Case studies 11, 12, 15 (heart attack, failure, and disease) Flashcards
(38 cards)
Heart failure
- No longer able to pump adequate amount of blood
- The ventricles fail to maintain cardiac output to adequately perfuse the tissues
(chronic and acute)
forward heart failure
reduced blood flow to tissues → reduced renal blood flow → activates renin-angiotensin-aldosterone mechanism → salt and water retention to increase blood volume and venous pressure → edema
backward heart failure
blood “back ups” in veins draining to the heart → increased venous pressure, congestion, edema
congestive heart failure etiology
Any type of heart disease that cause - myocardial weakness - restrictions to pumping - increased after load (AKA EVERYTHING)
left side heart failure
- Left ventricle is failing
- Blood backs up in pulmonary circulation
- Pulmonary congestion and more pronounced respiratory difficulties occur
right side heart failure
- Right ventricle is failing
- Blood backs up in systemic circulation
- Liver and spleen enlarge and peripheral edema is more prominent
Pulmonary edema
- Fluid accumulation in the lungs
- Caused by left-sided heart failure
- Causes an increase in blood hydrostatic pressure in the pulmonary capillaries
Pleural effusion
- Excess accumulation of fluid in the pleural space
- Eventually the same processes will lead to fluid leaking into the pleural space and causing the effusions
Pitting edema
Swelling in which a persistent depression is left when pressure is applied
Hepatomegaly
- Systemic venous congestion impairs the drainage of blood from the liver into the inferior vena cava
- Blood vessels in the liver become congested with blood
- the liver enlarges
Natriuretic Peptides in Heart Failure
- Peptides are released from stretched cardiac muscle
- Results from overdistention or elevated pressure in cardiac chambers
- promote urinary loss of salt and water, counteracting the effects of the renin-angiotensin-aldosterone system
Type B natriuretic peptide (BNP)
- released from ventricles is more significant physiologically than atrial peptide
- Measurement helpsdistinguish dyspnea due to heart failure (high BNP) from dyspnea caused by pulmonary disease (no significant BNP elevation)
Benign Prostatic Hyperplasia
The prostate enlarges and, because it surrounds the urethra, it causes constriction of the urethra and obstructs the outflow of urine
Acute myocardial infarction (MI)
Necrosis of myocardial tissue caused by the development of severe ischemia
Precipitating event often involves the disruption of an atheromatous plaque
often involves muscles of the LV and septum
Transmural infarct
full-thickness infarct from endocardium to epicardium, usually from clot in major coronary artery
Subendocardial infarct
only part of wall undergoes necrosis
cardiac arrest may result from
- Arrhythmia
2. Asystole
acute MI classical symptoms
- Severe chest pain often radiating to left shoulder, arm, or jaw - Diaphoresis - Shortness of breath/Breathlessness - Anxiety - Nausea and vomiting - Lightheadedness, dizziness, fatigue - Signs of falling cardiac output
who is most likely to experience atypical MI symptoms
women
elderly
people with diabetes
myoglobin
- A heme containing protein found in cardiac and skeletal muscle
- It is released early from damaged cardiac cells
- Increase within 2-4 hrs of injury
- Peak within 6-12 hrs
- Return to baseline 24-36 hrs
creatine kinase
enzyme in muscle and brain
CKMB
- Isoenzyme of CK found mainly in cardiac muscle
- Increase within 3-12 hrs of injury
- Peak within 24 hrs
- Return to baseline 24-72 hrs
troponin
- Muscle protein complex
- Consists of 3 subunits
Troponin T and I each have a subtype specific to cardiac muscle - Increase within 3-13 hrs of injury
- Peak within 24-48 hrs
- Return to baseline 5-14 days
MI early treatment
MONA oxygen aspirin morphine nitroglycerine
