path 1 Flashcards
describe the blood flow thru the heart
- Right atrium
- tricuspid valve
- tright ventricle
- pulmonic valve
- pulmonic veins
- left atrium
- mitral valve
- Left ventricle
- aortic valve
- aorta
Define Congestive Heart failure
- characterized by variable degrees of DECREASED CARDIAC OUTPUT AND TISSUE PERFUSION, as well as pooling of bloodin venous system which may cause pulmmonay edema, peripheral edema or both
- CHF occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure
What are the most common causes of Heart failure
- Coronary artery disease –> myocardial infarction
- High blood pressure
Define Acute Heart failure
- Happens suddenly (think heart attack)
- can be immediately life threatening because the heart doesn’t have time to undergo compensatory mechanisms
describe chronic heart failure
- long term conditions
- associated with the heart undergoing adaptive responses (DILATION, HYPERTROPHY) to a precipitating cause
- these adaptive responses, however, can be deleterious in the long-term and lead to worsening condition
how is ultrasound used
- looks at flow through the heart
- allows for calculation of ejection fraction
Describe the Systolic dysfunction
- Ejection fraction is LOW (heart is DILATED/ENLARGED VENTRICLES)
–> enlarged ventricles fill with blood
–> ventricles pump out less than 40-50% of blood (LOW EJECTION FRACTION IN SYSTOLE)
describe DIASTOLIC DYSFUNCTION
- Ejection fraction is normal (thickened wall and LESS VOLUME)
- The stiff ventricles fill with LESS BLOOD THAN NORMAL
- The ventricels pump out about 60% of the blood (normal), but the amount may be LOWER THAN NORMAL (SYSTOLE)
What are the stages of CHF
- Stage A = patietns at high risk for developing HF in the future but no functional or structural heart disorder
- Stage B = a structural heart disorder but no symptoms at this stage
- Stage C = previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment
- Stage D = advanced disease requiring hospital-based support, a heart transplant or palliative care
describe the response to HF
- Release of ATRIAL NATRIURETIC PEPTIDE (B-Type natriuretic peptide) –> over 100 = HF occuring
- Activation of renin-angiotensin-aldosterone system (flow to kidney is reduced/low volume state)
- Release of norepinephrine by adrenergic cardaic nerves of autonomic nervous system
–> increase HR and augment myocardial contractility and vascular resistance
describe Left sided CHF
- Will produce SYMPTOMS
–> Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
- Pulmonary congestion and edema (HF cells present)
- Dilation of left atrium
- reduction in renal perfusion and CNS (in severe left sided CHF)
Describe Right sided CHF
- Will produce SIGNS
–> Blood backs up into the venous system resulting in JVD, Pitting edema, congestive hepatosplenomegaly, pleural, pericardial or peritoneal effusions
- usually results in pulmonary hypertension (cor pulmonale)
- congestion of kidney and CNS
Describe Biventricular CHF
- Both sides are failing, so combo of both
- Most common cause of RIGHT HEART FAILURE is due to LEFT SIDED HEART FAILURE causing pulmonary edema leading to pressure on the rgiht heart leading to BIVENTRICULAR CHF
what are some treatments for CHF
- Diuretics
- angiotension converting enzyme inhibitors
- Beta1-adrenergic blockers
- mechanical assist
- cardiac transplant (advanced, irreversible heart failure)
describe Ischemic heart disease (IHD)
- MOST CAUSES CAUSED BY OBSTRUCTIVE ATHEROSCLEROTIC LESIONS in coronary arteries
- Insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries and variable degrees of superimposed acute plaque change, thrombosis and vasospams
- SUBENDOCARDIUM IS MOST VULNERABLE
what are the modifiable and nonmodifiable risk factors for atherosclerosis
- Nonmodifiable = incerasing age, male gender, family history, genetics
- Modifiable
- hyperlipidemia, hypertension, cigarrette smoking, diabetes
describe the formation of Atherosclerosis
- Endothelial injury/dysfunction causes binding of monocytes which will become macrophages
–> macrophages take up lipid and become foam cells which form fatty plaques
–> recruitment of smooth muscle cells precursors excrete extracellular martrix and fibroblasts
describe vulnerable plaque
- Soft with lipid filled core; most often eccentric; most often only 40-60% stenotic
- Prone to rupture due to plaque hemorrhage or to fibrous cap disruption
Ischemia vs Infarction
- ISCHEMIA - reversible cellular injury
–> therapeutic salvage may be possible
- Infarction - irreversible injury
–> myofiber coagulative necrosis
what are the symptoms of IHD
- Angina pectoris
- myocardial infarction
- chronic IHD with heart failure
- sudden cardiac death
describe Myocardial Ischemia
- Define = insufficient oxygen supply to myocardial fibers
- REVERSIBLE CONDITION, the result of:
–> decrease myocardial blood supply or..
–> increased myocardial oxygen demand
- Diagnose via Tredmill test: see if they have angina during exercise
Define stable (typical) angina
- produced by physical activity, emotional excitement or any other cause of increased cardiac workload resulting in an imbalance in coronary perfusion relative to myocardial demand
- relieved by resting or administering nitroglycerin
Define Unstable or crescendo angina
- pattern of increasing frequent pain, often of prolonged duration, that is precipitated by progressively lower levels of physical activity or that even occurs at rest
- caused by disruption of an atherosclerotic plaque with superimposed partial thrombosis.
define Prinzmetal variant angina
- Episodic myocardial ischemia that is caused by coronary artery spasm
- the angina attacks are urnelated to physical activity, heart rate or blood pressure
- responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers
describe the ankle brachial presure index (ABPI)
- ratio of the pressure difference from ankle to arm
- ratio should be equal
–> when it starts reducing (lower pressure in ankle and higher pressure in arm) indicates peripheral vascular disease (atherosclerosis)
describe teh symptoms of myocardial infarction
- Chest pain - levines sign (clenchig their fist over sternum),
–> pain radiates to left arm, lower jaw, neck, right arm, back or epigastrium
Dyspnea
- weakness, light-headedness, nausea, vomiting and palpitations
- loss of consciousness and sudden death
descrie the EKG changes in MI
- ST elevation = MI
- ST depression = Ischemia
What happens with tissue death
- Onset of myocardial infarction
- plasma membrane of necrotic myocytes becomes leaky
- molecules leak out of cell into circualtion
–> troponin will leak out and is measurable and indicates cell death (YOU DON”T GET IT WITH ISCHEMIA)
–> CK-MB is another marker to follow in order to make sure the patient does not REINFARCT
Patient presents with chest pain OR anginal equivalent symtpom, how would you decide what it is.
Why is timing so important in an MI
- If you get to patient within 30 mins you can salvage the muscle and reperfuse the area (no muscle death)
- If you want longer, the more cell death you develop
What vessels are most likely to have an MI
- LEFT ANTERIOR DESCENDING (40-50%)
–> infarcts involve the anterior wall of LEFT VENTRICLE near apex; anterior portion of ventricular septum and the apex circumferentially
- RIGHT CORONARY ARTERY (30-40%)
–> infarcts involve the inferior/posterior wall of left ventricle; posterior portion of ventricular septuml and the inferior/posterior right ventricular free wall
- LEFT CIRCUMFLEX (15-20%
- Lateral wall of left ventricle except the apex
describe histology post MI
- 1-4 hrs = wavy fiber pattern
- 12-24 hr = early coagulation and nerosis
- 1-3 days = lots of neutrophils
- 3-7 days = as neutrophils go away, the macrophages dominant
–> RISK OF MYOCARDIAL RUPTURE
–> switches from acute to chronic
- OLDER = scar tissue develops
What are the three scenarios leading to Myocardial rupture
- Rupture of free wall of LV = CARDIAC TAMPONADE
–> decreases ability to fill and contract
- Rupture of papillary muscle –> acute mitral valve incompetence
–> valvular disease suddenly
- Rupture of ventricular septum –> acutely acquired VSD
–> ventricular septal defect (increases volume to lungs)
Dressler’s syndrome
- 2-weeks post myocardial infarction, but can be delayed for a few months
–> inner material leaks out and starts developing an immune reaction which leads to pericarditis weeks after MI
describe pathogenesis of pericarditis
- Can occur shortly after MI due to area of infarct rubbing against the peritoneum causing inflammation
