Bikman - Heart Path Flashcards
What is heart failure? Early and final stages?
Heart cannot pump blood sufficient to meet body’s needs. Generally occurs on one side.
Early stages, compensations can occur:
- Catecholamines
- Frank-Starling mechanism
- Hypertrophy
Eventually:
- Ischemia
What is the Frank-Starling mechanism?
The more time the heart has to fill, the stronger it will contract
Where does R heart failure manifest?
Below the heart
Where does LHF (left heart failure) manifest?
Above the heart
What are some common causes of LHF?
- Systemic hypertension
- Mitral or aortic valve disease
- Primary heart diseases
What are some heart changes observed in LHF?
- LV hypertrophy**
- LV dilation
- LA may be enlarged
What are some consequences of LHF?
- Dyspnea - hard time breathing
- Orthopnea - hard time breathing in certain positions
- Enlarged heart, increased HR
- Rales - fluid accumulating in lung space
- Mitral regurgitation, systolic murmur
What are some common causes of RHF (right heart failure)?
- Cor Pulmonale ( HF due to lung failure)
- Some congenital heart diseases
What are some heart changes observed in RHF?
- RV hypertrophy
- RV dilation
- RA may be enlarged
What are some consequences of RHF?
- Peripheral edema
- Hepatomegaly
- Splenomegaly
Outline the series of events that cause cor pulmonale.
HF due to lung failure, causing RHF.
RV enlargement due to pulmonary hypertension (from primary lung disorder).
There is less O2 in the alveolar capillaries, causing alveolar constriction. The R side of the heart has to do more work since the alveoli constriction increases pressure.
What are the 3 categories of congenital heart disease and what diseases fall under each category.
Left to right (L2R)
- ASD
- VSD
- PDA
Right to left (R2L)
- Tetralogy of Fallot
- Transposition of great arteries
Coactation
- Aortic coarctation
Atrial Septal Defect (ASD)
Too much blood going to the lungs
- May cause pulmonary hypertension
- Sending too much blood to the lungs
- Mixing of oxygenated and deoxygenated blood
Ventricular Septal Defect (VSD)
Too much blood going to the lungs
- Most common
- Most close spontaneously
- Size and location matters
- The higher towards the base the defect is, the more problematic it will be with mixing of blood
Patent Ductus Arteriosus (PDA)
Too much blood going to the lungs
- Allows flow from PA to aorta in the fetus
- Generally closes by day 2 of life
- Size matters
- Moving blood from the aorta and into the pulmonary arteries
Tetralogy of Fallot
Most common cause of cyanotic congenital heart disease.
- VSD
- Pulmonary stenosis
- Overriding aorta
- RV hypertrophy
All 4 of these phenomena happen together
Transposition of great arteries
Requires atrial or ventricular shunt to live.
Embryonic lethal in absence of shunt
Coarctation
Aortic coarctation.
- Narrowing of aorta
- Causes cyanosis and low BP systematically
- Size of blockage matters
What is Ischemic Heart Disease and what are the 4 conditions associated with it? How is the coronary artery blood flow reduced?
Usually a result of reduced coronary artery blood flow.
Myocardial perfusion can’t meet demand.
- By thrombus
- Critical stenosis
- Angina pectoris
- Acute MI
- Chronic IHD
- Sudden cardiac death
What is Angina Pectoris and what are the three types?
Ischemic heart disease.
Intermittent chest pain.
- Stable
- Most common
- Pain on exertion
- Fixed narrowing of CA - Prinzmetal (variant)
- Pain at rest
- CA spasm - Unstable (pre-infarction)
What is acute MI and what are clinical features?
Ischemic heart disease.
Necrosis of myocardium from ischemia.
- Affects 1.5M/year.
- Mostly due to CA thrombosis <20-30min
- Prompt reperfusion can salvage myocardium
Clinical Features:
- Severe, crushing chest pain
- Not relieved by nitroglycerin
- Sweating, nausea
Elevation of what molecule precedes acute MI and why?
CK-MB increases within 2-4hrs, returns to normal within 72 hours.
Cardiomyocytes have a lot of CK-MB, so if they are damaged, CK-MB spills out of cells.
What gross changes may be absorbed with acute MI?
- Mottling - coagulation necrosis
- Mottling - coagulation necrosis; neutrophils come in
- Yellow infarct center - Neutrophils die, macrophages come to eat dead cells
- Yellow center, red borders - granulation tissue
- Scar - collagen
What are the two types of acute MI?
- Subendocardial infarction
- Affects 1/3-1/2 of heart wall
- Inner wall more affected because blood supply goes first to outer wall - Transmural infarction
- Affects more than 1/2 of heart wall
- More serious