cardiovascular Flashcards
Right side HF
when the heart can’t pump enough blood to the lung to get oxygenated
Ticagrelol (Brilinta):
Reversible and noncompetitive inhibitor of ADP P2Y12 receptor on platelet surface thus preventing activitation of GPIIb/IIIa leading to reducing platelets aggregation.
- MD of ASA > 100mg reduce effectiveness of Brilinta and should be avoided.
- Use is CI is ICH, PU bleeding.
- Surgery: D/C > 5days prior to operations
- CI in pregnancy
Main indications for VKAs are
Atrial fibrillation Acute coronary syndrome Heart failure Prosthetic heart valve Stroke Deep vein thrombosis Pulmonary embolism Antiphospholipid syndrome
Difference between valvular Afib & non-Valvular Afib:
- Valvular AF: AF in the setting of moderate-to-severe mitral stenosis (potentially requiring surgical intervention) or in the presence of an artificial (mechanical) heart valve. Valvular AF is considered an indication for LONG-TERM anticoagulation with warfarin.
- Non-valvular AF does not imply the absence of valvular heart disease. Instead, as used in the present focused update, non-valvular AF is AF in the absence of moderate-to-severe mitral stenosis or a mechanical heart valve.
Ranolazine (Ranexa)
Exerts antianginal and anti-ischemic effects without changing hemodynamic parameters (heart rate or blood pressure).
Inhibits the late phase of the inward sodium channel (late INa) in ischemic cardiac myocytes during cardiac repolarization reducing intracellular sodium concentrations and thereby reducing calcium influx via Na+-Ca2+ exchange. Decreased intracellular calcium reduces ventricular tension and myocardial oxygen consumption.
It is classified as: Partial fatty acid oxidation inhibitors (pFOX inhibtor): which enhances the efficiency utilization of oxygen.
Nitroglycerine (glycerly trinitrate):
The active ingredient is dynamite. It primarily reduces cardiac oxygen demand by decreasing preload through release of Nitric oxide (similar MOA of nitroprusside) thus, producing a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. It is firstly undergoes dinitration in the liver to 2 dinitrate (glyceryl trinitrate) which has the vasodialatory effects and then to mononitrates which is less active.
**use in rectal fissures, intra-anal administration results in decreased sphincter tone and intra-anal pressure.
First pass effect after oral administration is 90% !!!
Continuous IV infusion: Tolerance to the hemodynamic and antianginal effects can develop within 24 to 48 hours of continuous use. Nitrate-free interval (10 to 12 hours/day) is recommended to avoid tolerance development; gradually decrease dose in patients receiving nitroglycerin for prolonged periods to avoid withdrawal reaction.
Calcium Channel Blockers:
blocking L-type calcium channels leading to vasodialation and decrease afterload thus decreasing oxygen demand.
Verapamil and Diltiazem: also decrease heart rate and contractility. Thus, its use is beneficial in Arrhythmia.
Mechanism of QT prolongation associated with Ranexa:
Ranolazine inhibits the rapid delayed rectifier potassium current (IKr) thus prolonging the ventricular action potential duration and subsequent prolongation of the QT interval.
Ivabradine (PROCORALAN)
Antianginal through the blockage of the pacemaker Na channel (If) in SA node thus reducing Heart rate
It used for HF with EF<35% who are not responding to beta blockers and has sinus rythm of >70
SE: Luminous phenomena due to the fact that in the Retina of the eye there are If channels, bradycardia, AV block, Afib.
CI with CYP450 inhibitors i.e. verapamil
***Doses are based on HR
Major effect of digitalis on AV node and the ECG include:
increase AV node refractory period
Inverted T-wave
Short QT intervals
HF treatment include:
1.Cardiac Glycosides.
2.Diuretics: effective early treatment for both systolic and diastolic HF. (initial treatment is always Lasix)
Spironolactone is the only agent proved to reduce mortality in long standing HF
- ACEI & ARBS (they have NO positive inotropic effects however they reduce water retention, decrease aldosterone and vascular resistance.
- Beta-blockers: Carvedilol showed to prolong life on HF patient despite its negative inotropic action on the heart.
- Vasodilators: Isobide dinitrates, Hydralazine, Nestiride(Natriuretic peptides with diuretics effects) ) which is used in acte failure only through IV route.
- PDE-5 inhibitors: by increasing cAMP leading to vasodialation
- Beta1 selective agonist: Dobutamine which has positive inotropic effects
Patients with HF have a lesser response to a given dose of diuretic than normal subjects due to main two reasons:
- decreased diuretic delivery to the kidney due to low renal blood flow.
- Increased sodium reabsorption at other sites due to hypoperfusion-induced activation of the RAAS & sympathetic nervous systems.
Cardiac Glycosides Founded by William Withering from …………………………………
Founded by William Withering from foxglove plant (Digitalis)
Anti-ischemic and analgesic therapy:
M: morphine however its use demonstrated negative effects on anti-platelets.
O: Oxygen: in patients with PO2 less than 90%
N: nitroglycerine to elevate chest discomfort.
A: ASA+ P2Y12 inhibitors.
It is a cardenolide meaning it contains a steroid and a lactone ring
It has a positive inotropy in cardiac myocytes
Cardiac Glycosides
Cardiac troponins are more ……………. and ………………… markers of cardiomyocyte injury than (CK), (CK-MB), and myoglobin.
Cardiac troponins are more sensitive and specific markers of cardiomyocyte injury than creatine kinase (CK), its myocardial band isoenzyme (CK-MB), and myoglobin.
Stroke volume (SV) is defined as:
amount of blood pumps from each ventricles at each heartbeat.
SV= EDV - ESV
SV depends on: EDV( filled volume before contraction) and ESV (volume of blood remaining after ejection) and Contractility.
Normal SV= 70ml
Difference between infarction and ischemia:
- Ischemia is a restriction in blood supply leading to tissue damage. “absence of blood supply” . Treatment focuses on increasing blood flow to the heart. Reversible damage.
- Infarction aka heart attack: tissue death due to obstructed blood flow in the coronary arteries such as thrombus or rupture of blood vessels. Irreversible damage.
***Hypo perfusion—> ischemia—-> infarction
MOA of Digoxin:
- Blocks Na/K ATPase leading to increased intra-cellular Na levels which lead to stimulation of the Na calcium exchange pump leading to accumulation of Ca+2 levels within the cell thus, exerting its effects of increased contractility.
- Increase vagal tone, which results in decreased conduction through the SA & AV nodes
-Has narrow therapeutic window.
