Cardiac Pathology 1 Flashcards
Aging and the Heart
1) MYOCARDIUM and CHAMBERS
- Decreased LV chamber SIZE
- Increased EPICARDIAL FAT
- Myocardial changes:
a) LIPOFUSCIN and BASOPHILIC degeneration
b) Fewer myocytes, INCREASED COLLAGEN FIBERS
2) VALVES:
- Aortic and mitral valve annular CALCIFICATION (Can form Embolus)
- Fibrous THICKENING
- Mitral Valve LEAFLETS BUCKLING TOWARDS left Atrium → INCREASED left atrium size
- Lambl excrescences
3) VASCULAR CHANGES:
- Coronary ATHEROSCLEROSIS
- STIFFENING of the Aorta
Congestive Heart Failure
1) Occurs when the heart is UNABLE TO PUMP BLOOD AT A RATE TO MEET PERIPHERAL DEMAND, or can only do so with increased filling pressure.
2) MAY RESULT FROM:
- LOSS of myocardial CONTRACTILE FUNCTION (SYSTOLIC dysfunction)
- LOSS of ABILITY to FILL the VENTRICLES during diastole (DIASTOLIC dysfunction)
Cardiac Hypertrophy
1) Cardiac myocytes become HYPERTROPHIC when:
- Sustained PRESSURE or VOLUME OVERLOAD
- Sustained TROPHIC SIGNALS (β-adrenergic stimulation)
2) In the setting of PRESSURE OVERLOAD:
- Myocytes become THICKER, and the LEFT VENTRICULAR WALL THICKNESS INCREASES CONCENTRICALLY!!!!!
3) In the setting of VOLUME OVERLOAD:
- Myocytes ELONGATE, and the VENTRICULAR DILATION is seen
4) Hypertrophy of Myocytes ISN’T ACCOMPANIED by a MATCHING INCREASE IN BLOOD SUPPLY
- Even though the Hypertrophied Heart’s ENERGY DEMANDS HAVE INCREASED
5) “The hypertrophied heart is VULNERABLE TO ISCHEMIC RELATED DECOMPENSATION”
** Best measure of Cardiac Hypertrophy is the WEIGHT OF THE HEART!!!!!!
Left Sided Heart Failure
1) Can be SYSTOLIC or DIASTOLIC FAILURE
2) Most commonly a result of:
- Myocardial Ischemia
- Hypertension
- Left-sided valve disease
- Primary myocardial disease
3) Clinical effects are due to:
- CONGESTION in the PULMONARY CIRCULATION
- DECREASED TISSUE PERFUSION
4) DECREASED EJECTION FRACTION may result in DECREASED Glomerular Perfusion
- Stimulating RELEASE of RENIN → INCREASED VOLUME
- PRERENAL azotemia
5) ADVANCED CHF may lead to DECREASED CEREBRAL PERFUSION
- Hypoxic ENCEPHALOPATHY!!!
Left Sided Heart Failure
Morphologic Changes
Morphologic changes are variable (dependent on the inciting cause):
1) Left ventricular HYPERTROPHY
2) Left Ventricular DYSFUNCTION → Left Atrial DILATION
- This can lead to ATRIAL FIBRILLATION, stasis, thrombus
3) PULMONARY CONGESTION and EDEMA
◦ Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Right Sided Heart Failure
**** MOST COMMON CAUSE IS LEFT-SIDED HEAR FAILURE***
1) ISOLATED Right-sided FAILURE RESULTS from ANY CAUSE of Pulmonary HYPERTENSION:
- Parenchymal lung Diseases
- Primary pulmonary Hypertension
- Pulmonary Vasoconstriction
Primary Right Sided Heart Failure
1) Pulmonary CONGESTION is MINIMAL
2) The VENOUS SYSTEM is markedly CONGESTED:
a) Liver congestion (NUTMEG LIVER)
b) Splenic congestion → SPLENOMEGALY
c) EFFUSIONS involving peritoneal, pleural and pericardial spaces
d) EDEMA, especially in dependent areas (e.g., ankles)
e) RENAL CONGESTION
Ischemic Heart Disease
1) Results from INSUFFICIENT PERFUSION to meet the metabolic demands of the myocardium.
2) BLOOD to the MYOCARDIUM is supplied by the CORONARY Arteries, so any DISRUPTION of Coronary flow may result in ischemia.
3) Ischemia may result in:
- MYOCARDIAL INFARCTION
- ANGI pectoris
- Chronic ischemic heart disease, with heart failure
- SUDDEN CARDIAC DEATH
4) LEADING CAUSE OF DEATH in the US*****, and Greater than 90% are secondary to Atherosclerosis
- Chronic vascular OCCLUSION
- Acute plaque change
- Thrombus
Angina Pectoris
** Transient, often RECURRENT CHEST PAIN induced by MYOCARDIAL ISCHEMIA INSUFFICIENT to induce MYOCARDIAL INFARCTION.
Three clinical variants:
1) STABLE ANGINA:
- Stenotic OCCLUSION of CORONARY ARTERY!!!!!
* * PAIN WITH EXERCISE*
- “Squeezing” or BURNING sensation, relieved by rest or vasodilators
2) PRINZMETAL VARIANT ANGINA:
- EPISODIC coronary artery SPASM, relieved with VASODILATORS
3) UNSTABLE (or “crescendo”) ANGINA:
- PAIN, INCREASING in Frequency, Duration and Severity, eventually at rest
* ** PAIN AT REST ***
- Usually RUPTURE OF A PLAQUE, with a PARTIAL THROMBUS
- 50% may have EVIDENCE OF MYOCARDIAL NECROSIS
Myocardial Infarction
1) AGE DISTRIBUTION and RISK factors mirror those of atherosclerosis in general, because nearly 90% of infarcts are caused by an ATHEROMATOUS PLAQUE
2) Other causes include:
- Embolus
- Vasospasm
- Ischemia secondary to vasculitis, shock, hematologic abnormalities
Myocardial Infarction- Presentation
” Classic” Presentation
1) PROLONGED CHEST PAIN (>30 min)
- Crushing, stabbing, squeezing, tightness
- RADIATING DOWN LEFT Arm, or to LEFT Jaw
2) DIAPHORESIS
3) Dyspnea
4) Nausea-vomiting
5) Up to 25% are asymptomatic
Acute Myocardial Infarction Location, Size and Features depend on
- The site, degree and rate of OCCLUSION of the artery
- SIZE of the area perfused
- DURATION of occlusion
- Metabolic and oxygen NEEDS of the area at risk
- Extent of COLLATERAL BLOOD FLOW
- Presence of ARTERIAL SPASM
** Infarct can be TRANSMURAL in 6 to 24 Hours!!!!**
Coronary Vessels and Areas of Infarct
1) LAD (40-50%)
- Apex, LV anterior wall, ANTERIOR two thirds of SEPTUM
2) RCA (30-40%)
- RV free wall, LV posterior wall, POSTERIOR third of SEPTUM
3) LCX (15-20%)
- LV LATERAL WALL
Morphologic Evolution of MI
1) 4 to 24 hrs: Coagulation Necrosis
2) 1 to 3 Days: Many PMNs
3) 7 to 10 Days: Phagocytosis of Dead Cells/ Debris
4) 10 to 14 Days: Granulation Tissue
5) Greater than 2 Months: Dense Collagen
Reperfusion
1) RESTORING BLOOD FLOW to an area of ISCHEMIA and impending infarction
- An attempt to LIMIT THE INFARCT size by rescuing at risk myocardium
* CONTRACTION Bands
2) Thrombolysis, angioplasty and stent placement, CABG
