WEEK 3 Cardiovascular Meds Flashcards
1
Q
How is the reestablishment of balance between myocardial O2 supply and demand accomplished when taking meds for ischemic heart disease?
A
Decreasing HR or SBP to reduce O2 demand
2
Q
What are other goals of taking meds for ischemic heart disease besides reestablishing balance?
A
- Increasing arterial lumen size
- Removal of thrombus from coronary artery
- Decrease coronary spasm
- Increase O2 supply
3
Q
What are the goals of taking meds for heart failure?
A
- Maintain CO
- Regulate fluid/salt
- Decrease preload & afterload
- Increase cardiac contractility
- Reduce cardiac workload
4
Q
Describe the differences between stage A-D heart disease.
A
- A: No structural heart disease
- B: Structural heart disease
- C: Symptomatic heart disease
- D: Severely symptomatic
5
Q
What are the goals of taking meds for arrhythmias?
A
- Inhibit abnormal impulse formation & conduction by altering membrane permeability to specific ions
- Slow down repolarization or prolong refractory period
6
Q
How are arrhythmias classified?
A
- Ionic gates they control: Na+, K+, Ca+, Cl-
- Location: Myocardial pacemaker cells (SA, AV)
7
Q
What are the goals of taking meds for HTN?
A
- Reduce fluid volume
- Limit SNS activity
8
Q
Why should SNS activity be limited in HTN?
A
- Vasodilation
- Reduce CO
- Reduce effects of RAAS system @ kidney –> vasodilation & reduce fluid volume
9
Q
What do B blockers (B-antagonists, sympatholytic) do?
A
Reduce B-receptor binding sites of epinephrine & norepinephrine
10
Q
Describe what a selective B blocker does to B1.
A
Decreases HR & contractility @ the heart
11
Q
Describe what a selective B blocker does to B2.
A
Bronchoconstriction & vasoconstriction @ lungs & peripheral muscles
12
Q
Describe what a B-blocker does to A1 or A2 receptors.
A
Vasodilation @ gut
13
Q
What do nonselective B blockers do?
A
Block all receptors (B & A)
14
Q
Who should avoid taking nonselective B blockers and why?
A
PVD (peripheral vascular disease) & COPD because blocking B2 will make their conditions worse
- PVD: Constricting already narrow vessels
- COPD: Shortness of breath
15
Q
For people taking B blockers, how is their exercise tolerance affected?
A
Decreased with increased fatigue
16
Q
What 4 conditions are B-blockers clinically indicated for?
A
- HTN
- Ischemic heart disease
- Heart failure
- Arrhythmias
17
Q
What are some side effects of B blockers?
A
- Sedation (fatigue, depression)
- Thrombocytopenia
- Masks symptoms of hypoglycemia
- Reduced thermoregulatory response (overheating)
- Hyperglycemia
- Smooth muscle spasm (bronchospasm & cold extremities)
- Exaggerated cardiac responses
18
Q
Why are masked symptoms of hypoglycemia & reduced thermoregulatory response side effects of B blockers?
A
Sympathetic output blocked
19
Q
Which exaggerated cardiac responses can be seen when taking B blockers?
A
- Bradycardia
- Orthostatic hypertension (SBP drop of 20, HR rise of 30)
- Heart block
- Excess negative inotropic effect
20
Q
What 4 conditions are calcium channel blockers clinically indicated for?
A
- Ischemic heart disease
- Arrhythmias
- BP control
- Reduction of infarction in patients with non-Q wave infarcts
21
Q
Calcium channel blockers have very few side effects other than what?
A
Negative inotropic effects
22
Q
When taking calcium channel blockers, what may be necessary to use during exercise as HR responses may be blunted?
A
RPE
23
Q
What suffix do calcium channel blockers have?
A
-pine
24
Q
How do calcium channel blockers decrease arterial BP?
A
- Smooth muscle relaxation
- Vasodilation –> decreases afterload
25
Myocardial __________ causes influx of Ca++ which increases HR & contractility.
Ischemia
26
How do Ca++ blockers reduce O2 demand?
- Reduce intracellular Ca++
- Slows HR
- Strength of contraction
27
What 3 conditions are nitrates clinically indicated for?
- HTN
- Ischemic heart disease (angina)
- Heart failure
28
What effects do nitrates exert?
- Slow HR
- Reduce blood to heart by vasodilation --> reduce preload
- Cause heart to contract with less force
- Lower BP with less resistance in heart --> reduce afterload
29
How does nitrate feel for the patient after taking it?
Burning on tongue with chest pain relief within 5 min
30
How does angina occur?
Lack of O2 stimulates pain receptors in heart
31
What do nitrates tend to have in their name?
Nitr
32
What are some side effects of nitrates?
- Hypotension
- Dizziness
- Reflex tachycardia
- Flushing of skin
- Nausea/vomiting
33
How are nitrates administered? Which way is typically used for emergencies?
Enteral or parenteral:
- Oral
- Sublingual
- Percutaneous spray
- Intravenous
34
Where can ischemic pain radiate to?
- Shoulder
- In between scapulae
- Arm
- Throat
- Jaw
- Anywhere above umbilicus
35
What can be seen on ECG to indicate ischemia?
ST segment downward shift > 0.5 mm
36
What are the 2 types of angina?
- Stable
- Progressive
37
Describe stable angina.
- Pain free at rest & can be relieved with nitrates
- Several minutes
- Reliably predict activities that will provoke (increase O2 demand)
38
Describe unstable angina.
- Onset unpredictable or accelerating in frequency, severity, or intensity
- May happen at rest
- Longer than 15 min
- Progression of disease
39
Describe Prinzmetal's (variant) angina.
- Only at rest, often early morning
- ST elevation on ECG
- Result of cardiac vasospasm (transient decrease in artery diameter)
- Treated with Ca++ blockers
40
Which 3 meds are used for angina? How do they fix the issue of supply vs demand?
- Nitrates: Increase blood flow, decrease venous return
- B blockers: Decrease HR & workload
- Ca2++ blockers: Maintain coronary artery vasodilation & limit spasms
41
Which surgeries are used to help with angina?
- Heart catheterization
- CABG
- Angioplasty
42
What type of agent is used when there's blood clot formation in coronary artery at time of plaque rupture for stroke or MI patients?
Thrombolytic
43
What is rate pressure product? What does it estimate?
- SBP x HR
- Myocardial workload (don't go over 10,000)
44
How do thrombolytic agents break scaffold of blood clots?
Convert plasminogen to plasmin
45
What is the ideal time frame in which thrombolytics should be given?
Within 30 min but at the latest: 120 min (2 hrs)
46
What are some side effects of thrombolytic agents?
- Ventricular arrhythmias due to rapid reperfusion
- Excessive bleeding (high intensity resistance training, shaving, venipunctures)
- Hemorrhagic CVA
- GI or GU bleeding
47
What type of agent is used as primary & secondary preventative measure to prevent thrombus formation by decreasing platelet adherence at site of injury?
Anti-platelet
48
Which anti-platelet is common in post-op patients?
Plavix
49
What do anticoagulants do?
- Prevent clots or emboli
- Inhibit thrombin
50
Which anticoagulants are common?
- Heparin
- Coumadin
- Pradaxa
- Xarelto
- Eliquis
- Lovenox
51
True or False: Increased risk of bleeding is only with thrombolytic & anti-platelet agents.
False
## Footnote
All 3 so also anticoagulants
52
What 2 conditions are diuretics clinically indicated for?
- HTN
- Heart failure
53
What effects do diuretics exert?
- Decrease circulating blood volume (preload)
- Improve ventricular length-tension relationship --> improve contractility
- Reduce cardiac demand
- Decrease reabsorption of water & Na+ @ kidneys
54
What suffix do diuretics have?
-ide
55
Action of diuretics is at various sites along...
- Renal tubules
- Loop of Henle
56
Which is the most potent diuretic?
Lasix (loop diuretic)
57
Which diuretic is mild & works at proximal tubules?
Carbonic anhydrase inhibitors
58
Which diuretic is mild & works on collecting tubules & ducts?
K+ sparing
59
Which diuretic is moderate & may cause hypokalemia & glucose intolerance & works on distal convoluted tubules?
Thiazides
60
Proximal & distal convoluted tubules diuretics also inhibit KCl across where?
Ascending loop of Henle
61
Why is there caution with aerobic exercise when taking diuretics?
- Hypotension (because of fluid loss)
- Arrhythmias (because of K+ loss)
62
What medicine is used to lower blood sugar for T2D & has cardioprotective effects?
Sodium-glucose transporter inhibitors
63
What cardioprotective effects do sodium-glucose transporter inhibitors have?
- Reduce BP
- Lower hospitalization due to heart failure, less CV deaths
- Reduces kidney disease
- Weight loss
64
What type of medicine are these?
- Inxokana (canaglifozin)
- Farxiga (dapagliflozin)
- Jardiance (empagliflozin)
Sodium-glucose transporter inhibitors
65
What are some side effects of sodium-glucose transporter inhibitors?
- Hypoglycemia
- Hypotension
- UTIs
- Diabetic ketoacidosis with normal/slightly high blood glucose
66
What 2 conditions are drugs that affect RAAS clinically indicated for?
- HTN
- Heart failure
67
Drugs that affect RAAS can be considered as vaso(dilators/constrictors) & anti-HTN.
Dilators
68
What are some examples of drugs that affect RAAS?
- Angiotensin-converting enzyme inhibitors (ACE)
- Angiotensin receptor blockers (ARB) & neprilysin inhibitors
- Aldosterone antagonists
69
What do ACE inhibitors prevent? Why?
Conversion of angiotensin I --> II because II causes:
- Vasoconstriction --> increase BP
- Renal water & sodium retention
- Aldosterone stimulation
70
What suffix do ACE inhibitors have?
-ril
71
Where do ARBs limit the effects of angiotensin II?
Vasoreceptors of arterial beds
72
What suffix do ARBs have?
-sartan
73
What is a combo ARB & neprilysin inhibitor used for patients with HF?
Entresto (sacubitril/valsartan)
74
What do neprilysin inhibitors do?
- Reduce abnormal remodeling
- Promote diuresis
- Vasodilation
- Na excretion/K retention
75
What are some side effects of ACE inhibitors & ARBs?
- Hypotension
- Light headedness
- Dizziness
- Angioedema (life threatening)
- Hyperkalemia
- Persistent dry cough
76
What effects do aldosterone antagonists exert?
- Decrease renal fluid & Na+ retention/increase Na+ excretion
- Mild diuretic
77
What are some side effects of aldosterone antagonists?
- Hyperkalemia
- Orthostatic hypotension
78
Spironolactone is a type of what medicine?
Aldosterone antagonist
79
What type of drug is clinically indicated for heart failure & increases contractility?
Positive inotropes
80
What type of drugs are these?
- Cardiac glycosides
- Sympathomimetics
- Phosphodiesterase
Positive inotropes
81
Which receptors do positive inotropes stimulate?
B
82
Which type of positive inotrope is especially for dilated cardiomyopathy & a fib?
Cardiac glycosides
83
Cardiac glycosides increase intracellular ____ to increase contractility.
Ca++
84
What do cardiac glycosides have negative effects on? How?
- Chronotropy (decrease HR)
- Dromotropic (increase conduction delay SA --> AV & PR interval)
85
What type of drug are digitalis & digoxin?
Cardiac glycosides
86
How is toxicity possible with cardiac glycosides?
- Decreased renal function
- Altered GI absorption
87
What are some GI signs of digitalis toxicity?
- Anorexia
- Nausea
- Vomit
- Diarrhea
88
What are some neuro signs of digitalis toxicity?
- Malaise
- Fatigue
- Vertigo
- Insomnia
- Depression
- Colored vision
- Facial pain
89
What are some CV signs of digitalis toxicity?
- Palpitations
- Arrhythmias
- Syncope
90
What are some signs of hematologic toxicity?
- High digoxin/low K+
- Altered BUN/creatinine
91
How do patients feel with digoxin toxicity? How about if taking it for a fib?
- Vague symptoms of not feeling well
- A fib: Irregular pulse
92
How does digoxin control a fib?
Increased PR interval
93
When taking digoxin, a fib with resting HR of more than ___ bpm may need to be reassessed by doctor.
110
94
How long should resting pulses be taken for if patient has heart rhythm irregularities?
1 min
95
Which patients should avoid taking digoxin?
Those with 2nd or 3rd degree AV block
96
What condition are sympathomimetics clinically indicated for?
Acutely compromised heart failure patient to improve CO in critical care setting
97
What effects do sympathomimetics exert?
- Mimic actions of SNS
- Minimize possibility of sympathetic receptor desensitization
98
Which type of sympathomimetics stimulates influx of Ca+ into myocardium to increase contractility & increases SA & AV node firing & conduction?
Selective B1 (dobutrex, levophed)
99
Which type of sympathomimetics increases contractility & reduces afterload due to vasodilation?
Nonselective B1 & B2 (adrenaline chloride, isuprel)
100
Which type of sympathomimetics is used when heart failure is present with hypotension to stimulate B1 myocardial, D1, & a vascular receptors to increase CO & BP?
Dopamine (inotropin)
101
Phosphodiesterase inhibitors are used for patients who did not respond to sympathomimetics or cardiac glycosides with a combo of what?
- Severe CHF
- Need for contraction strengthening
102
What is the name of the drug that acts as a + inotrope & vasodilator to promote preload/afterload balancing?
Inocor (phosphodiesterase inhibitor)
103
What 3 conditions are vasodilators clinically indicated for?
- HTN
- Heart failure
- Ischemic heart disease
104
What 3 types of drugs are considered vasodilators?
- Ca++ blockers
- ACE inhibitors
- Nitrates
105
What type of drug are these?
- Apresoline
- Loniten
- Hyperstat IV
- Hydralazine IV
- Milrinone IV
Vasodilators
106
What do arterial vasodilators do? How about venodilators?
- Arterial: Reduce afterload
- Venodilators: Reduce preload
107
Venodilators are effective for __________ HTN.
Diastolic
108
Which type of vasodilator is used to manage HTN & not heart failure?
A adrenergic antagonist
109
What type of drug are these?
- Minipress
- Hytrin
A adrenergic antagonist
110
What are some side effects of A adrenergic antagonist?
- Reflex tachy
- Compensatory increase in blood volume
111
Which type of vasodilator is nipride?
Nitric oxide donor
112
What do venodilators reduce?
Venodilators reduce preload.
113
What type of hypertension are venodilators effective for?
Venodilators are effective for diastolic hypertension.
114
Which type of vasodilator is used to manage hypertension and not heart failure?
A adrenergic antagonist.
115
What type of drugs are minipress and hytrin?
A adrenergic antagonists.
116
What are some side effects of a adrenergic antagonists?
- Reflex tachy
- Compensatory increase in blood volume
117
What type of vasodilator is nipride?
Nipride is a combined arterial and venous vasodilator.
118
What does nipride treat and how?
Nipride treats severe heart failure by reducing preload and afterload, which reduces O2 demand.
119
What effects does morphine exert as a vasodilator?
- Decrease preload
- Mild vasodilation
- Reduces anxiety and effort with severe heart failure
- Reduces metabolic demand
120
What happens with compensatory sympathetic activation as a side effect of vasodilators?
- Tachycardia
- Vasoconstriction
- Increase aldosterone
- Elevated plasma renin
121
Which drug can be used to combat side effects of vasodilators?
B blockers.
122
Where are the baroreceptors that work with the kidney to regulate blood pressure located?
- Medulla
- Kidney
- Aortic arch
- Carotid artery
123
What happens to heart rate and cardiac output under hypertension conditions?
Heart rate and cardiac output are decreased to correct hypertension.
124
Which drugs help control hypertension?
- SNS blockers (B & a)
- Ca++ blockers
- ACE inhibitors (also ARB blockers & aldosterone antagonists)
- Vasodilators
- Diuretics
125
What three conditions are class I membrane stabilizers (xylocaine) clinically indicated for?
- Ventricular tachy
- Supraventricular tachy
- Atrial fibrillation
126
What do class I membrane stabilizers do and why?
They reduce Na+ influx into the cell, making it harder to reach action potential (depolarization).
127
What two conditions are class II membrane stabilizers (B-blockers) clinically indicated for?
- Ventricular arrhythmia
- Supraventricular arrhythmia
128
What do class II membrane stabilizers do?
They block sympathetic excitation of the heart to control rhythm.
129
What two conditions are class III membrane stabilizers (cordarone) clinically indicated for?
- Ventricular tachy
- Supraventricular tachy
130
What do class III membrane stabilizers do?
They make myocardial cells less responsive to stimulation.
131
In patients with hemodynamic instability, what is the antiarrhythmic medication often used?
Amiodarone.
132
What are some side effects of membrane stabilizers?
- Exacerbation of arrhythmias
- Sinus bradycardia
- Photosensitivity
- Hepatotoxicity
- Hypothyroidism
133
Anti-arrhythmics slow down what by blocking potassium?
They slow down repolarization. If the slowdown is too much, another arrhythmia can occur since another impulse can come in.
134
What do class IV membrane stabilizers (Ca++ blockers, isoptin, calan) do?
- Decrease pacemaker activity of depolarized cells
- Prolong refractory period
135
What does digitalis do in terms of anti-arrhythmics?
- Enhance parasympathetic tone in a healthy heart
- Depress sympathetic actions of a failing heart
- Slows heart rate and depresses AV node conduction
136
What condition is digitalis especially helpful for?
Atrial fibrillation.
137
How can digitalis have a side effect of arrhythmias?
- Increased Ca++
- Loss of K+ leading to bradycardia
- Increased speed of repolarization leading to tachycardia
138
What is the name of the drug clinically indicated for bradydysrhythmias?
Atropine.
139
What does atropine do?
- Block pre-ganglionic cholinergic receptors on cardiac muscle
- Blocks PNS/vagal tone, increasing heart rate
140
What is the name of the drug that is clinically indicated for supraventricular tachycardia?
Adenosine.
141
What does adenosine do?
It slows conduction in the re-entry pathway through the AV node, decreasing heart rate.
142
Patients who receive hydroxychloroquine or azithromycin in combination with antiarrhythmic drugs are at risk of prolonged what interval and torsades de pointes?
QT interval.
