Cardiology Concepts and ECG Interpretations
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Questions and Answers

What is the definitive treatment for AVNRT?

  • Vagal maneuvers
  • Catheter ablation targeting the slow pathway (correct)
  • Catheter ablation of the accessory pathway
  • Administration of beta-blockers

Which feature is indicative of Slow-Fast AVNRT on an ECG?

  • Narrow QRS complex with retrograde P waves (correct)
  • Regularly spaced R-R intervals
  • Presence of T-wave inversions
  • Wide QRS complex

Which of the following is the first-line therapy for the acute termination of AVNRT?

  • Adenosine
  • Vagal maneuvers (correct)
  • Calcium channel blockers
  • Catheter ablation

What condition can increase the risk of gastroesophageal reflux disease (GERD)?

<p>Weak lower esophageal sphincter (D)</p> Signup and view all the answers

What effect does hypocalcemia have on the myocardial contractions?

<p>Decreases myocardial contractions due to decreased calcium-induced calcium release. (D)</p> Signup and view all the answers

What triggers transient relaxation of the lower esophageal sphincter in GERD?

<p>Alcohol consumption (D)</p> Signup and view all the answers

Which of the following ECG manifestations is associated with hypocalcemia?

<p>Prolonged QT interval. (A)</p> Signup and view all the answers

How does hypernatremia primarily influence depolarization?

<p>It slightly speeds up depolarization and may shorten action potential duration. (B)</p> Signup and view all the answers

Which of the following is NOT a complication associated with untreated GERD?

<p>Increased gastric acid production (D)</p> Signup and view all the answers

Which ECG feature may be observed in severe cases of hyponatremia?

<p>Prolonged PR interval. (C)</p> Signup and view all the answers

Which of these factors can contribute to the development of GERD?

<p>Transient lower esophageal sphincter relaxation (C)</p> Signup and view all the answers

What is the expected effect of hypermagnesemia on cardiac conduction?

<p>Slows down conduction but does not affect ECG. (A)</p> Signup and view all the answers

What role does delayed gastric emptying play in GERD?

<p>It prolongs the potential for reflux to occur. (B)</p> Signup and view all the answers

What is a potential ECG manifestation of hypomagnesemia?

<p>Early afterdepolarization. (D)</p> Signup and view all the answers

Which of the following best describes the effect of hyponatremia on overall cell excitability?

<p>Decreases overall cell excitability. (B)</p> Signup and view all the answers

How does hypernatremia affect the QRS complex?

<p>It may cause a mild increase in QRS amplitude. (D)</p> Signup and view all the answers

What are the components of Charcot's Triad?

<p>Fever, Jaundice, RUQ Pain (D)</p> Signup and view all the answers

Which treatment is considered emergent for jaundice caused by biliary obstruction?

<p>Emergent ERCP (C)</p> Signup and view all the answers

What does MRCP stand for and what is its primary use?

<p>Magnetic Resonance Cholangiography, for bile duct visualization (D)</p> Signup and view all the answers

In the liver lobule structure, what is the role of the sinusoids?

<p>Receive mixed blood from the hepatic arteriole and portal venule (A)</p> Signup and view all the answers

Which of the following best describes the function of hepatocytes?

<p>Store nutrients and produce bile (C)</p> Signup and view all the answers

Which of the following statements about the portal triad is true?

<p>It consists of a hepatic arteriole, a bile ductule, and a portal venule. (D)</p> Signup and view all the answers

What additional symptoms are included in Reynold's Pentad?

<p>Hypotension and altered mental status (B)</p> Signup and view all the answers

What is the anatomical path of blood from the abdominal aorta to the hepatic vein?

<p>Abdominal aorta → Celiac trunk → Common hepatic artery → Portal vein → Central vein (A)</p> Signup and view all the answers

What ECG manifestation is commonly associated with hypokalemia?

<p>Prolonged QT interval (D)</p> Signup and view all the answers

Which type of cells has a longer refractory period due to the presence of a plateau phase?

<p>Cardiac myocytes (C)</p> Signup and view all the answers

What mechanism is primarily activated due to decreased renal perfusion during lactate accumulation?

<p>Renin-Angiotensin-Aldosterone System (A)</p> Signup and view all the answers

What does the absolute refractory period (ARP) indicate?

<p>Cell is completely unexcitable (D)</p> Signup and view all the answers

Which symptom is NOT commonly associated with lactate accumulation and metabolic acidosis?

<p>Elevated blood pressure (C)</p> Signup and view all the answers

During which phases are fast Na⁺ channels inactivated leading to the ARP?

<p>Phase 0, 1, and 2 (C)</p> Signup and view all the answers

How does catecholamine release affect myocardial oxygen demand?

<p>Increases heart rate and afterload (C)</p> Signup and view all the answers

What physiological role does the long refractory period serve in the ventricles?

<p>It prevents tetanic contractions (D)</p> Signup and view all the answers

What characterizes the effective refractory period (ERP)?

<p>Cell can depolarize but not propagate (A)</p> Signup and view all the answers

What is the primary consequence of elevated left ventricular end-diastolic pressure (LVEDP)?

<p>Backflow of blood into pulmonary circulation (D)</p> Signup and view all the answers

Which treatment option is typically used to support mechanical circulation?

<p>Intra-aortic balloon pump (IABP) (D)</p> Signup and view all the answers

What is the primary determinant of the refractory period in nodal cells?

<p>Recovery of L-type Ca²⁺ channels (D)</p> Signup and view all the answers

What happens to the voltage-gated Na⁺ channels during phases of an action potential?

<p>They cycle through resting, activated, and inactivated states (D)</p> Signup and view all the answers

What effect does high blood osmolarity have on antidiuretic hormone (ADH) release?

<p>Enhances ADH release (D)</p> Signup and view all the answers

Which hemodynamic parameter is expected to be LOW in the context of lactate accumulation?

<p>Cardiac Output (CO) (D)</p> Signup and view all the answers

What is a potential sequela of high myocardial oxygen demand coupled with low oxygen delivery?

<p>Worsened myocardial injury (C)</p> Signup and view all the answers

What is the primary function of Kupffer cells in the liver?

<p>Immune surveillance and breakdown of old red blood cells (D)</p> Signup and view all the answers

Which zone of the liver lobule is most resistant to ischemia?

<p>Zone 1 (Periportal Zone) (D)</p> Signup and view all the answers

What is the role of stellate cells in the liver?

<p>Storage of fat and fat-soluble vitamins (B)</p> Signup and view all the answers

What metabolic activities are primarily associated with Zone 3 (Centrilobular Zone)?

<p>Detoxification and lipogenesis (C)</p> Signup and view all the answers

Which liver condition is characterized by chronic damage leading to fibrosis?

<p>Cirrhosis (C)</p> Signup and view all the answers

Which statement regarding the Space of Disse is correct?

<p>It serves as an exchange space between sinusoids and hepatocytes. (D)</p> Signup and view all the answers

Which zone of the liver lobule is the least oxygenated and most vulnerable to damage?

<p>Zone 3 (Centrilobular Zone) (B)</p> Signup and view all the answers

What is a hallmark of lobular injury in hepatic diseases?

<p>Loss of lobular structure (D)</p> Signup and view all the answers

What condition is characterized by the obstruction of bile flow due to gallstones in the common bile duct?

<p>Choledocholithiasis (B)</p> Signup and view all the answers

Which symptom is typically associated with cholangitis due to biliary obstruction?

<p>Severe jaundice (C)</p> Signup and view all the answers

What is the primary purpose of performing an MRCP in the diagnosis of gallstone disease?

<p>To confirm the presence of CBD stones non-invasively (B)</p> Signup and view all the answers

Which laboratory finding is most indicative of cholestasis due to biliary obstruction?

<p>Markedly elevated ALP/GGT levels (C)</p> Signup and view all the answers

What complication can occur if choledocholithiasis is left untreated?

<p>Cholangitis or pancreatitis (A)</p> Signup and view all the answers

What effect does hyperkalemia have on the duration of the action potential?

<p>It shortens the action potential duration. (C)</p> Signup and view all the answers

What is an ECG manifestation associated with hypokalemia?

<p>U wave. (A)</p> Signup and view all the answers

How does hypercalcemia primarily affect the refractory period of cardiac myocytes?

<p>It decreases the refractory period. (C)</p> Signup and view all the answers

What clinical risk is associated with prolonged QT interval as a result of hypokalemia?

<p>Torsade de pointes. (C)</p> Signup and view all the answers

What happens to the resting membrane potential (RMP) during hyperkalemia?

<p>It becomes more positive. (A)</p> Signup and view all the answers

What is a significant effect of hypocalcemia on the myocardial contraction process?

<p>Decreased strength of contraction. (C)</p> Signup and view all the answers

How does the T wave manifest on an ECG during hyperkalemia?

<p>It shows a sine-wave pattern. (C)</p> Signup and view all the answers

What effect does calcium-induced calcium release have on myocardial contractility during hypercalcemia?

<p>Increases myocardial contractility. (C)</p> Signup and view all the answers

What is a consequence of H. pylori infection on the stomach lining?

<p>Increased damage to acid-producing cells (C)</p> Signup and view all the answers

What is the primary effect of chronic NSAID use on the stomach?

<p>Reduced prostaglandin production (C)</p> Signup and view all the answers

How does smoking affect the gastric mucosa?

<p>Increases acid production (B)</p> Signup and view all the answers

What leads to duodenal ulcer formation in the context of H. pylori infection?

<p>Increased acid flow into the duodenum (A)</p> Signup and view all the answers

What effect does damage to the acid-producing cells have in the stomach?

<p>Reduced acid production (B)</p> Signup and view all the answers

What role does urease play in H. pylori infection?

<p>Increases inflammation (C)</p> Signup and view all the answers

Which of the following leads to hypochlorhydria in diffuse gastritis?

<p>Damage to the parietal cells (C)</p> Signup and view all the answers

What is a common effect of NSAIDs on the gastric mucosal lining?

<p>Decreased blood flow to the gastric mucosa (D)</p> Signup and view all the answers

Which phase of the myocyte action potential is characterized by rapid depolarization due to sodium influx?

<p>Phase 0 (Rapid Depolarization) (C)</p> Signup and view all the answers

During which phase does the calcium-induced calcium release (CIRC) occur?

<p>Phase 2 (Plateau Phase) (C)</p> Signup and view all the answers

What is the primary ion flow during Phase 3 of the myocyte action potential?

<p>Increased K⁺ efflux (A)</p> Signup and view all the answers

What is maintained by the Na⁺/K⁺-ATPase during the resting membrane potential?

<p>A negative charge inside the cell (C)</p> Signup and view all the answers

Which phase corresponds with the T wave on the ECG?

<p>Phase 3 (Rapid Repolarization) (A)</p> Signup and view all the answers

What initiates depolarization in cardiac myocytes?

<p>Na⁺ and Ca²⁺ entering the cell (B)</p> Signup and view all the answers

Which phase is responsible for maintaining a stable myocardium contraction duration?

<p>Phase 2 (Plateau Phase) (B)</p> Signup and view all the answers

At what membrane potential do voltage-gated Na⁺ channels begin to open?

<p>-70 mV (B)</p> Signup and view all the answers

What is the primary function of Phase II reactions in drug metabolism?

<p>To convert lipid-soluble toxins into water-soluble forms (D)</p> Signup and view all the answers

Which of the following enzymes is involved in alcohol metabolism?

<p>Acetaldehyde dehydrogenase (A), Alcohol dehydrogenase (C)</p> Signup and view all the answers

What is the role of Kupffer cells in the liver?

<p>To filter pathogens and debris from the blood (B)</p> Signup and view all the answers

What primarily determines coagulation times, specifically the Prothrombin Time (PT)?

<p>The presence of Factor VII (B)</p> Signup and view all the answers

How does the liver contribute to glucose homeostasis?

<p>By regulating insulin and glucagon interactions (D)</p> Signup and view all the answers

Which process is NOT performed by the liver in the context of detoxification?

<p>Synthesizing steroid hormones (D)</p> Signup and view all the answers

Which type of compounds does the liver primarily convert through Phase I reactions?

<p>Lipid-soluble metabolites to active forms (B)</p> Signup and view all the answers

What are the major polar groups that drugs are conjugated with during Phase II reactions?

<p>Various polar groups via transferase enzymes (A)</p> Signup and view all the answers

What condition is indicated by severe hepatocellular damage and may lead to mixed hyperbilirubinemia?

<p>Hepatitis (D)</p> Signup and view all the answers

Which symptom is NOT commonly associated with cholelithiasis?

<p>Persistent RUQ pain lasting more than 6 hours (A)</p> Signup and view all the answers

What is a key differentiating factor between cholecystitis and cholelithiasis?

<p>Cholecystitis involves inflammation and infection. (B)</p> Signup and view all the answers

Which are risk factors for developing cholelithiasis?

<p>Females over 40 years old (C)</p> Signup and view all the answers

Which of the following statements about Dubin-Johnson Syndrome is true?

<p>It is characterized by defective hepatic transport, leading to conjugated hyperbilirubinemia. (A)</p> Signup and view all the answers

What is a common complication associated with untreated cholecystitis?

<p>Gallbladder perforation (C)</p> Signup and view all the answers

Which symptom is often used to diagnose cholecystitis?

<p>Murphy's Sign (B)</p> Signup and view all the answers

In what condition does bile stasis occur due to gallstone obstruction?

<p>Cholecystitis (C)</p> Signup and view all the answers

Flashcards

Lactate accumulation

Leads to metabolic acidosis in the body.

SNS compensatory mechanism

Increased heart rate (tachycardia) and vasoconstriction (increased SVR) to compensate for low blood flow, raising myocardial oxygen demand.

RAAS compensatory mechanism

Activated by low blood pressure, it increases systemic vascular resistance (SVR) and fluid retention, leading to congestion.

ADH compensatory mechanism

Conserves water, increasing preload, but exacerbates heart failure congestion.

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Metabolic acidosis symptoms

Low blood pressure (hypotension), fast heart rate (tachycardia), cold clammy skin, shortness of breath (SOB), altered mental status (AMS), and low urine output (UO).

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Hemodynamic profile in metabolic acidosis

Low cardiac output (CO), mean arterial pressure (MAP), and mixed venous oxygen saturation (SvO2); high systemic vascular resistance (SVR), central venous pressure (CVP), and pulmonary capillary wedge pressure (PCWP).

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Treatment for metabolic acidosis

Inotropes, vasopressors, mechanical support (e.g., IABP, Impella), revascularization (PCI, CABG).

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IABP (Intra-Aortic Balloon Pump)

A mechanical device that improves cardiac function by increasing coronary perfusion during diastole and reducing afterload during systole.

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Absolute Refractory Period (ARP)

The time during an action potential when a cell is completely unresponsive to a new stimulus.

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Effective Refractory Period (ERP)

The period where a stimulus might trigger a weak depolarization, but it won't spread to other cells.

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Refractory Period Myocytes

The time during an action potential when a heart cell is resistant or unresponsive to a new stimulus.

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Voltage-gated Na⁺ Channels

Channels that control sodium flow; crucial for action potentials, influenced by the membrane potential.

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Prolonged QT Interval

A longer-than-normal time for the heart's electrical activity between a beat's start and end.

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Torsades de Pointes

An irregular and dangerous heart rhythm associated with a prolonged QT interval.

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Nodal Cells

Heart cells that initiate electrical signals (pacemaking), having a shorter refractory period than other heart cells.

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Hypokalemia

Low potassium in the blood, linked with heart rhythm issues and ECG changes like a prolonged QT interval.

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Hypocalcemia Effect on Cardiac Action Potential

Hypocalcemia prolongs the plateau phase (phase 2) of the cardiac action potential, increasing action potential duration and refractory period. This leads to decreased myocardial contractions and negative inotropy (reduced contractility).

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Hypocalcemia ECG Manifestation

Hypocalcemia causes a prolonged QT interval, increasing the risk of torsades de pointes, a potentially fatal heart rhythm disorder.

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Hypernatremia Effect on Depolarization

Hypernatremia slightly speeds up depolarization (phase 0) of the cardiac action potential; this may shorten the action potential duration.

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Hypermagnesemia Effect on ECG

Severe hypermagnesemia can prolong the PR interval and widen the QRS complex due to slowed conduction.

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Hypomagnesemia Effect

Hypomagnesemia affects potassium handling, which potentially promotes early afterdepolarization, a situation with increased risk for arrhythmias.

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Hyponatremia Effect on Depolarization

Hyponatremia slightly slows down depolarization (phase 0) and may increase action potential duration, affecting cell excitability. Severe cases can cause flattened or broad QRS complexes.

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Hyponatremia ECG Manifestation

Hyponatremia can lead to prolonged PR intervals (due to slowed conduction).

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Sodium Derangement ECG Effects

Sodium imbalance generally causes subtle changes to the ECG, primarily affecting depolarization (phase 0).

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Kupffer Cells

Specialized macrophages in liver sinusoids involved in immune response and red blood cell breakdown.

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Bile Canaliculi

Small channels between hepatocytes where bile is secreted and transported to bile ducts.

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Space of Disse

Exchange space between sinusoids and hepatocytes allowing nutrient/waste exchange.

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Stellate Cells

Liver cells storing fat-soluble vitamins (A, D, E, K) and involved in liver repair.

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Zone 1 (Periportal)

Liver zone near portal triad, receiving most oxygenated blood; active in oxidative metabolism.

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Zone 3 (Centrilobular)

Liver zone near central vein receiving least oxygen; active in glycolysis, detoxification.

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Cirrhosis

Chronic liver damage leading to scarring and disruptive liver structure.

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Hepatic Diseases

Conditions causing liver damage, often involving lobular injury.

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AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

Reentrant tachycardia that occurs within the AV node, involving two pathways with different conduction speeds.

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Slow Pathway (AVNRT)

A slower conduction pathway in the AV node with a shorter refractory period. It is part of the loop used for reentrant tachycardia in AVNRT.

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Fast Pathway (AVNRT)

Normal conduction pathway in the AV node with rapid conduction and slow refractory period. Part of the loop used for reentrant tachycardia in AVNRT.

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GERD (Gastroesophageal Reflux Disease)

Chronic condition where stomach contents flow back into the esophagus, resulting in symptoms like heartburn.

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Lower Esophageal Sphincter (LES) Dysfunction

Failure of the LES to prevent reflux of stomach acid triggered by meals, alcohol, or food.

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Increased Intra-Abdominal Pressure

Higher abdominal pressure that may force stomach acid back into the esophagus.

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Catheter Ablation (AVNRT)

A definitive treatment for AVNRT that targets the slow pathway that creates the reentrant loop.

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Adenosine (AVNRT)

First-line medical treatment for acutely terminating AVNRT by blocking the AV node.

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Jaundice Cause

Elevated conjugated bilirubin in the blood, leading to yellowing of the skin and eyes, and dark urine and pale stools.

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Charcot's Triad

A medical finding characterized by fever, jaundice, and right upper quadrant (RUQ) pain, often associated with severe liver disease.

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Reynold's Pentad

Charcot's Triad plus hypotension (low blood pressure) and altered mental status (AMS).

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Liver Lobule

Structural and functional unit of the liver, shaped like a hexagon.

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Portal Triad

A key component of the liver lobule, consisting of the hepatic arteriole, portal venule, and bile ductules.

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Hepatocyte Plate

Rows of liver cells within the liver lobule, crucial for detoxification and bile production.

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Sinusoid

Capillary-like spaces between hepatocyte plates, where blood from the hepatic artery and portal vein mixes and exchanges substances with hepatocytes

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Treatment for Cholangitis

Emergent ERCP (Endoscopic Retrograde Cholangiopancreatography) for diagnostic and therapeutic purposes, along with broad-spectrum IV antibiotics, often Piperacillin-Tazobactam (Zosyn) as a single agent or ceftriaxone + metronidazole as a combination.

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Choledocholithiasis

Presence of gallstones in the common bile duct, leading to obstruction of bile flow.

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Cholangitis

Infection of the biliary tree caused by obstruction, usually by gallstones, leading to bile stasis and bacterial infection.

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What does elevated ALP/GGT indicate?

Elevated ALP/GGT levels indicate cholestasis and biliary obstruction, suggesting a problem with the flow of bile.

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What are the symptoms of choledocholithiasis?

Symptoms include severe right upper quadrant pain, nausea and vomiting, jaundice due to conjugated hyperbilirubinemia, dark urine, and pale stools.

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What is the standard treatment for choledocholithiasis?

Ultrasound is used for diagnosis, MRCP is the gold standard, ERCP is done for stone removal, and elective cholecystectomy is performed to prevent recurrence.

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Hyperbilirubinemia

Increased bilirubin levels in the blood, causing yellowing of the skin and eyes, and dark urine and pale stools.

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Biliary Obstruction

blockage of the bile ducts, leading to the buildup of bile in the liver and gallbladder.

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Liver Disease

Conditions affecting the liver's function, leading to impaired excretion of bilirubin.

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Cholelithiasis

Presence of gallstones in the gallbladder, often asymptomatic but can cause biliary colic.

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Cholecystitis

Inflammation of the gallbladder, usually caused by gallstones blocking the cystic duct.

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Biliary Colic

Intense, intermittent pain in the right upper quadrant of the abdomen, typically triggered by fatty meals.

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Murphy's Sign

Sharp pain in the right upper quadrant upon palpation during inspiration, indicative of cholecystitis.

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H. pylori Infection

A bacterial infection that colonizes the stomach lining, leading to various complications including ulcers and gastritis. It damages the protective mucus layer, increases inflammation, and alters acid production.

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Gastritis

Inflammation of the stomach lining, often caused by H. pylori infection, NSAID use, or other factors.

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Duodenal Ulcer

A sore or erosion in the lining of the duodenum, often caused by excessive acid exposure, commonly due to H. pylori infection or NSAID use.

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Gastric Ulcer

A sore or erosion in the stomach lining, usually caused by a combination of factors including H. pylori infection, NSAID use, and lifestyle factors.

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NSAIDs and Gastric Mucosa

Nonsteroidal anti-inflammatory drugs (NSAIDs) can damage the protective lining of the stomach by reducing prostaglandins, decreasing mucus and bicarbonate secretion, and impairing blood flow. This can lead to ulcers.

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Lifestyle Factors and Ulcers

Smoking, alcohol consumption, and stress can contribute to the development and worsening of ulcers by impairing mucosal healing, increasing acid production, and disrupting the digestive system.

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Hyperacidity

Excessive acid production in the stomach, often caused by increased gastrin production, which can lead to ulcers and other problems.

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Hypochlorhydria

Reduced acid production in the stomach, often caused by damage to acid-producing cells, which can weaken the protective mucus layer and contribute to ulcers.

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Resting Membrane Potential

The electrical charge across the membrane of a cardiac myocyte when it's not actively conducting an impulse. This is typically around -90mV.

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Depolarization

The process of the cell membrane becoming less negative (more positive) due to the influx of positive ions like sodium (Na⁺) and calcium (Ca²⁺).

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What is the threshold potential?

The minimum voltage that must be reached for a cardiac myocyte to initiate an action potential. It's around -70 mV.

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Phase 0: Rapid Depolarization

The initial phase of the cardiac action potential where there's a rapid influx of sodium ions (Na⁺) through voltage-gated sodium channels, making the cell membrane less negative (more positive).

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Phase 2: Plateau Phase

A period of prolonged depolarization where calcium ions (Ca²⁺) enter the cell through L-type calcium channels while potassium ions (K⁺) exit. This balance creates a plateau.

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Phase 3: Rapid Repolarization

The phase where the cell returns to its resting membrane potential (-90mV) as potassium ions (K⁺) rapidly exit through open potassium channels.

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Calcium-Induced Calcium Release (CIRC)

The process where calcium ions entering the cell through L-type calcium channels trigger the release of calcium from the sarcoplasmic reticulum (SR).

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What is the key role of Phase 2 (Plateau Phase)?

The plateau phase is essential for prolonging the contraction of the cardiac myocytes, allowing sufficient time for the heart to pump blood effectively.

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Hyperkalemia's Effect on Repolarization

High potassium levels in the blood speed up repolarization (phase 3) of the heart's action potential, making it shorter. This makes the resting membrane potential (RMP) less negative, bringing the cell closer to the threshold for triggering a new action potential.

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Hyperkalemia's ECG Manifestations

Hyperkalemia shows up on an ECG as peaked T waves (due to accelerated repolarization), a shortened QT interval (faster repolarization), flattened P waves or their disappearance in severe cases, and a widened QRS complex. In extreme cases, a sine wave pattern can appear, leading to ventricular fibrillation.

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Hypokalemia's Effect on Repolarization

Low potassium levels in the blood slow down repolarization (phase 3) of the heart's action potential, making it last longer. This makes the resting membrane potential (RMP) more negative, making it harder for the myocyte to reach the threshold and initiate a new action potential.

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Hypokalemia's ECG Manifestations

Hypokalemia is reflected on an ECG as flattened T waves, a prolonged QT interval (slower repolarization), and a U wave, a secondary deflection after the T wave. This prolongation of the QT interval can lead to torsades de pointes, a fatal heart rhythm.

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Hypercalcemia's Effect on Action Potential

High calcium levels in the blood shorten the plateau phase (phase 2) of the heart's action potential, making it shorter overall, thus reducing the refractory period. It also enhances the release of calcium from the sarcoplasmic reticulum, boosting myocardial contractility.

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Hypercalcemia's ECG Manifestations

High calcium levels are seen on an ECG as a shortened QT interval, indicating faster repolarization.

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Non-Nodal Electrolyte Derangements

Electrolyte imbalances, like potassium (K+) or calcium (Ca2+) derangements, can cause significant changes to the shape of the ECG curve, affecting action potential duration, repolarization speed, and overall electrical activity of the heart.

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ECG Manifestations of Electrolyte Derangements

ECG changes associated with electrolyte imbalances are usually specific, allowing us to identify the underlying problem. For instance, peaked T waves strongly suggest hyperkalemia, while a prolonged QT interval could indicate hypokalemia, hypercalcemia, or other conditions. Understanding these ECG patterns is essential in diagnosing and managing potential cardiac issues related to electrolyte disturbances.

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Phase I Metabolism

The initial phase of drug metabolism in the liver, where enzymes like cytochrome P450 (CYP450) add or unmask functional groups, making the drug more polar and potentially active, inactive, or toxic.

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Phase II Metabolism

The second phase of drug metabolism in the liver, where enzymes like UGT and GST attach polar molecules to drugs or their metabolites, making them inactive and easier to excrete in urine.

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Prolonged Prothrombin Time (PT)

A lab test that measures how long it takes for blood to clot, specifically assessing the extrinsic and common pathways of coagulation, primarily dependent on Factor VII. It is prolonged in liver dysfunction due to reduced production of clotting factors.

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Bilirubin Metabolism

The liver breaks down hemoglobin from old red blood cells into bilirubin, which is then conjugated and excreted in bile. Problems with this process can lead to jaundice.

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Cholesterol Excretion

The liver eliminates excess cholesterol through bile, which is then excreted in the stool. This helps to regulate blood cholesterol levels.

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Alcohol Metabolism

The liver breaks down ethanol (alcohol) through enzymes like alcohol dehydrogenase and acetaldehyde dehydrogenase. Excessive alcohol consumption can damage the liver over time.

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Glucose Storage

The liver stores glucose as glycogen, which can be broken down into glucose for energy needs when blood sugar levels are low.

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Study Notes

Acute MI (Different Coronary Arteries)

  • Acute MI usually begins with coronary artery disease (CAD), characterized by atherosclerotic plaque formation in coronary arteries.
  • Plaque consists of cholesterol, inflammatory cells, and connective tissue within arterial walls.
  • Plaque rupture or erosion triggers a cascade of events:
    • Activation of platelets
    • Release of Tissue Factor (Factor III)
    • Conversion of Factor X to Xa
    • Conversion of Factor II to IIa
    • Conversion of Factor I to Ia
    • Formation of a thrombus (partial or complete obstruction).
  • Thrombus leads to myocardial ischemia.
  • Reduced or absent blood flow deprives myocardial tissue of oxygen and nutrients.
  • Ischemia affects the subendocardial layer, furthest from the blood supply and with the highest oxygen demand, most susceptible to irreversible injury.
  • Myocyte necrosis releases intracellular contents (troponin, CK-MB) into the bloodstream.
  • Inflammatory response & leukocytes infiltrate the affected areas to remove dead cells and prolong injury.

Stable Angina, Angina Pectoris, Unstable Angina, NSTEMI, STEMI

  • Stable angina: Predictable chest pain related to exertion or stress.
  • Angina Pectoris: General term for angina, which is chest pain caused by reduced blood flow to the heart muscle.
  • Unstable angina: Chest pain that is new, more severe, and occurs at rest or with less exertion than previously tolerated.
  • NSTEMI (Non-ST-elevation myocardial infarction): Coronary artery blockage, but the blockage is not complete.
  • STEMI (ST-elevation myocardial infarction): Complete coronary artery blockage, leading to irreversible myocardial damage & necrosis.

Cardiac Shock

  • Pump failure caused by:
    • MI (most common)
    • HF
    • Myocarditis
    • Valve dysfunction
  • Reduced cardiac output → hypotension.
  • Impaired coronary artery perfusion → worsening ischemia.
  • Reduced organ perfusion → tissue hypoperfusion leads to ischemia and anaerobic metabolism
  • Metabolic acidosis: lactate buildup.
  • Kidney injury, altered mental status (brain), and impaired liver metabolism (jaundice)
  • Systemic Hypoperfusion triggers circulatory failure and possible sepsis.

Cardiogenic Shock Compensation Mechanisms

  • Sympathetic nervous system activation
    • Increased heart rate
    • Vasoconstriction
    • Increased blood pressure
  • Renin-angiotensin-aldosterone system (RAAS) activation
    • Maintaining blood pressure by retaining sodium & water.

Pulmonary Edema (Associated with Hypertensive Crisis)

  • Elevated LVEDP (Left Ventricular End Diastolic Pressure)
  • Increased capillary hydrostatic pressure
  • Reduced oncotic pressure
  • Impaired lymphatic drainage

Starling Forces

  • Movement of fluid between capillaries and surrounding tissues.
  • Relationship between capillary hydrostatic pressure (Pc), interstitial hydrostatic pressure (Pi), capillary oncotic pressure (πc), and interstitial oncotic pressure (πi)
  • Net filtration pressure (NFP) = (Pc - Pi) - (πc - πi).
  • Increased pressure → more fluid, leading to edema.

Cardiogenic Shock Treatment

  • Restore hemodynamic stability (fluids, vasopressors)
  • Treat underlying cause
  • Support (monitoring vital functions & managing complications).

Cardiac Tamponade

  • Obstructive shock caused by fluid accumulation in the pericardial sac
  • Pericardial effusion compresses the heart → reduced cardiac output (reduced CO).
  • Symptoms include dyspnea, hypotension, and muffled heart sounds.
  • Echocardiogram → pericardial effusion, diastolic collapse of the right heart chambers

Cardiac Tamponade Treatment

  • Pericardiocentesis → remove the accumulated fluid form the pericardial sac
  • Consider inotropes and in cases of worsening, mechanical support (if needed)

Relationship between CO, SVR, and BP

  • MAP = CO x SVR (mean arterial pressure = cardiac output x systemic vascular resistance)
  • Increased CO: raises BP if SVR remains constant.
  • Decreased CO: lowers BP if SVR doesn't compensate.

Frank-Starling Law

  • Relationship between preload, contractility and stroke volume • Increasing preload (stretching of cardiac fibres) → proportionally increases stroke volume up to an optimum point.
  • At high preload, overstretched fibers do not respond effectively → reduced contractility → reduced stroke volume.

Left Ventricular Hypertrophy (LVH), Concentric vs. Eccentric (FORMATIVE)

  • Concentric: Increased wall thickness with a relatively smaller chamber size triggered by pressure overload. (e.g. hypertension or aortic stenosis)
  • Eccentric: Increased wall size and chamber enlargement with normal or even decreased wall thickness triggered by volume overload as a compensation. (e.g., valvular regurgitation and high-output states).
  • Both lead to impaired relaxation and filling
  • Clinical presentation depends on the predominant mechanism

Aortic Stenosis

  • Narrowing of the aortic valve → increased afterload.
  • Reduced stroke volume and cardiac output
  • Blood pressure increases due to increased afterload and reduced stroke volume
  • EKG findings consistent with these effects

Mitral Stenosis

  • Narrowing of the mitral valve → reduced preload.
  • Reduced stroke volume and ventricular filling → reduced cardiac output

Cardiac Action Potential

  • Phase 0: Rapid depolarization mediated largely by fast sodium channels (voltage-gated sodium channels) resulting in rising action potentials
  • Phase 1: Early repolarization, rapid potassium efflux through these voltage-gated channels resulting in early phase of repolarization
  • Phase 2 Plateau phase, the slow calcium influx balances potassium efflux, contributing to prolonged contraction required for effective ejection of blood from the heart
  • Phase 3: Rapid repolarization, voltage gated potassium channels open further, triggering the efflux of potassium ions
  • Phase 4: Resting membrane potential, maintained by sodium-potassium ATPase, responsible for returning the cells to a resting potential after each contraction

Nodal Action Potential

  • Phase 4: the slow spontaneous depolarization period, characterized by a slow influx of sodium and calcium ions, which gradually raise the membrane potential towards the threshold potential
  • Phase 0: depolarization from the influx of fast sodium and calcium ions, eventually initiating the firing of an action potential
  • Phase 1: very brief and small repolarization, triggered by the closure of sodium channels and the opening of the potassium channels, which causes slight drop in membrane potential
  • Phase 2: plateau phase, occurs because calcium influx (through L-type calcium channels) balances potassium efflux
  • Phase 3: rapid repolarization, which is due to the closing of the calcium channels and a major efflux of potassium.
  • Phase 4: resting membrane potential, occurs rapidly from the movement of potassium to the outside of the cell.

Refractory Period (Nodal)

  • ARP (absolute refractory period): period before the cell can be excited by a stimulus
  • ERP (effective refractory period): period where the cell may respond to a stimulus by depolarizing minimally and not for propagation of the action potential
  • RRP (relative refractory period): period following the ARP where the cells respond to stronger than normal stimuli by initiating an action potential.

Prolonged QT Interval (ECG Manifestations)

  • Hypercalcemia: Short QT interval, faster repolarization.
  • Hypocalcemia: Prolonged QT interval, slower repolarization.
  • Hypokalemia: Flattened T waves, prolonged QT interval, slower repolarization.
  • Hyperkalemia: Peaked T waves, shortened QT interval, rapid repolarization.
  • Prolonged PT (prothrombin time) and INR (international normalized ratio)
  • Decreased production of clotting factors
  • Liver dysfunction → impaired synthesis of coagulation factors → prolonged clot formation (hemorrhage potential)
  • Vitamin K deficiency could occur in patients with cholestasis (obstruction of the bile ducts) → impairment in Vitamin K absorption.
  • DIC (disseminated intravascular coagulation) - a serious and sometimes life-threatening condition

Liver Function Tests Elevated ALT, AST, ALP (and GGT) & Bilirubin

  • ALT (alanine aminotransferase, a measure of hepatocellular injury)
  • AST (aspartate aminotransferase, a measure of hepatocellular injury)
  • ALP (alkaline phosphatase, indicates cholestatic processes, as commonly found in the bile ducts.)
  • GGT (gamma-glutamyl transpeptidase) → enzyme found in the bile ducts so high values suggest cholestasis
  • Bilirubin (elevated levels suggest the liver is not excreting it efficiently → jaundice potential)

Portal Hypertension

  • Increased resistance to blood flow in the liver → elevated pressure in the portal vein. Common causes are cirrhosis, portal vein thrombosis.
  • Complications include ascites, varices (enlarged veins), and hepatic encephalopathy

Varices

  • Dilated, and weakened veins. Common sites are esophagus and stomach.
  • Due to portal hypertension Risk of bleeding → hematemesis, melena.
  • Endoscopy (gold standard for detection and grading)
  • Medical management: non-selective Beta blockers; endoscopic variceal ligation (EVL)

Medications that interfere with Liver Function

  • Many medications, including NSAIDs (nonsteroidal anti-inflammatory drugs), other medications → can strain the liver if administered too often or in high doses.

Hyperbilirubinemia

  • Jaundice: yellowing of skin, sclera & mucous membranes due to elevated bilirubin levels
  • Pre-hepatic: RBC lysis → unconjugated bilirubin
  • Hepatic: Impaired bilirubin conjugation → Mixed (unconjugated & conjugated) bilirubin
  • Post-hepatic: Obstruction of bile ducts → conjugated bilirubin

Cholangitis/Cholecystitis

  • Cholangitis: Inflammation of the common bile duct. Often caused by gallstones obstructing the duct, infection in the bile ducts.
  • Cholecystitis: Inflammation of the gallbladder, likely from gallstones obstructing the cystic duct.

Nerve Conduction (general)

  • Action potentials travel along the sarcolemma and into the T-tubules via myofibrils leading to the release of Ca++ initiating contraction
  • Depolarization → opening of voltage-gated channels → Na+ inflow → K+ outflow

Cholinergic Crisis/ Myasthenia Crisis

  • Cholinergic crisis due to excessive acetylcholine at the neuromuscular junction, leading to muscle weakness, fasciculations, and excessive sweating.
  • Myasthenia Crisis → muscle weakness due to insufficient acetylcholine at the neuromuscular junction → caused by medications/ disease processes impacting acetylcholine receptors at the NMJ.

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NUR 201 Patho Final Study Guide PDF

Description

Test your knowledge on the treatment of AVNRT and its associated ECG features. This quiz covers conditions like GERD, hypocalcemia, and various electrolyte imbalances affecting cardiac function. Challenge yourself with scenarios and questions based on clinical practices.

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