Lecture review Flashcards
What contributes to coronary blood flow rate?
- perfusion pressure
- perfusion time
- vascular resistance
What contributes to myocardial O2 supply?
Coronary blood flow rate
Oxygen content of blood
As perfusion goes ↓, resistance vessels _____________
If perfusion goes ↑, resistance vessels _____________
what is this process called?
As perfusion goes ↓, resistance vessels dilate, so flow is maintained in spite of lower pressure
If perfusion goes ↑, resistance vessels constrict, so you don’t overperfuse the tissue
- AUTOREGULATION
As perfusion goes ↓, resistance vessels _____________
If perfusion goes ↑, resistance vessels _____________
what is this process called?
As perfusion goes ↓, resistance vessels dilate, so flow is maintained in spite of lower pressure
If perfusion goes ↑, resistance vessels constrict, so you don’t overperfuse the tissue
- AUTOREGULATION via arteriolar resistance vessels
What happens to pressure if stenosis increases?
P will drop (across the stenosis)
ie: 100 –> 70
body can compensate with arteriolar resistance vessels
- Oxygen supply may be compromised by what two things?
Anemia: less hemoglobin per ml blood
Hypoxemia: incomplete saturation of hemoglobin
What happens to perfusion P with hypotension?
decreased perfusion pressure
- ie hypovolemia (massive bleeding) or septic shock
Cardinal symptom of acute MI
- what should we keep in mind though?
severe unremitting chest discomfort at rest (not angina) - more severe, longer)
- 25-30% of MIs are silent
Cardinal symptom of acute MI
- what should we keep in mind though?
severe unremitting chest discomfort at rest (not angina) - more severe, longer)
- 25-30% of MIs are silent
- 1/3 of pts die suddenly
What mediators are released in AMI that can result in pain?
Adenosine, lactate from ischemic myocardial cells onto local nerve endings
but ischemia in AMI persists → necrosis → substances accumulate → activate nerves for longer periods
Possible Physical findings of AMI:
Possible Physical findings of AMI: (173)
- S4 - S3
Systolic murmur sometimes if:
○ Ischemia induced papillary muscle dysfxn → mitral valvular insufficiency (regurg)
○ Infarct ruptures through IV septum → VSD
• Drugs to treat coronary heart disease:
○ Lipid-modifying: - Statins ○ Anti-platelet: - Aspirin, clopidogrel ○ Anti-anginal: - Nitrates, beta blockers, CCBs ○ LV dysfunction: ACEI or ARBs
• Drugs to treat coronary heart disease:
○ Lipid-modifying:
- Statins
○ Anti-platelet:
- Aspirin, clopidogrel
○ Anti-anginal:
- Nitrates, beta blockers, CCBs
○ LV dysfunction:
- ACEI or ARBs
Primary prevention of anginal attacks
start a statin if LDL cholesterol > 190mg/dl
- aspirin
Secondary prevention after MI:
- Aspirin with or w/o clopidogrel or other thienopyridines (clop/thi esp after MI)
- Statins
- Beta blockers
- ACE inhibitor
- Smoking cessation
Profibrinolytics
- examples
- good to treat _____
profibrinolytics: tPA, uPA
Good to treat STEMI (not UA, or NSTEMI)
Problems with stents
Stents are thrombogenic, so a combo of oral antiplatelet agents (aspirin + clopidogrel) is crucial after implantation
Which vessels are commonly used for grafts?
○ Internal mammary artery
○ Saphenous vein
Primary prevention of anginal attacks
- start a statin if LDL cholesterol > 190mg/dl
- aspirin
How to acutely treat stable angina vs unstable angina
stable:
- Anti-anginal (nitrates, BBs)
- Anti-hypertensives
- Statins
- Antiplatelets (aspirin)
- if symp not relieved –> cor angiography
Unstable:
- Hospitalization
- IV nitroglycerin
- Usually early Cath / cor intervention
- Anti-anginal (nitrates, BBs)
- AntiTHROMBOTICS (aspirin, heparin ect)
How to acutely treat stable angina vs unstable angina vs acute STEMI
stable:
- Anti-anginal (nitrates, BBs)
- Anti-hypertensives
- Statins
- Antiplatelets (aspirin)
- if symp not relieved –> cor angiography
Unstable:
- Hospitalization
- IV nitroglycerin
- Usually early Cath / cor intervention
- Anti-anginal (nitrates, BBs)
- AntiTHROMBOTICS (aspirin, heparin ect)
AMI:
- Immediate aspirin, nitroglycerin, maybe BBs
- Reperfusion therapy ASAP: Coronary angioplasty if poss, or thrombolytic if not.
Activated SMC actions
- ↑ed inflammatory cytokines (IL-6, TNF) → ↑ed Leukocyte Prolif and LAM expression
- ↑ed ECM synthesis
- ↑ed migration/prolif into subintima (almost like a malignancy)
Good fxn of NO is activating cGMP to vasodilate, what is a negative fxn?
Recognize that abnormal endothelium and promote inflammatory state
How is activation of SNS in normal endothelium beneficial? How can it be bad?
Normal: activate SNS → ↑ blood flow → ↑ NO → vasodilate
- relaxation effect of NO outweighs direct a-adrenergic constrictor effect of catecholamines
Abnormal endo: impaired NO → inappropriate vasoconstriction
