Fetal Circulation
Cardiac Pathophysiology - Part 1
Congenital
Heart Disease
NRS 232 - Pathophysiology I
Cyanotic & Acyanotic Defects
Perfusion
Transposition of the Great Arteries
Ventricular Septal Defect
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
Consequences of Impaired Perfusion
2
3
1
4
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
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
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
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
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"