Ischemic Heart Disease and Conduction Disorders (PATHO)

Heart

• Size of fist

  • Located in mediastinum

  • Base: Upper part

  • Apex: Pointed end

• Acute coronary syndrome (ACS)

• 
  

• Due to ischemia

• Myocardial infarction (MI)

• 
  

• Prolonged ischemia leading to cell death

• Heart wall

• 
  

• Epicardium: 

  • Outer

• Myocardium:

  • Muscle

• Endocardium: 

  • Lines interior

Coronary Arteries

• Right and left

• Left coronary artery

  • LAD: 

    • Left anterior descending

• Exercise

  • Increases coronary collateral vessels

Exercise and the Heart

• Increases coronary circulation

• 
  

• Right atrium

• 
  

• 
  

• Receives deoxygenated blood 

• 
  

• Right ventricle

• 
  

• 
  

• Pumps blood to lungs

• 
  

• Left atrium

• 
  

• 
  

• Receives blood from pulmonary veins

• 
  

• Left ventricle

• 
  

• 
  

• Pumps blood to body

• Two circuits

• pulmonary

• 
  

• 
  

• Low pressure system, RV to LA

• Picks up oxygen at lungs

• Two circuits

• systemic

• 
  

• 
  

• High pressure system, LV to RA

• Delivers oxygen to body tissues

• Systolic

• 
  

• Contraction

• SBP: Systolic blood pressure

• Diastolic

• 
  

• Relaxation

• DBP: Diastolic blood pressure

Conduction System Overview

• Sinoatrial node (SA node)

  • Pacemaker

• AV node

• Bundle of His

• Bundle branches

• Purkinje fibers

Phase 0 cardiac muscle action potential

Fast sodium channels open

Increase potential from −90 mV to +20 mV

Phase 1 Cardiac Muscle Action Potential

Peak

Abrupt closure fast sodium channels

Phase 2

Cardiac Muscle Action Potential

Plateau

Slow sodium-calcium channels

Phase 3
Cardiac Muscle Action Potential

Repolarization,

K+ channels open

Phase 4

Cardiac Muscle Action Potential

Resting potential

Na+/K+ pump

Refractory Period

• Absolute refractory period

  • Cells cannot be re-stimulated

  • Phases 0, 1, 2, part of 3

• Enables heart to relax without being reactivated

  • Time for heart to fill with blood

  • Protects against fatal arrhythmias

Electrocardiogram

• Electrical activity of the heart

  • X-axis: Time and Y-axis: Millivolts

• Standard waveforms

• p wave

• qrs complex

• t wave

• 
  

• P wave

• 
  

• Atrial depolarization

• 
  

• QRS complex

• 
  

• Ventricular depolarization

• 
  

• T wave:

• 
  

• Ventricular repolarization

• 12-Lead ECG

• 
  

• 12 different views of electrical activity of heart

Acute Coronary Syndrome (ACS)

• Ischemia of heart

  • Unstable angina

  • Myocardial infarction

• Angina pectoris

• 
  

• Chest pain due to myocardial ischemia

• Two main types:

  • Unstable angina

  • Chronic stable

Angina Pectoris

unstable

• 
  

• New episode or increased severity

• Not relieved with rest

• Medical emergency

Angina Pectoris

• Chronic stable

• 
  

• Consistent, chronic pain

• Self-medication with nitroglycerin

Angina Pectoris

other forms

• 
  

• Prinzmetal’s and microvascular angina

Unstable Angina

• Incidence increasing in United States

• Cause:

  • Myocardial ischemia

    • Blood clot (coronary thrombosis)

    • Atherosclerotic plaque

    • Coronary artery vasospasm (Prinzmetal’s)

    • Microvascular obstruction

• Risk factors: 

  • Arteriosclerosis

  • Same risk factors for developing arteriosclerosis

Unstable Angina pathophysiology

• 
  

• Cardiac tissue oxygen demands exceeds delivery

  • Lactic acid formation 

• Coronary thrombus—blockage

• Prinzmetal’s angina

  • Vascular spasm

• Ischemia with no obstructive coronary artery (INOCA)

  • Microvascular angina

• Anemia

  • Can also result in angina

Unstable Angina s&s

• 
  

• Chest pain brought on by exertion

  • Crushing sensation on left side of chest

  • Levine’s sign

  • Pain radiating to shoulder, jaw, and down the arm

  • Pain precipitated by exertion or stress

    • Lasts approximately 1 to 5 minutes

    • No change with alterations in position, respiration, or cough

• Anginal equivalents

  • Signs of MI that differ from classic angina

  • Dyspnea, feeling faint, epigastric pain, dizziness

Unstable Angina  diagnosis

• 
  

• Tests similar to those for arteriosclerosis 

• Additional tests:

  • ECG

  • High sensitivity C-reactive protein (hs-CRP)

  • Cardiac enzymes

  • High sensitivity cardiac troponin (hs-cTn)

• 
  

• Chest x-ray, cardiac angiogram, cardiac catheterization, and coronary computed tomographic angiography (CCTA)

• Exercise stress test

Unstable Angina treatment

• 
  

• Relieve symptoms

• Prevent progression (MI)

• Oxygen

  • Administered with angina if SaO₂ <95%

• Nitrates: Vasodilators

• Aspirin: Decrease platelet adhesion 

INOCA: Treatment

• Microvascular angina 

• Treated differently than other forms of angina

  • Anti-lipidemia statin agents

    • With ACE inhibitor or ARB 

  • Thromboxane A2 (TXA2) inhibitors

Angina: Surgical and Endovascular Options

• Percutaneous coronary intervention (PCI)

• Percutaneous transluminal coronary angioplasty (PCTA)

  • Uses catheter with balloon on tip

  • Angioplasty

    • Inflated balloon pushes plaque against arterial wall

  • Atherectomy

    • Catheter with blade reduces plaque

• 
  

• Stent

  • Maintains open vessel

  • Drug-eluting stents

• 
  

• Coronary artery bypass graft (CABG)

• 
  

• Creates new routes around occlusions

• Saphenous vein of leg often used

• Triple, quadruple, or quintuple bypasses may be performed

• Traditionally

  • Cardiopulmonary heart pump used

• Currently

  • “Off pump” procedures 

Prinzmetal’s Angina

• AKA: Variant or vasospastic angina

• Differences than “typical” angina

  • Angina while at rest

  • Not always associated with typical CAD risk

    • Except for:

      • Cigarette smoking 

      • Inflammatory states (high levels of hs-CRP levels)

  • Small percentage of patients, concurrent conditions:

    • 
      

    • Migraine headaches, Raynaud’s phenomenon

Prinzmetal’s Angina:Unclear etiology

• 
  

• Lack of nitric oxide

• Endothelial dysfunction

• Not always associated with typical CAD risks

• Risk for MI, ventricular arrhythmias, and sudden death

Prinzmetal’s Angina  diagnosis adn treatment

• 
  

• 24-hour cardiac monitoring

• Coronary angiography

• Cardiac enzymes

• Treatment: 

  • Nitrates 

  • Calcium channel blockers

Chromic Stable Angina

• Recurring episodes of chest pain

  • Transient myocardial ischemia

  • Quiescent atherosclerotic plaque

• Surgical intervention for CAD not an option

• Treatment:

  • Nitroglycerin preparations: Tablet, sprays

  • Nicorandil: K+ channel activator 

  • Ranolazine: Inhibits the late Na+ current, improves myocardial relaxation 

  • Ivabradine: Reduces firing rate of SA node

Acute Myocardial Infarction

• Prolonged cardiac tissue ischemia

• Irreversible damage

• Due to:

  • Atherosclerotic plaque

  • Thrombus

  • Increased myocardial demand

Type 1 MI

Spontaneous due to plaque or thrombus

TYPE 2 MI

Lack of oxygen to meet demands

Not due to atherothrombotic occlusion

TYPE 3 MI

MI death before cTn measurement

Type 4 MI

MI due to stent insertion (within 48 hours)

Type 5 MI

MI due to CABG

MI Damage

• Location

• Length of time

  • Greater than 30 minutes of ischemia causes irreversible damage

• Available collateral circulation

MI Damage zone of injruy

• 
  

• Surrounds zone of ischemia

• Some recoverable cells

• Necrotic cells

  • Altered electrical activity (ECG changes)

  • Release cellular contents (cardiac markers such as troponin)

Reperfusion Injury

• Ischemic myocardial tissue

  • Can sustain damage by normalized levels of oxygen and nutrients

• Known as “myocardial stunning”

  • Reperfusion injury

    • May be due to oxidized free radicals from WBCs

• Arrhythmias and reduced contractility

MI Signs and Symptoms

• Crushing chest pain

• Levine’s sign

• Pain radiating to shoulder, jaw, down left arm

• Sweating, nausea, anxiety

• Anginal equivalents

• “Silent MI”

  • No signs or symptoms

MI Diagnosis: ECG

• ECG: Cannot confirm MI

• Examine for ST segment changes

  • STEMI: ST segment elevation myocardial infarction 

    • MI completely through the heart wall

  • NSTEMI: Non-ST segment elevation myocardial infarction 

    • MI subendocardial and not completely through the heart wall

MI Diagnosis: Blood Test

• CPK-MB: Cardiac enzyme

  • Rise within 4 hours of MI, subside over 3 to 4 days

• cTnI: Cardiac protein

• hs-cTnI:

  • High sensitivity cardiac troponin (hs-cTn) assay 

  • Highly specific for cardiac muscle necrosis

    • 1-hour turnaround time: Fairly accurate

    • 3-hour level: 100% final

MI Diagnosis: using blood tests

• 
  

• Confirm cardiac biomarker

• Then, use ECG to categorize as STEMI or NSTEMI 

MI Diagnosis: Tests other than Blood or ECG

• Echocardiogram

• Radionuclide myocardial perfusion

Anti-platelet medications MI

Aspirin and P2Y12 receptor inhibitors

Beta adrenergic blockers MI

Decrease HR, myocardial oxygen demand

Calcium channel antagonists MI

Decrease coronary arteriole constriction

Nitrates MI

Vasodilation

Morphine MI

Pain

Thrombolytic agents MI

Break up clot

Anticoagulants MI

Reduce clotting

Pecutaneous coronary intervention MI

Restore flow

• Dysrhythmia

• 
  

• Risk greatest after onset of MI symptoms

• Reentry

  • Ischemic areas do not conduct impulses as expected

  • Impulses may “re-activate” already depolarized areas

  • Excitable activation sequence occurs, disrupting normal rhythm 

  • Heart destabilized electrically

• Papillary muscle rupture

• 
  

• If in LV, mitral valve affected

  • Mitral insufficiency (regurgitant murmur) 

  • Backup of blood into left atrium and pulmonary circulation

  • Dyspnea, crackles may develop

• Thromboembolism

• 
  

• Poorly contracting heart chambers cause stagnant blood, increasing risk for clot formation

• Ventricular aneurysm and rupture

• 
  

• Weakened, bulging area of heart wall

• May rupture, surgical intervention needed

• Pericarditis

• 
  

• Occurs 2 to 3 days post-MI

• Pericardial friction rub, stabbing pain with inspiration

• May occur as component of Dressler’s syndrome

  • Hypersensitivity reaction to tissue necrosis in MI

• Heart failure

• 
  

• Ability to generate sufficient pressure is compromised

• LV

  • Hypotension; fluid backs up in pulmonary circulation

• RV

  • Fluid backs up in systemic circulation leading to jugular vein distention and peripheral edema

• Cardiogenic shock

• 
  

• Acute (MI) accounts for 81% of patients in cardiogenic shock

• Heart failure progresses to cardiogenic shock

• Ventricles fail to pump sufficient blood

  • BP, cardiac output drop

  • Hypoperfusion of organs leading to failure

cardiac Inflammation and Infection

• Infectious endocarditis

• Myocarditis

• Pericarditis

Infectious Endocarditis (IE)

• Normally bacterial

  • Staphylococcus aureus

• Damages valves

• Risk factors 

  • Prosthetic valves, pacemakers, intravascular devices, IV drug usage

  • Pneumonia, pyelonephritis, dental procedures can be a source of microorganisms

Infectious Endocarditis (IE)  vegetation

• 
  

• Develops on valve

• Fragments can break off and enter bloodstream

  • Septic emboli

• Different potential causes account for different categories of endocarditis

• 
  

• Examples: Prosthetic valve endocarditis, IVDA endocarditis, etc.

• Different organisms associated with the different causes

• Native valve endocarditis

  • Group A beta hemolytic Streptococcus (GABHS)

• Native valve endocarditis (NVE)

Infectious Endocarditis (IE) 

• 
  

• Acute and subacute

• Prosthetic valve endocarditis (PVE)

early adn late

Infectious Endocarditis (IE contunied

• IV drug abuse (IVDA) endocarditis

• Pacemaker IE

• Health-care-acquired IE

Infectious Endocarditis (IE) 

• Acute or subacute infection

• New, different sounding heart murmur

  • Important sign

  • DIAGNOSIS

• 
  

• Blood labs and echocardiographic findings

  • Multiple blood samples, as infectious agent may be difficult to detect in blood

• Duke Criteria

Infectious Endocarditis (IE) trearment

• 
  

• Antibiotics

  • IV 6 weeks or longer

  • High doses of oral and depot antibiotics may be viable

• Blood cultures:

  • Should be repeated daily until sterile

• Persistent fever despite antibiotic therapy may be due to paravalvular or extracardiac abscesses

• Surgical intervention

Myocarditis

• AKA: Inflammatory cardiomyopathy

• Mild disorder to lethal

  • Viruses common cause

    • Influenza, herpesvirus, hepatitis

  • Autoimmune diseases; toxin exposure

myocarditis symptoms

• 
  

• Fever, myalgia, arthralgia, palpitations

• Pericardial friction rub

• S3 gallop

Myocarditis

• Diagnosis

• 
  

• CBC, ESR, CRP

• cTnI may be elevated

• Viral antibody titers should be measured

myocarditis treatment

• 
  

• Reduce myocardial workload

• Activity restricted for 6 months or more

• Reduce heart workload

  • ACE inhibitors, inotropic agents

Pericarditis

• Inflammation of pericardium and epicardium

• Pericardial effusion

• 
  

• Fluid surrounding the heart

• Cardiac tamponade

• 
  

• Fluid accumulation begins to compress the heart

• Acute pericarditis

• 
  

• Presents in manner similar to MI

• May be caused by viral and bacterial infections

• May occur post-MI

• Dressler’s syndrome

• 
  

• Specific form of pericarditis after MI

Pericarditis Effusion presentation

• 
  

• Chest pain, fever, pericardial friction rub

• Pain worsens with deep breathing

• Beck triad: Hypotension, jugular vein distention, muffled heart sound

• Pulsus paradoxus: Decrease in SBP by 10 mm Hg or more with inspiration

• Diagnosis

  • Echocardiogram, cardiac MRI

• Treatment depends on etiology

Dysrhythmias and Conduction Disorders

• Disruption in electrical signal

  • Supraventricular: SA node, atria, AV node

  • Ventricular: Bundle of His, bundles branches, Purkinje fibers, and ventricle muscle

  • Tachyarrhythmias: Heart beats excessively fast

  • Bradyarrhythmias: Heart beats excessively slow

  • Heart block: Conduction system impulse blocked

    • Most commonly at the AV node

    • Complete heart block:

      • Atria and ventricles beat independently of each other

Atrioventricular Block

• Anterior and inferior wall MI

• SA atrial impulse fails to be conducted to the ventricles

• Prolonged PR interval

Atrial Fibrillation

• Most common arrhythmia

  • Absence of coordinated, rhythmic atrial contractions

  • Multiple irregular fibrillatory P waves 

• May or may not stimulate a rapid ventricular response

Atrial Fibrillation  surgical approcahes

• Increase the risk of clot formation and stroke

  • Surgical approaches

    • Obliterate the left atrial appendage, where clots tend to occur 

    • Devices:

      • Watchman and Amplatzer cardiac plug

Premature Ventricular Contraction (PVC)

• Sporadic PVCs

  • Most common arrhythmia post-MI

• Ventricle beats independently

• Widened QRS complex

Premature Ventricular Contraction (PVC)  how does it occur

• May occur singularly or

• Patterns

  • Bigeminy, trigeminy, quadrigeminy

• Sporadic, infrequent PVCs do not require treatment

Premature Ventricular Contraction (PVC) increases concern:

• 
  

• Two sequential PVCs (couplets)

• PVCs >10 per hour

• Treatment:

  • Medical: Beta-blockers, calcium channel blockers

  • Catheter ablation

Ventricular Tachycardia

• Series of widened QRS waves

  • Without P or T waves

  • Rapid, ineffective ventricular contractions

  • Rate greater than 100 bpm  

  • Does not allow for effective pumping 

• Dyspnea, palpitations, and lightheadedness

Ventricular Fibrillation

• May be precipitated by PVC falling on the T wave, interrupting refractory period

  • Rhythm degenerates

  • Fibrillation = quivering

  • Contraction is uncoordinated, with no effective pumping

• Loss of consciousness, death may occur