Cardiac conditions And Meds Flashcards
What are the stages of SYSTOLIC HTN
< 120 - Normotensive
120-140- pre HTN
140-159 Stage 1
160- 180 Stage2
180 + stage 3
What are the stages of DIASTOLIC HTN
< 80 - Normotensive
80 -90- pre HTN
90-99 Stage 1
100-120 - stage 2
120+ stage 3
Nitrates- name common uses and mechanism of action
Relief of angina- GTN spray and sublingual/buccal tablets- rapid acting
Prevention of angina- ISMN, GTN patch- long acting
Mechanisms:
Peripheral vasodilation – reduces preload – reduces myocardial oxygen demand
Coronary artery vasodilation - improves endocardial blood flow – increases myocardial oxygen supply
Calcium channel Blockers- name indication and mechanism of action of Non Rate limiting CCB
Non Rate limiting CCB- Indication- hypertension
Mechanism: block calcium channels of smooth muscle
Arterial dilation reduces systemic vascular resistance and myocardial oxygen demand
non cardiac specific
amlodipine, felodipine, nifedipine
Calcium channel Blockers- name indication and mechanism of action of Rate limiting CCB
Rate limiting CCB- Indication- hypertension, angina, arrhythmias
Mechanism: block calcium channels of smooth muscle
and reduce myocardial contractility- reduced myocardial oxygen consumption
Slow sinus node and AV node conduction
Reduced HR = reduced myocardial oxygen demand
caution with other selective rate controlling drugs e.g. bisoprolol.
– verapamil and diltiazem
Nicorandil- what is its indication and mechanisms
prophylaxis and treatment of stable angina
Mechanisms: Dual mechanisms
Potassium channel opening action to provide vasodilation
Nitrate component promotes venous dilation
dual mode of action avoids some of tolerance seen with long term nitrates.
Aspirin- indications and mechanisms
Stops platelet aggregation and clot formation
Mechanism: A non-selective cyclo-oxygenase (COX) inhibitor- Inhibits thromboxane A2 (TA2) formation
Clopidigrel- indications and mechanisms
Stops platelet aggregation and clot formation
Used in dual antiplatelet therapy with aspirin e.g post MI
Mechanism: Antagonist at adenosine diphosphate (ADP) receptors- blocking it reduces aggregation
ticagrelor- indications and mechanisms
Stops platelet aggregation and clot formation
Used in dual antiplatelet therapy with aspirin e.g post MI
Mechanism: stops the action of ADP
Ticagrelor vs clopidogrel
not a prodrug
faster onset
more potent inhibition of platelet aggregation
name 3 common antiplatelets drugs
Aspirin
Ticagrelor
Clopidogrel
which common class of drugs are used to lower cholestrol?
STATINS
Simvastatin
Atorvastatin
Rosuvastatin
Statins- indications and mechanisms
Decreases cholesterol production and increases LDL clearance
Other actions:
Stabilises plaque
Improves endothelial function
Prevents thrombus formation
mechanism- Inhibit hydroxy-methylglutaryl-coenzyme A reductase (HMG-CoA)
HMG coenzyme a is an essential cholesterol precursor
Primary prevention - Atorvastatin 20mg nocte
Post myocardial infarction (MI) - Atorvastatin 80mg nocte
Atorvastatin and pravastatin can be given AM due long action of onset in cases of poor adherence nocte.
many interaction- avoid grapefruit juice
Beta-(adrenoreceptor) blockers- indication and mechanisms
Indications- hypertension, Angina, MI (secondary prevention), aryhthmias e.g. AF
Mechanism: antagonist to Beta 1 receptor
Decrease myocardial oxygen requirements by:
slowing heart rate
reduce force of contraction
reduce blood pressure
caution with other rate control drugs
caution in Severe asthma- can block beta 2 receptors
what is the role of the Renin angiotensin Aldosterone system (RAAS) ?
RAAS plays a role in regulating blood pressure/volume, maintaining sodium concentration and the right amount of water in the blood
how does the RAAS moderate BP?
A reduction in blood pressure is detected by the kidneys
Renin - released by the kidneys, stimulates the formation of angiotensin I in the liver - this inconverted to Angiotensin II in lungs by angiotensin converting enzyme
Angiotensin II - stimulates the release of aldosterone from the adrenal cortex and causes direct vasoconstriction- increase in BP
Aldosterone - stimulates reabsorption of sodium and water- increase BP
Which two classes of drugs act on RAAS to lower BP ?
ANGIOTENSIN – CONVERTING ENZYME (ACE) INHIBITORS
e.g. Ramipril, Captopril, Enalapril, Lisinopril, Perindopril
ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)
e.g. Candesartan, Eprosartan, Irbesartan, Olmesartan, Valsartan
THESE TWO DRUGS SHOULD NOT BE USED TOGETHER !
how do ACE inhibtors lower BP?
they inhibit ACE in the lungs and thus Angiotensin II formation.
how do ARBs lower BP?
they block receptors and are angiotensin II receptor antagonists.
Management HTN “with” T2DM any age/origin
management HTN “without” T2DM < 55yrs - not black African/African-Caribbean.
step 1 ACE/ARB
Step 2 in addition to ACE/ARB add CCB or thiazide diuretic (THD)- in HF offer THD
step 3 ACE/ARB + CCB + THD
Step 4 consider adherence, specialist help
consider spironolactone- K < 4.5mmol
consider alpha/beta blocker - k >4.5 mmol
Management HTN “without” T2DM > 55yrs
Or all age black African/African-Caribbean “without” T2DM
step 1 CCB
Step 2 in addition CCB add ACE/ARB or thiazide diuretic (THD)
step 3 ACE/ARB + CCB + THD
Step 4 consider adherence, specialist help
consider spironolactone- K < 4.5mmol
consider alpha/beta blocker - K >4.5 mmol
Which oral anticoagulants are vitamin k antagonist
Warfarin - most common
Inhibits Vitamin K Reductase
Prevents degradation of vitamin K to its active form- stops phase of clotting cascade.
older generation -Acenocoumarol and Phenindione
which are the common direct oral anticoagulants (DOACs)
Rivaroxaban, Apixaban and Edoxaban– Factor Xa inhibitor
Dabigatran – direct thrombin inhibitor
All have rapid onset and offset of action, so adherence is paramount
What are drawbacks when using warfarin ?
Narrow therapeutic range- can be condition specific
Slow onset of action- 3 -5 days before therapeutic
Long elimination half-life
Multiple drug and dietary interactions- including herbal and over counter preparations
Monitoring required- INR regularly
Difficult to manage peri-operatively- long half life.
Inconvenient and/or unsuitable for some patients
Large commitment of resources in primary and secondary care
What are drawbacks of DOACs ?
Specific contraindications and cautions for DOACs
Renal impairment- renally excreted
Extreme body weight eg. Apixaban only in BMI < 40, < 120 kg
Pregnancy - animal studies showed crossed placenta.
Advice re: contraception in women of child-bearing age
Adherence- short halve life - can soon be non therapeutic
Specialist indications- not suitable in mechanical valves, sinus venous thrombosis and cancer, antiphospholipid syndrome
Peri-operative management
Important patient education whom are taking
any oral anticoagulation
Importance of regular administration
Always seek medical advice when starting new treatments or any new diet regimes
Work by stopping blood clotting formation- Report any signs or symptoms of Bruising or Bleeding
If you miss a dose, do not double up !!!!
Carry patient alert card
When to anti coagulate - CHA2DS2VASc Score
CHA2DS2-VASC >1 anti-coagulate for women or > 2 for men
CHA2DS2-VASC ≤1no treatment
Must consider a risk of bleeding assessment such as the by calculating the HAS-BLED score
Consider HASBLED score when anticoagulating
Bleeding risk classification:
0-1 low risk
2 intermediate risk
≥ 3 high risk
NOTE: A score of 3 or more is not a contraindication to oral anticoagulation but these patients require extra care
