HEART DRUGS & ECGs Flashcards
potassium-sparing diuretics that inhibit aldosterone activation
Spironolactone (Aldactone) and eplerenone (Inspra)
first-line drugs for chronic HFrEF
ACE inhibitors
ACE inhibitors block the RAAS by inhibiting the conversion of angiotensin I to angiotensin II. They reduce afterload and SVR and inhibit the development of ventricular remodeling by inhibiting ventricular hypertrophy.
MED For patients who are unable to tolerate ACE inhibitors
angiotensin II receptor blockers (ARBs) are recommended.
They prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. ARBs promote afterload reduction and vasodilation.
directly block the negative effects of the SNS (e.g., increased HR) on the failing heart
β-Blockers
reduce symptoms of fluid overload and congestion in both HFrEF and HFpEF
Diuretics
Diuretics reduce edema, pulmonary venous pressure, and preload.
Digoxin (Lanolin)
inhibits Ca from leaving the cardiac cell which allows complete emptying of ventricles
decreases heart rate by inhibiting Na, K pump
digoxin toxicity: hypokalemia, hypercalcemia, and hypomagnesemia
Check apical HR for one minute prior to administration, hold if < 60
Normal Digoxin Level
0.5-2 ng/mL
loop diuretics
furosemide
used to treat Acute decompensated heart failure ADHF in the absence of hypotension
Vasodilators
Nesiritide (Natrecor): Recombinant form of Brain Natriuretic Peptide (BNP) that causes arterial and venous dilation.
Nitroglycerin
main effects include a reduction in pulmonary artery wedge pressure and decrease in dyspnea. Because the primary adverse effect is symptomatic hypotension, BP is carefully monitored.
Vasodilators
Nesiritide (Natrecor): Recombinant form of Brain Natriuretic Peptide (BNP) that causes arterial and venous dilation.
Nitroglycerin
primary venodilator that reduces circulating blood volume. It also improves coronary artery blood flow by dilating the coronary arteries
nitroglycerin
NTG reduces preload, slightly reduces afterload (in high doses), and increases myocardial O2 supply.
increase myocardial contractility and are used for patients with evidence of cardiogenic shock or with low CO
Inotropic agent:
Dobutamine: selective β-agonist that works mainly on the β1-receptors in the heart and does not increase Systemic Vascular Resistance
Milrinone: has both inotropic and vasodilator properties. Milrinone improves myocardial contractility, increases CO, and reduces BP (decreases afterload).
Peripheral Artery Disease (PAD) Sx
Thin, shiny, and taut skin
Loss of hair on the lower legs
Diminished distal pulses
Pallor of foot with leg elevation
Reactive hyperemia of foot with dependent position
Intermittent claudication ( ischemic muscle pain is caused by exercise, resolves within 10 minutes or less with rest, and is reproducible. The ischemic pain is due to the buildup of lactic acid from anaerobic metabolism. Once the patient stops exercising, the lactic acid clears, and the pain subsides.)
Paresthesia
Pain at rest (w/ advanced disease)
meds for Peripheral Artery Disease (PAD)
Angiotensin-converting enzyme (ACE) inhibitors
Antiplatelet agents
Aspirin (ASA)
Clopidogrel (Plavix)
are examples of
Antiplatelet agents
a type of anticoagulant (blood thinning drugs) that work by binding selectively and reversibly to the clotting factor Xa
Factor Xa inhibitors
Factor Xa plays a crucial role in the blood clotting mechanism when you get an injury by forming a mesh to prevent loss of blood. However, clots can form within the body and cause blockages in the arteries, veins, and heart causing heart attacks and stroke.
Venous Thromboembolism (VTE) MEDS
Vitamin K antagonists (VKAs)
Thrombin inhibitors (both indirect and direct)
Factor 10a (Xa) inhibitors
Vitamin K Antagonist
Warfarin
Patients receiving warfarin with an INR of 5.0 or more are at increased risk for bleeding. For VKA-related bleeding, treatment with prothrombin complex concentrate (human) (Kcentra), IV vitamin K and/or fresh frozen plasma is recommended.
Do not give antiplatelet drug or NSAIDs with warfarin as these increase bleeding risk.
Thrombin Inhibitor
enoxaparin (Lovenox)
Low-Molecular-Weight Heparin (LMWH)—subc injection
Monitor CBC count at regular intervals.
Antidote: Protamine neutralizes the effects of LMWH.
Promotes urine flow by inhibiting the reabsorption of 3-5% of luminal sodium as well as natriuresis and diuresis
Thiazide Diuretics
risk of hypokalemia, alkalosis
interacts w/ digoxin and NSAIDs
Inhibits the sodium-potassium-chloride co-transport and reduces their reabsorption
Works on the ascending loop of Henle
Treats hypertension and edema with Chronic Heart Failure (CHF) and Chronic Kidney Failure (CKD)
Loop Diuretics (mide) Ex: furosemide
can be given IV
Increases diuresis without causing potassium loss. Check serum potassium level before giving, contact provider is level is high and request supplemental potassium
Monitor strict I/O and daily weights.
spironolactone is a
Potassium Sparing Diuretics
(Aldosterone Antagonists)
induces gynecomastia by decreasing testosterone production, increasing peripheral conversion of testosterone to estradiol, and displacing estradiol from sex hormone-binding globulin. Discontinuation of treatment usually results in resolution of gynecomastia.
disrupts the movement of calcium through the calcium channels into the arteries and heart
Provides strong contractions of muscles. Restricting flow decreases strength of contractions and relaxes blood vessels
Treats hypertension, angina by opening constricted bloods; reduces heart rate
Dihydropyridine calcium channel antagonists (dipines)
Ex: Amlodipine
Rapid acting, potent peripheral dilators
Non-Dihydropyridine
Calcium Channel Blockers
Normal Sinus Rhythm (NSR)
P-wave before every QRS complex
Heart Rate 60-100, regular rhythm
Normal P-wave axis (upright in leads 1 and 2)
PR interval remains constant (Between 0.12 and 0.20 seconds)
Sinus Tachycardia (ST)
same as norm sinus except Heart Rate > 100 bpm (100-180), regular rhythm
May affect cardiac output/ preload.
Check lab work (K+, Mg, Ca+)
May need rate control drug if tachycardia is frequent or uncontrolled.
Sinus Bradycardia (SB)
same as norm sinus except Heart Rate < 60 bpm, regular rhythm
May affect cardiac perfusion.
Check lab work (K+, Mg, Ca+)
May need atropine (anti-cholinergic) if vagal stimulation
May be a heart block.
May need pacemaker if severe or chronic.
Premature Atrial Contractions (PAC)
looks like theres 2 P waves. One big almost immediately after T wave and a small one right after
P-wave is ectopic. Originates outside the SA node.
Compensatory pause after the PAC.
Usually, no interventions needed.
Supraventricular Tachycardia (SVT)
P-wave is not observed. HR > 100, but many times 160+
Dysrhythmia originates at or above the AV node.
Stable vs. Unstable? Unstable=symptomatic. May need IV fluid resuscitation. May need adenosine or cardioversion.
Atrial Fibrillation (A. Fib)
QRS surrounded by a bunch of squiggles
Irregularly irregular rhythm, variable ventricular rate
Absence of an isoelectric baseline.
Atrial Flutter (A. Flutter)
QRS surrounded by a bunch of POINTY squiggles (SAW TOOTH)
Atrial rate 250-350
Premature Ventricular Contraction (PVC)
P/T wave become GIANT wave that dwarfs the QRS wave
Unusually long wave
Usually not life-threatening
Bigeminy: happens every other beat
Trigeminy: happens every third beat
Treatment is based on symptoms
Could cause heart enlargement or clots
Can feel like chest “fluttering”
Premature Ventricular Contraction (PVC)- Multifocal
P/T wave become GIANT wave that dwarfs the QRS wave BUT ALSO is inverted, then comes way up from baseline and settles before the QRS wave
Junctional Rhythm
Absent P-wave
Normal, narrow QRS complex. Regular rhythm.
Can create bradycardia
Pacemaker if symptomatic w/ bradycardia
Ventricular Tachycardia (VT)
grave stones
Ventricular Fibrillation (VF)
chaotic, not really returning all the way to baseline giant skinny waves
Rate is 150-500 bpm, no effective perfusion.
Amplitude decreases with duration (coarse VF to fine VF)
Immediate Intervention
Ventricular defibrillation
CPR
ACLS algorithm
Asystole
straight line
Cardiac arrest rhythm. Heart standstill.
No electrical activity
P-waves, QRS complexes are absent
No pulse. Asystole is confirmed in 2 separate leads when pronouncing death.
Pulseless Electrical Activity (PEA)
You see electrical activity on the ECH but the heart isn’t mechanically pumping
Initiate CPR
Atrial Pacemaker
Presence of pacer spike prior to the P-wave
Ventricular Pacemaker (V-paced)
little tiny spike right before the T wave
Atrial- Ventricular Pacemaker (AV-paced)
Presence of 2 pacer spikes prior to the P and QRS-wave
Creates wide QRS
Pacemaker- Failure to Capture
