Cardiac Pathology

1. Congestive Heart failure
2. Ischemic heart dx
3. Hypertensive heart dx
4. Cardiac tumors

- ventricle is unable to pump the normal vol. of blood out that is delivered to it in diastole-->leading to inc amt of blood left in vent at end of diastole-->causing inc end-diastolic press-->and subsequent inc in venous press
- hence body not receiving sufficient blood supply

PATHOLOGY
- main event is dilatation of L vent
- inc L vent lumen-->inc in L vent diastolic press-->inc in pulmonary venous press-->inc pulmonary capillary press-->causing acute edema and congestion of lungs (transudate)--->if persists can lead to chronic congestion and edema of lungs

Hemosiderin Laden macros (heart failure cells) w/n alveoli

BROWN INDURATION of lungs

1. Dyspnea (due to dec lung compliance from the congestion & edema in the lungs)
2. Arrythmias

1. systemic HTN
2. Mitral or Aortic valve insufficiency
3. Ischemic heart disease
4. Primary dx of myocardium

dilatation of R vent--> inc R ventricular venous press-->inc systemic venous press (first seen in SVC and IVC)-->systemic venous congestion

1. distended neck veins
2. hepatomegaly or splenomegaly
3. inc freq of DVT
4. soft tiss edema (feet and legs usually or can be generalized)

1. Left sided HF (MOST COMMON)
2. Intrinsic lung parenchyma dx or pulmonary lung dx (basically prob getting blood to lung to be oxygenated)
3. Tricuspid or Pulmonic valve dx
4. Congenital Heart dx

T

transudate present - frothy, bluish, bubbling liquid. liquid is acellular.

- CHF
- Pneumonia

- Non-inflammatory (basically an ultrafiltrate of blood)
- low protein content
- low specific gravity

- Inflammatory
- high protein content
- high specific gravity

Brown Induration

L-sided HF

congestion of abdominal viscera
- liver (zone 3)
---acute sinusoidal congestion
---chronic hepatocyte atrophy
---"Nutmeg-like" appearance
---fibrosis called "cardiac cirrhosis"
-and soft tiss edema

Nutmeg-like
-due to chronic congestion of sinusoids (filled w/ erythrocytes)
- atrophy of hepatocytes

PITTING EDEMA

-DVT (femoral vein) secondary to chronic venous stasis due to congestion
**thrombus can embolize and head for R side of heart of lungs

- atherosclerosis of coronary arteries

male >60
female >70
**can also be in young adults due to drug abuse (cocaine)

- HTN
- DM
- smoking
- inc LDL

critical stenosis of >75% due to...
--fixed narrowing of atherosclerosis
(may cause ANGINA- intermittent chest pain)
--acute arterial thrombosis superimposed on atherosclerotic plaque occluding artery leading to coagulative necrosis & MI
--acute change w/n existing plaque such as hemorrhage

intermittent chest pain

LAD>>RCA>LC

T

eccentric (variable) wall thickening rather than concentric

-ONLY the intima
- media and adventitia are sparred

lipid and collagen

fibrin and platelets

blue trichrome

thrombus formation

MI

myocardial necrosis due to occlusion of segment of coronary art

- most common cause of death in US
- 1/3 are fatal
- of fatal MIs 50% die on way to hospital

1. Progressive (evolves over time hrs-wks)
2. Ischemic (block oxy blood to tiss)
3. Coagulative (protein denaturation > enzymatic digestion
4. Necrosis (cell death, tiss death)

- ER
- Mitos

20-30 min of occlusion

- anterior LV and anterior 2/3 of IVS (interventricular septum)
- RARELY in RV

- area of myocardial necrosis
- extent of necrosis

GROSS: NO change no lesions
HISTO: wavy myocardial fibers

GROSS: dark spots
HISTO: coagulative necrosis

GROSS: pale yellow
HISTO: neutros present

GROSS: yellow, well defined area of infarct
HISTO: lysis of dead muscle cells begin to dissappear. early phagocytosis by macros

**VERY critical period

GROSS: soft & pale - shrunken, purple
HISTO: Granulomatous tiss = prominent capillary growth. phagocytosis of necrotic muscle. collagen gets deposted by FIBROBLASTS (basically trying to heal)

GROSS: dense fibrous scar (white & firm)
**remains for life

- jaw, shoulder
- NO, can feel like worsening indigestion

1. papillary muscle dysfunction/rupture (usually early)
2. rupture of infarct (usually early)
3. mural thrombi (thrombus on endocardium)
4. acute pericarditis
5. ventricular aneurysms
6. L vent failure
7. arrythmias (most common 75-95%)

ARRYTHMIA

Hemopericardium - blood accumulating in pericardium

cardiac tamponade-->ventricular fibrillation

you would hear a friction rub

- dark and sunken infarct
- dilated ventricles

- hypertrophy of L vent

> 450 gm (normal = 300-350gm)
> 2cm (normal = 1.5cm)

- concentric wall hypertrophy
***unlike in Ischemic Heart Disease where atheroscerlotic plaque leads to eccentric artery wall thickening in coronary arteries

1. MM- skel muscle (MOST available)
2. MB- cardiac muscle>>>skel muscle
3. BB- brain & GI tract (least available)

- MB
- rises 2-4 hrs, peaks @ 18 hours, normal @ 48 hours

- Troponin I
- it rises quickly in injury and stays elevated longer (4-7 days)

- if LD1>LD2 suggests myocardial ishemia
(normal heart LD1<LD2)
**LD1 rises in 3 days

1. Creatine Kinase (mainly MB)
2. Troponin (mainly Troponin I)
3. Lactate Dehydrogenase

- hypertrophic myocardial fibers w/ BOXCAR NUCLEI

- kidney--> granular cortex due to HTN and the resulting hyaline ARTERIOLOSCLEROSIS
- brain--> hypertensive hemmorhage

1. Metastatic
--10% pts w/ disseminated cancer. --metastasize from lung & breast.
--most freq involve PERICARDIUM.
2. Primary
--Benign & very uncommon
--ATRIAL MYXOMA most common in this grp. appears in LA causing mass to create "ball valve" obstruction. see Stellate cells histologically.

- ATRIAL MYXOMA
- Left Atrium
- Stellate cells

syncope & sudden death