Cardiovascular System Overview

• Negative inotropic effect decreases heart contractility, while a positive inotropic effect increases it.

Circulatory System

• Deoxygenated blood flows into the right atrium, then the right ventricle, and then into the pulmonary artery, which leads to the lungs for oxygenation.
• Oxygenated blood returns via the left pulmonary artery to the left atrium, then to the left ventricle, and finally to the aorta.

Nodes of the Heart

• The SA node (upper right atrium) acts as the pacemaker of the heart.
• The AV node (lower right atrium) slows down the impulse, controlling the speed of conduction.

Cardiac Action Potential

• Sodium (Na+) ions are responsible for depolarization.
• Calcium (Ca+) ions facilitate contraction.
• Potassium (K+) ions are responsible for repolarization.

Fluid Shift Within Cells

• Hydrostatic Pressure, driven by the heart, pushes fluid out of the capillary.
• Oncotic Pressure, driven by albumin (plasma protein), pulls fluid into the capillary.
• Filtration Pressure is the net force on fluid, determined by the balance between hydrostatic and oncotic pressures.

Factors Affecting Heart Rate

• The more the heart pumps, the more oxygen it requires.
• Preload (volume): Increased by fluid overload, causing the heart to work harder due to more blood return.
• Afterload (pressure): Increased by hypertension, resulting in higher resistance and increased effort for the heart to contract.
• Contractility: Increased by a greater influx of calcium.

RAAS System

• When BP drops, the SNS stimulates the kidneys to release renin.
• Renin activates angiotensinogen, creating angiotensin I, which is then converted to angiotensin II by ACE (from the liver).
• Angiotensin II constricts vessels and increases blood volume.
• Ultimately Angiotensin + ACE = Angiotensin II.

ACE Inhibitors (captopril)

• Works against the RAAS system to stop ACE from converting Angiotensin I into Angiotensin II, decreasing BP and fluid volume.
• Useful in heart failure by decreasing afterload and preload when the left ventricle can’t empty or pump blood out.
• Therapeutic Action (TA): Blocks ACE, decreasing BP and aldosterone production with a slight increase in K+.
• Indications: Hypertension, heart failure (decreases cardiac workload), diabetic nephropathy, and left ventricular dysfunction after MI.
• Drug-to-Drug Interaction: NSAIDs decrease the antihypertensive effects, while K+ supplements and K+ sparing diuretics can cause hyperkalemia.
• Cautions and Contraindications: History of allergic reaction, impaired renal function, acute HF, and salt/volume depletion.
• Assessment: Monitor potassium levels (3.5-5), BP, pulse (for hypotension), BUN, and creatinine.
• Adverse Effects (AE): Persistent dry cough, angioedema (swelling of face, mouth, eyes), and hyperkalemia.

ARB’s (losartan)

• Angiotensin II Receptor Blockers (end in -sartan) vasodilate to decrease BP, blocking the activation of ANGIO II type 1 (at receptor).
• Binds with angio II receptors in the adrenal cortex to block vasoconstriction and aldosterone release, thus lowering BP.
• Carries a lower risk for elevated K+ levels,
• Angiotensin II type 1 receptor sites: angiotensin II binds here to vasoconstrict & trigger aldosterone release.
• Therapeutic Action: Blocks the binding of angiotensin II in vascular smooth muscle and adrenal glands, preventing vasoconstriction and aldosterone release.
• Indications: Hypertension, diabetic nephropathy with elevated creatinine and proteinuria in type 2 DM & HTN, heart failure (decreases preload & afterload).
• Drug-to-Drug interaction: NSAIDS (will decrease HTN effects of the meds); K+ supplements (drug will already increase K+, so this will elevate it even more); K+ sparing diuretics
• Cautions and Contraindications: Hx of allergic reaction; impaired renal function; hepatic dysfunction (liver won’t metabolize); hypovolemia (bc blocking aldosterone (holds salt & water))
• Assess: potassium levels (3.5-5), BP & pulse (watch for hypotension), BUN & creatinine.
• AE: less common cough; angioedema (from allergies; swelling of face, mouth, eyes); hyperkalemia
• Results in vasodilation, excretion of Na and H2O, retention of K+, and decreased proteinuria.

Renin Inhibitors (aliskiren)

• Directly inhibits renin, preventing the conversion of angiotensinogen to angiotensin I.
• REMEMBER: kidney releases renin when BP is low; angiotensinogen (protein created & produced in liver) to create ANGIOTENSIN I, then ACE, then Angiotensin II = vasoconstricts & aldosterone released.
• Therapeutic Action: Directly inhibits renin, preventing the conversion of angiotensinogen to angiotensin I.
• Indications: Hypertension, diabetic nephropathy with elevated creatinine and proteinuria in type 2 DM & HTN, heart failure (decreases preload & afterload).
• Drug-to-Drug Interaction: ACE inhibitors and ARBs (high risk for high K+ levels)
• Cautions and Contraindications:
• Assess: potassium levels (3.5-5), BP & pulse (watch for hypotension), BUN & creatinine.
• AE:risk for hyperkalemia; angioedema w/ respirator involvement; renal impairment

Calcium Channel Blockers (diltiazem)

• Class IV antiarrhythmic drug that decreases BP and cardiac workload, working in blood vessels with a less negative inotropic effect.
• Blocks calcium channels to prevent calcium from passing through, causing vasodilation.
• Cardiac Nodal Tissues (SA NODE: slow down the heart rate *negative chronotropic effect) (*AV NODE: slow down speed of conduction of electrical impulses negative dromotropic effect)
• Calcium channel blockers inhibit movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering action potential and blocking muscle cell contraction (calcium causes contraction in action potential).
• Therapeutic Action: Inhibits calcium movement across cardiac and arterial muscle cells, slowing the action potential, decreasing myocardial contractility, and dilating arterioles.
• Indications: Hypertension, angina (blocking, coronary vasospasm, atherosclerosis), cardiac dysrhythmias (vasodilates), tachyarrhythmias (decreases action potential from calcium).
• Drug-to-Drug Interaction: Avoid grapefruit juice due to risk of drug toxicity.
• Cautions and Contraindications: Heart block, sick sinus syndrome, heart failure, and acute MI.
• Assess: Monitor potassium levels (3.5-5), BP & pulse (watch for hypotension), BUN & creatinine.
• Adverse Effects: Peripheral edema, bradycardia, AV block.
• Interventions: Implement lifestyle changes, monitor renal and fluid status, check electrolytes, monitor pulse rate and BP daily, advise reporting dizziness or fainting, avoid abrupt cessation, and monitor glucose levels.

Vasodilators (nitroprusside)

• Used IV in emergencies for severe hypertension that hasn't responded to other treatments.
• Therapeutic Action: Acts directly on vascular smooth muscle to cause vasodilation and a drop in BP.
• Indications: Severe hypertension, acute heart failure.
• Cautions and Contraindications: Conditions worsened by sudden BP drop (PVD, CAD, HF, tachycardia).
• Assess: BP, chest pain.
• Adverse Effects: Retrosternal pressure, palpitations, cyanide toxicity (deadly).