68

What are the compensatory mechanisms for heart failure?

Back 68

Ventricular hypertrophy- increased end-diastolic pressure, wall tension. Increased inotropy, ejection volume. Increase in sympathetic ANS activity, renin-angiotensin-aldosterone system.

Front 69

Digitalis

Back 69

Direct inhibitor of Na+/K+ ATPase pump, resulting in increased intracellular Na+.

Indirect inhibition of sodium-calcium exchanger, resulting in increased intracellular Ca2+.

Thus increased actin-myosin cross linking, decreased SA node firing, increased AV node refractory period. (Increased inotropy but decreased chronotropy?)

Narrow margin of safety. Can cause arrhythmias, GI discomofrt, headaches, dizziness, emesis, anorexia. Treatment of digitalis AEs by antiarrhythmic drugs, digoxin binding antibodies (digifab)

Front 70

Milrinone

Back 70

PDE3 inhibitor. Increases cAMP (and thus inotropy and peripheral vasodilation).

(Remember that phosphodiesterase normally converts cAMP to AMP).

IV admin only, for acutely ill hospitalized patients with HF.

Front 71

Dobutamine

Back 71

Selective beta-1 agonist. For acutely decompensated HF. Can't use chronically because tolerance and will work the heart too hard

Front 72

Ivabradine

Back 72

HF novel therapy. SA node inhibitor- prolongs diastolic depolarization. Not to be administered to pts with atrial fibrillation (but many HF pts have this!).

Front 73

Sacubitril/Valsartan

Back 73

Neutral endopeptidase inhibitor (allows heart stimulating enzymes to remain in the heart longer without being broken down by the endopeptidase Neprilysin) PLUS an angiotensin II receptor blocker. Neprilysin also breaks down angiotensin, so inhibiting it will increase angiotensin in the body. Thus you need the Valsartan to block angiotensin II receptors.

Front 74

How are glomerular filtration, tubular secretion, and tubular reabsorption measured?

Back 74

Filtration- creatinine and inulin

Secretion- PAH and penicillin

Reabsorption- glucose

Front 75

GFR value

Back 75

120-125mL/min

Front 76

Carbonic anhydrase inhibitors

Back 76

Target the proximal convoluted tubule, which reabsorbs most Na but is very ineffective drug.

Front 77

Loop diuretics which part of nephron?

Back 77

Thick ascneding loop of henle

Front 78

Thiazides target which part of nephron?

Back 78

Distal convoluted tubule

Front 79

Furosemide (Lasix), ethacrinic acid

Back 79

Loop diuretic targeting ascending loop of Henle where 20-30% of Na is reabsorbed. Most effective, leading to excretion of 20-25% of filtered Na rather than 1% normally excreted.

Mechanism- inhibits Na/K/2Cl cotransporter, leading to Na excretion. Also K and Ca excretion. Thus bad for osteoporosis. Need extra Ca plus vitamin D.

Tx for hypertension (only for patients not responding to thiazides or antihypertensive drugs), peripheral edema, acute pulmonary edema, ascites, acute renal failure, hyperclacema, hyperkalemia, anion overdose (Fluoride, iodide).

AEs: Hypokalemia, hypocalcemia, carb intolerance and hyperuricemia, deafness (dose dependent and rare). DI: blocked by NSAIDs! NSAIDs impair kidney function. For long term use of NSAIDs in hypertensive pts, consider acetaminophen adjunct.

Front 80

Thiazides

Back 80

Target distal convoluted tubule (5-10% of Na). Eliminate Na/K/H, not calcium. Actually decreases calcium excretion, so first choice in osteoporosis pts.

AEs: Hypokalemia, metabolic alkalosis, hyperglacemia/glucose intolerance, hyperuricemia (gout!), hyperlipidemia, hypercalcemia. Also DI with NSAIDs like lasix

Front 81

K-sparing diuretics

Back 81

Aldosterone antagonists (Spironolactone), and non-aldosterone antagonists- Na channel blockers (Amiloride, triamterene).

Mild diuresis (2-3% excretion), target late distal tubule/collecting duct. Weak, usually used in conjunctions with other diuretics to counter-balance K loss.

Spironolactone can also be used to treat primary or secondary aldosteronism

Remember that aldosterone usually causes reabsorption of Na and H2O

Front 82

Acetazolamide, dorzolamide

Back 82

Carbonic anhydrase inhibitors. Less HCO3- in lumen causes decreased Na+ reabsorption. Targets proximal convoluted tubule (area with highest reabsorption). Nevertheless, not very effective as diuretic, so

-used topically for glaucoma (decrease IOP), -urine alkalinization (maintain acid substances in urine, such as uric acid, myoglobin, hemoglobin),

-and to treat metabolic alkalosis.

AE: Metabolic acidosis, hypokalemia

Front 83

Mannitol

Back 83

Osmotic diuretic. Increase osmolarity in blood so water moves from tissue into blood. Decreases edema, intracranial pressure/hemorrhagic stroke. Increases voemia, which decreases viscosity and renin secretion. Demand on heart, bad for pt with heart failure or high BP. Do not use for treatment of peripheral edema! Can cause pulmonary edema in pts with HF! Mainly for treatment of brain edema, renal failure.

Front 84

Horsetail

Back 84

Herbal diuretic. AE: nicotinic toxicity. Avoid in smokers or pts on smoking cessation program.

Front 85

Dandelion

Back 85

Herbal diuretic. AE: increased risk of bleeding in pts on blood thinners. Reduces GI absorption of ciprofloxacin

Front 86

List 2 proinflamm cytokines and 2 adhesion molecules that contribute to atherosclerosis

Back 86

IL-1, TNF-alpha. LAM, ICAM-1.

Front 87

What two classes or drugs are used to treat high plasma lipids?

Back 87

Anti-platelet drugs- ASA, dipyridamole, clopidogrel, ticlopidine

Anti-lipid drugs- bile acid-binding resins, cholesterol absorptions inhibitors, fibrates, statins, nicotinic acid derivatives, PUFAs

Front 88

How are lipoprotein complexes formed?

Back 88

Apoproteins bind phospholipids. Triglycerides and cholesterols are stored inside this spherical shell. Makes lipids more stables and water (blood) soluble.

Front 89

Apo B-100

Back 89

An apoprotein (zip code) found only in lower density lipoproteins. Not found in HDL!

Front 90

Plasmin

Back 90

Cause fibrin breakdown! Dissolution of clot. Relevant to atherosclerosis.

Front 91

Tranexamic acid

Back 91

Topical solution to stop bleeding. Don't swallow!! Can cause clotting!

Front 92

Apo (a) (not ApoA)

Back 92

a highly atherogenic apoprotein (as bad as ApoB-100). Blocks plasminogen from activating into plasmin, so fibrin isn't broken down.

Front 93

Lipoprotein lipase

Back 93

Found in tissues, breaks down chylomicrons to use the fats. Lowers serum lipids. Stimulated by exercise, lowered by smoking.

Front 94

Conditions that contribute to high LDL (secondary dyslipidemia)

Back 94

Hypothyroidism, nephrotic syndrome, anti-rejection meds (cyclosporine, sirolimus, tacrolimus)

Front 95

Conditions that contribute to low HDL (secondary dyslipidemia)

Back 95

TIID, smoking, lack of phys activity

Front 96

Conditions that contribute to high TG (secondary dyslipidemia)

Back 96

TIID, alcohol, chronic kidney disease, hepatocellular disease, pregnancy, abdominal obesity, OCP, estrogen, retinoids, steroids, beta blockers, thiazides, cyclosporine, sirolimus

Front 97

How do statins work?

Back 97

Reduce cholesterol in endogenous pathway. Inhibits HMG-CoA reductase which creates cholesterol. Also excites the LDL receptors, to mop up LDL from blood into hepatocytes. Thus decreased synthesis of cholesterol in liver, decreased liver secretion of VLDL, and increased liver uptake high affinity LDL receptors

Front 98

AEs of statins

Back 98

Myopathy and mylagia. Myositis and rhabomyolysis. Hepatotoxicity and elevated transaminases. GI, dizziness.

DI: CYP3A4 inhibitors (trizaole antifungals, erythromycin, grapefruit juice. CYP2C9 inhibitors (NSAIDs, warfarin, phenytoin).

Taking these meds will cause increase in blood statin levels, increased AEs.

Front 99

Colestipol, cholestyamine, colesevelam

Back 99

Bile acid-binding resins to lower cholesterol. Decrease absorption of bile acids, increase CYP7A1 (increase in bile acids and decrease in cholesterol in liver), and upregulate LDL receptors in liver.

AEs: decrease ADEK, acidic drug uptake. Nausea, vomiting, steatorrhea.

Only lipid-lowering drugs safe during pregnancy.

Front 100

Ezetimibe and plant sterols

Back 100

Cholesterol absorption inhibitors. Inhibit dietary and biliary cholesterol absorption in the intestine (transport protein Niemann-Pick C1-Like1). Also potentiates statins.

No inhibition of vitamin absorption like resins do! Di: cyclosporine.

Front 101

Fenofibrate, bizafibrate

Back 101

Fibrates. Drug of choice for lwoering TG, preventing TG related pancreatitis. Peroxisome proliferator-activated receptor- alpha (PPAR-alpha) agonist.

AEs: GI, caution in pts with liver of kidney disease, pregnant and lactating women, myositis when combined with statins!

Front 102

Niacin (B3, nicotinic acid)

Back 102

Decreased production of VLDL, LDL, and TG. Drug of choice to increse HDL.

AEs: flushing, pruritis (lower in extended reelase), rare hepatotoxicity.

DI: Anti-hypertensive drugs

Front 103

Fish oils/omega 3 PUFAs

Back 103

Alpha-linolenic acid (ALA) derivatives. DHA, EPA. Decreases LDL production and TG. Increases HDL somewhat.

Front 104

Plant sterols/omega-6 PUFAs

Back 104

GLA (gamma-linolenic acid). Less effective for CVD than omega-3's.

Front 105

Which lipid lowering drugs are best for lowering LDL?

Back 105

Statins, resins, omega-3's, and cholesterol absorption inhibitors, and omega 6 and 9 (in order of effectiveness)

Front 106

Which lipid-lowering drugs are best for lowering TG?

Back 106

Fibrates, niacin, and omega-3's (in order of effectiveness)

Front 107

Which lipid-lowering drugs also raise HDL?

Back 107

Niacin and fibrates mostly. Omega 3's and stains too. (in order of effectiveness)

Front 108

Early after depolarization (EAD)

Back 108

Very strong impulse during the refractory period. Only partial, because the fibres had not been fully relaxed yet. Increases number of heart beats.

Front 109

Delayed after depolarization

Back 109

Premature depolarization after recovery but slightly too early. Also raises number of heart beats.

Front 110

1st degree AV block

Back 110

PR interval increased, more than 0.2 sec

Front 111

2nd degree AV block

Back 111

Some QRS's missing. Multiple P waves without QRS following (2:1-3:1)

Front 112

3rd degree AV block

Back 112

Complete AV block. Atrial and ventricular depolarization. Controlled by separate pacemakers. Multiple P waves, never initiating a QRS wave. The QRS wave will spontaneously appear due to spontaneous contraction of ventricles.

Front 113

Conduction re-entry

Back 113

Scar tissue conducts some impulses at a different rate and may cause retrograde conduction along Purkinje fibres. Bad!

Front 114

Quinidine, lidocaine

Back 114

Anti-arrhythmic drugs. Sodium channel blockers. Good at blocking retrograde (re-entry) impulses. Increases effective refractory period.

AEs: quinidine increases plasma digoxin, thrombocytopenia. Other Na channel blockers (class Ic) is contraindicated in CAD- increases mortality.

If lidocaine is given systemically (by mistake) in dentistry, can cause antimuscarinic effects. CYP2D6 inhibitors (relevant to opioids)

Front 115

Which is the most commonly used antiarrhythmic drug?

Back 115

K channel blockers.

Front 116

Amiodarone

Back 116

K channel blocker- antiarrhythmic drug. Prolongs AP and effective refractory period. Blocks Na and Ca channels, alpha and beta adrenoreceptors.

AEs: Pulmonary fibrosis (serious), GI intolerance, ataxia, prolonged QT, torsades de pointes

Front 117

Sotalol

Back 117

Antiarrhythmic drug. Non selective beta blocker that prolongs AP and effective refractory period.

Front 118

Verapamil, diltiazem

Back 118

Ca channel blockers, can be used as antiarrhythmic drugs. Decreases sinus rate and AV node conduction. Negative inotropy, so monitor CAD/HF pt.

Front 119

Digoxin as antiarrhythmic

Back 119

Na/K ATPase and Na/Ca inhibitor. Increase ERP and vagal activity (PSympathetic), and decreased conduction velocity in Purkinje fibres

Front 120

Adenosine as antiarrhythmic

Back 120

Regulates potassium channels via GPCRs. Potassium is allowed to escape, thus creating negativity in the cells, inhibiting muscle contraction. Also causes the inhibition of calcium channel opening. Result: heart relaxation or vasodilation and longer ERP.