Week 3 Flashcards
A constellation of symptoms that results from myocardial oxygen demand being greater than the supply.
Angina
Class 1 angina:
Proven CAD without symptoms
Class 2 angina:
Angina with unusually strenuous physical activity.
Class 3 angina:
Angina during the routine physical activity.
Class 4 angina:
Angina during minimal activity and rest.
MOA of an ACEI:
Inhibits the affect the enzyme responsible for converting angiotensin I to angiotensin II. Blocking the production of angiotensin II results in vasoconstriction and sodium and water retention, thus reducing preload, afterload, and increasing EF.
What to monitor with ACEI?
Renal function and serum potassium
Contraindications for ACEI:
Pregnancy, bilateral renal artery stenosis, renal insufficiency, hyperkalemia (k greater than 5.5), and sever hypotension
Adverse events of ACEI:
Hypotension (first-dose effect), worsening renal function, hyperkalemia, cough, angioadema, rash
Why are beta blockers effective in managing angina?
They are effective due to the reduction in the workload of the heart and the overall decrease in myocardial oxygen demand and consumption. They reduce heart rate and myocardial contractility at rest and during periods of normal exercise.
What drugs have complementary effects on myocardial oxygen supply and demand and are often used together?
Nitrates and beta-blockers
Types of beta-blockers:
1: cardioselective- block only beta1 receptors
2. Noncardioselective- block both beta1 and beta2 receptors
Contraindications for beta blockers:
Asthma (reactive airway disease), AV block (unless pacemaker), symptomatic hypotension/bradycardia
Adverse events of beta blockers:
Hypotension (first-dose effect), fluid retention/worsening of the failure, fatigue, bradycardia/heart block, can mask symptoms of hypoglycemia.
Teaching points of beta blockers:
Do not stop abruptly- reduce dose
Discontinue only in severe cases
Why are CCB effective in treatment of angina?
Due to vasodilators effects on the coronary and peripheral vessels. Depending on the agent they have the potential to depress cardiac contractility, heart rate, and conduction.
CCB have a positive or negative inotropic effect?
Negative inotrope- decreases contractility
CCB should NOT be used in what?
Heart failure
Because CCB do not cause substantial venous dilation they do no reduce what?
Preload
Types of CCB?
- Nondihydropyridines
2. Dihydropyridines
Which type of CCB reduce HR by slowing contraction through the SA and AV nodes and depress cardiac contractility?
Nondihydropyridines
These have more antianginal properties, used to treat arrhythmia, with minimal effect on BP.
Nondihydropyridines: verapamil and diltizem
Dihydropyridines have no effect on what?
HR
Nondihydropyridine CCB can cause what adverse events:
Constipation, edema
Adverse events of CCB:
Edema, fatigue, dizziness, HA, flushing, and gingival hyperplasia
Antiplatelet therapy includes:
ASA therapy
Thienopyridine (plavix-clopidogrel) therapy
ASA MOA:
Inhibits platelet activation through irreversible enzyme antagonism to block prostaglandin synthesis.
Thienopyridines MOA:
Reduced ADP-induced platelet activation. Works on receptors.
In patients with stable angina, the risk of MI can be lowered with:
Daily ASA therapy
Adverse events of ASA:
Dyspepsia, bruising, and bleeding
Plavix- clopidogrel is recommended for:
Prevention of MI in angina patients who have contraindications to ASA
Plavix has better what then ASA?
GI tolerance
This drug can be used alone or in combo with nitrates, BB, CCB, or ACEI.
Ranolazine
When to use Ranolazine?
Chronic treatment of angina only when all other modalities are tried.
MOA of ranolazine:
Thought to block late-phase sodium channels, which remain open during hypoxia or ischemic events. By blocking these it decreases calcium overload and breaks the cycle of ischemia.
Adverse events of ranolazine:
QT prolongation, dose-related dizziness, HA, constipation, nausea, palpitations, vertigo, peripheral edema, hypotension. Less common: angioedema and renal failure
Nitrates are used to:
Halt an acute angina attack, to prevent predictable episodes, and for chronic treatment to prevent episodes.
MOA of nitrates:
Cause dilation throughout the vasculature- in the peripheral veins as well as coronary arteries. When dilated the veins return less blood to the heart, thereby decreasing LV filling and preload. This decreases workload of the heart.
Nitrates do not affect the cardiac function but rather:
Decreases workload of the heart and increases myocardial oxygenation
Can you develop tolerance with prolonged nitrate use?
Yes
Nitrates are contraindicated in:
Anemic/volume depleted patients, head trauma, issues with hemorrhage
Adverse events of nitrates?
Vasodilatory effects: HA, flushing, dizziness, weakness, and orthostatic hypotension. Reflex tachycardia: results as the heart compensates for the bp drop
Examples of long and short-acting nitrates:
Long-acting: isordil, indur, NTG transdermal
Short-acting: NTG spray and tabs
All patients with angina use:
Short-acting nitrate, ASA
First-Line therapy in angina:
BB+ lifestyle+ ASA+ short-acting nitrate
Second line therapy in angina:
CCB or combo therapy (CCB + BB or long-acting nitrate + BB)
Third-line therapy for angina:
CCB + BB + long-acting nitrate
Types of heart failure:
Systolic dysfunction- ventricular contraction/ejection- failure of the pump with low EF
Diastolic dysfunction- ventricular filling/relaxation- stiff ventricle/ inadequate SV
In patients with a reduced EF what drugs should be used to prevent HF?
ACEI or ARBS
In patients with MI and a reduced MI what drugs should be used to prevent HF:
BB with a statin
Class I HF:
Patients may have symptoms of HF only at levels that would produce symptoms in normal people- no limitations
Class II HF:
Patients may have symptoms of HF on ordinary exertion- slight limitations- comfortable at rest
Class III HF:
Patients may have symptoms of HF on less than ordinary exertion- marked limitations
Class IV HF:
Patients may have symptoms of HF at rest- severe limitations
ACEI are used in HF for:
Patients with LV systolic dysfunction and an EF less than 35-40%.
First-line in HF
ACEI reduce:
Preload and afterload
What ARB is most studied in heart failure?
Losartan- decreases BP, SVR, pulmonary capillary wedge pressure, and heart rate. Raises cardiac index
BB should be used in HF treatment:
After an MI- improves function
What BB for HF?
Carvedilol- improves BP and cardiac output in stages B and C
Metoprolol
Diuretics do what in HF?
Reduce preload by decreasing extracellular fluid volume that can be used to manage HTN, which will then reduce afterload
Digitalis has a positive or negative inotropic effect?
Positive inotrope- increases contractility
Digitalis is not good for what type of HF?
Diastolic HF with hypertrophic cardiomyopathy.
Digitalis is good for this Hf:
A-fib induced HF due to its Na pump effect and subsequent rate control.
What stage should dig be used in HF?
Stage C only
Adverse events of digitalis?
Dig toxicity, anorexia, N/V, HA, fatigue, malaise, disorientation, confusion, delirium, seizure, and visual disturbances. Followed by cardiac symptoms manifested by arrhythmia.
Contraindications for digitalis:
Dig toxicity, advanced A-V block without a pacemaker, bradycardia/ sick sinus with pacemaker, PVCs/VT, marker hypokalemia, WPW with a fib
Spironolactone is an:
Aldosterone antagonist
Spironolactone is used:
For stage C only and with recent or current symptoms despite ACEI, diuretics, digoxin, and BB
Contraindications of spironolactone:
Hyperkalemia and renal insufficiency
Nitrates are used in HF:
In stage C with hydralazine when intolerant to an ACEI
Hydralazine is a:
Vasodilator that works directly on smooth muscle to dilate the blood vessel; very effective on arterioles; some NO donation, which has been shown to trigger vasodilation
Hydralazine is used in HF:
In stage C with nitrates when intolerant to ACEI.
Not used alone
Hydralazine should be with:
Diuretic and BB due to high incidence of fluid retention and elevated HR
Medications that can exacerbate HF:
NSAIDS steroids Hormones Lithium Anti-hypertensives BB Arrhythmics TCA CCB Cardiac toxins
First line therapy in HF:
ACEI or ARB with or without diuretic
Second line therapy in HF:
ACEI or ARB and BB with a diuretic
In patients with mild heart failure, use a potassium sparing diuretic when serum K is less than 4
Third line therapy in HF:
ARB, BB, aldosterone antagonist, diuretic, and digoxin
2 strategies for management of dysrhythmias:
- Rate control
2. Rhythm control
Rate control consists of:
Use of AV Nodal agents (class 2 and 4) Primary strategy for patients over 65, with CAD, with contraindications to antiarrhythmic drugs, unsuitable for cardioversion, or without CHF.
Rhythm control consists of:
Use of antiarrhythmia meds (class 1 and 3) Primary strategy for patients that are symptomatic, presenting for the first time with AF and can pinpoint the exact time the symptoms began within 48-72 hours, secondary to a treated/corrected precipitation, or with CHF
Class I AAD drugs are:
Sodium channel blockers- membrane stabilizing agents
Class II AAD drugs:
Beta-blockers
Beta blockers are useful in treating what arrhythmia:
Supraventricular tachycardias
Class III AADs:
K channel binders- prolongs depolarization
Class IV AADs:
Calcium channel blockers
Used for a fib/a flutter
Class V AADs:
Others:
Digoxin- excellent for a fib induced HF
