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Fetal Circulation

Cardiac Pathophysiology - Part 1

Congenital

Heart Disease

NRS 232 - Pathophysiology I

Cyanotic & Acyanotic Defects

Cyanotic

  • Right to left shunting

Acyanotic

  • Left to right shunting

Perfusion

Transposition of the Great Arteries

Ventricular Septal Defect

Left to right

Cyanotic

Transposition of the Great Arteries

Cyanotic

Tetralogy of Fallot

The flow of blood through arteries and capillaries

  • Delivering nutrients & oxygen to cells
  • Removing cellular waste products

Acyanotic

Right to left

Consequences of Impaired Perfusion

2

3

1

4

Necrosis vs. Apoptosis

Cyanotic

Supply vs. Demand

Ischemia!

Exemplar - Coronary artery perfusion

Risk Factors for Impaired Perfusion

Modifiable:

  • Smoking - Nicotine vasoconstricts
  • Elevated serum lipids - Contribute to atherosclerosis
  • Sedentary lifestyle - Contributes to obesity
  • Obesity - Increases risk for DM II & atherosclerosis
  • Diabetes mellitus - Increases risk of atherosclerosis
  • Hypertension - Increases work of myocardium

Non-modifiable:

  • Age - Increases with age
  • Gender - Men > women
  • Genetics - Family history

Endocardial

Disorders

Coronary

Heart Disease

Symptoms of Impaired Perfusion

Pain:

  • Ischemic pain
  • Chest - MI
  • Legs - PAD

Dyspnea:

  • Interference with O2 transport to tissues
  • LHF

Dizziness/Fainting:

  • Orthostatic hypotension
  • Atherosclerosis of the carotid arteries

Edema:

  • Excessive fluid in interstitial spaces
  • RHF
  • Incompetent veins

Insufficient delivery of oxygenated blood to the myocardium (ischemia) due to atherosclerotic changes of the coronary arteries

Atherosclerosis

Infective endocarditis

  • Invasion & colonization of endocardial structures by microorganisms resulting in inflammation from a portal of entry
  • Vegetations - Erosion of the valve leaflets, and embolization
  • Splinter hemorrhages

Diagnosis of MI

Rheumatic heart disease

  • Acute inflammatory disease following infection with group A beta-hemolytic streptococci
  • Antibodies directed against the antigen are also directed against self-tissues due to cross-reactivity
  • Diffusely affects connective tissue in the joints, heart, & skin
  • Carditis affects all layers of the heart
  • Clumping of platelets & fibrin on heart valves - scarring & shortening

Cardiac Enzymes

  • Troponin I
  • Myoglobin
  • CK-MB

12-Lead ECG Changes

& Location of Injury

ECG Changes

  • Q-wave
  • ST segment changes
  • T-wave changes

Central & Peripheral

Janeway Lesions

Treatment of Myocardial Infarction - MI

Decrease O2 demand

  • Activity restriction - Rest & relaxation techniques
  • Preload & afterload reduction - NTG = dilation of veins > arteries
  • Heart rate control - SNS antagonists/beta blockers
  • Pain control - NTG = dilation of coronary arteries & arterioles; morphine only if pain is severe & unrelieved (morphine = delayed response to antiplatelet therapy)

Angina vs. Acute Coronary Syndrome

http://circ.ahajournals.org/content/127/7/861

Systemic Vegetative Embolization

NOTE: Ischemic myocardial pain receptors travel with 8th cranial nerve & 1-4 dorsal root ganglia along with sensory neurons from jaw, neck, & arm - "Referred pain"

Vegetations on

mitral valve

Renal infarcts

Increase O2 delivery to ischemic tissues

  • Antiplatelet treatment - ASA & others
  • Anticoagulant treatment - UFH or LMW heparin
  • NTG - Increase cardiac collateral circulation
  • Reperfusion
  • Thrombolytic/fibrinolytic treatment
  • Percutaneous coronary intervention (PCI)
  • Angioplasty
  • Stent placement
  • Bypass surgery
  • O2 administration - For sats <90%, respiratory distress, high-risk features for hypoxia (hyperoxia = coronary vasoconstriction)
  • Stabilize plaque - Statin therapy

Vegetations on Prosthetic Valves

Cerebral infarct

Emboli in iliac arteries

Acute Coronary Syndrome:

1. "Unstable" Angina

  • Plaque rupture, but occlusion is partial, or clot is dissolved prior to death of myocardial tissue = negative enzymes

2. Myocardial Infarction (MI)

  • Occlusion is complete & thrombus persists long enough for development of irreversible damage to myocardial cells = positive enzymes

Angina - "Stable"

  • Precipitated by events that increase myocardial demand - Exercise, stress, SNS activation, increased preload/afterload/heart rate/muscle mass
  • Stenosed arteries dilate poorly in response to O2 demand
  • Responds to rest & NTG - cardiac & peripheral vasodilation

Myocardial Ischemia

Scar tissue

Antiplatelet therapy!

Reperfusion therapy!

Valvular Disorders:

Stenosis & Regurgitation

Mitral Regurgitation

References

Stenosis

  • Pressure work
  • Hypertrophy
  • Etiologies
  • Mitral - Rheumatic heart disease
  • Aortic - Rheumatic heart disease, senile calcifications

Copstead, L. & Banasik, J. (2018). Pathophysiology (6th ed.). St. Louis, MO: Elsevier.

Giddens, J. (2016). Concepts for nursing practice (2nd ed.). St. Louis, MO: Elsevier Mosby.

Kahn Academy video on YouTube.

Burcham, & Rosenthal. (2016). Lehne's pharmacology for nursing care (8th ed.). St. Louis, MO: Saunders Elsevier.

UpToDate database retrieved through the OHSU Library.

YouTube videos embedded on some slides.

Volume work = Dilation at first, then hypertrophy

  • Volume work
  • Dilation
  • Etiologies
  • Mitral - Rheumatic heart disease, inflammation of muscles/chordae tendonae
  • Aortic - Rheumatic heart disease, infective endocarditis

Aortic Regurgitation

- Pressure Waves

Pressure work = Hypertrophy at first, then dilation

Bounding pulse

Wide pulse pressure

Check out "Law of Laplace"

versus "Starling's Law"

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