2P07 Class 8

What blood pressure threshold defines hypertension?

A systolic blood pressure of 140 mm Hg or higher, or a diastolic blood pressure of 90 mm Hg or higher.

What is the primary difference between primary and secondary hypertension?

Primary hypertension has no single identifiable underlying cause, whereas secondary hypertension is directly attributable to a specific, correctable cause.

What happens to secondary hypertension once its specific underlying cause is identified and corrected?

The hypertension is removed.

Which two main physiological factors must increase to elevate arterial blood pressure?

Cardiac output or systemic vascular resistance (SVR).

What is considered the hallmark physiological abnormality of hypertension?

Increased systemic vascular resistance (SVR).

Approximately what percentage of people develop hypertension when consuming a high-sodium diet?

Approximately 20%.

How does excessive sodium intake contribute to fluid retention in hypertension?

It alters the pressure-natriuresis relationship, leading to water retention.

In the Renin-Angiotensin-Aldosterone System (RAAS), elevated plasma renin activity correlates with which biochemical conversion?

The conversion of angiotensinogen to angiotensin I.

What three major cardiovascular and endocrine effects are directly caused by Angiotensin II?

Arterial constriction, vascular hypertrophy, and induction of aldosterone secretion.

What is the primary action of aldosterone on renal function?

It promotes the reabsorption of sodium and water by the kidneys.

What three cardiorenal responses are triggered by Sympathetic Nervous System (SNS) activation during stress?

Increased vasoconstriction, elevated heart rate, and increased renin release.

How does hyperinsulinemia affect nitric oxide function in blood vessels?

Elevated insulin impairs nitric oxide-mediated vasodilation.

What structural change occurs in blood vessels due to insulin acting as a growth hormone?

Vascular hypertrophy.

Which specific subclass of Endothelin produced by endothelial cells acts as a potent vasoconstrictor?

Endothelin-1 (ET-1).

Which two endothelial-derived substances involved in vascular tone regulation may be impaired in hypertensive individuals?

Nitric Oxide and Endothelin-1 (ET-1).

What inflammatory and metabolic substances are secreted by enlarged adipocytes in visceral adipose tissue?

Leptin, proinflammatory cytokines, and reactive oxygen species.

What are the four core goals of nursing care considerations for hypertension?

1. Achieve and maintain target BP; 2. Understand and accept the therapeutic plan; 3. Experience minimal or no adverse therapeutic effects; 4. Be confident in managing the condition.

What are the six key elements included in home and ambulatory care for hypertension?

Nutritional therapy, medication therapy, physical activity, home BP monitoring, tobacco cessation, and stress management.

In cardiac electrophysiology, what is automaticity?

The ability of cardiac cells to initiate an electrical impulse spontaneously and continuously.

In cardiac electrophysiology, what is contractility?

The ability of cardiac cells to respond mechanically to an electrical impulse.

In cardiac electrophysiology, what is conductivity?

The ability of cardiac cells to transmit an electrical impulse along a membrane in an orderly manner.

In cardiac electrophysiology, what is excitability?

The ability of cardiac cells to be electrically stimulated.

What heart rate defines Sinus Bradycardia?

A sinoatrial (SA) node impulse rate of less than 60 beats per minute.

When does Sinus Bradycardia become clinically problematic?

When the client exhibits symptoms of inadequate tissue perfusion.

What heart rate defines Sinus Tachycardia?

A sinoatrial (SA) node impulse rate of more than 100 beats per minute.

Where does the electrical impulse originate in a Premature Atrial Contraction (PAC)?

From an ectopic focus in either of the atria outside the SA node.

Where must an ectopic focus originate to cause Paroxysmal Supraventricular Tachycardia (PSVT)?

Anywhere above the bifurcation of the bundle of His.

What dynamic mechanism causes Paroxysmal Supraventricular Tachycardia (PSVT)?

A re-entrant phenomenon.

What does the term 'paroxysmal' signify in PSVT?

Sudden onset and termination.

Where does the ectopic focus originate in Atrial Flutter?

From a single ectopic focus in the right atrium.

What electrophysiological mechanism causes Atrial Fibrillation?

Totally disorganized atrial electrical activity caused by many ectopic foci.

Where do Junctional Dysrhythmias originate relative to the AV node?

Outside of the AV node.

What P-wave abnormality occurs in Junctional Dysrhythmias due to retrograde conduction?

An abnormal P wave.

Where does the ectopic focus originate in Premature Ventricular Contractions (PVCs)?

In the ventricles.

What occurs during Ventricular Tachycardia when ectopic foci repeatedly fire?

They repeatedly initiate ventricular contractions, overriding the primary pacemaker.

What electrical mechanism causes Ventricular Fibrillation?

Rapid, chaotic firing of many ectopic foci in the ventricles.

What defines Asystole?

The total absence of ventricular electrical activity.

What defines Pulseless Electrical Activity (PEA)?

The presence of electrical activity on the monitor without corresponding mechanical myocardial activity.

What is the primary underlying cause of Coronary Artery Disease (CAD)?

Atherosclerosis.

In which arterial wall layer do lipid deposits accumulate during CAD development?

The intima of the artery.

Which two pathological processes are central to the development of CAD?

Endothelial injury and inflammation.

What composes the yellow-tinged fatty streak stage of CAD?

Lipid-filled smooth muscle cells within the arterial intima.

What factors stimulate smooth muscle proliferation and arterial wall thickening during fibrous plaque formation?

Low-Density Lipoproteins (LDLs) and platelet-derived growth factors.

How does fibrous plaque formation impact coronary blood flow?

It narrows the vessel lumen, reducing blood flow.

What is the main physiological role of Low-Density Lipoproteins (LDLs)?

Delivering cholesterol to peripheral tissues.

How do hepatic receptors regulate serum LDL levels?

By binding circulating LDL and limiting endogenous liver synthesis.

What initial step triggers endothelial cells to express adhesion molecules that bind inflammatory cells?

Endothelial cell injury and inflammation.

What causes the oxidation of LDL accumulated within the vessel intima?

Toxic oxygen free radicals generated by activated macrophages during the inflammatory process.

How are foam cells formed within the vessel intima?

Macrophages enter the intima and engulf oxidized LDL.

How do fatty streaks induce progressive damage to the arterial wall?

By generating toxic oxygen free radicals, recruiting T lymphocytes to drive autoimmunity, and secreting inflammatory mediators.

What triggers smooth muscle cell migration over the fatty streak to form a fibrous plaque?

Growth factors released by macrophages.

What is the most dangerous stage of an atherosclerotic lesion?

The complicated lesion.

What event immediately follows the rupture or ulceration of a fibrous plaque?

Platelets accumulate and adhere to the inner wall, forming a thrombus.

Which receptor is expressed on activated exposed platelets to bind fibrinogen and cause further aggregation?

Glycoprotein IIb/IIIa receptors.

Under what condition does Acute Coronary Syndrome (ACS) develop?

When myocardial ischemia is prolonged and not immediately reversible.

Which three clinical entities are included under Acute Coronary Syndrome (ACS)?

Unstable angina, non-STEMI, and STEMI.

At what percentage of arterial lumen narrowing does coronary blood flow become impaired enough to impede cellular metabolism during increased demand?

Narrowing of 50% or more.

How many seconds of complete coronary occlusion cause myocardial ischemia?

10 seconds.

For approximately how long can cardiac myocytes sustain ischemic conditions before infarction occurs?

Approximately 20 minutes.

What three electrocardiography (ECG) changes signal myocardial ischemia?

ST segment depression, T wave inversion, or ST segment elevation.

At which spinal cord levels do afferent sympathetic nerves enter to transmit chest pain in stable angina?

Levels C3 to T4.

What physiological mechanism causes Prinzmetal's (variant) angina?

Vasospasm of one or more large coronary arteries.

Which two inflammatory markers are typically elevated in clients with Prinzmetal's angina?

C-reactive protein (CRP) and Interleukin-6 (IL-6).

What key clinical characteristics distinguish Unstable Angina from Stable Angina?

Unstable angina is new in onset, occurs at rest, or presents with an increasingly worsening pattern.

What key pathological outcome distinguishes a Myocardial Infarction from Unstable Angina?

Prolonged vessel occlusion resulting in myocyte necrosis and cell death.

What is the anatomical extent of tissue damage in a subendocardial infarction (non-STEMI)?

Damage is limited to the inner endocardial layer.

What is the anatomical extent of tissue damage in a transmural infarction (STEMI)?

Infarction covers the entire depth of the myocardium.

Within how many seconds of complete blood flow cessation are myocardial oxygen reserves depleted?

Within approximately 8 seconds.

Why is the accumulation of lactic acid during anaerobic metabolism particularly problematic for myocardium?

The myocardium is highly sensitive to pH alterations and has poor buffering capacity.

Which key intracellular electrolytes are lost from myocytes during acute myocardial oxygen deficits?

Potassium, Calcium, and Magnesium.

Why are elevated levels of Free Fatty Acids (FFAs) harmful during ischemic catecholamine release?

High FFA levels are harmful to cell membranes.

How does Angiotensin II activation during myocardial ischemia alter vascular tone and structure?

It increases peripheral vasoconstriction, promotes fluid retention, and causes myocardial structural remodeling.

What cellular mechanism triggers myocyte death during reperfusion injury?

Release of toxic oxygen free radicals, calcium flux, and pH changes that open mitochondrial permeability transition pores.

Which specific enzyme and structural protein are released into circulation upon irreversible necrotic myocyte injury?

Creatine phosphokinase-myocardial bound (CPK-MB) and troponins.

What is myocardial stunning?

A temporary loss of contractile function in surviving tissue surrounding the site of infarction.

How does recurrent angina prior to an MI benefit myocardial tissue survival?

It prepares the myocardium to deal with oxygen deprivation, decreasing stunning and preserving cells.

List four key functional changes of the heart that are dictated by the size of a myocardial infarct.

1. Decreased contractility; 2. Altered left ventricular compliance; 3. Decreased stroke volume/ejection fraction; 4. Increased left ventricular end-diastolic pressure (or SA node malfunction).

What inflammatory event occurs at the infarction site 24 hours post-MI?

Leukocyte infiltration of the necrotic area, where neutrophils use proteolytic enzymes to break down necrotic tissue.

What is the structural condition of the wound matrix 10 to 14 days post-MI?

A weak, soft, and vulnerable collagen matrix has developed.

How long after a Myocardial Infarction is necrotic tissue fully replaced by strong, non-contractile scar tissue?

After 6 weeks.

MI Pathophysiology:

What time period for - Weak, soft and vulnerable collagen matrix is developed

10-14 days

MI Pathophysiology:

What time period for - Leukocyte infiltration of necrotic area and neutrophils use proteolytic enzymes to break down necrotic tissue

24 hours

Size of infarct dictates significance of function change including:

1. decreased contractility and altered wall motion

2. altered left ventricular compliance

3. decreased stroke volume

4. decreased ejection fraction

5. increased left ventricular end diastolic pressure

6. sinoatrial node malfunction

term - the clinical manifestation of reversible ischemia caused by narrowing of the lumen

angine (chest pain)

During a myocardial infarction, explain what happens to glycogen and which system takes over and explain

• glycogen reserves are quickly depleted

• anaerobic metabolism take over resulting in increased production and accumulation of H+ and lactic acid

• this is a problem because myocardium is highly sensitive to pH alterations and has poor buffering capacity