Module 7

What is preload

The volume of blood in the ventricles at the end of diastole that stretches the heart before it contracts.

What increases preload

Fluid overload or venous constriction.

What decreases preload

Dehydration, hemorrhage, or nitrates that dilate veins.

What is afterload

The resistance the heart must overcome to eject blood during systole.

What increases afterload

Hypertension or vasoconstriction.

What decreases afterload

Vasodilators or medications that lower vascular resistance.

What is contractility

The strength of the heart's contraction independent of preload.

What factors improve contractility

Inotropes like dobutamine or digoxin.

What factors reduce contractility

Acidosis, hypoxia, or myocardial ischemia.

What is stroke volume (SV)

The amount of blood pumped from one ventricle with each heartbeat (normal 60-100 mL).

What determines stroke volume

Preload, afterload, and contractility.

What is cardiac output (CO)

The total amount of blood the heart pumps per minute (CO = HR × SV).

What happens when cardiac output is low

Fatigue, hypotension, poor perfusion, and decreased organ function.

What do baroreceptors do

Detect changes in blood pressure and adjust heart rate and vessel tone.

Where are baroreceptors located

In the carotid sinus and aortic arch.

What do chemoreceptors respond to

Changes in oxygen, carbon dioxide, and blood pH levels.

What is the RAAS system

The renin-angiotensin-aldosterone system that increases blood pressure by causing vasoconstriction and fluid retention.

What activates the RAAS system

Low blood pressure, low sodium, or reduced renal perfusion.

What do ACE inhibitors do

Block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and blood pressure.

What do ARBs do

Block angiotensin II receptors, leading to vessel relaxation and reduced afterload.

What do natriuretic peptides (ANP/BNP) do

Promote sodium and water loss to decrease blood volume and pressure.

What condition raises BNP levels

Heart failure due to overstretching of the heart chambers.

What do beta-blockers do

Block beta-1 receptors in the heart to lower heart rate, contractility, and oxygen demand.

When are beta-blockers commonly used

Hypertension, angina, heart failure, and after myocardial infarction.

What do calcium channel blockers (CCBs) do

Block calcium entry into muscle cells, causing vasodilation and reduced heart rate.

What are calcium channel blockers used for

Hypertension, angina, and supraventricular tachycardia (SVT).

What side effects are associated with calcium channel blockers

Edema, bradycardia, dizziness; avoid grapefruit juice.

What do nitrates do

Relax venous smooth muscle, decreasing preload and relieving angina pain.

What should patients avoid while taking nitrates

Phosphodiesterase-5 inhibitors (e.g., sildenafil) due to severe hypotension risk.

What do diuretics do

Increase sodium and water excretion to reduce fluid volume and blood pressure.

What should nurses monitor when giving diuretics

Electrolytes (especially potassium), I&O, and daily weight.

What does digoxin do

Increases contractility and slows the heart rate by affecting the AV node.

What are signs of digoxin toxicity

Nausea, vomiting, vision changes (yellow-green halos), and bradycardia.

What do vasodilators do

Relax arterial smooth muscle to reduce afterload and improve cardiac output.

What should nurses assess when giving vasodilators

Continuous blood pressure; watch for reflex tachycardia.

What vital sign must always be checked before giving a beta-blocker or CCB

Heart rate — hold if below 60 bpm or systolic BP < 90 mmHg.

Why is daily weight important for cardiac patients

It helps detect fluid retention early in heart failure.

How much weight gain should be reported to a provider

2 pounds in a day or 5 pounds in a week.

Why are electrolyte levels important in cardiac pharmacology

Imbalances can cause arrhythmias and increase toxicity risk for drugs like digoxin.

What are early signs of poor perfusion

Cool extremities, decreased urine output, altered mental status, weak pulses.

Hypertension, CAD, Heart Failure, Tachyarrhythmias

β-Blockers ↓ HR, ↓ contractility, ↓ O₂ demand.

Hypertension, Heart Failure

ACEIs / ARBs / Vasodilators ↓ Ang II → vasodilation → ↓ BP.

Heart Failure, CKD, Hypertension

ACEIs / ARBs / ARNIs ↓ preload/afterload, ↓ remodeling.

Angina, Hypertension, Arrhythmia

CCBs block Ca²⁺ channels → ↓ contractility, ↓ BP, ↓ angina.

Heart Failure, Pulmonary Congestion, Volume Overload

Nitrates / Diuretics ↓ preload, ↓ pulmonary pressure.

Atrial Fibrillation, SVT, Ventricular Tachyarrhythmias

Antiarrhythmics, β-Blockers, CCBs, Digoxin stabilize rhythm.

Heart Failure, Shock, Cardiomyopathy

Positive Inotropes (Digoxin, Dobutamine, Milrinone) ↑ Ca²⁺ → ↑ contractility, ↑ cardiac output.

Coronary Artery Disease, Angina, MI

Nitrates, CCBs, Antiplatelets, Statins dilate arteries, prevent thrombosis, and stabilize plaques.

Chronic Hypertension

Combination Antihypertensives (ACEI + CCB ± Diuretic ± β-blocker) lower CO or SVR → restore normal MAP and prevent organ damage.

Atherosclerosis, Endothelial Dysfunction

Statins / Antiplatelets enhance NO production, reduce LDL oxidation, and prevent plaque rupture and clot formation.

HTN, CAD, HF, Tachycardia

Beta-blockers press the brake → slow, steady, efficient beats.

HTN, HF

ACEIs/ARBs relax vessels → easier pumping, lower BP.

HF, CKD, HTN

Diuretics / ACEIs / ARBs make kidneys release salt & water → less volume.

Angina, HTN, Arrhythmia

Calcium blockers limit calcium → heart & vessels relax.

HF, Pulmonary Congestion

Nitrates / Diuretics drain extra fluid → easier breathing.

AFib, SVT, Tachyarrhythmia

Antiarrhythmics calm signals → steady rhythm again.

HF, Shock

Inotropes make each beat stronger → better circulation.

CAD, Angina, MI

Nitrates / Statins / Antiplatelets open or clear arteries → restore oxygen.

Chronic HTN

BP meds reset control → protect brain, heart, kidneys.

Atherosclerosis

Statins / Aspirin smooth and protect lining → prevent clots.