Exam II Flashcards
Myocardial ischemia: Reperfusion injury can occur when introducing new blood during an MI.
Common manifestations of Reperfusion injury include:
- Myocardial stunning
- Microvascular dysfunction
- Lethal reperfusion injury
_________ occurs when there is myocyte injury and death. It is associated with contraction band necrosis (myofibril contraction + reperfusion induced Ca2+ injury)
Lethal Reperfusion Injury
Heart Failure drugs:
- Thiazides and Thiazide-like diuretics inhibit the ________ cotransporter in the DCT. This ultimately decreases Na reabsorption (inc. exretion of Na and water)
- They also increase expression of _____ calcium channels (increasing Ca2+ absorption and subsequent transport to the interstitium via NCX1)
- Na/Cl- (NCC)
- TRPV5
- -hypercalcemia
Heart failure drugs: Diuretics help to decrease the volume overload in HF (dec. congestive symptoms). They are also used in HTN and edema.
What are the effects of diuretics in HF?
- Loop diuretics (furosemide)
- -higher efficacy in HF - Thiazide-like diuretics (metolazone, chlortalidone)
- -more potent than thiazides (hydrochlorothiazide)
- -longer duration w/ fewer side effects
- -good at night - K+ sparing diuretics (spironolactone)
- -less useful in acute decompensated HF
NOTE: Do NOT improve mortality or morbidity
NOTE 2: Thiazides and K+ sparing often combined w/ Loop
Angina drugs - Ca2+ channel blockers:
_____ (amlodipine, felodipine) decrease arteriolar tone and systemic vascular resistance (TPR). This helps to decrease arterial and intraventricular pressure.
- dec. wall tension
- dec. O2 demand
Dihidropyridines
amlodipine, felodipine
Endocarditis: Infective endocarditis is classified in several ways:
- Temporal evolution
- Infection site
- Cause of Infection/Pre-disposing risk factor
True/False - With regard to the cause of infection, Intravenous drug abuse (IVDA), prosthetic heart valves and congenital abnormalities may be involved.
True
Myocarditis: When would you suspect viral myocarditis?
Px presents w/ recent febrile illness, prominent myalgia followed by angina-like chest pain, dyspnea or arrhythmia.
Dx: Elevated troponin
Initial Injury: 2ndary to direct invasion by the virus
NOTE: further injury w/ IL-1, TNF, anti-heart Abs
Heart failure drugs: Diuretics help to decrease the volume overload in HF (dec. congestive symptoms). They are also used in HTN and edema.
What are the effects of diuretics in HF?
- Loop diuretics (furosemide)
- -higher efficacy in HF - Thiazide-like diuretics (metolazone, chlortalidone)
- -more potent than thiazides (hydrochlorothiazide)
- -longer duration w/ fewer side effects
- -good at night - K+ sparing diuretics (spironolactone)
- -less useful in acute decompensated HF
NOTE: Do NOT improve mortality or morbidity
NOTE 2: Thiazides and K+ sparing often combined w/ Loop
These K+ sparing diuretics induce
- hyperkalemia
- metabolic acidosis
Amiloride/Triamterene (non-steroidal)
Amiloride: 1st pass
Heart Failure: The following describes heart failure on what side?
- dyspnea (difficulty w/ inspiration)
- bibasilar inpiratory crackles
- -“cardiac asthma”
- rust-colored sputum (heart-failure cells)
- pulmonary edema
Left sided heart failure
- juxtacapillary J receptors - rapid shallow breathing
- fluid collects around bronchioles – expiratory wheezing “cardiac asthma”
Endocarditis: Remember, infective endocarditis usually affects L. side of heart (mitral). If the right side is involved, IV drug abuse.
The most common cause is bacteremia (infection). Patients often present with a fever of unknown origin***.
What are the most common infective species and ways to diagnose?
- S. aureus (MC)
- -high virulence
- -previously damaged or normal - Strep Viridans (2nd MC)
- -low virulence
- -infect previously damaged valve
Diagnosis:
- -blood culture
- -Echo
- -fever (unknown origin)
- -heart failure MC cause of death
Myocarditis: Chagas Disease: In acute Chagas disease, cardiac damage results from direct invasion of myocardial cells and subsequent inflammation. It is mild in most, but can lead to progressive cardiac failure. How is it diagnosed?
Dx: find organisms in blood
NOTE: Following acute phase, many become asymptomatic, which can last lifetime
Anti-arrhythmics: True/False - Flecainiade (Class IC) can be used during pregnancy and is a first line choice for fetal SVT
True
Endocarditis: Libman-Sacks and Non-bacterial thrombotic endocarditis are non-infectious vegetations, meaning they did not occur from bacterial or viral infection.
Describe these forms of endocarditis, how they arise, and what they affect
- Libman Sacks
- sterile, warty lesions
- systemic lupus
- lesions: either side of valve
- Tri and Mi valves
* deformity - Non-bacterial thrombotic
- non-deforming sterile veg.
- platelets and fibrin
- due to procoagulant circulating mucin (pancreatic/colon cancer)
* *embolize w/ infarct
Heart failure drugs: PDE inhibitors are contraindicated with which of the following drugs?
a. digitalis
b. heparin
c. warfarin
d. insulin
e. tizanidine
Answer: Tizanidine (muscle relaxant)
Also: Selegiline (MAO inh.); Anagrelide (thrombocytosis)
—dec. b.p. and inc. side effects
Myocardial Ischemia: True/False Over the ensuing weeks to months, infarcted tissue is replaced by dense scar tissue (type I). This tissue is not able to contract.
It can be stained with Trichrome stain.
True
Heart Failure drugs: B1 blockers not only can be used to treat HTN, but can also be used to treat HF.
What are the actions of B-blockers on the heart? in blood vessels?
- Heart:
- -competitive antagonists of B1-receptors (sympathetic)
- slow heart rate and force of contraction (dec. b.p., dec. SA node)
-blocks NE/E
- Blood vessels:
- inc. dilation
- dec. b.p.
Angina drugs: True/False: O2 requirements inc. where there is an increase in HR, contractility, arterial pressure or ventricular volume
True
NOTE: cardiac muscle cannot develop appreciable O2 debt during stress and repay it later
Rheumatic fever: Diagnosis of a patient with rheumatic fever usually as follows:
“Patient presents with known group A strep pharyngitis followed 2-3 weeks by one or more of the other manifestations”
What is the criteria for diagnosis?
Need 2 major OR 1 major/2 minor criteria
Minor:
- -fever
- -arthralgia
- -raised erythrocyte sedimentation (ESR)
- -C-reactive protein
- -Leukocytosis
- -ECG w/ prolonged PR
- -previous episode of RF
Myocardial Ischemia: Describe the pathologic finding during acute MI 3-7 days post-MI
Gross:
–Red (hemorrhage - necrotic area; granulation tissue)
Microscopic:
- -macrophages remove necrotic debris
- -Risk of rupture:
- —free wall: cardiac tamponade
- —mitral regurgitation (papillary muscles rupture)
- —interventricular septum (VSD – L to R shunt)
Myocardial Ischemia: Atherosclerosis is the major cause of Myocardial Ischemia.
What again are the risk factors for atheroslerosis?
-Age (male >45; female >55)
-Family history of premature CHD
(1st degree male relative <55 or female <65)
-Lipid abnormalities (inc. LDL)
-Smoking ***
-HTN
-Diabetes mellitus
-elevated serum homocysteine levels
-metabolic syndrome (3x inc. risk for coronary atherosclerosis; 3/5 Dx)
NOTE: HDL >60 = reduced risk
Angina drugs - Nitrates and Nitrites: In unstable angina, these drugs dilate _______ coronary arteries and thus reduce myocardial O2 demand.
dilate epicardial coronary arteries
*can also prevent platelet aggregation
Myocardial Ischemia: Prinzmetal angina also known as _________ is pain associated with myocardial ischemia. It is caused by focal or diffuse spasm of the SM of a coronary artery.
Vasospastic angina
- hyperreactivity of vascular SM
- can involve normal or atherosclerotic vessels
Myocardial Ischemia: True/False - During an MI, necrosis involves half of the thickness of the myocardium within 2-3 hours of onset. Usually, by 6 hours, ischemia is transmural.
True
Heart Failure Drugs: Thiazides can induce vasodilation via activation of Ca2+ induced _____ channels. This hyperpolarizes the membrane, closing L-type Ca2+ channels and causes SM relaxation (vasodilation)
K+ channels
- hyperpolarize
- dec. Ca2+ release
- vasodilation
Describe the steps for managing atrial flutter/fibrillation and paroxysmal supraventricular tachycardia
- Carotid sinus massage/valsalva
- -if hemodynamically stable
2-4. Drugs to slow ventric. rate
a. beta blockers, Ca2+ blockers, digoxin, adenosine
2-4. drugs to convert atrial rhythm
–ibutilide, dofetilide, sotalol
3-4. cardioversion if drugs don’t work (plus aspirin)
–or as 1st choice
- Long term management** FOR EXAM
- Catheter/surgical oblation or pacemaker
Anti-arrhythmics: Afterdepolarizations are believed to result from abnormal calcium influx during or immediately after phase ______ of ventricular action potential. They can lead to extrasystoles and tachycardia.
- Early afterdepolarizations (EAD’s) are often _____ induced which is why it can be a dangerous trigger for arrhythmia
- Late or delayed (DAD’s) are often ____ induced, which is why tachycardia can trigger an arrhytmia.
- EAD: bradycardia induced
2. DAD: tachycardia induced
Heart Failure Drugs: Thiazides can induce vasodilation via activation of Ca2+ induced _____ channels. This hyperpolarizes the membrane, closing L-type Ca2+ channels and causes SM relaxation (vasodilation)
K+ channels
- hyperpolarize
- dec. Ca2+ release
- vasodilation
Ischemic Heart: Myocardial Ischemia (ischemic heart disease) is the leading cause of death in the U.S.
It results from an imbalance between myocardial O2 supply and cardiac demand. Atherosclerosis of the coronary arteries (coronary heart disease) can cause decreased perfusion to the heart, and thus, cause cardiac myocytes to be deprived of adequate O2 supply.
What are clinical presentations of Ischemic heart disease (coronary heart disease/myocardial ischemia)?
- Angina pectoris
- -most common
- chest “pain” from ischemia tissue injury
* *inc. risk of infarction
* *discomfort, heaviness, rubber band, elephant - MI
- -ischemic necrosis of heart muscle
* heart attack - Chronic ischemia
- -results in heart failure
- -need O2 for contraction; not getting it - Sudden cardiac death
A 59 year old female presents to the clinic with syncope, angina and dyspnea. Upon auscultation, you can hear a crescendo-decrescendo that radiates to the carotids.
What is the most likely valvular disorder?
aortic stenosis
- commissural fusion
- calcified valve (hydroxyapetite)
- schistocytes (fragmented RBC’s)
Myocardial Ischemia: Thrombosis of the RCA can lead to this.
Common features include:
- bradycardia (right. coronary supplies AV, SA)
- hypotension
- Rt. heart failure
- preserved LV function
RIght ventricular MI
The following describes what valvular disorder?
- opening snap
- history rheymatic fever
mitral stenosis
Heart Failure Drugs: What are common side effects of Thiazides?
Common:
- Most common:
- headaches, blurred vision
- postural hypotension
- allergies (sulfonamide) - Others:
A. electrolyte imbalance (hypokalemia; metabolic alkalosis; hypercalcemia; hyponatremia; prolonged use)
B. metabolic imbalance
(dec. insulin = insulin tolerance; hyperuricemia = gout)
Heart Failure drugs: Phosphodiesterase inhibitors include amrinone and milrinone.
They are positive inotropes and are considered 2nd line agents for CHF.
When are they most used?
- IV
- short term management of acute HF and refractory HF
*milrinone higher activity than amrinone
The following describes what valvular disorder?
- holocystolic
- history of rheumatic fever
- radiates to axilla
Mitral regurg.
Myocardial Ischemia: Angina results from ischemia (loss of blood flow to the heart).
Ischemia leads to acidosis and decreased ATP formation. This loss of ATP impairs Na/K+ pumps, and leads to cell swelling and release of chemical mediators (adenosine) that stimulate pain receptors.
Where can the pain be felt?
- chest, neck, lower jaw, down left arm
* Referred pain – dermatomes that correspond to same segments as the heart (C7-T4 sympathetic afferents)
Herat failure drugs: B-adrenergic agonists are sympathomimetic drugs that stimulate the sympathetic nervous system.
What are examples of these drugs and their features?
- Dopamine
- -non-specific
- -D1 = D2 > B > a
- -vasodilation - Dobutamine
- -selective
- B1 > B2»_space; a
- -increases renal perfusion
- extremely strong (IV)
- not 1st line meds
- mainly in life threatening situations (acute HF; refractory HF; severe failure following MI, cardiogenic shock)
Heart Failure Drugs: WHat are the most common side effects of ACE inhibitors?
- dizziness, hypOtension
- dry cough***
- skin rashes
- fever
- hyperkalemia
NOTE:
- -Fetal toxicity (2nd-3rd trimester)
- -angioedema (rare)
- -acute renal failure
**NO CNS effects (No BBB)
Angina drugs: True/False: O2 requirements inc. where there is an increase in HR, contractility, arterial pressure or ventricular volume
True
Myocardial Ischemia: STEMI involves ST segment elevation and new Q wave formation.
Common complications of STEMI include
- Cardiogenic Shock
- Lethal arrhythmias
- Heart Failure
- Rupture
- Mural thrombus
- Pericarditis
Rupture usually occurs between days 3-7 (wall is the weakest). There are 3 possibilities:
a. Anterior wall rupture
b. Posteriomedial papillary muscle rupture
c. Interventricular septum rupture
Describe these
- Rupture (days 3-7 (weakened wall))
a. ant. wall rupture (MC)
- -thrombosis of LAD, cardiac tamponade
- -rapid/fatal
b. posteromedial papillary muscle dysfunction
- -due to inferior MI (thrombosis of rt. coronary artery)
- -acute onset of mitral regurg./LHG
c. Interventricular septim rupture
- -thombosis of LAD
- -Left to R. shunt (RHF)
- -inc. O2 in RV
Heart Failure: Most ACE inhibitors are pro-drugs that must be activated.
Which of the following is not a pro-drug?
a. Captopril
b. Benazepril
c. Lisinopril
d. Quinapril
Answer:
Captopril (short acting)
Benazapril (intermediate)
Lisinopril (long acting)
Myocardial Ischemia: Chest discomfort described as pressure, heaviness, squeezing. It is typically diffuse, with gradual onset and offset after 2-5 minutes.
It is the most common clinical manifestation of myocardial ischemia.
Angina pectoris
*other symptoms: nausea, fatigue, diaphoresis, SOB
NOTE: usually middle aged males; females w/ menopause
Tx: Nitroglycerin (venodilation)
Rheumatic Fever: RF is a multi-system disease that occurs from an autoimmune reaction against ______. This affects multiple organ systems including joints, heart, skin and brain.
Nearly all manifestations resolve, EXCEPT valbular heart damage (chornic rheumatic heart disease)
Group A strep
Myocardial Ischemia:
- What would we see in a patient who has >70% of the vascular cross sectional area?
- What would we see in a patient who has 90% stenosis?
- Asymptomatic at rest; Chest discomfort (Angina) w/ activity (mowing, shoveling snow)
- Ischemia even at rest
- -chronically ischemic
Anti-arrhythmics: List the anti-arrythmic drugs associated with the classes listed:
Class I Class II Class III Class IV Other
Class I: Na2+ channel blockers
Class II: B- blockers
Class III: K+ channel blockers
–prolong effective refractory period (prolong action potential)
Class IV: Ca2+ channel blockers
Others: digoxin, adenosine and Mg Sulfate
Heart Failure: A form of heart failure that is normally due to a non-compliant (stiff ventricle).
Ejection fraction is normal at rest (dec. SV and LVEDV), but is decreased with exertion.
Diastolic Heart Failure
(HFpEF)
-S4 heart sound (secondary to blood enterning non-compliant ventricle)
Causes:
- LVH
- Hypertrophic cardiomyopathy
- Restrictive cardio (amyloidosis)
Myocardial Ischemia: A form of tissue death associated with rupture of atheromatous plaque within a coronary artery.
- thrombogenic necrotic material within the plaque is exposed
- platelets adhere to exposed material
- thrombus forms, occluding blood flow
- *ischemic necrosis of cardiac myocytes
Myocardial infarction
*ischemic necrosis of cardiac myocytes (due to plaque rupture in coronary artery)
Tx: Aspirin prevents further thrombosis (inhibits COX-1 which inhibits Thromboxane A-2)
Anti-arrhythmics: These class IV drugs are non-Dihydropyridine Calcium channel blockers.
They block Ca2+ channels in the heart and vascular SM. They are used to Tx supraventricular tachycardia.
Verapamil and Diltiazam
NOTE: Verapamil preferred during pregnancy
Rheumatic heart disease: _________ refers to the long term sequelae of acute RF (rheumatic fever). Over decades, patients commonly develop calcification and fibrosis of heart valves (esp. the mitral valve) leading to stenosis w/ resistance to flow.
Over time, inc. LA pressure leads to dilatation of the LA (inc. risk of atrial fibrillation)
Chronic rheumatic heart disease
- inc. fibrosis of leaflets (commissural fusion)
- inc. LA pressure and dilatation (atrial fib risk)
- pulmonary HTN
- leads to RVH (risk eventual R. sided HF)
Angina drugs: Ranolazine is a last choice drug for angina.
It works by inhibiting ____ influx in the heart, leading to reduced Na/Ca exchange and dec. calcium overload.
Ranolazine
*slight reduce in O2 demand
The following describes what valvular disorder?
- holosystolic
- IVDA
Tricuspid regurg.
Heart failure drugs: What are the adverse effects of Beta blockers?
- bradycardia
- hypOtension
- SOB
- drowsiness, depression
- Reynaud’s (numb cold)
- sexual dysfunction
- bronchospasm (non-selective)
**Glucagon (Tx B-blocker overdose)
Anti-arrhythmics: This drug blocks the Na/K pump current -
- positive inotropic effect
- -negative chronotropic effect (not causing bradycardia).
It CAN be used during pregnancy.
Digoxin
Myocardial Ischemia: Sudden onset of severe, crushing retrosternal discomfort that lasts > 30 minutes.
It is NOT relieved by Nitroglycerin and can have radiating pain down the inner left arm, into the jaw, shoulder and epigastrium.
Acute MI
- referred pain C7-T4 sympathetics/dermatomes
- diaphoresis, anxiety, hypotension
Anti-arrhythmic drugs: True/False: Most anti-arrhythmic drugs are pro-arrhythmic
True
Myocardial Ischemia: Myocardial Oxygen supply is determined by two main factors:
- blood flow through coronary arteries
- oxygen carrying capacity
What affects oxygen carrying capacity?
- Severe anemia
- -dec. cell count = dec. O2 - Decreased O2 saturation
- -Hb issues (CO poisoning; Methemoglobinemia)
Anti-arrhythmics: This Class III drug is:
- given intravenously (IV)
- converts patients with atrial flutter or fibrillation to a normal sinus rhythm.
- inc. risk of patient harm (if error)
Ibutilide
NOTE: can cause torsade de pointes
**heightened risk of significant patient harm (if used in error)
Heart Failure: True/False - The type of heart failure (systolic or diastolic) can be determined by ejection fraction
True
- low EF (<0.5) = systolic
- normal EF (>0.5) = diastolic
NOTE:
- systolic: impaired contraction/ejection
- diastolic: impaired relaxation/filling
Anti-arrythmic drugs: Class IA anti-arrhythmic drugs are used when other Tx do not work. These act as open channel blockers (inc. QRS depolarization) and include the drugs:
- Disopyramide
- Procainamide
- Quinidine
- Disopyramide
- -not used much
- -6hrs - Procainamide
- -IM and IV only in U.S
- -3rd level choice
- -lasts 7hrs; cleared in 6 - Quinidine
- -life threatening arrhytmias
- -not used often
Heart failure: True/False - Left sided abnormal heart sounds/murmurs do NOT increase with inspiration, but intensity of R. sided murmurs DO increase on inspiration
True
Rinspiration
Lexpiration
Heart failure drugs: List the drug interactions with dobutamine
- Monoamine oxidase inhibitors (anti-depressant)
- -inc. catechols
- -inc. dobutamine side effects
* dec. dose of dobutamine
NOTE: no interaction with CV drugs
Anti-arrhythmics: True/False - Class IV drugs slow the AV node conduction velocity and prolong the AV node refractory period. Thus, they terminate AV node re-entry that causes supraventricular tachycardia
True
Myocardial Ischemia: What is the most common trigger for plaque rupture w/ regard to acute coronary syndrome, angina and MI? What determines onset?
Trigger: sympathetic nervous system
–HR and BP
(physcial/sexual activity, anger, anxiety, work stress, cocaine, war/terror)
Onset: circadian rhythm of biological pathways
**MI’s most common in the morning
NOTE: vulnerability of plaques to rupture (content of lipids and inflamm cells) is the MOST important
Angina drugs: Which of the following is a method for modifying risk factors for coronary atherosclerosis?
a. smoking cessation
b. reduce obesity
c. diabetes management
d. reduce HTN
e. reduce hyperlipidemia
f. gradual intro to exercise
All of the above
Heart Failure drugs: What are the 4 stages of Heart failure?
- Stage 1
- -breathlessness/tiredness
- -brisk walk or jog (exertion) - Stage 2
- -comfortable when resting
- -heart races/breathlessness when walking or taking stairs - Stage 3
- -palpitation or tiredness
- -difficulty with simple tasks (getting out of a chair)
Stage 4
- -heart and breath inc. at rest
- -tiredness at rest
- -anxiety and palpations all the time
Anti-arrhythmics - Class C drugs: Flecainide can induce bronchospasm and seizures while Propafenone causes agrnulocytosis and anemia.
When are Class IC drugs most commonly used?
Severe supraventricular arrhythmias and/or life threatening ventricular arrhythmia
NOTE: PVC’s in otherwise normal hearts should NOT be given flecainide
(perfectly controlled rhythm and rate leads to increased mortality and morbidity)
Anti-arrhythmics: Re-entry is characterized by retrograde conduction of an impulse into previously depolarized tissue. It is normally caused by a unidirectional conduction block in a bifurcating conduction pathway.
What are the 3 necessary requirements/events for re-entry to occur?
- obstacle to normal AP conduction
- unidirectional block (dec. conduction of the impulse anterograde; normal conduction retrograde)
- conduction time through the retrograde pathway MUST exceed the refractory period of the re-entered tissue
Heart Failure: What are the most common side effects of vasodilators?
- headache, nausea, diarrhea, flushing, hypotension
- tachycardia (due to hypotension)
- inc. RAAS
- countered by B-blockers and diuretics
NOTE: prolonged use of hydralazine at high doses = lupus like syndrome
NOTE 2: Nesiritide can induce renal failure; inc. risk of mortality; no arrhythmias
Endocarditis: Infective endocarditis is usually caused by bacterial infection of the endocardial surface of the heart.
It primarily affects the cardiac valves and sometimes involves the mural endocardium. What is the mechanism by which it damages the valves?
- Fibrin/platelets adhere to valve
- -damaged area – forms clot - Bacteremia leads to infection of clot
- Organisms within clot proliferate
- -vegetation (friable - break off and form emboli) - Infection and subsequent host immune response damages valve leaflets
- -or chordae tendinae
- -heart murmur
Angina drugs:
What drugs serve as the drug of choice for treating variant (vasospastic) form of angina
Calcium Channel blockers
— relieve and prevent coronary artery spasm, increasing coronary blood flow.
NOTE: nifedipine/nimodipine = inc. reflex tachycardia
Myocardial Ischemia: Because the myocardium cannot increase O2 extraction, an increase in O2 demand requires increased perfusion (blood flow).
Which of the following are determinants of oxygen demand?
a. HR
b. myocardial contractility
c. myocardial wall tension
d. systolic b.p. (afterload)
All of the above
- Wall tension:
- -product of preload and myocardial muscle mass
- -inc. tension = inc. O2 demand
*Also: physical activity, thryotoxicosis (e.g. hypothyroidism), aortic stenosis, cocaine/amphetamines inc. O2 demand
Heart Failure Drugs: What is the mechanism of action of Antiotensin Receptor Blockers (ARBs: AT1RWhat inhibitors)?
-Relax Vascular SM
(dilation; inc. flow; dec. afterload)
- dec. aldosterone (dec. preload)
- dec. NE (dec. sympathetic)
NOTE: Valsartan (AT1R inhibitor); Sacubitril (pro-drug; active neprilysin inhibitor – breaks down natriuretic peptides)
Heart failure drugs: Which of the following is a positive inotropic drug?
a. B1-adrenoceptor agonist (dobutamine)
b. digitalis (digoxin and digitoxin)
c. ACE inhibitors (lisinopril)
d. ARBs (candesartan)
Answer: A and B
- B1 agonists (dobutamine)
- Phosphodiesterase inhibitors (amrinone, milrinon)
-DIgitalis (digoxin, digitoxin)