Hypertension Flashcards
1
Q
What/how controls the heart beat? Where is it located?
A
SA Node
- Located in right atrium
2
Q
What is the job of the AV Node?
A
Gateway for electrical impulse into ventricles (delays ventricular contraction*)
Only way for an impulse to trigger ventricles in a healthy heart
3
Q
Describe the process of AV Node conduction? What drugs are used to decrease contraction?
A
The AV NODE DELAYS ventricular contraction
–> Allows one impulse in at one time, delays LUB-DUB to allow the ventricle to fill with blood
BETA-Blockers and Non-DHP CCB (non-hydromonium Calcium Channel Blcokers) –> Slow the conduction slower
4
Q
What is AV block? What drugs are C.I.?
A
AV Block –> Conduction delayed for too long
Non-DHP-CCB and Beta-blockers
5
Q
What ion causes muscle contraction?
A
Calcium
6
Q
More calcium entering a cell is indicative of…..
A
stronger contraction (inotropy/contractility)
7
Q
Faster calcium entry into a cell is indicative of…
A
faster contraction (chronotropy/heart rate)
8
Q
A cardiac muscle cannot contract again until….
A
Muscle cannot contract again until repolarization occurs
9
Q
What is an ECG?
A
Graph of electrical activity in heart
10
Q
ECG’s are the test of choice for _____ Why?
A
Most sensitive and effective test to determine if having heart attack or not
11
Q
The QRS complex measures….
A
Depolarization of ventricles
12
Q
In a normal ECG, what is the width of the QRS complex?
A
Narrow
13
Q
A wide QRS indicates what?
A
Tell tale sign that ventricular impulse did not originate AV node
14
Q
The QT interval indicates…..
A
Represents the time it takes from ventricular contraction until repolarization –> Full cycle
15
Q
What is the risk of QT prolongation?
A
Risk for ventricular arrhythmia
16
Q
The T-Wave is responsible for….
A
REPOLARIZATION of ventricles
17
Q
What are the four approaches to asses blood pressure?
A
- Automated Office Blood Pressure (unattended)
- Office Blood Pressure Monitoring (attended)
- Ambulatory Blood Pressure Monitoring
- Home Blood Pressure Monitoring
18
Q
AOBP Blood Pressure is considered high when….
A
Displayed mean SBP ≥ 135 mmHg or DBP ≥ 85 mmHg is high
19
Q
OBPM blood pressure is considered high-normal and high when…..
A
Mean SBP 130-139 mmHg or mean DBP 85-89 mmHg is high-normal
Mean SBP ≥ 140 mm Hg or DBP ≥ 90 mmHg is high
20
Q
ABPM is considered high when…..
A
Mean awake SBP ≥ 135 mmHg or DBP ≥ 85 mmHg or mean 24-hour SBP ≥ 130 mmHg or DBP ≥ 80 mmHg are high
21
Q
HBPM is considered high when…..
A
Mean SBP ≥ 135 mmHg or DBP ≥ 85mm Hg are high and associated with an increased overall mortality risk
22
Q
Home Blood pressure Monitors Benefits
A
Considered highly accurate
AND
Highly correlated with usual resting BP levels
23
Q
For home blood pressure monitoring, the home values reference is….
A
< 135/85
24
Q
What are guidelines for blood pressure monitoring as set out by the Candian Hypertension Guidelines?
A
- Sitting position
- Back Supported
- Arm bare and supported
- Use an appropriate sized cuff
- Middle of cuff at heart level
- Lower edge of cuff 3 cm above elbow crease
- Do not talk or move
- Legs uncrossed
- feet flat on floor
- Traditionally recommended to avoid exercise, caffeine, or a full bladder prior to taking BP (30min).
25
Home Blood Pressure monitoring conditons....
Resting, --> stimulation/stimulants/irritants
Duplicate measures
26
Timing for patient of Home Blood Pressure Monitoring
Before doses of medication (troughs)
Morning and night (estimate 24 hr control)
27
Duration of Home Blood Pressure
One week blocks during times of interest
Do not have to measure every day for extended periods if stable.
28
What body part is blood pressure monitoring is preferred? Exception?
- Arm BP are preferred
- Validated wrist devices may be used for BP estimation ONLY in patients with large arm circumference when standard arm methods cannot be used (Grade D recommendation from Canadian hypertension guidelines)
29
High Blood Pressure during activity is (useful/bad) because....
↑ blood flow = ↑oxygen and
glucose delivered to muscle.
Very useful -->Run faster, hit harder, yell louder, etc…
Regular activity (with rests!) will trigger cellular changes (e.g., ↑protein, ↑ mitochondria)
30
High blood pressure during rest is (useful/bad) because....
↑ afterload = ↑ energy to pump blood
Wastes energy
Fatigues tissues/cells --> adverse changes over long term
Damages specific tissues/cells
31
High blood pressure is defined as.....
Continuous high blood pressure readings at rest
32
Damage as a result of hypertension is usually as a result of....
↑ afterload
Arterial damage
33
Hypertension risk increase with:
a) Diabetes
b) Age
c) Arthritis
d) Cancer
AGE
34
Hypertension is a ____ -factorial problem and can result due to....
MULTI
Fluid and electrolyte balance
RAAS
Natriuretic hormone
Electrolyte imbalance (e.g. Na*)
Renal dysfunction / poor renal perfusion
Sympathetic nervous system / baroreceptor function
Increased SNS activity
Metabolic syndrome
Hyperinsulinemia/insulin resistance, abdominal obesity, low HDL, high BP, high Tg
Vascular endothelial function
Prostacyclin, Nitric Oxide production
35
Since Hypertension is multifactorial, drug tx often involves...
Multiple agents
Chronically increased’d BP results from multiple factors, no single factor predominates
Thus, single antihypertensive drug regimens often have limited success in control (-10/-5 average)
36
Single Anti-hypertensives on average, lower blood pressure by....
10/-5 average
37
Hypertension is often commonly associated with.....
Metabolic Syndrome
38
Secondary hypertension definition
is high blood pressure that's caused by another medical condition
39
Is Hypertension often due to significant damage of a single system?
Rarely, HTN is caused by significant dysfunction of a single system
40
In secondary hypertension, hypertension is commonly not recognized until?
Often not recognized initially until patients show resistance to conventional treatment
41
Treatment resistant hypertension definition
“Treatment resistance” in hypertension is usually defined as lack of BP control despite a combination of 3 antihypertensive medications, one of which being a diuretic.
42
Risk factors for hypertension are often... and therefore..... is important
SILENT, SCREENING
43
In which stage of life would the identification of HTN have the biggest impact to lifespan?
Earlier stages of life
44
Is hypertension a disease?
Hypertension is a risk factor for disease; but it is not a disease itself
45
Modifiable risks for developing hypertension....
Obesity
Poor dietary habits
High sodium intake
Sedentary lifestyle
High alcohol consumption
High-normal blood pressure
Diabetes or metabolic syndrome (“pre-diabetes”)
46
The main goal of tx for blood pressure
Preventing life-threatening cardiac consequences
47
3 goals of tx for hypertension (specific)
- Reduce/prevent myocardial cell dysfunction
- Reduce/stabilize artherosclerosis burden and endothelial cell dysfunction
- Reduce/prevent weakened vessel walls
48
Canadian Guidelines for Optimal Blood Pressure
less than 120/80
49
Normal Blood Pressure Values
less than 130 (systolic) and/or 85(diastloic)
50
High-Normal Blood Pressure
130-139 --> Systolic
and/or
85-89 diastolic
51
Grade 1 (mild hypertension) guideline values
140-159 and/or 90-99
52
Grade 2 (moderate hypertension) guideline values
160-179 and/or 100-109
53
Grade 3 (severe) hypertension values
Greater than or equal to 180 and/or greater than or equal to 110
54
Isolated systolic hypertension is defined as....
Greater than or eqaul to 140 and/or less than 90
55
For diagnosis of hypertension....
Must be high at rest
Unrelenting/ consistent
56
Hypertension diagnosis requires.....
Requires the physician to find if blood pressure is consistent and/or unrelenting
57
Hypertension can be directly diagnosed from blood pressure readings when....
Mean office BP ≥ 180/110 mmHg or hypertensive emergency
No need for additional BP assessment to make the hypertension diagnosis
Diagnose with hypertension and initiate treatment
58
What is normotensive?
No hypertension at office/clinic/hlthcare setting and no hypertension at home/nonhlthcare/ABPM Setting
59
Sustained hypertension is...
Hypertension at office/clinic/hlthcare setting and hypertension at home/nonhlthcare/ABPM Setting
60
Masked hypertension is....
No hypertension at office/clinic/hlthcare setting and hypertension at home/nonhlthcare/ABPM Setting
61
White coat hypertension is...
Hypertension at office/clinic/hlthcare setting and no hypertension at home/nonhlthcare/ABPM Setting
62
Think of white coat hypertension when....
- Young age
- Lean/healthy body weight
- No other risk factors or target organ damage
- No family history
- Blood pressure is high in clinic examinations
- Someone you wouldn't expect to have htn
63
One should think about masked HTN when....
Older age
Overweight / sedentary lifestyle
Has other conditions (e.g., diabetes, kidney dysfunction) or other target organ damage
Possibly positive family history
Blood pressure is NORMAL in clinic examinations.
Someone you WOULD expect to have HTN
64
Metabolic syndrome consists of....
“Metabolic syndrome” (at least 3 of)
Insulin resistance / incr’d blood sugar
Low HDL
Abdominal obesity
High triglycerides
High blood pressure
65
Before starting tx of hypertension, a ___ assesment should be done beacuse....
Blood pressure may be treated differently depending on the patients short-term risk of a life-threatening event
It is essential that a risk assessment be undertaken before treatment is determined
66
CV Non-modifiable risk factors of hypertension
Age ≥55 years
Male
Family history of premature
cardiovascular disease
(age <55 in men and
<65 in women doubles FRS)
67
CV Modifiable risk factors include...
Sedentary lifestyle
Poor dietary habits
Abdominal obesity
Dysglycemia (or diabetes)
Smoking (even 2nd hand)
Dyslipidemia
Stress
Hypertension
68
People at the highest risk for CV events will demonstrate....
Target organ damage
69
Target Organ Damage Includes
Cerebrovascular disease
Hypertensive retinopathy (would only know if you got an eye exam)
Left ventricular dysfunction (more about function)
Left ventricular hypertrophy (enlarged left ventricle; but, nothing about function – slow change over time )
Coronary artery disease
CKD
Peripheral Artery Disease
70
Target organ damage is a sign that damage....
Has already occured
71
What is the framingham risk calculator?
A widely used tool to assess overall CV risk in Canada
A simple algorithm estimates an individual’s 10-year risk of experiencing a major CV event (MI, stroke, etc) or death.
72
What are limitations of the framingham risk score?
Just an estimate
Poor performance in extremes of age (young, old)
10-year risk may not always correlate to lifetime risk
73
Are high blood pressure readings an emergency? What should we do?
No
Check technique and re-take BP
Ask patient if they are experiencing symptoms
If no signs/symptoms of danger, ask patient to make an appointment within a day or two. Might have to go to walk-in clinic
74
What are some symptoms of concern in regards to a high blood presusre reading?
1) Neurologic
2) Cardio-repsiratory
3) Any symptoms suggestive of major CV event
75
Neuroligic sx may include:
Severe headache, numbness, weakness, slurred speech,
Vision problems
76
Cardio-respiratory sx:
Chest pain, difficulty breathing
77
A hypertensive emergency is defined as:
Situations where BP should be reduced within hours
BP ≥180 / ≥130 AND
papilledema or other target organ changes
78
A hypertensive emergency is when.... Examples?
>180 systolic &/or >130 diastolic
Situations that require immediate BP reduction as target organ damage PLUS sx
E.g. hypertensive encephalopathy, intracranial bleed, unstable angina/MI, acute heart failure
79
At the physicians office, a clinical assessment will include
Physical Assesment
Labratory testing/Imaging
80
Jugular Venous pressure (JVP) indicates
Indirect assessment of right atrial pressure
81
Edema will indicate
May represent ‘volume’ or tissue-specific fluid
82
Pulse indiactes
Heart rate
Pressure/circulation (feet) --> pedal Pulses
83
heart sounds indicates
Normal: S1 = systole (lub); S2= diastole (dub)
Not normal: murmur, S3 or S4 (may indicate disease)
84
Bruit indicates
an audible vascular sound associated with turbulent blood flow
- Carotid and renal
85
What conditions can increase volume?
HF, Kidney Disease and hypertension (to a lesser degree)
86
JVP is a test used to asses....
assessed to gauge volume/preload
87
Is JVP a good estimate? When is it used?
JVP is a rough assessment but conducted routinely –esp in HF patients
88
JVP normal values....
Normal is < 2cm above sternal angle
pressure can be crudely examined by looking at it
89
peripheral Pulses can be used for....
arms and legs (if diminished – may mean reduced stroke volume or PAD)
90
The ankle-brachial indecx means....
– if less than 0.9 means PAD (peripheral arterial disease --> atherosclerosis in peripheral blood vessels)
91
What does pressure in ABI indicate?
Weak pedal (feet) pulses -->Unhealthy finding
Strong pedal findings --> Blood pressure in top is same as bottom part of body --> Probably healthy arteries that are npt obstructed
If blocked artery, weak pedal pulse
Ideally --> Ankle and arm should be the same
92
ABI is calculated by....
ankle pressure divided by arm pressure
93
What are the 2 heart sounds?
S1 (Lub)
S2 (Dub)
94
S1 indicates....
First heart sound – start of ventricular contraction
95
S1 is due to....
Due to closure of the mitral and tricuspid valves
96
S2 indicates.... and is due to....
2nd heart sound – closure of aortic and pulmonic valves during to ventricular relaxation
97
What are the abnormal heart sounds? What do they indicate?
S3 and S4 are not normal heart sounds and may indicate presence of problem. (abnormal heart sounds)
98
Heart murmurs result from....
Result from ‘turbulent flow’ within the heart
99
What is a bruit? How can it be detected?
Bruits also represent turbulent flow
Stethoscope can pick up bruits in some arteries such as carotid or renal artery
100
In a healthy veseel, flow should be....
Flow through a healthy (unobstructed) vessel should be silent
101
When analyzing a pt's hypertension, a pharmacist should look for what cause of the HTN? Examples?
- Drug induced BP elevations
NSAIDS
Corticosteroids (glucocorticosteroids and anabolic steroids)
Oral contraceptives and sex hormones
Decongestants (stimulants)
Certain antidepressants (MAOI’s, SNRI’s, SSRIs)
Stimulants (e.g., methylphenidate, dextroamphetamine)
Excessive alcohol
102
How do NSAIDS raise BP?
Inhibition of renal Pg production
Lowers renal perfusion (constriction of afferent arteriole)
103
How do steroids raise bp?
Mineralocorticoid effect (i.e., acts like aldosterone)
104
How do hormonal contraceptive raise bp?
Triggers angiotensinogen production from liver
105
How do decongestant, certain anti-depressants and stimulants raise bp?
SNS activity (vasoconstriction +/- ↑CO)
106
How does alcohol raise bp?
In excess only. Impairs ADH + (increased over long term leading to water retention) other mechanisms likely important
107
Summarize Candian HTN Guidelines Risk Strat and Targets
High Risk - >20%
Intermediate Risk --> 10-19%
Low Risk --> <10%
FRS
108
According to the Canadian Hypertension Guidelines, a high risk patient is.....
Individuals over 50 and with sbp 130-180 mmHg and with one of the following:
a) Clinical or sub-clinical CV disease
b) CKD (Proteinuria <1g/d, or EGFR 20-50)
c) Estimated 10-year global risk >15%
d) Age> 75 years
109
High Risk Patient Blood Pressure for Intitiation of Tx
>130 mmHg
110
Diabetes Mellitus High Risk BP to initiate tx
> 130/80 mmHG
111
Moderate-to-high risk BP to initiate tx
>140/90
112
Low-risk to initiate tx
>160/100 mmHg
113
High risk target BP
<120
114
Diabetes BP Target
<130/80
115
Moderate-High BP target
<140/90 mmHg
116
Low risk BP target
<140/90 mmHg
117
First Line tx of Hypertension (adults)Diastolic +/- Systolic
1) Thiazide and thiazide-like diuretic
2) ACE-i
3) ARB
4) Long-acting CCB
5) B-blockers
6) Single Pill combo
118
Which diuretics are preferred? Why?
Long acting diuretics like indapamide and chlorthalidone are preferred over shorter acting diuretics like hydrochlorothiazide
119
Are ebta-blcokers first line? Age?
B-blcokers are not indicated as first line for age 60 and above due to increased risk of stroke
120
Should shor acting nifedipine be used?
NO - Increased risk of stroke and MI
121
The recommended single pill options are:
a) ACE-i combined with CCB
b) ARB with CCB
c) ACE-I or ARB combined with a diuretic
122
What are some non-pharm tx?
- Being more physically active
- Weight reduction
- Moderation in alcohol intake
- Eating Behaviour
- relaxation Techniques
- Smoking cessation
123
When should combo tx be started?
BP drugs are WIMPY (sometimes do not get 10/5 drop)
Combinations often required in 2/3 patients
Adding therapy usually preferred over switching
Lifestyle modification might be a big help
124
What mechanism should be used for combo?
AB-CD rule
AB --> (Renin-active) --> Beta-adrenergic blocker, ACE, ARB
CD --> THiazide diuretic, long-acting calcium channel blocker
125
Should an ACE and ARB be used together?
NO --> May be dangerous (angioedema and hyperk+)
126
Caution should be taken when combining a.... Why?
Non DHP-CCb and a beta-blocker
Both can decrease heart rate
127
What is the most notable evidence based combo?
DHP-CCB and ACE Inhibitor
128
What is the major difference between Ace's and ARB's?
Biggest difference is frequency of cough with ACEI (higher than ARB)
129
ARBS suffix
Sartan's
130
ACE-inhibitor suffix
Pril's
131
When should ACE's and ARB's be avoided?
Pregnancy
Bilaterial renal artery stenosis (predispose people (narrow renal arteries on both sides) can be harmed by ACE’s and ARB’s)
Hyperkalemia (All RAAS drugs increase K+)
132
What is the ladder for adding on therapy?
If partial response to monotx --> Add on tx --> Triple or Quadruple TX
133
If blood pressure is not controlled, consider non-drug issues such as....
Non-adherence
Secondary HTN
Interfering drugs/lifestyle
White coat effect
134
Triple tx should always include....
a diuretic
135
Treatment resistance is defined as a poor blood pressure response despite:
3 antihypertensive drugs used in combination
One of the drugs is a diuretic
Non-adherence/white coat is ruled out
136
Tx-Resitant HTN TX. What is causing tx resistance? Which one achieves the greatest effect? WHy?
Spironolactone (or MRA) -->Most success achieved here --> Very weak bp reducing effects in uncomplicated hypertension. Reasoning: Tx resistance is due to aldosterone excess
Clonidine / methyldopa (alpha-2 agonists)
Hydralazine/minoxidil (vasodilators) + beta-blocker
137
What are some causes of tx resistance?
Hyperaldosterism
Pheochromocytoma (unregulated SNS activity)
CKD
Renovascular Disease
Obstructive Sleep Apnea
Hyper/Hypo-thyroidism
138
Hyperaldosterism tx
MRA's or K+ sparing diuretics
139
Pheochromocytoma Tx
Alpha-blockers (alpha-1 ANtagonists - Prazosin, doxazosin, terazosin) +/- Beta-blockers (surgery is required)
140
CKD TX
manage as recommended
141
In renovascular disease, which drugs should be avoided?
Caution with ACE and ARB's
142
In obstructive sleep apnea and hyper/hypo-thyroidism, tx involves....
Correcting underlying problem
143
ISH is common in what population....
Elderly
144
ISH is due to...
Stiff arteries do not accommodate systolic pressure
Creates a high “pulse-pressure” (SBP – DBP)
145
The target of ISH
<140 mmHg systolic BP
146
What meds are used in ISH?
1. Thiazide Diuretic
2. ARB
3. LOng acting CCB
Then Dual Tx
Then triple or Quadruple Tx
147
In ISH, caution should be taken when DBP drops below....
Caution if DBP drops < 60mmHg (esp in patients with coronary atherosclerosis)
148
Diuretics MOA and Examples
Thiazides – block NaCl transporters in the distal
convoluted tubule. May work for mild sodium retention
but often results in compensatory increased sodium
and water reabsorption in the proximal tubule --> Chlorthalidone, Hydrochlorothiazide, Indapamide, Metolazone
o Loops – blocks Na/K/Cl transporter in the ascending
loop of Henle. Preferred for brisk and immediate
diuresis --> Furosemide, ethacryniuc acid, bumetanide
o Potassium sparing – decrease Na reabsorption in the
collecting duct. Small effect but may be used adjunct.
--> MRA's (eplenerone, sprinolactone), K+ sparing (Amiloride, Triamterene)
ENAC Blockers:
- Amiloride
- Triamterene
Aldosterone Receptor Antagonists:
- Spironolactone
- Eplerenone
149
Electrolytres and Diuretics
150
TZD Adverse Effects
Dehydration, Hypokalmeia, Nauseuam, Hypotension, Hypomagnesemia, Hyponatremia, Hyperglycemia (more with tzd's), Hyperuricemia (GOUT), Rash, HYpercalcemia (Kidney STones)
151
TZD Drug Int. and Monitoring
Lithium Increase
Digoxin - Toxicity if K+ depleted n
Corticosteroids (hypokalmeia),
NSAIDs - Reduced diuretic effecr, renal toxicity
Loop Diuretics - HYpoK+, Hypomagnesemia, Dehydration, Renal dysfx
Monitor renal function (less effective if GFR below 45 m,l/min), electrolyrtes
152
Loop Diuretics A/E and monitoring
Dehydration, HypoK+, Hypocalcemia, Hypomagn, nausdeua, hypotension, hyperglycmeia (less than tzds), weakness, fatigue, rash, ototoxicity (higher doses)
Monitor e-
153
Loop DCiuretics DI
Lithium, DIgoxin, Corticosteroids, NSAIDs, TD Diuretics
154
MRA ADverse Effects
Dizziness, Rash, HyperK+, Dehydration, Nauseua
SPI>>Eplenerone - Gynecomastia, ED, abnormal menstruation
155
MRA Drug Int
Acei/ARB/NSAID/TMP-SMX - Incraesed K+
156
When do thiazides become ineffective? What should be done?
Reduced effectiveness if CrCl <30m/min (switch to loop)
157
What electrolytes should be cautioned in TZD diuretics?
↓ K and ↓Na the most common electrolyte disturbance
↓ Mg and ↓ Cl also possible
May ↑ calcium (differs from loop diuretics which ↓ Ca)
158
Thiazides and Blood Sugar
May ↑ blood sugar slightly (but does NOT cause risk)
159
Thiazide and Uric Acid
May ↑ uric acid (caution in people with hx of gout)
160
TZD and urination
May ↑ urinary frequency (likely minimal with TZD)
161
D.I. of thiazide diuretics
caution with other BP reducing drugs
Electrolyte interactions (K, Na)
162
Convienience of TZD. When should they be dosed?
Once daily dosing – dose in AM to reduce nighttime urination
163
C.I. of TZD
Consider other options in people with low K or low Na
“Sulfa” allergy – Antibiotic sulfa allergies usually do not cross react. Avoid if reaction was severe (steven’s johnsons, etc)
Caution if hypercalcemia is present
164
Do diuretics differ in lowering blood pressure?
YES
- Some better handle blood pressure and some eliminate more fluid
165
What are the classses of diuretcis and their role in tx?
Thiazides --> best for BP reduction --> Less impact on RAAS, 24 hours of action
Loop --> best for fluid excretion
K sparing --> K+ supplement --> late late distal tubule --> Not good at lowering bp
166
What is a common consequence of diuretic tx?
Hypokalemia
167
What are the TZD drugs? GFR effects?
Ineffective if GFR<30:
Chlorothialidone
Hydrochlorthiazide
More effective in reduce renal function:
Indapmaide
Metolazone
168
What are some other causes of hypokalmeia?
Inadequate K intake (elderly)
High dietary Na+ intake --> High RAAS itself causing K+ loss
Hypomagnesemia
Prolonged diarrhea (laxatives)/vomiting
Hyperaldosteronism (i.e., secondary HTN)
Heart failure (HF)
Catecholamines
Insulin
169
Low K+ Thresolds for TX (IMPORTANT)
<3.0 mmol/L --> Always undesirable
3.0-3.5 --> Usually treated
3.5-4.0 --> Action may be taken
170
Persistent Hypokalemia has been associated with....
has been associated with a higher risk for death in many patient groups (esp HF and CKD).
171
What can be done if K+ is low due to a diuretic?
General measures
- Reduce sodium intake
- Increase K intake (dietary)
Lower diuretic dose
Discontinue diuretic if K seriously low
Add K sparing drugs
- BB, ACEI/ARB, K-diuretics --> All interrupt RAAS
Add K supplement
172
Is Hyperkalmeia serious?
YES
↑ K is also a potential cause of serious harm
Caution must be taken in replacing K AND using drugs that increase K levels.
173
How much of daily intake of K+ do the kidneys excrete?
Normal functioning kidneys excrete 90% of daily K intake
174
Hyperkalemia effects on ECG
- Widening of P-R interaval (conduction delay)
- Loss of p-wave
- Conduction delay through ventricles (widening of QRS)
175
What is the most feared complication of hyperkalmeia?
Ventricular arrhythymia
176
What drugs increase K+?
RAAS drugs,
NSAIDs,
vitamins/supplements,
K sparing diuretics,
Trimethoprim and sulfamethoxazole
177
What are some pt factors that may cause hyperkalmeia?
CrCl <60ml/min
Baseline K >4.5mmol/L
178
What defecit often accompanies hypo-K?
Magnesium
179
In Hypokalmeia, is dietary repletion sucessful?
Often not successful to correct hypoK (ok for prevent’n
180
Indications implicating complicated HTN include....
Diabetes with nephropathy
Diabetes w/t nephropathy
Non-diabetic Kidney disease
Coronary Heart Disease
Heart Failure
Left ventricular hypertrophy (LVH)
Stroke or transient ischemic attack (TIS)
181
Diabetes Threshold and Target BP
Threshold equal or over 130/80 mmHg and target below 130/80
182
Diabetes with renal dysfunction should be treated with....
Microalbuminuria, renal Disease, CVD, or additional CVD risk factors
- ACE or ARB (1st Line)
Second LIne:
ACEi + DHP-CCB - ACCOMPLISH
- Addition of DHP-CCB preferred over diuretic as add on
ACEi + TZD
ARB + DHP-CCB
ARB + TZD
183
Diabetes w/t comorbities tx...
ACE, ARB, DhP-CCB, or TZD
If using a combo, DHP CCb is preferred over a TZD
184
In CKD, what drugs are first line?
ARB and ACE
185
How can hypertension cause kidney disease?
Long-standing hypertension + diabetes increases risk for chronic kidney disease (↑ pressure can damage glomerulus)
Filtering function is damaged (E.g., protein escapes!)
186
Kidney damage progresses (slow/fast) as a result of HTN and can cause....
SLOWLY
↓rate of glomerular filtration
↑ serum creatinine (easily excreted in healthy state)
Difficulties excreting fluid and toxins
Leakage of protein, large molecules
187
nephropathy refers to....
Protein (albumin) escapes from glomerulus
188
RAAS Summary
Angiotensinogen converted to angiotensin I by Renin. ACE converts Angiotensin I to ANgiotensin II
189
Renin secretion occurs due to...
Reduced renal artery blood flow/pressure
Increased sympathetic stimulation
190
Angiotensin II is responsible for...
- Increased contraction
Vasoconstriction (especially efferent artery)
- Aldosterone secretion
Vasoconstriction:
Angiotensin II constricts blood vessels, leading to a rise in blood pressure. (especially efferent arteriole)
Increased Blood Volume:
It promotes the retention of sodium and water by the kidneys, increasing blood volume and contributing to higher blood pressure.
Stimulates Aldosterone Release:
Angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that further increases sodium and water retention.
Thirst and Salt Cravings:
It triggers the sensation of thirst and the desire for salt (sodium) through the hypothalamus.
Stimulates Vasopressin (ADH) Release:
Angiotensin II stimulates the release of antidiuretic hormone (ADH), also known as vasopressin, from the pituitary gland, which causes the kidneys to reabsorb water.
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How do ACE and ARB's protect the kidney?
- Decrease efferent constriction, decrease pressure at glomeruls
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What are the 3 types of HTN seen in preganancy?
1. Pre-eclampsia
2. gestanional HTN
3. Chronic HTN
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Pre-eclampsia is....
High BP with proteinuria
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pre-eclampsia onset
Onset after 20 weeks of pregnancy
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pre-eclampsia and mother and baby health? Can progress to?
ASsociated with poor outcomes for baby and mother
Can progress to seizures (eclampsia)
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gestational HTN is....
High BP without proteinuria after 20 weeks
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Chronic HTN is...
HTN was present before pregnancy began
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First-line Tx in pregancy. Other safe options:
Labetalol
Methyldopa and long acting oral nifedine
Safe:
Propranalol
Metoprolol
Hydralazine
Clonidine
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2nd Line Tx in pregancy
Combination 1st Line (Labetalol, Nifedipine XR, Methyldopa)
Clonidine, Hydrazlaine, and thiazide diuretics
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Should ACE and ARB's be used in pregancy?
NO
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Lactation First Line and 2nd Line TX
Labetalol, methyldopa, long-acting nifedipime, enalapril or catopril,
2nd line --> combo
Monitor baby for adverse effects
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centrally ACting Agents include...
Alpha-2 Adrenergic Agonists
Clonidine & Methyldopa
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Centrally Acting Agents MOA and results
Stimulate alpha-2 rec’s in the brain
Lowers sympathetic outflow
Increases vagal tone (cholinergic effects)
Results in
Lower HR / Cardiac output (CO)
Lower BP
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Where is that alpha-2 receptor located?
pre-synaptic terminal
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When stimulated, a-2 receptors.... a-2 agonists.....
When stimulated, shuts down further release of messengers into the SNS nerve fibre
Decrease sympathetic discharge from CNS
↓ circulating NE, and ↓ SNS nerve transmission
Lowers blood pressure and heart rate
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S/e of alpha-2 agonists...
Sedation – cause should be obvious
Dry mouth anti-cholinergic drugs
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Monitoring S/e of all BP medications
BP (if feeling s/e, take it in 4 wks)
Outcomes (kidney, heart, arteries)
Dizziness / headache / hypotension
Orthostatic Hypotension (OH)
Reduction >20 / > 10 upon standing
Erectile dysfunction
Arterial dysfunction very common cause
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ACE's and ARB's should be monitored for...
K+ levels
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ACE's should be monitored for....
Cough
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TZD Diuretics should be monitored for...
gout, electrolytes, SCr, urination
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DHP CCB's should be monitored for....
edema
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BB and Non-DHp CCB should be monitored for....
heart Rate
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Alpha-2 agonists should be monitored for....
Fatigue
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Vasodilators should be monitored for....
Tachycardia
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Beta-1 Selective Blocker Examples
Most commonly used agents in this sub-type:
Atenolol (Tenormin)
Bisoprolol (Monocor)
Metoprol (Lopressor)
Others:
Acebutolol (also has ISA – discussed later)
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Non-selective Beta-Blockers
Nadolol
Pindolol
Propranolol
Timolol
Sotalol - Class III anti-arrthymic (Class 2 and 3 anti-arrthymics preferred fro SVT's)
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What is different about carvediol? Indication?
- Non slective BB that also blocks alpha-1
- Indicated for heart failure with LVSD
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Beta-Blockers effectivenss in uncomplicated HTN
Minimal role in UNCOMPLICATED patients
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When would a beta-blocker be considered?
Might consider if individual presents with high heart rate (after excluding conditions associated with tachycardias)
BB are extremely protective in certain ‘complicated’ cases (i.e., people with HF, afib, ACVD, etc)
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Vasodilator Classes
Alpha blockers (sympathetic NS) (ALpha-1 Blockers - Doxazosin, Prazosin, Terazosin)
DHP Calcium Channel Blockers
Smooth muscle relaxants --> Need diuretic and beta-blocker to prevent reflex tachcardyia (Hydralazine, Minoxidil)
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B-2 receptors When stimulated lead to....
Vasodilation
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Alpha-1 receptors when stimulated lead to....
Vasoconstriction
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Alpha-1 Antagnosits MOA
Stimulation causes smooth muscle around vessel to contract
Actions blocked by alpha-1 antagonists --> prevent constriction
May play an important role in circulation
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Alpha-1 blocker Examples
Doxazosin, prazosin, terazosin
"osins"
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Are Alpha-1 blockers first line?
Not recommended for first line b/c shown less effective than others (ALLHAT)
Can be used for add-on therapy
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What condition are alpha-1 blockers useful for?
Used frequently for Benign prostatic hyperplasia (BPH)
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Which vasodilators are indicated as first-line?
- DHP-CCB
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When are other vasodialtors used?
Other agents are avoided EXCEPT as add-on therapy for people with treatment resistance – ALWAYS in combination with beta-blockers to prevent reflex tachycardia
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Can an ACE be used in someone who has normal BP?
You will see ACEI recommended in most patients at “high-risk” for CV events
EVEN if their BP is normal.
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Which is more effective:
ACE + TZD
ACE+ DHP CCB (when is this used)
ACE + DHP-CCB according to ACCOMPLISH
High Risk Pt's --> DIABETES
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ACE/ARB in CKD Benficial?
Benefit to kidneys increases in people with more severe disease
In lower risk people (i.e., lower SCr/higher GFR) other drugs appear to provide similar protection
Some BP-independent benefits on kidneys are likely in higher risk situations
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is renal harm possible from ARBS and ACE's?
YES
- Decrease Angiotensin II
- Decrease GFR
↓ GFR means lower ability to excrete fluid (i.e., edema, incr’d BP, etc)
if not resolved,
Acute renal failure can result (rarely)
Nephron ‘collapse’ due to lack of pressure
Urine production halted
Toxins and fluid accumulate over short term (acutely)
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When starting an ARB, which tests should be orderd and how often?
Obtain SCr and K within 1 – 2 weeks of starting drug (or increasing dose)
SCr is EXPECTED to increase from baseline - SHould not be > 30% from baseline
BP and edema should get better – not worse after ACEI or ARBs
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After starting and ACE or ARB, Scr should increase but should be less than....
30%
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ACEi/ARB Cautions
Reduced BP
Dry cough in 5-20% due to bradykinin accumulation (**ACEI only**)
Risk of hyperkalemia due to aldosterone inhibition
↓ kidney (renal) perfusion in vulnerable patients (hemodynamic)
Teratogenicity
Angioedema (ACEI primarily – <1% either way)
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USes of MRA
Resistant HTN
Heart failure
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MRA Cautions
↑ potassium
“Hormonal effects” – partially stimulates progesterone and androgen receptors: (gynecomastia, impotence, menstrual irregularities)
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BETA-Blcokers Slectivity
B1-selective (slay) (Bisoprolol, Metoprolol)
B1 and B2 (i.e., non-selective)
B1 and B2 AND alpha-1 (Carvedilol AND Labetolol) - Greater effect on BP
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Cautions of BEta-Blockers
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CCB Types
Non-DHP – So like BB except for systolic heart failure - worsens HF episodes
Block CO but do not block the reflective sympathetic nervous system)
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Short ACting Acei
Enalopril and captopril are the shortest acting ACEi – Enalapril can be dosed BID (Captopril is the lowest here - BID-TID)
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What to do if 15-20 mmHg off target?
15-20 off target – can recommend two drugs
AB-CD
ACEi/ARB + CCB or TZD
B-Blcoker + CCB or TZD (+ ACEi post MI/HF)
DHP-CCB + ACEi/ARB OR*** Beta-Blocker
Diuretics + ACEi/ARB OR Beta-Blocker
Amlodipine favoured in high risk (High Risk: ACEi, CCb (amlodipine) preferred in high risk)
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Resistant HTN Defintion
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Most common Secondary cause of HTN and SCreening
Primary aldosteronism 20% of resistant HTN
Screening
Plasma renin activity (blood test) LOW in Primary aldosteronism
Plasma aldosterone concentration HIGH in primary aldosteronism
Guidelines – Suggest empiric tx with spironolactone – Can go to sprinolactone as drug of choice after 1st line therapy (3 drugs) – Typical expected net step in tx resistant HTN
Primary Aldosterone – Potassium is low – Aldosterone eliminates potassium from the renal system – Urine – Would present with hypokalmeia
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First Line TX Resistant HTN
Lower sodium intake – People may be sodium sensitive – May reduce HTN in some individuals
Increase fitness/activity/exercise
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Drug Modifications TX Resistant HTN
Consider switching diuretic to chlorthalidone (long acting TZD) if GFR >30ml/min --. Long-standing recommendation
Consider adding spironolactone (first line “empiric drug”)
Spironolactone is expected to have the biggest effect on BP in Resist HTN
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Oher possible drugs to add in resistant HTN
Vasodilators – use with HR controllers
Alpha blockers
Hydralazine/minoxidil (not currently recommended routinely)
HR blockers (if HR elevated)
BB
NonDHP CCB
Clonidine/methyldopa
Amiloride or eplerenone (as alternatives to spironolactone)
Anti-anxiety medications such as SSRI’s if anxiety or depressive symptoms
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Timing of BP Measurement
Mornig and NIght - 24 Hour Assesment
Identify a wearing off effect of anti-hypertensive
Take it before or at the same time
BID if wearing off effect – Morning and night – Evening BP is good – Evening vs morning contrasted –
If uncontrolled at both – dose change
If just one – Split dosing – wearing off or tolerability can split spironolactone
