Week 5 Cardiac A

Flashcards for Cardiac A: Own-Time (week 5) lecture notes.

Cardiovascular System Function

To circulate blood throughout the body, delivering oxygen and nutrients to cells and removing waste products like carbon dioxide.

Cardiovascular Disease (CVD)

Umbrella term for diseases of the heart and blood vessels, including stroke and coronary artery disease.

Coronary Heart Disease (CHD)

A subcategory of CVD, referring to conditions affecting the heart's structure and function, primarily involving the coronary arteries through atherosclerosis.

Arteriosclerosis

A condition characterised by the thickening and stiffness of arterial walls.

Atherosclerosis

A common form of arteriosclerosis characterised by soft deposits of intra-arterial fat and fibrin along the vessel wall that hardens over time.

Fatty deposits (plaques) build up inside the walls of arteries. This makes the arteries narrow and stiff, reducing blood flow which can lead to heart attacks, strokes, or poor circulation

Hypertension (HT)

Condition in which blood pressure is consistently >140mmHg (systolic) and/or >90mmHg (diastolic).

Dyslipidaemia

An imbalance of lipids, such as cholesterol, low-density lipids (LDLs), triglycerides, and high-density lipids (HDLs).

Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome is a term used to describe a range of conditions caused by sudden, reduced blood flow to the heart.
It is usually due to a blocked coronary artery, and it’s a medical emergency.

It includes:

1. Unstable Angina

2. Non-ST Elevation Myocardial Infarction (NSTEMI)

3. ST Elevation Myocardial Infarction (STEMI)

Non-ST Elevation Infarction (NSTEMI)

Caused by prolonged ischaemia that leads to myocardial cellular death, without ST elevation on ECG but with detectable cardiac biomarkers.

ST Elevation Myocardial Infarction (STEMI)

ST segment will be elevated above the baseline on the 12-lead ECG; considered a life-threatening emergency.

Angina

Angina is chest pain or discomfort that happens when the heart muscle doesn’t get enough oxygen-rich blood.

It’s not a disease itself — it’s a symptom of coronary artery disease (CAD), usually due to narrowed or blocked coronary arteries.

Stable Angina

Predictable, transient chest discomfort precipitated by exertion or emotional stress, relieved by rest or medication (nitro-glycerine (GTN)) within a few minutes.

Unstable Angina

Chest pain that is new in onset, occurs at rest, and/or has a worsening pattern.

ECG

Electrocardiogram - a visual representation of the electrical conduction system of the heart.

Sinus Rhythm (SR)

Most common rhythm seen in healthy hearts, generated by the sinoatrial (SA) node.

Characteristics:

• Rate: 60-100 bpm

• Regularity: regular

• P wave: upright, rounded

• PR interval: 0.12-0.20 seconds (3-5 small squares)

• QRS complex: narrow >0.12 seconds (unless a ventricular conduction delay exists)

• Origin: sinus node

Atrial Fibrillation (AF)

The most common arrhythmia, resulting from abnormal electrical simulation in the atria and often resulting in an irregular ventricular contraction

Pharmacology of Hypertension

Drugs used to treat HT, generally fall into the class of:

• Diuretics

• Beta-Adrenergic Blockers

• Renin-Angiotensin-aldosterone inhibitors (i.e ACE inhibitors),

• Calcium Channel Blockers.

Statins

The most commonly used drug to treat dyslipidemia; works directly in the liver by competitively inhibiting HMG-CoA reductase

Pharmacology for ACS, Angina & AF

Anti-anginal drugs with the main physiological action of vasodilation. The most common medication used in this family of drugs is the organic nitrates

Non atheromatous arteriosclerosis

No atheromatous which means no atheroma or fat build up of the arteries which hardens due to age related scarring called fibrosis

Monkeberg's arteriosclerosis

The artery wall becomes hardened from calcium deposits

Hyaline arteriolosclerosis

Affects the small arteries and arterioles in people with diabetes. The artery wall thickens, narrows and weakens that can result in reduced or blocked blood flow

Hyperplastic arteriolosclerosis

This conditions leaves protein deposits along the artery wall that causes the arteries to thicken and narrows. People with hypertension have a higher risk of developing this condition

Pathophysiology of Atherosclerosis development

• 1. Endothelial Injury (Damage to artery wall)

  • The endothelium is the smooth inner lining of arteries.

  • It gets damaged by things like:

    • High blood pressure (hypertension)

    • High cholesterol (especially LDL)

    • Smoking

    • Diabetes

• 2. Inflammation Begins

  • After the damage, white blood cells (monocytes) move to the area.

  • These cells enter the artery wall and become macrophages, which start "eating" up cholesterol (especially LDL).

• 3. Fatty Streak Formation

  • The macrophages filled with fat turn into foam cells.

  • These foam cells create fatty streaks, the earliest sign of plaque buildup.

• 4. Plaque Formation

  • Over time, more fat, cholesterol, calcium, and immune cells build up.

  • A fibrous cap forms over this buildup, creating a plaque.

• 5. Plaque Growth and Narrowing of Arteries

  • As the plaque grows, it narrows the artery, reducing blood flow.

  • This causes ischemia (lack of oxygen) to tissues downstream — e.g., heart, brain, or limbs.

• 6. Plaque Rupture and Clot Formation (Thrombosis)

  • If the plaque breaks open, it triggers the clotting process.

  • A blood clot (thrombus) can form and block the artery completely → this can cause a:

    • Heart attack (if in coronary arteries)

    • Stroke (if in brain arteries)

    • Peripheral arterial disease (if in leg arteries)

Pathophysiology of hypertension

1. Narrowing (constriction) of blood vessels

• Blood vessels become less flexible or narrow, making it harder for blood to flow.

• This increases resistance → blood pressure goes up.

2. Overactive sympathetic nervous system

• The "fight or flight" system is overactive.

• Causes the heart to pump harder and blood vessels to constrict.

• Leads to increased heart rate and blood pressure.

3. Increased blood volume

• Often due to kidneys not working properly.

• Kidneys may retain too much salt (sodium) and water.

• More fluid = more blood volume = higher blood pressure.

4. Hormone imbalances (RAAS system)

• The Renin-Angiotensin-Aldosterone System (RAAS) helps control blood pressure.

• If it's overactive:

  • Renin from kidneys → causes production of angiotensin II (tightens blood vessels)

  • Aldosterone → causes salt and water retention

• This all leads to higher blood pressure.

Clinical manifestations of hypertension

• Dizziness, fatigue

• Palpitations and dyspnoea (difficulty breathing)

• Retitnal changes, papilloedema

• CHD/Angina/AC

Pathophysiology of Angina

• 1. Oxygen Demand vs. Oxygen Supply

  • The heart muscle needs oxygen to work properly.

  • When the oxygen demand is greater than the oxygen supply, the heart becomes ischemic (starved of oxygen).

  • This causes pain — this is angina.

• 2. Atherosclerosis is the main cause

  • Fatty plaques build up inside coronary arteries (atherosclerosis).

  • These plaques narrow the arteries, reducing blood flow to the heart, especially during exercise or stress when the heart needs more oxygen.

• 3. Temporary Ischemia, Not Permanent Damage

  • In angina, the reduced blood flow is usually temporary and doesn’t cause permanent heart damage (unlike a heart attack).

Pathophysiology of unstable angina

• 1. Plaque Rupture

  • In unstable angina, a plaque (fatty deposit) in a coronary artery becomes unstable and ruptures.

  • This causes the body to form a blood clot (thrombus) at the rupture site.

• 2. Partial Blockage of the Coronary Artery

  • The clot doesn’t fully block the artery, but it partially reduces blood flow to the heart muscle.

  • Because of this reduced oxygen supply, the heart becomes ischemic (oxygen-starved), especially during rest or mild activity.

• 3. Ongoing Ischemia, No Cell Death (Yet)

  • The ischemia causes chest pain, but there is no actual death of heart muscle cells at this stage (unlike in a heart attack).

  • However, it can progress quickly to a full heart attack (myocardial infarction) if the clot grows and fully blocks the artery.

Sinus Bradycardia characteristics

• Rate: Less than 60 bpm

• Regularity: Regular

• P wave: Upright, rounded

• PR interval: 0.12-0.20 seconds (3-5 small squares)

• QRS complex: narrow >0.12 seconds

• Origin: sinus node

Sinus tachnycardia characteristics

• Rate: Greater than 100 bpm

• Regularity: Regular

• P wave: Upright, rounded

• PR interval: 0.12-0.20 seconds (3-5 small squares)

• QRS complex: narrow >0.12 seconds

• Origin: sinus node

Occasinal (paroxysmal) AF

Atrial fibrillation and associated symptoms may come and go, usually lasting for a few minutes to a hours. The patient may or may not require treatment. 

Persistent AF

Atrial fibrillation lasts longer than a week and can become permanent. Treatment can include cardioversion, however, as the duration is generally unknown, medications would be the first treatment option.

Permanent AF

The rhythm has become a permanent condition for the patient, and the normal heart rate cannot be restored with interventions. At this stage, the patient will require specific medications to prevent the associated complications of AF (such as thrombus formation).

Causes of atrial fibrillation

• 1. Hypertension (High Blood Pressure)

  • Most common cause. Puts stress on the atria and can stretch them.

• 2. Coronary Artery Disease (CAD)

  • Blocked arteries reduce oxygen to the heart and can trigger arrhythmias.

• 3. Heart Failure

  • Weak pumping of the heart causes pressure to back up into the atria.

• 4. Valvular Heart Disease

  • Especially mitral valve disease, which affects blood flow between the atria and ventricles.

• 5. Post-Heart Surgery or Cardiac Procedures

  • Irritation or inflammation around the heart after surgery can trigger AF.

• 6. Congenital Heart Defects

Pathophysiology of atrial fibrillation

1. Electrical signals in the atria become chaotic

• Normally, the heart’s rhythm is controlled by the sinoatrial (SA) node, the natural pacemaker in the right atrium.

• In AF, multiple abnormal electrical impulses fire rapidly from different areas in the atria, especially near the pulmonary veins.

• These impulses override the SA node.

2. Atria quiver instead of contracting properly

• Because the electrical signals are disorganised, the atria don’t contract effectively — they quiver (fibrillate).

• This leads to inefficient blood flow from the atria to the ventricles (lower chambers).

3. Irregular ventricular response

• The chaotic signals are sent to the atrioventricular (AV) node, which filters and sends some signals to the ventricles.

• This causes the ventricles to beat irregularly and often too fast.

• The result: an irregular and often rapid pulse.

What this means for the body:

• Less effective pumping: Poor atrial contraction reduces how much blood is pushed into the ventricles.

• Blood pooling in the atria: Increases risk of blood clots, especially in the left atrial appendage.

• Clots can travel: This raises the risk of stroke if a clot moves to the brain.

• Reduced cardiac output: Especially in people with heart failure or other heart conditions.

Beta blockers

Also called beta-adrenergic blockers, medications that slow the heart down and reduce blood pressure.
They are commonly used to treat:

• Hypertension (high blood pressure)

• Angina

• Heart failure

• Atrial fibrillation

• Post-heart attack

How Do They Work?

1. Block the effects of adrenaline (epinephrine)

   • Beta blockers block beta receptors in the heart and blood vessels.

   • Normally, adrenaline binds to beta receptors to make the heart beat faster and stronger.

   • By blocking these receptors, beta blockers slow down the heart rate and reduce the force of contraction.

2. Result: ↓ Blood Pressure and ↓ Heart Workload

   • Slower heart rate → less cardiac output

   • Lower force of contraction → less pressure on the blood vessels

   • Overall, this helps to lower blood pressure and reduce strain on the heart.

Common beta blockers:

• Metoprolol

• Atenolol

Angiotensin- Converting Enzyme (ACE) Inhibitors

Help lower blood pressure and reduce strain on the heart.
They are commonly used to treat:

• Hypertension (high blood pressure)

• Heart failure

• After heart attacks

• To protect the kidneys, especially in people with diabetes

How Do ACE Inhibitors Work?

To understand this, think of the Renin-Angiotensin-Aldosterone System (RAAS), which helps regulate blood pressure:

1. When blood pressure drops, the kidneys release renin.

2. Renin converts a protein in the blood to angiotensin I.

3. ACE (angiotensin-converting enzyme) then converts angiotensin I into angiotensin II.

4. Angiotensin II causes:

   • Vasoconstriction (tightens blood vessels) → raises BP

   • Release of aldosterone → holds onto salt and water → increases blood volume

💊 ACE inhibitors block the enzyme that makes angiotensin II.
✅ This leads to:

• Vasodilation → wider blood vessels → lower BP

• Less aldosterone → less fluid retention → reduced blood volume

Common ACE inhibitors:

• Perindopril

Angiotensin II Receptor Blockers (ARBs)

ARBs (Angiotensin II Receptor Blockers) are medications that help lower blood pressure by relaxing blood vessels and reducing fluid retention.
They are used to treat:

• Hypertension (high blood pressure)

• Heart failure

• Kidney protection in diabetic patients

• After heart attacks (in some cases)

How Do ARBs Work?

To understand ARBs, you need to know about Angiotensin II — a hormone that raises blood pressure.

Here’s how it works:

1. The body makes angiotensin II when blood pressure is low.

2. Angiotensin II causes:

   • Vasoconstriction (tightening of blood vessels) → raises BP

   • Aldosterone release → kidneys keep salt and water → increases blood volume and BP

💊 ARBs block the receptors that angiotensin II normally binds to.

✅ So:

• Blood vessels stay relaxed and open → lower blood pressure

• Less aldosterone → less salt and water retention → reduced blood volume

Common ARBS:

• Losartan

• Candesartan

Calcium Channel Blockers (CCBs)

Calcium Channel Blockers (CCBs) are a class of medications that work by blocking calcium from entering cells in the heart and blood vessels. This reduces contraction strength, relaxes blood vessels, and lowers blood pressure.

How They Work:

• Calcium is essential for muscle contraction, including the heart and blood vessels.

• CCBs prevent calcium from entering smooth muscle cells in the blood vessels, leading to vasodilation (widening of blood vessels).

• They also reduce heart rate and contractility, making them useful for conditions like hypertension and angina.

Types of CCBs:

1. Dihydropyridines (e.g., amlodipine, nifedipine)

   • Primarily affect blood vessels, leading to vasodilation.

   • Used for hypertension and angina.

2. Non-Dihydropyridines (e.g., verapamil, diltiazem)

   • Affect both heart rate and blood vessels.

   • Used for arrhythmias, angina, and hypertension.

Diuretics

Help the body get rid of excess sodium and water by increasing urine production. They are commonly used to treat hypertension, heart failure, edema, and other conditions where fluid retention is an issue.

Types of Diuretics & How They Work:

1. Thiazide Diuretics (e.g., hydrochlorothiazide, chlorthalidone)

   • Act on the distal convoluted tubule in the kidneys.

   • Used for hypertension and mild edema.

   • Monitor for hypokalemia (low potassium) and dehydration.

2. Loop Diuretics (e.g., furosemide, bumetanide)

   • Act on the loop of Henle, causing stronger diuresis.

   • Used for severe edema, heart failure, and kidney disease.

   • Can cause hypokalemia, dehydration, and ototoxicity (hearing issues).

3. Potassium-Sparing Diuretics (e.g., spironolactone, amiloride)

   • Act on the collecting ducts to prevent potassium loss.

   • Used for heart failure and hyperaldosteronism.

   • Watch for hyperkalemia (high potassium).

Statins

Statins are cholesterol-lowering medications that work by inhibiting HMG-CoA reductase, an enzyme involved in cholesterol production in the liver. They help reduce low-density lipoprotein (LDL) cholesterol, often called "bad cholesterol," and can slightly increase high-density lipoprotein (HDL) cholesterol, or "good cholesterol."

How Statins Work:

• Block the enzyme HMG-CoA reductase, reducing cholesterol synthesis.

• Increase the liver's ability to remove LDL from the bloodstream.

• Help stabilise plaques in arteries, reducing the risk of heart attacks and strokes.

Ani-anginal medications (acute ischaemic therapies)

Anti-anginal medications, also known as acute ischaemic therapies, are drugs used to relieve chest pain (angina) and improve blood flow to the heart. These medications help manage coronary artery disease (CAD), myocardial infarction (heart attack), and other conditions related to ischemia (lack of oxygen supply to the heart).

Types of Anti-anginal Medications

1. Nitrates (e.g., Nitroglycerin, Isosorbide dinitrate)

   • Mechanism: Dilates blood vessels, reducing oxygen demand and improving blood flow.

   • Used for: Acute angina relief and long-term prevention.

   • Nursing Considerations: Watch for hypotension, headache, and dizziness; store sublingual tablets properly.

2. Beta-Blockers (e.g., Metoprolol, Atenolol)

   • Mechanism: Reduces heart rate and contractility, lowering oxygen demand.

   • Used for: Chronic angina, post-myocardial infarction therapy.

   • Nursing Considerations: Monitor heart rate and blood pressure, watch for bradycardia and fatigue.

3. Calcium Channel Blockers (CCBs) (e.g., Verapamil, Diltiazem, Amlodipine)

   • Mechanism: Relaxes blood vessels and reduces heart workload.

   • Used for: Prinzmetal's angina (vasospastic angina), stable angina.

   • Nursing Considerations: Watch for hypotension, edema, and dizziness.

4. Ranolazine (e.g., Ranexa)

   • Mechanism: Modifies sodium and calcium channels to reduce ischemic damage.

   • Used for: Chronic angina (when other therapies are insufficient).

   • Nursing Considerations: Monitor QT interval, avoid grapefruit juice.

5. Antiplatelet Agents (e.g., Aspirin, Clopidogrel)

   • Mechanism: Prevents platelet aggregation, reducing clot formation in arteries.

   • Used for: Acute coronary syndrome (ACS) and secondary prevention of ischemia.

   • Nursing Considerations: Watch for bleeding risk, GI irritation, and bruising.

Anti-platelet and Anti-thrombotic Medication

Anti-platelet and anti-thrombotic medications are blood-thinning agents used to prevent blood clots in patients at risk of conditions like stroke, heart attack, deep vein thrombosis (DVT), or pulmonary embolism (PE). They work by interfering with different clotting mechanisms.

1. Anti-Platelet Medications

These drugs prevent platelets (small blood cells involved in clotting) from clumping together, reducing the risk of arterial thrombosis. 🔹 Examples:

• Aspirin – Inhibits thromboxane A2, reducing platelet aggregation.

• Clopidogrel (Plavix) – Blocks ADP receptors on platelets, preventing activation.

• Ticagrelor (Brilinta) – Similar to Clopidogrel but has reversible action.

• Prasugrel (Effient) – Stronger than Clopidogrel, used for acute coronary syndrome (ACS).

2. Anti-Thrombotic (Anticoagulant) Medications

These drugs prevent blood clot formation by interfering with the coagulation cascade (clotting factors in the blood). 🔹 Examples:

• Heparin – Inhibits thrombin and fibrin formation; used for DVT, PE, ACS.

• Enoxaparin (Lovenox) – Low-molecular-weight heparin, with fewer bleeding risks.

• Warfarin (Coumadin) – Blocks vitamin K-dependent clotting factors; requires INR monitoring.

• Direct Oral Anticoagulants (DOACs):

  • Apixaban (Eliquis) & Rivaroxaban (Xarelto) – Factor Xa inhibitors (used for atrial fibrillation, DVT).

  • Dabigatran (Pradaxa) – Direct thrombin inhibitor.