Anti-Angina Flashcards
● Due to blockage or imbalance of the oxygen supply and demand is too much on the heart
● If oxygen supply cannot keep up with the demand
MYOCARDIAL INFARCTION
What is the primary symptom of Myocardial Infarction?
Angina Pectoris
○ Chest pain
○ Pain over the myocardium
○ Which is associated with Ischemic Heart Disease or Myocardial Ischemia
Myocardial ischemia main dysfunction is when you have
atherosclerosis or when there is blockage inside the arteries
● Increase lipid deposition in subendothelial space which gives way to plaques (early plaque) in the arterial lining/blood vessels
● Leads to endothelial dysfunction with decrease production of Nitrous Oxide (NO) which is a vasodilator
● Less vasodilation, increase risk of platelet adhesion
● Influx of lipid scavenger cells, necrosis, sterile inflammation
● Proliferation of smooth M cells, calcification and narrowing of blood vessel by inc plaque formation
ATHEROSCLEROSIS
What are the triggering factors for atherosclerosis?
Cases wherein symptoms will come up:
○ Acute inflammation: viral infection (Influenza)
○ Blood Pressure (BP) peaks during exercise or
emotional stress
Factors that determine progress of Coronary Artery Disease
● Most important: Concentration of lipids in blood
○ Familial hypercholesterolemia
- family disorder; high level of lipids even with strict diet and exercise
○ More fatty food, higher conc. Of lipids in the blood; bad lipids LDL, VLDL
● Endothelial dysfunction
● Blood Pressure (high)
● Activity of inflammatory system
● Reactivity of pro- and anti-thrombotic systems
Patient with Coronary Artery Disease (CAD) advised
● Lipid profile: At a certain age needs to be check (LDL, HDL/good cholesterol, VLDL)
○ There are some patients who have low HDL; Typically female patients have high HDL until they reach menopause. Afterwhich, as we all know, the cardiovascular risk factors of females equal those of the males after menopausal. Typically, women are really protected while they are still menstruating.
○ It’s important to remember that, when patients have low HDL, we advise them to drink fish oil or to eat fish more.
● Exercise regularly
○ Ideally, around 4-5 times a week, even 30 minutes or even just walking
● Stop smoking
● BP and body weight control
● Treatment with statins, aspirin, Beta blockers
● Annual vaccinations against Influenza
○ Nowadays, also COVID vaccinations
What is the primary symptom of Ischemic Heart Disease?
Angina Pectoris
It is due to an imbalance in the myocardial oxygen
supply-demand relationship
Angina Pectoris
Angina Pectoris is c/b:
Caused by:
○ Increase myocardial oxygen demand
■ As when you exercise because usually that’s when your angina or your symptoms will come out when exercising or under stress
○ Decrease in myocardial oxygen supply
■ Presence of plaques or vasospasm
What happens in progressive decrease in vessel radius (coronary atherosclerosis)?
Impair coronary blood flow
○ Angina will occur when myocardial O2 demand increases
When there is an abrupt decrease in blood flow?
○ Coronary thrombosis
○ Localized vasospasm
Signs and Symptoms of Angina Pectoris
● Heavy, pressing, substernal discomfort often radiating to left shoulder, flexor aspect of left arm, jaw or epigastrium
● Key is Management: If the patient is complaining of Angina, you have to be very fast. When the patient already has Myocardial infarction, the golden rule is that, within an hour, you have to stop the progression of your infarction so you will not end up with dead myocardial tissue which is now very difficult to treat
● May have atypical symptoms
● Some of them may complain, not of chest pain but some may complain of cough, or back pain or sometimes dyspnea, and they don’t really complain of chest pain, so we have to investigate further.
Women, elderly, and diabetics
● We all know that beta blockers and some calcium entry blockers like your verapamil and diltiazem, decreases the heart rate and contractility leading to an increase in oxygen demand
● Your nitrates and your calcium entry blockers also can affect your preload and afterload also leading to decrease in oxygen demand
Does vasodilators increase oxygen supply?
Yes.
They don’t have any effect on the oxygen demand because they do not per say have any effect on the heart. They do have an effect on your blood vessels, they dilate the blood vessels to improve coronary blood flow, increasing the oxygen supply.
● Any imbalance of the two will now lead to your
ischemia.
You now have an anaerobic metabolism, and the accumulation of your substance P, as well as increase in glycolysis, lactate, and pyruvate formation, what is now triggered?
sympathetic nerve endings are now triggered. So, it will all lead to pain and that’s when the patient will complain of angina.
This is typically a person with angina. If you notice, he or she will complain of tightness or pain in the chest. Usually, they will hold a fist to the left side of their chest, typically that is what they complain of.
● But sometimes there are also other causes of chest pains, it’s not just angina. One of the more common causes may be your gastroesophageal reflux disease (GERD), pancreatitis. There are a lot of causes but the main thing that you should rule out immediately when you have patients complaining of chest pain is your ischemia or in the worst case scenario, a myocardial infarction.
What are the types of angina?
- Typical Stable Angina
- Variant Angina
- Unstable Angina
● Pathology: (this is caused by) fixed atherosclerotic narrowing of an epicardial coronary artery
● Depending on where the narrow portion or the block is, that’s where you get your symptoms
Typical Stable Angina
● Usually this is caused by a focal/diffuse coronary spasm episodically reduces coronary flow
○ there is no block but there is usually a focal or decreased coronary spasm of the artery which reduces the coronary blood flow
● AKA Prinzmetal’s Angina
● Usually this is reversed by Nitrates or Ca++ blockers
Variant Angina
● This one is dangerous because it is an acute coronary syndrome
● Episodes of angina at rest and when there is a change in character, frequency, and duration of chest pain and precipitating factors in patients with previously stable
angina
● Caused by episodes of increased epicardial artery tone
● Small platelet clots occurring in the vicinity of an atherosclerotic plaque
● High risk of MI and death
○ Or this may be a precursor to a greater cardiac event in the near future where the patient may have an impending MI. If you have a massive MI, that’s very difficult to treat already, usually that will lead to death
of the patient.
Unstable Angina
WAYS BY WHICH DRUGS RELAX VASCULAR SMOOTH MUSCLE
● Increase cGMP
○ NO
■ Nitroprusside
■ Nitrates
● Decrease Intracellular Ca+2
○ Ca++ channel blockers
○ β-blockers
● Stabilizing or preventing depolarization of vascular SM cell membrane
○ Minoxidil
○ Nicorandil
● Increase in cAMP in vascular smooth muscle cells
DRUGS FOR ANGINA
● Nitrovasodilators
● Β-adrenergic receptor antagonists
● Ca+2 channel antagonists
● All approved antianginal agents function by improving the balance of myocardial oxygen supply and demand
○ Increasing supply by dilating the coronary
vasculature
○ Decreasing demand by reducing cardiac work
Other Treatment
● Stabilize the plaque
○ Anti-platelet agents (Aspirin, Clopidogrel)
○ Statins
■ Lowers down cholesterol
○ Ranolazine
■ Chronic Angina
■ Direct effects on cardiac myocyte Na+
channels
● Β-adrenergic Antagonists
○ Decreased mortality by reducing incidence of sudden cardiac death associated with M.I. and ischemia
TREATMENT FOR CARDIAC FACTORS
● Aspirin
● Other antiplatelet agents:
○ Clopidogrel
○ Abciximab
○ Tirofiban
○ Eptifibatide
● Lipid-lowering agents
● ACE Inhibitors
○ Patients with impairment of cardiac systolic function
● Coronary Artery Bypass Surgery (CABG)
○ More than 2 vessels, or vessels are too small for a stent to be inserted; DM- small vessel disease
● Angioplasty
● Coronary Artery Stent Deployment
● Give drugs that either increase blood flow to the heart
○ Decrease left ventricular wall tension, heart rate or contractility
TYPICAL ANGINA
Prevention of coronary spasm
Variant/Vasotonic Angina
Correcting the tendency to intracoronary thrombosis
Unstable Angina
ORGANIC NITRATES
● Nitroglycerin
● Isosorbide dinitrate
● Isosorbide 5-mononitrate
○ There are all emergency medications which elderly individuals or people with high risk should have with them all the time.
○ These are life saving drugs.
NITROGLYCERIN GENERAL ACTION:
● In patients with stable angina, it produces dilatation of veins and dilatations of collaterals leading to a decrease in oxygen consumption.
● For patients with heart failure, dilation of your arteries (reduction of afterload) and dilation of veins leading to a decrease preload, so this will result in a reduction of your left ventricular end diastolic pressure, reduction in wall stress, and reduction of mitral regurgitation.
● For patients with acute coronary syndrome, dilatation of arteries, dilatation of collaterals, and produces antiaggregation of your platelets leads to an increased O2 supply.
MECHANISM OF ACTION OF NITRATES:
Source of NO (Nitric Oxide) -> activates guanylyl cyclase -> Increased levels of cGMP -> Dephosphorylation of myosin light chain, decreased cytosolic Ca++ -> smooth muscle
relaxation
EFFECTS OF NITRATES:
● Relaxation of vascular smooth muscle.
● Low concentrations will dilate the VEINS more than the arteries.
● Decreased venous return -> Decreased L and R ventricular chamber size and end-diastolic pressure.
● Relieve anginal pain by dilating coronary artery -> increased coronary blood flow.
● Angina due to coronary artery spasm
○ Epicardial coronary arteries dilate, particularly regions affected by spasm which will relieve your angina.
MECHANISM OF RELIEF OF SYMPTOMS OF ANGINA:
● Reduction in myocardial work and O2 demand
🠊 Primary effect in chronic stable angina.
● The problem with nitrates is that you will have vasodilation of all the blood vessels in the body
🠊 the patient will now experience the side effects.
● Responses evoked by vasodilation.
○ Tachycardia (baroreceptor reflex, compensatory mechanism)
○ Orthostatic Hypotension (direct extension of venodilator effect)
○ Throbbing headache (meningeal arteries
vasodilation)
Frequently repeated/continuous exposure to high doses of organic nitrates -> marked attenuation of most pharmacologic effects
TOLERANCE
Reduced capacity of vascular SM to convert nitroglycerin to NO
True Vascular Tolerance
Activation of mechanisms
Pseudotolerance
MANAGEMENT
● Interrupt treatment for 8-12 hours/day
● Omit night dose in patients with exertional angina
TOXICITY/UNTOWARD RESPONSES
● Secondary to actions on the CVS
● Headache
○ Common, can be severe
○ Decreases over a few days if treatment is continued and controlled by decreasing dose
● Transient episodes of dizziness, weakness, other manifestations associated with postural HPOT- esp. if patient is standing immobile
○ occasionally progress to loss of consciousness accentuated by alcohol
● Drug Rash
● Cause methemoglobinemia at high blood concentrations
● Cause “Monday Disease”
● Alternating development of tolerance and loss of tolerance
● Headache, tachycardia and dizziness every Monday
Nitrates
● Immediate exposure to amyl nitrite
● IV administration of Na nitrate ->
increase methemoglobin level -> removes significant amount of cyanide
● IV Na thiosulfate
Cyanide Poisoning
● Inhibitor of PDE5 (phosphodiesterase – 5)
● Improve erectile function in patients with various causes of erectile dysfunction
● S/E: headache, flushing, rhinitis, dyspepsia
● Has significant and potentially dangerous
interaction with nitrates
● Nitrates produce profound increases in cyclic GMP -> dramatic reductions in BP
● Should not be prescribed to pts receiving any form of nitrate
● Question pts about Sildenafil use w/in 24H before nitrates are administered
Interaction with Sildenafil (Viagra)
THERAPEUTIC USES OF ANGINA
● Diseases that predispose to angina should be treated
○ Hypertension
○ Anemia
○ Thyrotoxicosis
○ Obesity
○ Heart failure
○ Cardiac arrhythmias
○ Acute anxiety, acute emotional stress
● Smoking cessation
● Avoid overeating
○ Get BMI to normal levels
● Avoid exposure to sympathomimetics (nasal decongestants)
● Lose weight
● Maintain a low-fat, high fiber diet, low sodium diet
● Correct hypertension and hyperlipidemia
● Daily aspirin or clopidogrel
● Avoid exposure to serotonin-receptor agonists for migraine (Sumatriptan)
● Most commonly used drug for rapid release of angina
● Tablets, capsules, sublingual powder, spray, aerosol
● Onset of action: 1-2 mins
● Initial dose: 0.3 mg
○ Relieves pain w/in 3 min
○ Seek medical attention if 3 tab taken over a 15 min period do not relieve a sustained attack → indicative of MI or unstable angina (need to bring the patient to the hospital)
■ That is what I mentioned with having the
golden rule wherein you can still stop the
damage to the cardiac muscle, you give your
Nitrates. If you don’t have nitrates, you can
give Aspirin or any form of vasodilator (beta
blockers/ calcium channel) so that you will help dilate the vessels while transporting the patient to the hospital.
SHORT ACTING NITRATES
Nitroglycerin
● Provide prophylaxis against anginal episodes in patients w/ more than occasional angina, especially if they have to undergo exercise
● For px who experience angina and wants to exercise, they usually take long-acting nitrates prior to exercising, prophylaxis
LONGER ACTING NITRATES
● Most useful drug given sublingually
● Onset of action: 1-2 min
● Initial dose: 0.3 mg – relieve pain w/in 3 min
● Absorption limited in pts w/ dentures or dry mouths
○ Because the absorption may be limited
● Tablets kept in glass containers (colored glass containers; not plastic), protected from moisture, light and extremes of temperature
● Seek medical attention when 3 tablets taken over a 15-min period do not relieve a sustained attack
● How will you know that the Nitroglycerin is not expired?
○ The active tablets should produce a burning sensation under the tongue when you take it
SUBLINGUAL ADMINISTRATION
Nitroglycerin
ORAL ADMINISTRATION
● Prophylaxis against anginal episodes in patients with occasional angina
○ For oral administration usually with the long acting nitrates
● Effects: peak at 60-90 min (last for 3-6 hrs)
○ Ideally before the patient undergoes exercise or any stress-related activities, they have to take nitroglycerin approximately an hour or 2 hours before doing an exercise and the effects will last for 3-6 hours.
CUTANEOUS ADMINISTRATION
● Relieve angina
● Prolong exercise capacity
● Reduce ischemic ST depression with exercise for >/= 4 hrs
● Nitroglycerin ointment (2%) applied to skin (2.5-5 cm) with a thickness of 1-2 inches and spread in a uniform layer
● Effects: apparent w/in 30-60 min (last 4-6 hrs)
○ Approximately 30 minutes to an hour before, you should apply already
● Particularly useful for nocturnal angina or patients experiencing angina while sleeping
TRANSMUCOSAL/BUCCAL ADMINISTRATION
Inserted under upper lip above incisors
● More dangerous angina
● New-onset exertional angina
● Increase in the usual pattern of angina
● Rest angina
● ECG: elevation/depression of ST segment, variable T-wave abnormalities
● IV nitroglycerin is given
○ allows high concentrations of drug to be attained rapidly
UNSTABLE ANGINA
● Disruption of coronary plaque
↓
● Local platelet aggregation
● Thrombosis at arterial wall
↓
● Partial/total occlusion of vessel
○ The patient will be having myocardial infarction already
● You may end up with partial or total occlusion of vessels.
○ If total occlusion of vessel, that means the patient will be having a myocardial infarction already
ACUTE CORONARY SYNDROME
TREATMENT
● All of them should be done in the hospital:
○ Antiplatelet agents;
○ Antithrombotic agents (Heparin);
○ Anti-integrin Tx; and if that fails, you do
○ Stents
○ Coronary bypass surgeries
MYOCARDIAL INFARCTION
● Reduce size of infarct
● Preserve/retrieve viable tissue by decreased O2 demand of myocardium
○ That is why there is the presence of the ________ wherein you have to stop further progression of the infarction so that you will not end up with a dead myocardium which will end up a with a pt having congestive heart failure
● Prevent vent remodeling – lead to HF
● Transdermal of oral nitrates – safe, well tolerated in the setting of MI
○ Have beneficial effect on pain
○ Do not provide survival advantage
● Variant (Prinzmetal’s Angina)
○ Long acting nitrates with Calcium channel blockers
CALCIUM CHANNEL ANTAGONISTS
● 5 Classes:
○ Phenylalkylamines (Verapamil)
○ Benzothiazepine (Diltiazem)
○ Dihydropyridines (Nicardipine, Nifedipine,
Isrardipine, Amlodipine, Felodipine, Nisoldipine, Nimodipine)
○ Diphenylpiperazine
○ Diarylaminopropylamine (Bepridil)
● The more important of these Calcium channel antagonists are the dihydropyridines, verapamil, and diltiazem
● MOA of Calcium channel blockers - inhibit Ca++ influx through L-type channel into smooth muscle cells -> impair responses to contractile stimuli -> vasodilation -> decreased BP
○ Which is why it is a very effective drug in
hypertension
● L-type Ca++ channel - slow voltage channel dominant in heart and smooth mm - contain several drug Rs
● Dihydropyridines bind to a-1 subunit Rs site
● Non-dihydropyridines bind to another Rs site in same subunit that is closely related but not identical
● Vascular smooth muscle are the most sensitive to calcium channel blockers
○ Smooth mm of GIT, Bronchi, Uterus - also responsive but to a lesser extent
■ In OB, we use it to treat preterm labor. Nowadays it is the main drug which we give to patients with preterm labor since there are no other agents given PO which can produce relaxation of the uterus as effectively as Nifedipine.
○ Skeletal muscle NOT affected, since it uses intracellular pools of Ca to support
excitation-contraction coupling and doesn’t require as much transmembrane Ca influx.
● Difference in vascular sensitivity among Ca blockers
○ DHPs - greater vasoselectivity relative to cardiac effects, than do nonDHPs.
■ Do not have prominent effects to the heart; the effects are more on the vascular muscles
○ NonDHPs - prominent cardiac depression = minimal to (-) tachycardia due to direct (-) chronotropy and (-) inotropy
● In vascular system, arterioles - more sensitive to DHPs than veins -> decreased PVR (Peripheral vascular resistance) without change in venous tone -> uncommon
orthost HPOT
● Rank of potency as vasodilators:
○ DHPs > non-DHPs (Verapamil > Diltiazem)
● Decreased PVR -> generally evokes sympathetic tachycardia to variable degrees
○ DHPs -> (+) tachycardia, especially when drug is rapidly absorbed
○ Ex: Sublingual route - Nifedipine
■ Discontinued due to tachycardia which
worsens angina
CLINICAL USE
Anginas
● Variant, exertional
● Relieves vasospasm, Increased CBF, decreased Myocardial demand (decreased BP, HR, and contractility)
○ DHPs especially Nifedipine + 𝞫-blockers
○ NonDHPs — Verapamil, Diltiazem
■ Reduces angina but CAUTION in
combination with 𝞫-blockers
● Both drugs are cardiac depressants or
they have (-) chronotropic and inotropic
effects on the heart
● Due to delay AV conduction, AV block,
severe bradycardia, presence of LV
dysfunction
TOXICITY/UNTOWARD RESPONSES
● Due to excessive vasodilation
○ Dizziness, hypotension, headache, flushing, digital dysesthesia, nausea
● Constipation, peripheral edema, coughing, wheezing, pulmonary edema
● Nimodipine - muscle cramps
● Nifedipine - worsened M ischemia
○ Result from excessive HPOT and decreased coronary perfusion, especially if you let the patient take it sublingually
● Exacerbation of GERD
● Nifedipine - Worsening MI
● Worsening of angina — due to excessive HPOT, decreased coronary perfusion
THERAPEUTIC USES: CALCIUM CHANNEL ANTAGONISTS
● Variant Angina
● Exertional Angina
● Unstable Angina
● Effective in reducing the severity and frequency of attacks of exertional angina
○ Fall in myocardial oxygen consumption at rest and during exertion
● Improves survival in patients who had an MI
● Not useful for vasospastic angina
○ This is the vasospasm in the blood vessels so you’ll have to treat the vasospasm
● Cardioprotective — timolol, metoprolol, atenolol, propranolol
Β-ADRENERGIC RECEPTORS ANTAGONISTS
THERAPEUTIC USES
● Reduce recurrent episodes of ischemia
● Reduce risk of progression of acute MI
COMPARISONS OF ANTIANGINAL THERAPEUTIC STRATEGIES
Combination of Agents
● Lower doses
● Increased effectiveness
● Reduced incidence of side effects
Nitrates and Adrenergic Receptor Antagonists
● Very effective in the treatment of typical exertional angina
● Additive efficacy — result of one drug blocking the adverse effects of the other agent on net myocardial oxygen consumption
β-blockers
● Block baroreceptor mediated reflex tachycardia and (+) inotropic effects of nitrates
Nitrates
● Increased venous capacitance -> attenuate -> Increased left ventricle end-diastolic volume associated with β-blockers
CONDITION
Systemic HPN
RECOMMENDED (and Alternatives) For Angina:
β-adrenergic (Ca++ channel antagonist)
Migraine or Vascular HA
RECOMMENDED (and Alternatives) For Angina:
β-adrenergic (Ca++ channel antagonist)
Asthma or COPD w/ bronchospasm
RECOMMENDED: Verapamil or Diltiazem
DRUGS TO AVOID: β-adrenergic
Hyperthyroidism
RECOMMENDED: β-adrenergic
Raynaud’s phenomenon
RECOMMENDED: Long-acting, slow-release Ca++ channel
DRUGS TO AVOID: β-adrenergic
IDDM
RECOMMENDED: β-adrenergic long acting,
slow-release Ca++ channel
NIDDM
RECOMMENDED: Long acting, slow-release Ca++ channel
DRUGS TO AVOID: β-adrenergic
CHF
● Mild (LVEF >=40%)
● Mod ‒ Severe (LVEF <40%)
RECOMMENDED:
● β-adrenergic
● Amlodipine or Felodipine (nitrates)
DRUGS TO AVOID:
● Verapamil, Diltazem
● Reduce incidence of MI in pts w/ chronic stable angina
○ Long term use can produce bleeding ulcers
● Dose: 160–325 mg
Aspirin
● A newer drug
● Tx of Acute Coronary Syndromes
● Inform the patient to take daily for his lifetime
Clopidogrel
Primary choice in patients with angina
Prasugrel, Ticagrelor, Cangrelor-inhibit platelet aggregation
● Reduces Sx, prevents infarction in unstable angina
● Usually given to hospitalized patients
Heparin
● Selective late-sodium current inhibitor
–> inhibits subsequent Ca++ overload within myocyte (hallmark of an ischemic cell)
–> decreased diastolic tension
● MARISA (Monotherapy Assessment of Ranolazine in Stable Angina) trial
○ Increased total exercise duration
○ Increased time to onset of angina during exercise
○ Increased exercise time to onset of 1.0 mm
ST-segment depression
● CARISA (Combination Assessment of Ranolazine in Stable Angina) trial
○ Increased exercise time and longer periods of exercise until symptom onset
● ERICA (Evaluation of Ranolazine in Chronic Angina) study
○ Fewer angina episodes
● Works by improving regional blood flow in areas of myocardial ischemia
● Exerts little effect on HR and BP
● T ½ – 7 hours
● Dose: 500 mg BID
● Approved either as primary or combination tx for chronic stable angina
● Contraindicated in patients with cirrhosis and those taking strong inhibitors or inducers of CYP3A
● Most common adverse effects: dizziness, headache, constipation, nausea
● Very minor dose-related prolongation of the QTc interval
RANOLAZINE
● If (“funny current”) inhibitor
● Acts by reducing heart rate in a mechanism distinct from beta blockers or calcium channel blockers
● INITIATIVE (International Trial on the Treatment of Angina) trial
○ Noninferior to Atenolol with respect to exercise duration, time to limiting angina and time to angina onset
● ASSOCIATE (Efficacy and Safety of Ivabradine on Top of Atenolol in Stable Angina Pectoris) trial
○ Significant improvement in exercise time, time to angina, & ischemic threshold compared to atenolol
● Administered orally at 5 or 7.5 mg BID
● Acts on If expressed in SA node-mixed NA+K+inward current activated by hyperpolarization & modulated by ANS
○ Regulates pacemaker activity in SA node
○ Greater heart reductions at higher doses
● For treatment of chronic, stable angina and for patients in sinus rhythm who cannot take beta blockers (generally a second line agent to beta blockers) or patients who have inadequate HR control (<60 beats/min) while on beta blockers
● Also for off label treatment of inappropriate sinus tachycardia
● Contraindicated in patients with sick sinus syndrome and those taking inhibitors of CYP3A4
● Side effects: significant bradycardia or heart block
● 15% of patients - luminous phenomena or phosphenes
○ Sensations of enhanced brightness in fully maintained visual fields
■ Mild and fully reversible upon stopping the intake of the drug
IVABRADINE
● Fatty acid oxidation inhibitor
● Increases cardiac metabolic efficiency
○ Shifts cardiac metabolism toward increased dose of glucose (more oxygen efficient)
Trimetazidine
● K+ channel activator
● Arterial and venous dilator -> improves coronary blood flow
Nicorandil
Rho-kinase inhibitor, vasodilator
Fasudil
Example of a 𝛽-blocker with the highest intrinsic sympathomimetic activity?
Pindolol
Are nitroglycerides available over-the-counter?
○ They might ask for a prescription. If you have elderly patients, these are really life saving drugs.
○ It’s really important for the golden hour that you have to be able to save and preserve as much cardiac function because the cardiac muscle is very difficult once it’s damaged and it may end up in heart failure for the patient.
○ I’m not sure if it’s over the counter but you should be able to buy it easily with a prescription
○ You have to remember the important ways to keep it:
■ Glass (Colored containers)
■ Away from sunlight and moisture at all times
Which Beta Blocker 2 is given to patients with Glaucoma?
Timolol
Conditions for which Beta blockers are useful?
Anxiety disorders, Migraines, Hyperthyroidism, Hypertension
Which Beta blocker has a very short half-life that you can give especially if you just need blockage for a very short time?
Esmolol
Remember, for patients with diabetes it is best to give Beta 1 selective blockers and not the non-selective beta blockers (ex: Propranolol)
Propranolol - not also good for patients with diabetes, COPD, and asthma
Which calcium channel should you use with caution when giving beta blockers?
Verapamil or Diltiazem
○ These two are cardiac depressant calcium channel blockers
Which diuretic is the most commonly used for initial treatment of mild hypertension?
Hydrochlorothiazide
Which diuretic is used more as a diuretic agent because it causes profound diuresis?
Furosemide
Which diuretic has an effect on progesterone receptors so it causes gynecomastia, impaired sexual drive in men as well as menstrual irregularities in females?
Spironolactone
What is the most serious side effect of thiazides?
Hypokalemia
When you have a patient who develops hypokalemia during treatment, what is your best management? Will you give oral potassium supplementation? Potassium sparing diuretics? or Potassium sparing diuretics only?
Potassium sparing diuretics only (you
don’t give potassium)
When you have a patient with hepatic cirrhosis, what is the diuretic of choice?
Furosemide
When nitroglycerin is taken orally instead of sublingually, the time of onset is slower because there is a big chance that it will be destroyed by the gastric acid so it might not have an effect ideally
It is given sublingually because there are a lot of blood vessels under the tongue so you have direct absorption and it will go directly to your vascular system.
Angina does not immediately become myocardial infarction. Angina is like a warning symptom to a possible progression to MI. It warns you that you have ischemic heart disease. Ideally, you should get ECG.
○ If there is sign of ischemia in ecg, aside from other laboratories (blood chemistry), the best thing to do is treadmill stress test or stress echo. Either treadmill or bicycle.
○ If there is no ischemia then you probably have GERD or peptic ulcer disease because they have similar symptoms.
○ Gall bladder stones can also present as angina or ischemia.
○ Ideally, if you have high risk for angina or ischemia you will generally have high risk of developing MI later on.
■ So you have to cut down cardiovascular risk factors, especially women. Once you become menopausal, your cardiovascular risk factors are the most important to correct. You have to do lifestyle modifications.
■ If you are overweight, you have to lose weight.
■ If you are diabetic, manage your diabetes and hypertension. These things can lead to hypercholesterolemia leading to your plaques in your blood vessels which will lead to angina and later on possible MI.
