CAD, HF, Acute CS & AF Flashcards
What is the role of GTN?
- Vasodilator, given for angina pectoris
- Causes venous dilatation to reduce cardiac preload
- Decreasing cardiac oxygen demand
- GTN is metabolised into NO in smooth muscle cells
What are the adverse effects of Nitrate drugs?
- venous pooling
- leads to postural hypotension, from supine to sitting position
- dizziness and headaches
What are the types of Angina?
- Stable angina (most common)
- Unstable Angina
- Prinzmetal Angina
What is stable angina?
- Most common type of angina
- Induced by exercise, heavy meals, cold and emotional stress
- Controlled well by GTN & other anti-anginal drugs
What is unstable angina?
- Occurs at rest
- May be induced by little exercise or stress
- Occurs due to possible thrombus formation on ruptured atheromatous plaque
- Causing partial occlusion of CA
-Patient at risk of full occlusion of CA and MI
What is prinzmetal angina?
- rare form of angina
- spasm of CA’s
- may occur in patient’s with minimal atherosclerotic damage and rarely progresses to MI
Why is GTN administered as sublingual, skin patch or buccal spray and NOT as a tablet to swallow?
- Absorption of the drug in the gut will lead to metabolisation by the liver
- Limits the drug availability
Can a patient with Asthma be prescribed with Beta Blockers for angina (non-selective & selective)?
-No
- B- blockers have affinity for both B1 (cardiac) & B2 receptors (airways) on bronchial muscles
- This can lead to bronchoconstriction
- Even selective B- blockers can have some effect
What is the mechanism of action of Beta Blockers e.g. Propranolol?
- act on B1 and B2 receptors
- cause vasoconstriction & bronchoconstriction
- Block sympathetic effects on B1 & B2 receptors
- Causes small reduction in HR and CO; little effect on BP
- May be beneficial for some angina patients; reduces the response of B1 receptors to sympathetic stimulation during exercise, stress etc.
- Selective & Non-selective B-Blockers
How can you distinguish between Angina & MI?
- Angina goes away after rest and taking medication e.g. GTN
- MI patient still presents with symptoms
- Pain, pallor, sweating, nausea, hypotension with shock suggest complete occlusion of CA
- MI patient will have increased Troponin I & T with increased creatine phosphokinase
What is the MOA of Calcium Channel blockers (CCB’s)?
- Block L type Ca channels of vascular smooth muscles
- Reduces Ca concentration in smooth muscles
- Leads to dilation of arteries due to reduced contractile activity
- CCB’s mainly act on arteries
- Dihydropyridines, e.g. Nifedipine, is useful for CA dilation
- Commonly used for prinzmetal angina
What ECG changes will be expected in Angina?
- ST segment depression
- Severe Angina may present with ST segment elevation for short duration
What is Angina Pectoris?
- Paroxysmal attacks of retrosternal chest discomfort, tightness, or pressure due to myocardial ischemia
- Pain may radiate to left arm, chin and jaw area
- Narrowed CA’s may not be able to dilate upon exercise, stress, cold etc
- Therefore, increased oxygen demand of cardiac muscles are not met, leading to ischemia
What is heart failure?
-heart is unable to pump enough blood
-Unable to meet the metabolic needs
- Ventricular dysfunction results in low cardiac output
-congestion of blood (backward failure) and poor systemic perfusion (forward failure)
-Disturbance of tissue fluid management; increased venous pressure
- therefore swelling of ankles is presented in patients
What is the significant underlying cause of Heart Failure?
Hypertension- leads to increased afterload which causes hypertrophy of ventricles and increased O2 consumption
- reducing cardiac efficiency
What are Thiazides? MOA?
- Thiazides are diuretics
- Reduce Na and Water reabsorption by acting on distal tube of Nephrons
- Block NaCl transporters
- This ultimately reduces blood volume
- Diuretics also act on vascular smooth muscles to cause dilation
- Both of these reduce BP and reduce peripheral edema
- Preload and afterload is also reduced
What are the symptoms of Right Sided Heart Failure?
- Abdominal bloating
- Nausea
- Loss of appetite
- Reduced tolerance to exercise
- Breathlessness
What are adverse effects of thiazide’s?
- hypokalaemia, hyperglycaemia & hyperurecaemia
What type of diuretics are prescribed when thiazides are not functioning well?
- Loop diuretics (stronger diuretic than thiazides)
- Better to introduce a stronger diuretic than increase dose of thiazides
- As therapeutic effect is lower and increased events of adverse effects
What is the MOA of loop diuretics?
- Blockage of Na+, K+, 2Cl-cotransporter in the thick ascending loop of Henle
-Diminishing concentration gradient between the (usually hypertonic) renal medulla and the cortex → concentration of urine is no longer possible → increased diuresis
-Decreased reabsorption of Ca2+ and Mg2+ - Increased PGE release (can be inhibited by NSAIDs)
Dilation of renal afferent arterioles → diuresis - General venodilation (rapid venous pooling) → ↓ cardiac preload
What are the adverse effects of Loop Diuretics?
- Similar to thiazides
-Hypokalaemia, Hyperglycaemia and Hyperurecaemia - Some patients may also present with hypovolemia & hypotension, which can develop to CV collapse
Define Myocardial Infarction
-obstruction of blood flow to cardiac muscles
-due to occluded CA’s leading to ischemia
-Interruption of blood flow to that area causes potential cell death of affected cardiac muscles
What is the MOA of Epinephrine on the heart?
- non-selective A & B receptor agonist
- acts on B1 receptors on cardiac muscles to stimulate contractions to increase CO
- doesn’t cause bronchoconstriction, as it relaxes airways
What is the MOA of aspirin?
- Aspirin is a NSAID which inhibits COX enzyme
- This prevents the release of PGs
- Whom are responsible for inflammation, temperature regulation, blood clotting etc.
- Aspirin aids to reduce fever, pain and stops blood clotting
Why is aspirin administered to patients after an MI?
- prevent risk of blood clotting in the circulation
What are the MOA of thrombolytic agents and use in MI e.g. streptokinase?
- “dissolve’ clots obstructing blood flow in CA’s to cardiac muscles
- Activates plasminogen to plasmin conversion; lyses clots
- Should be administered within 12 hours of infarction; ideally within 1st hour
-Given IV
What are the contraindications for thrombolytic agents?
- allergy to medication
- recent hemorrhage e.g. recent head injury with intracranial hemorrhage or had surgery
What is Furosemide? MOA?
- Loop diuretic
- Acts on ascending thick loop of Henle
- Acting on Na/Cl transporters
- Reduces Na and water reabsorption in collecting duct
- Large amounts of salt and water is excreted by the kidney
- Strong class of diuretics, able to improve pulmonary edema
What is atrial fibrillation?
- Common type of supraventricular tachyarrhythmia
-Characterized by uncoordinated atrial activation that results in an irregular ventricular response
What type of drug is Digoxin and what is its MOA?
- Cardiotonic agent
- Increases contractility of cardiac muscles
- Increases Ca concentration in cardiac muscles
- Acts on Na/K pumps in cardiac muscle; competes on K binding site
What are the adverse effects of Digoxin use?
-narrow therapeutic index
-therapeutic dosage is close to dosage causing toxicity
-may cause cardiac rhythm abnormalities
- GI disturbances, anorexia, nausea, CNS effects e.g. confusion and visual disturbances
What is the MOA of warfarin?
- Anticoagulant
- Structurally similar to Vit K which is needed for synthesis of prothrombin and other clotting factors
- Interferes with actions of Vit K and reduces risk of clotting
- Given for anticoagulant therapy for atrial fibrillation
