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cardiac output
Heart rate x stroke volume
the overall performance of the heart
- HR controlled by ANS (increased by SNS B1, decreased by PSNS)
preload
volume of blood present before contraction
- increase in preload, increases SV
afterload
Resistance heart must overcome to eject blood
- increase in afterload, decreases SV
stroke volume
The amount of blood ejected from the heart in one contraction
- determined by contractility (dilation and venous return)
starling's relationship
ventricular contraction is proportional to the muscle fiber length
- the more the heart stretches, the more forcefully it contracts allowing adequate BF
peripheral resistance
the opposition to flow that blood encounters in vessels away from the heart
- regulated by constriction/dilation of arterioles
arterial pressure
The pressure of the blood against the arterial walls
- peripheral resistance x cardiac output
RAAS
Renin is released by kidneys in response to decreased blood volume; causes angiotensinogen to split & produce angiotensin I; lungs convert angiotensin I to angiotensin II; angiotensin II stimulates adrenal gland to release aldosterone & causes an increase in peripheral vasoconstriction
Angiotensin II
high activity
- vasoconstriction of arterioles (increase BP)
- release of aldosterone --> Na+ and H2O retention (increase BP)
- hypertrophy and remodeling
renin
converts angiotensinogen to angiotensin I
ACE inhibitors
- reduce levels of Ang II
- cause vasodilation and reduce BV
- introduced after other BP drugs but reduce risk of cardio mortality caused by HTN similar to other drugs
captopril
ACE inhibitor
- used for MI and diabetic neuropathy
lisinopril
ACE inhibitor
- used for MI
ARBs
Angiotensin II Receptor Blockers
- used for HTN, heart failure, diabetic nephropathy
Losartan
ARB
- used for diabetic nephropathy
ARNI
Angiotensin receptor-neprilysin inhibitor
- for heart failure.
Valsartan/Sacubitril
ARNI
- for heart failure
- _____ blocks ang II causing dilation
- _____ blocks breakdown of natriuretic peptides produced in the body
- NOT given to those currently on ARBs or ACE inhibitors
Eplerenone
Selective aldosterone receptor blocker
- ONLY for HTN
calcium channel blockers
agents that inhibit the entry of calcium ions into heart muscle cells, causing a slowing of the heart rate, a lessening of the demand for oxygen and nutrients, and a relaxing of the smooth muscle cells of the blood vessels to cause dilation; used to prevent or treat angina pectoris, some arrhythmias, and hypertension
nifedipine
calcium channel blocker
- works in the arterioles
- dihydropyridine
Verapamil and Diltiazem
Class IV: calcium channel blocker (2)
- works in the arterioles and the heart
- decreases velocity of conduction in the heart, prolongs QT interval
vasodilators
medications that cause dilation of blood vessels
- decrease afterload and preload
hydralazine
vasodilator
- works on arterioles
- uses: HTN, hypertensive crisis, and heart failure
minoxidil
vasodilator
- works on arterioles
- uses: severe HTN and hair growth (rogaine)
sodium nitroprusside
vasodilator
- works on arterioles/veins
- used in hypertensive emergencies
hypertension
high blood pressure
- BP > 120/80
heart failure
a chronic condition in which the heart is unable to pump out all of the blood that it receives
- reduced CO, fluid retention, and ventricular dysfunction
Digoxin
cardiac glycoside
- increases force of contraction/cardiac output
- used for heart failure
Spironolactone
potassium-sparing diuretic; aldosterone antagonist (receptor blocker)
- used for heart failure
sotagliflozin
SGLT2 inhibitor
- prevents sugar and sodium absorption in body lowering stress on the heart
- reduces risk of CV death, hospitalization for heart failure, and urgent heart failure visits
dysrhythmias
antidysrhythmic drugs also cause _____
- not used as often
lengthen
many antidysrythmic drugs ____ the PR interval
quinidine
Class IA: sodium channel blocker
- antidysrythmic drug
- decreases conduction in atria, ventricles, and his-purkinje system
lidocaine
class IB: sodium channel blocker
- antidysrhythmic drug
propranolol
class II: B blocker
- antidysrhythmic drug
- effects B1 and B2 receptors
Bretylium
Class III: Potassium channel blocker
- short term therapy
- antidysrhythmic drug
- delays repolarization in the heart, prolongs QT interval
Amiodarone
class III: potassium channel blocker
- antidysrythmic drug
- delays repolarization in the heart, QRS widening, PR/QT lengthening
VLDL
Very Low-Density Lipoprotein, transports triglycerides.
LDL
bad cholesterol
HDL
high density lipoproteins (healthy type of cholesterol)
Statins (HMG-CoA Reductase Inhibitors)
decreased LDL, TG; increase HDL
- MOA: inhibits enzyme needed for cholesterol synthesis
nicotinic acid
decrease LDL and TG; increase HDL
- MOA: decrease VLDL (LDL are byproducts of VLDL)
bile acid sequestrants
Decreases LDL
Increases HDL
No change in TG
fibric acid (fibrates)
Has little to no effect on LDL
Increases HDL
Decreases TG
- MOA: accelerate clearance of VLDL thereby reducing TG
angina pectoris
chest pain, which may radiate to the left arm and jaw, that occurs when there is an insufficient supply of blood to the heart muscle
nitroglycerin
organic nitrate drug used in the treatment of angina
- stable angina: decrease O2 demand by dilating veins
- variant angina: increase O2 supply by relaxing vasospasm
beta blockers
decrease heart rate and dilate arteries by blocking beta receptors
- treats stable angina: decrease O2 demand by decreasing HR
- not used for variant angina
stable angina
chest pain that occurs when a person is active or under severe stress
- exertional angina
- goal of decreasing oxygen demand
variant angina
pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm
- goal of increasing oxygen supply
calcium channel
_____ ____ blockers can treat:
- stable angina: decrease O2 demand by dilating arterioles and decreasing HR
- variant angina: increase O2 supply by relaxing coronary vasospams
thrombus
stationary blood clot
fibrin
protein that forms the basis of a blood clot
plasmin
enzyme that dissolves clots
heparin
Helps antithrombin inactivate clotting factors
- suppresses formation of fibrin
- parenteral anticoagulant
- used in hospital and requires lab monitoring
- uses: pregnancy, surgery, MI
Low molecular weight heparins
Helps antithrombin inactive clotting factors
- suppresses formation of fibrin
- parenteral anticoagulant
- used in hospitals/home, does not require lab monitoring
- uses: DVT following hip/knee replacement
warfarin
Oral anticoagulant
- delayed onset of action
- antagonist of vitamin K (required by 4 clotting factors)
- use: prophylaxis of thrombosis
aspirin
Antiplatelet drug
- inhibits COX needed to synthesize thromboxane
adenosine receptor antagonist
Inhibits ADP-stimulated aggregation
- long term antiplatelet maintenance
glycoprotein IIb/IIa receptor antagonist
- antiplatelet drug
- block the final step of aggregation
- long term antiplatelet maintenance
streptokinase
removes thrombi (blood clots)
- made from streptococci
- thrombolytic drug
- use: MI and DVT
Alteplase (tPA)
thrombolytic agent
- removes thrombi (blood clots)
- tissue plasminogen activator
- made in a lab
MI
necrosis of the heart resulting from occlusion of a coronary artery
thrombolytics; antiplatelet
we use _____ and _____ drugs to treat MI