Lecture 3: Cardiac Pathology & Pharmacology Flashcards
1
Q
Fatty deposits (plaque) accumulate inside the artery wall: called what?
A
Atherosclerosis
2
Q
Where does arthosclerosis start?
A
Tunica intima
3
Q
Which layer of arteries is responsible for inflammatory responses?
A
Tunica Intima
You get plaque buildup which causes a tear in the tunica intima and causes an inflammatory response
4
Q
What is an ischemia?
A
Reduction of blood flow (not complete blockage)
5
Q
What diliniates myocardial infarction and ischemia?
A
Ishcemia is a partal blackage while infarction is complete
6
Q
KNOW: Atherosclerosis causes progressive hardening and narrowing of the coronary, cerebral, and peripheral arteries
* **Its very systemic
* If you have cornary artery disease or likely have cerebral / peripheral artery disease as well (because its a systemic disease) **
A
7
Q
KNOW: Atherosis (paste) = the fatty streak
* Consists of lipid-laden macrophages (foam cells) and smooth muscle cells
A
8
Q
Sclerosis definition
A
Hardening
9
Q
Does atherosclerosis indecrease or decrease blood vessel compliance?
A
Decreases
10
Q
KNOW: Progressive hardening / narrow in atherosclerosis comes from that inflammatory response. You have those fibroblasts that are in the tunica intimia, and in order to repair itself it keeps lying down more collagen, which leads to the hardening, essentially forming a fibris cap of thrombi over advanced plaqyes that have developed on the endothelial lining
The thrombus can block the entire artery or break of
A
11
Q
7 Recommendations for reducing the risk of coronary artery disease and cardiovasclar disease
A
1) Avoid cigarette smoking
2) Engage in appropriate PA
3) Maintain ideal body wt
4) Eat a healthy diet
5) Manage BP
6) Manage cholesterol
7) Manage fasting blood glucose
12
Q
KNOW: Emerging risk factors for cardiovascular disease:
1) Lipid-releated biomarkers; lipoprotein(a) and high lopoprotein-associated phospholipase A2
2) Inflammatory markers; interleukin-6, C-reactive protein, and others
3) kidney related biomarkers; microalbuminuria
4) Air pollution
5) Mediastinal radiation (think cancer radiation)
6) Human immunodeficiency viral infection (HIV) - causes increase radiation
7) Elevated homocysteine levels
8) Abdominal sleep (increased infllamation)
I think really anything that causes increase inflammatory response
A
13
Q
Atherosclerosis typically persents in one of four ways
A
1) Sudden cardiac death (typically from ventricular tachycardia –> ventricular fibriliation –> quivering of ventricle and not pumping enough blood out into body)
2) Chronic stable agina
3) Acute cornary syndrome (ACS)
* unstable angina
* ST-segment elevation myocardial infarction (STEMI)
* Non-STEMI
4) Cardiac muscle dysfunction
14
Q
What is angina
A
Not enough blood to supply metabolic demands
Substernal pressure anywhere from epigastric area to jaw
Squeezing tightness or crushing
Imbalance in supply and demand of myocardial O2
15
Q
How are angina symptoms controlled? (2)
A
Reducing the intensity of EX and taking sublingual nitroglycerin
16
Q
angina that has a well established onset (I get over this HR and it starts) is called
A
Chronic stable angina
17
Q
What is the most common syptom of acute coronary syndrome?
A
Chest discomfort for greater than 20 minutes
NOTE: its basically chest pain (kind of an umbrella term for lots of things)
18
Q
Whats dangerous stable or unstable angina
A
unstable
19
Q
Patient starts to have new chest pain 30 seconds into working out. What is this?
A
unstable angina
20
Q
KNOW: Acute myocardial infarction can be STEMI or non STEMI
A
21
Q
transient ischemic attack = stroke
aneurysm = outpocket of wall
A
22
Q
KNOW: Coronary Artery disease = when atherosclerosis hits coronary arteries
A
23
Q
Order of anginia that occurs w/ coronary artery disease
A
Unstable anginia –> resting anginia –> new onset anginia
24
Q
Coronary Artery Disease causes elevation of what thing?
A
Troponin 1
25
What is peripheral vascular disease?
Atherosclerosis of arteries AND veins
issue to getting blood there
26
Where is PVD most common?
Extremities (legs mostly)
27
Why is someone w/ cornoary artery disease likely to also have peripheral vascular disease (PVD)
Because atherosclerosis (which causes both) is typially systemic
28
Arterial Occlusive Disease = Peripheral vascular disease
29
What is arteriosclerosis?
Atherosclerosis of arterioles
30
What do symptomes of acute coronary syndrome signify?
Acute mycardial infarction, as a result of insufficient supply to cardiac muscle
symptoms indicate whats coming
31
What is angina pectoris?
Chest pain
32
**Is Angina Pectoris a symptom or a disaese? (Test)**
Angina Pectoris is a symptom not a disease
33
What kind of ischemia is angina?
Transient ischemia of cardiac m
Its ischemia that omes and goes
34
Does angina cause damage to cardiac muscle
No
35
KNOW: Angina can be one of the first warning signs that there is a cardiac issue
36
**4 causes of angina** Test
1) Demand of myocardium > blood supply = ischemia (not enough blood flow) --> happens w/ EX because you need more blood supply to the heart
* With angina, the vessels narrow, meaning you have an increased demand on that tiny space it can get through but a decreased supply
2) Increase O2 needs to myocardium
3) Decreased blood flow to heart
4) Increased CO
37
**Anginia equivalents (things that arent chest pain but indicate a coronary issue)** TEST
1) Shortness of breath
2) Nausea
3) Fatigue
4) Diaphoresis - excessive sweating
5) Pain other htan chest
EX: someone exercising and sweating perfusly for the amount of EX they're doing. Well that could indicate an angina equivalents, especially if that have any kind of cardiovascular issues in the past.
38
Exertional angina is also known as
Stable angina (comes on w/ EX)
39
**TEST** What do you do for someone with exertional (stable) angina that it comes on when they start exercising.
Record symptoms/vital and continue on w/ EX (maybe at a lower intensity)
40
**TEST** Do you continue EX w/ unstable angina?
Stop EX immediately.
NOTE: It could turn into stable angina, or it could lead to a myocardial infarction, we just dont know at this point. Needs to be tracked before we feel comfortable continuing EX.
41
**TEST** The question is essentially going to be diliniating between stable vs unstable angina, then your course of action.
42
Most common cause of angina?
What often triggers it?
Coronary artery disease (when artherosclerosis hits the coronary arteries)
Often triggered by EX or any kind of exertion because, exertion causes increased blood supply through a decreased area.
43
Remember, angina is just chest pain. However, it is typically caused by atherosclerosis. Name the different causes of angina
* How it happens w/ vessels
* How it happens w/ circulation
* How it happens w/ blood factors
Vessels: Atherosclerosis, hypertension, cardiomyopathy, CAD
Circulation: Arrhythmias, coronary spasms, aortic stenosis, hypotension, bleeding (trauma)
Blood factors: Anemia, hypoxia, polycythemia (wasnt really covered)
44
**TEST** a pt w/ chest pain doesnt always have angina. Know the differential diagnosis charts and be able to dilinate them out.
Probs focus mostly on s/s
pleural rub = sound w/ stethascope
RR = respiratory rate
45
46
**TEST** Reasons to stop or modify EX: - With CV Hx or angina
1) New onset of easily provoked chest pain (unstable angina)
2) Increasing episodes/intensity /duration of angina (unstable angina)
3) Discomfort elsewhere in the upper body
4) Syncope, dizziness, light-headedness
5) Severe sydden dyspnea (difficult breathing)
6) Severe fatigue or muscle pain
7) Nausea or vomiting
8) Back pain during exercise - further investigate if they've had cardiac risk factors that could be leading to this
9) Bone/joint pain or discomfort during or after EX
10)
47
**TEST** Symptoms of angina (15)
1) Temporary squeezing
2) Burning
3) Pressure
4) Heartburn
5) Indigestion
6) Chocking
7) Pallor (think turning blue_
8) Cyanosis
9) Cold
10) Moist skin
11) >6 arrhythmias (palpations or irregular beats) per hour
12) Oxygen saturation <90%
13) Resting HR 130 beats/mm (because heart rate trying to get CO back up)
14) Fall in systolic BP with increase workload (10 mmHg or more)
15) Rise in systolic BP > 250 mmHg or diastolic > 115 mmHg
** If you have any of the above + angina, discontinue exercise**
48
Angina scale
49
Will ECG be normal or abnormal with angina?
Normal, angina isnt affecting the electrical part unless its actually stopping the heart
50
For documentation what is our mnuemonic / fill in
OLDCART
* Onset
* Location
* Duration
* Charactersitics
* Accompanying symptoms
* Radiation
* Treatment
51
Drugs used to treat angina pectoris (4)
1. Organic Nitrates = first line of defense
2. Beta-Adrenergic Blockers
3. Calcium Channel Blockers
4. Anticoagulants
typically prescribed when you have something else + angina, however, you typically have angina + another pathology going on thats leading to angina
* Remember, angina is a symptom, not a pathology
52
What is the MOA for Organic Nitrates?
Dilate peripheral blood vessels, decreasing peripheral resistance so the afterload is decreased, making it easier for the heart to pump into the systemic vascular supply
53
How are organic nitrates typically administered and how long does it take to see affects?
Adminustred sublingally
Therapeutic effects within 2 minutes
54
What effect does the sublingual adminstration of organic nitrates spare the patient?
First pass effect
when taken orally it goes through GI system and into liver which breaks down medication
Sublingually, it just disolves and goes right into blood system, which is why its much faster than taking orally
55
Adverse effects and why nitro
Primary: HA, dizziness, orthostatic hypotension
* This is because the blood vessels are dilated, so, HA because increased BF, and dizziness / hypotension because blood pressure cannot be maintained w/ diliated vessels
Nausea is another possible side effect
NOTE: Transdermal is another possible application (patch on skin), however, isnt recommend because they can build a tolerance
* This is typically for people who need it all the time
56
Why would you want to sit a patient down before adminsitration of organic nitrates?
Because vasodilation causes hypotension, which can lead to them falling and causing some injury
57
**TEST** Sublingual organic Nitrates should be kept how
* Discard after how long?
* how many till you call 911
In OG bottle
* ROOM temp, no direct light
* Discard after 3 months
should be in original glass bottle, O2 starts breaking it down along w/ sunlight
Super important to discard after 3 months because if they have angina they need this medication to work
If they have adminstered 3 than call 911
58
What do Beta blockers do?
* How do they work?
Block beta-1 receports on the myocardium (act as antagonists)
**Block HR and force on contractions, which decreases the workload of the heart and demand of O2**
59
Beta blockers suffix
olol
60
What do selective beta blockers target?
What do non-selective beta receptors target?
Selective = Beta 1 receptors on the heart
* 1 heart --> targets the heart
Non-selective = block both beta 1 and beta 2 receptors
* 2 Lungs --> targets the lungs
61
**TEST** Patient taking non-selective betablockers is experienceing brochoconstriction, how can this be fixed?
Put them on selective beta blockers that only target the heart
go back to slide 35 and recap here
62
KNOW: If beta blockers are taken daily they will blunt HR/BP, so you can't use BP/HR to see how they're responding to EX. Going to have to use RPE scale (increased subjectivity)
63
Calcium channel blockers suffix
* 2 exceptions
End in Pine
Diltiazem
Verepamil
64
64
How do calcium blockers work?
* does it cause vasodilation or constriction
* Does it increase or decrease oxygen supply
Block entry of calcium into the smooth muscle within the vessels, which stops that interaction between actin and myosin because the troponin is never displaysed meaning that the interaction never takes places.
* Essentailly w/ this interaction relaxion/vasodilation occurs which inxcreases oxygen supply to myocardium (because of increased BF)
65
Why are whirlpools / hot tubs contraindicated when a pt is taking calcium channel blockers?
because calcium channel blockers cause vasodilation, and the hot tub / whirl pool also cause vasodilation, meaning there is entirely too much vasodilation occuring.
* they're already having vasodilation on the inside, now they're having it on the outside, and this can lead to a fall
66
Adverse effects of calcium channel blockers
HA, flushing, feelings of warmth, dizziness, peripheral edema, nausea, disturbances in cardiac rhythm, which can lead to reflex tachycardia
67
What ia reflex tachycardia?
HR increasing due to taking calcium channel blockers
A cardiac arrhythmia that occurs when the heart beats faster in response to decrease BP or blood flow) - and that vasodilation that calcium channel blockers cause = decrease in BP
68
True or false: patients taking nitroglycerine for angina should avoid PA, as exercise can worsen their symptoms
False
While exercise can worsen those symptoms, PA can help manage and decreaase those symptoms.
* They just need to know how to exercise the correct way
69
How should nitrogylcerine tablets be stored:
a) in the refigerator
b) in a warm and humid environment
c) in their OG container (to know when it expires [3 months]), away from light and moisture
d) in a pill cotainer
C
70
71
Force exerted on wall of vessels (arteries and arteroles)
BP
composed of systolic/diastolic
72
How is BP controlled
Hormones
73
RAS system controlled BP in short term or long term pathways?
Long term
74
Baroreflex controlled BP in a short term or long term manner?
Short term
75
To ways BP is controlled?
Baroreflex (short term)
RAS system (long term)
76
What does the baroreflex respond to?
Change in pressure (responds mostly to peripheral vascular resistance) - this is if you have blood loss and need a quick increase in BP, to make sure all vital organs are getting blood. Its quick, which is why its short term
77
Blood comes into the heart and fills the ventricle causing end diasoltic volume. What two things increase it?
1) Hypervolemia
2) Regurgitation of cardiac valves
78
What can increase BP, preload or afterload?
Afterload (its the resistance taht the left ventricle must overcome to circulate blood
79
What two things increase afterload?
1) Hypertension
2) Vasoconstriction
Basically the LV has to overcome more resistance when these two things are taking place, and it increases BP
80
What external organ in affect stroke volume?
Stroke volume is influenced by the kidneys desire to maintain homeostasis (I think through RAS)
81
Is SV affected by preload or afterload?
Both
82
What 3 things affect SV?
1) Preload
2) Afterload
3) Contractility (how hard it pumps to get the blood out)
83
**TEST** Shes going to ask about the things that affect preload/afterload/contractility. Learn the right side of this chart well
84
4 vasoconstricting hormones
1) Norepinephrine
2) Epinephrine
3) Angiotensin II
4) Vasopressin
85
What percent of the population is hypertensive?
50%
Silent killer, you don't have symptoms until its really bad
Leading cause of lost years of quality of life
86
What is the most common kidn of hypertension: Primary (essential), secondary, labile?
Primariy (90-95% of population has this one)
87
What causes primary (essential) hypertension?
No known cause, idiopathic
88
Which part of the vessels is increased w/ primary hypertension?
Increased arteriole resistance
89
What causes secondary hypertension
Occurs in the presence of a disease
Think, the person having a stroke, or spinal cord injury, liver issue, etc... anything that has caused damage
90
What is labile hypertension?
elevation of blood pressure with normal readings - think white coat syndrome
* might be increased now but normal later
91
92
What is malignant hypertension?
* What can it load to?
Same thing as a hypertensive crisis - marker of elevated BP reading of > 180 mmHG for systolic AND/OR > 120 mmHg diastolic
Leads to targeted organ damage
Stop EX here, if they've having symptoms they're going straight to the ER
93
KNOW: with hypertension sympathetic tone increases vasoconstriction of blood vessels
* arteriole resistance is increased
artioles regulate the pressure of blood going into capillary bloods where O2 exchange takes place. If the arterioles are constricted the blood will be flowing too quickly through it which will decrease the amount of gas exchange taking place (less O2) which will lead to an increase in the O2 demand
94
Explain the Renin-Angiotension-Aldosterone system (RAS)
* What triggers it to turn on?
* is it a long term or short term
* Once angiotensin II is in the body what 2 things start happening
Turned on w/ a drop in BP
Signals kidneys to release renin (which is an enzyme)
Renin goes and splits angiotensin (which is in the liver) into angiontensin 1 (which is an inactive hormone)
Angiotensin 1 goes to the lungs and is converted to angiontesin 2 by the angiotensin converting enzyme (ACE)
Angiontesin II is a powerul vasoconstrictor
once angiontesin II is in the body the **adreal gland** will start producting aldosterone and **pituitary gland** releasing the antidirectic hormone (ADH)
* both of these help with sodium reteintion and excretion of patissum
* That sodium retetntion is going to cause increased water retention which is going to cause vasoconstriction (I think she means increased BP)
Angiotensin II being in the blood stream also leads to vascular remodeling and hypertrophy; and decreased vascular compliance
Long term pathway
95
This chart is showing secondary hypertension
Impaired renal function: If kidneys arent working well they might just be producing a lot of renin which is causing increased hypertension
This renin will cause inappropriate activation of hormones that regulate salt and water excreetion by the kidney, causing increased BP
Excessive activation of the sympathetic NS can also lead tot his
Natriuresis = process of the kidneys excreting large amounts of sodium in urine, which lowers sodium levels in the blood
96
Who is high BP most common in (race)
97
What is the highest risk factor for cardiovascular disease mortality (thing that leads to dying of cardiovascular disease)
Hypertension
98
KNOW: risk factors for cardiovascular disease = alcohol, obesity, oral contraceptives (women)
Primary hypertension risk factors
* Modifiable = smoking
* non modifable = age, gender, ethnicity
Secondary hypertension risk factors
* Chronic kidney disease
* Drug induced/releated
99
S/S of hypertension
1) Often asymptomatic (called silent killer)
2) HA
3) Vertigo
4) Flushed face
5) Spontaneous epitaxis (nose bleed)
6) Blurred vision
7) Nocturnal urinary frequency
KNOW: If someone is taking medication for hypertension you really don't want them stopping it because they're typically asymptomatic and won't see a difference even though its elevating
* NOTE: they often won't like taking the medication and will want to stop
100
Best way to take blookd pressure for someone with labile hypertension?
24 hour blood monitor
can also take average of two or more readings taken on separate occasions
101
KNOW: labortoary tests will help more for secondary hypertension or anything else going on in the heart
* Think CBC, urinalysis, serum electrolytes, lipid profile and creatine, fasting blood glucose, thyroid stimulating hormone
102
**Most important non pharmaceutical treatment for hypertension**
#1 Physical activity or EX
* what we do
Can also do:
* Weight contorl
* Dietary modifications
* Decreasing use of alcohol and tobacco
* Behavior modification and stress manageemnt
103
What is the first line of defense for hypertension (anti-hypertensives)
* what are the other ones
Diuretics (help excrete the fluid) - first line of defense
sympatholytic drugs
vasodilators
Angiotensin-converting enzyme inhibitors
calcium channel blockers - these are ACE inhibitors - we want to stop that whole process to stop because it increases BP
104
**TEST:** What is our goal BP for someone on anti hypertensives (drugs that lower BP)
130/80 mmHg
goal is to achieve and maintain the lowest sage arterial blooc pressure without side effects
105
Antihypertensive drugs overview
106
What drugs increase the formation and excretion of urine?
Directics
Ability to increase renal excretion of water and sodium, thus decreasing fluid volume within the vascular system
107
Why won't patients no want to take diuretics?
Increases urination (they call it their "water pill" )
108
Diuretics work directly on which organ?
All diuretics exert their effects by acting directly on the kidney to increase water and sodium excretion
* Less water in the vessels = decreased BP
NOTE: This is the first drug used in hypertension and is inexpensive and works well in mild-to-moderate hypertension
109
**Diuretic drugs are subdivided into 3 categories. What are they?**
which one is most common
1) Thiazide Diuretics (most common)
2) Loop Diuretics
3) Potassium-Sparing Dieuretics
110
What is the advantage to potassium-Sparing diuretics and how does it work?
Advantage = reduces potassium loss and preventing hypokalemia (basically decreases cramps because it doesnt have the potassium loss that the others do)
They prevent the secretion of potassium into the distal tubule of the kidney --> which then it would be excreted into the urine
111
Thiazide diuretics act primarily on which portion of the which part of the kidney? and what do they do?
Act primarily on the early portion of the distal tubule of the nephron, where they inhibit sodium reabsoportion.
By inhibiting reabsorption, more sodium is retained within nephrone, creating osmotic force that retains more water in the nephron --> to be excreated as urine
NOTE: This is the most common dieurteic
112
Loop Diuretic
* Where does it act?
* how does it work?
Act primarily on the ascending limb of the loop of henle
Exert effect by inhibiting the reabsorption of sodium and chloride from the nephron, preventing reabsorption of water that follows electrolytes
113
Dieuretics - however, shes going to primarily be focusing on adverse effects
what do thiazide diuretics end in?
Ide/One
114
What is the most serious adverse effect of diuretics?
* name some others (4)
Fluid depletion and electrolyte imbalance (hyponatremia / hypokalemia)
Orthostatic hypotension - due to decreased fluid
GI disturbances and weakness-fatigue
Changes in mood and confusion - more applicable for older adults
115
Hyponatremia
Sodium depletion
116
Hypokalemia
Potassium depletion
117
Patient has a sudden decrease in BP. What pathway takes over to restore BP
Baroreceptors
118
Diuretics can cause a sudden decrease in blood volume (removed the fluid portion) and may cause a reflexive increase in cardiac output and peripheral vascular resistance because of the baroreflex activation
* The RAS system may also be activated causing further vasoconstriction
119
What is the most commonly prescribed diuretic?
Thiazide
120
Which two diuretics impair glucose and lipid metabolism, creating an issue for pts w/ type 2 diabetes?
Thiazide and Loop
So I guess prescribe potassium-Sparing Diuretics?
121
**TEST** two main things that beta blockers do
Decrease HR
Decrease force of myocardial contraction (contractility)
122
What do betablockers do to CO?
Decrease it
CO = SV*HR and both of those things are decreased w/ this drug
123
which part of the autonomic NS is changed w/ beta blockers and explain the mechanism.
Decreases sympathetic activity
It does this via
1) A central inhibitory effect on the brainstem
2) Decreased renin release from kidneys and within CNS
3) Impaired sympathetic activity in ganglia or at presynaptic adrenergic terminals
4) increased baroreceptor sensitivity
can be any combination of the above
it can complement other antihypertensives
* A combination of 3 drugs for hypertension is typically the best
124
Recent research shows a combination of which 3 drugs is best for hypertension.
calcium channel blockers
Anti-directs
Ace inhibitors
125
How to take someones BP
Feet uncrossed
Arm should be at heart level - SUPPORTED
Want them to be at resting position., not right after they've been walking around
126
127
**TEST** What drug is bad for people w/ asthma and why?
Non selective beta blockers because they bind to the B2 receptors in the lungs and cause bronchoconstriction
128
KNOW: Beta blockers are a sympathetic drug
129
KNOW: alpha blockers = sympathetic drug
130
How do Alpha blockers work?
Alpha blockers work by blocking alpha 1 adrenergic receptors on vascylar smooth muscle, will promote decrease in vascular resistance
I think its a symapthetic drug because in a sympathetic response these alpha receptors are turned on, but now they can't be turned on, which blocks vasoconstriction from happening.
131
Which drug would be recommended for BP if the pt has diabetes?
Alpha blockers, because they have the ability to improve blood lipid profiles (decreased triglycerides and total cholesterol, increased high density lipoprotein-cholesterol ratoi) and produce favorable effect on glucose metabolism and insulin resistance
remember, beta blockers are bad because they can impaire glucose breakdown, leaving it in the blood stream
132
KNOW: There are newer alpha receptor drugs that are better because they're slower release, keeping from having that suddent drop in BP (decrease orthostatic hypotension)
133
**What other pathology is treated w/ alpha receptors?**
Benign prostatic hypertrophy because decreases sympathetic mediated contraction of smooth muscle in the prostate gland
* reduction of muscle decreases constriction of ureter, improving urinary flow and ability to empty bladder
* because alpha receptors get rid of some of that sympathetic tone
134
135
Adverse effects of alpha blockers
1) Reflex tachycardia due to a decrease in peripheral vascular resistance --> prevented by administering with a beta blocker (slows down HR)
2) Increased risk of cardiac disease, including congestive heart failure (because it can increase the workload on the heart because of that vasodilation, causing more of that preload to the heart)
3) orthostatic hypotension
136
KNOW: Presynaptic Adrengeric Inhibitors = sympathetic drug
137
How do presynaptic adrengeric inhibitors work? (for hypertension)
what are adverse effects
Inhibits the release of noreepinephrine from the presynaptic termins of peripheral adrenergic neurons
* without epi/nor theres decrease vasoconstriction
Adverse: - these are basically the same for the anti hypertensive medications
*Orthostatic hypotension (too much of a decrease in BP)
GI distrubances such as nausea, vomiting, and diarrhea
138
KNOW: centrally acting agents = sympathetic drugs
139
How do centrally acting agents work as an anti hypertensive drug?
Work on vasomotor center in your brainstem (centerally not peripherally) which is the BP regulatory center
* Stimulation results in decrease in sympathetic discharge of heart and vasculature
140
Clonidine is a centrally acting agent. However, whats its other use? (2)
seziure / anxiety
141
Adverse effects of centrally acting agents
Dry mouth, dizziness, and sedation (sleepy)
142
Ganglionic blockers = sympathetic drugs
143
How do ganglionic bockers work as an antihypertensive drug?
* When are they used?
Decrease systemic sympathetic activity
Essentially nicotinic cholinergic antagonists, which block transmission at the junction between presynaptic and postsynaptic neurons in sympathetic and parasympathitc pathways
Used to decrease BP rapidly in certain emergencies such as acute aortic dissection or autonomic crisis in spinal cord injury.
144
adverse effects of ganglionic blockers
GI discomfort
Urinary retention
Visual disturbances
orthostatic hypotension
high doses, neuromuscular blocking activity
145
vasodilaters are antihypertensive drugs. How do they work?
Exert an inhibitory effect directly on vascular smooth muscle cells
* causing them to dilate so more blood can get through
146
Adverse effects of vasodilators?
1) Reflex tachycardia - due to the increased blood supply back to the heart
2) Dizziness, postural hypotension, weakness, nausea, fluid retention, and HA
147
**TEST** Vasodilators drugs (5)
Diazoxide (Hyperstat)
Hydralazine (Apresoline)
Fenoldopam (Corlopam)
Minoxidil (Loniten)
Nitroprusside (Nitropress)
148
How do calcium channel blockers work as anti hypertensive drugs?
Block calcium entry into vascular smooth muscles cells
Essentially its blocking the binding of calcium to troponin which means that actin and myosin heads cant articulate together, meaning that the sacromeres within the smooth muscle cannot contract, meaning decreased muscle tone, leading to more vasodilating = decreased BP
149
KNOW: calcium channel blockers lead to vasodilation and decreased vascular resistance, heart rate, and myocardial contraction force --> which reduces cardiac workload
150
Adverse effects of calcium channel blockers
1) Excessive vasodilation leads to swelling in feet and ankles - this can happen in any drug that causes vasodilation
2) Orthostatic hypotension - one of the most common side effects - make sure they're sitting
3) Abnoramilities in HR, reflex tachycardia
4) Dizziness, HA, nausea
150
What is the suffix for calcium channel blockers? except which 2
pine
Diltiazem
Verapamil
151
152
ACE inhibitors end in what suffix
Pril
153
how do ACE inhibitors work
They keep angiotension I from converting into angiotensin II because it stops that angiotensin converting enzyme, meaning that this system cannot increase BP
154
What is the name of our only direct renin inhibitor
Aliskiren (Tekturna)
155
Angiotensin II receptor blockers end in what suffix?
rtan
156
**TEST** When taking any medication that causes vasodilation (or blocks vasoconstriction) avoid activities producing widespread vasodilation (or use them very cautiously)
* think activities like whirlpool / hottub
* Exercise may cause vasodilation in skeletal musculature, which may potentiate the peripheral vasodiltion induced by antihypertensive drugs
If the patients takes beta blockers, cardiac responses to EX may be somehwat blunted becayse the myocardial repsonse to sympathetic stimulation will be deiminshed --> so you can't use these measures to test level of exerction
* Going to have to go w/ RPE
157
PT implications
Baseline BP should be taken and monitored
* great way to objectify interventions
PT education
* Diet
* Monitorying BP
* Fluid intake
* Stress level
* Pain could also be a stressor
Rehab concerns:
* orthostatic hypotension
* Weakness/fatigue
* confusion/mood changes
* Decreased maximal exercise capacity (beta blockers)
* edema and reflex tachycardia (vasodilators)
