Newman: Questions for CV disease and CAD Flashcards
What are the determinants of BP?
P = Q x R
*altering flow and resistance
the ability of the arterioles to clamp down ro relax
resistance
What substances can increase vascular resistance?
Norepi
Epi
Angiotensin II
What substances decrease vascular resistance
NO
prostacylin
T or F: Flow = Cardiac Output
True
CO =
SV x HR
quantity (CCs) of blood ejected from the left ventricle into the aorta every cardiac cycle
stroke volume
What are the determinants of SV?
preload, afterload, contractility
the volume of the left ventricle at the end of diastole
preload (EDV)
T or F: An increase in preload will increase blood pressure
T
Why would you insert a pulmonary artery catheter?***
to measure preload: ballon inflates in the (left ventricle?) and the preload can be measured (left ventricular end diastolic pressure)
A bigger left ventricle (dilation) will (increase or decrease) the afterload.
increase
The inherent ability of the heart to contract–is independent of preload and afterload
contractility
SV / EDV =
ejection fraction
A pt has an ejection fraction of 30%, is that good or bad?
bad
A pt has an ejection fraction of 70%, is that good or bad
good
renin is secreted fron JG apparatus in response to ____
dec Q, CO, SV
Angiotensin I goes thru the ____ and is converted to ang II by_____
lungs
converting enzyme
What 2 important things does angiotensin II do?
- potent vasoconstrictor (inc resistance)
2. stimulates the secretion of aldo from the adrenal glands
An decrease in the amount of angiotenisn II would (inc or dec) BP
decrease
What does aldosterone do?
causes reabs of Na and excretion K+
Would a person in HF want to have high or low levels of aldosterone?
low – do not was to reabsorb any more Na/H2O
A pt presents to you with chest pain only upon exertion and is relieved by rest.
What would a treadmill test tell you?
What would a cardiac catherterization tell you?
What pharm
treadmill: will increase HR and SBP, which exacerbate the exertional chronic stable angina
cardiac cath will tell you how blocked he is, but I don’t think he’s a candidate for this?
A pt has severe chest tightness which wakes him from sleep
normal ECG
acute coronary syndrome
You have 3 vessel coronary disease. What do you do now?
bypass–STAT!
pt presents to the ED with severe chest pain. the ECK reveals ST elevation in leads 2, 3, and avF what do you do?
cath?
3 syndromes of coronary disease
chronic stable angina
Acute coronary syndrome
ST elevation MI
62 yr old male walks his dog and gets tightness in chest with SOB. He sits down and the pain goes away.
Dx
chronic stable angina
Man carrying bag of groceries upstairs and it got better when he sat down.
Dx
chronic stable angina
tighness/contrictoion in chest + SOB + gets better when sits down/at rest
chronic stable angina
exertional symptoms
chronic stable angina
inadequate supply of blood to myocardium (heart blockages) and increased demand relative to the supply
chronic stable angina
2 major determinates of myocardial demand
systolic BP
HR
Effect of exercise on HR and systolic pressure
inc HR and inc systolic pressure
What reduces supply in chronic stable angina?
arthlerosclerosis
Wakes up with elephant sitting on chest pale sweating breathing hard *this is not dependent upon exertion
acute coronary syndrome
pathophys of acute coronary syndrome
arthlerosclerotic plaque narrown lumen –> ruptures–>
- increased constriction/resistance
- thrombotic state in which blood clots form at area of rupture
T or F: acute coronary syndrome is a problem of supply and demand
false
*there is no inc demand on the heart, just a problem with supply
What is the diff btwn MI and acute coronary syndrome?
in MI, there is ZERO perfusion/supply = CA is 100% occluded
Has ECG changes!
problem of supply and demand–inc demand will not lead to a proportinal inc supply
chronic stable angina
O2 supply is a function of ____
coronary blood flow
arthleroscloerotic plaque causes
inadeqate supply
Myocardial demand is a function of
systolic BP and HR
blockage restricts O2 supply when it takes up ___% of CA lumen
70%
heart pains are always more than _____mins and never more than ____mins (time)
5 mins; 30 mins
Heart pains assc with activities is better or worse prognosis
better prognosis
Chronic stable angina is assc with (inc or dec) catecholamines
inc catecholamins –> skin gets pale
= over sympathetic activity
angina pectoris/chronic stable angina assc with
diaphoresis
sense of breathlessness
T or F: heart pains almost always makes a person alter their activities
true
angina pectoris is a consequence of myocardial oxygen demand exceeding _____
myocardial oxygen supply
can replicates syndrome (see if gets pale, breaks out in sweat, pain, see EKG)
treadmill test
At the microscopic level in chronic stable angina, what is happening at microscopic level?
ishemia
etiologic factors other than artherlosclerosis that can cause an MI
injury
emboli
pt that woke up in middle of the night with an elephant on chest with normal ECG
acute coronary syndrome
*lack of complete occlusion of artery
pathophys of ACS
artherlosclerotic CA –> rupture –> platelets move in –> TXA2 made –> momentary vasoconstriction –> decrease in O2 supply/ischemia
artherlosclerosis –> ______ –> rupture –> _______
chronic stable angina
acute coroney syndrome
What causes the arthlerosclerotic plaque rupture in ACS?
endothelial activation smoking cytokines elevated glc (AGE) HTN
lead to
-vasoconstrion and platelet aggrgation –> rupture
vulnerable plaque vs stable plaque
vulterable have large lipid core, thin cap
stable: more smooth muscle cells and is more well formed
role of platelets in ACS
rupture of plaque –> paltelets rush in –> TXA2 produced –> vasoconstriction –> fibrin deposition
In ACS the ____ is the culprit
vessel
platelets are the 2nd most important part
rupture –> thrombus
ACS
What is the Tx of ACS
blood thinners (heparin)
MI and ACS presents similarly, what is the only distinguishing factor
ECG
severe prolong contriction of chest (may last an hour or 2)
very pale
very diaphortetic
difficulty breathing
acute MI
Complications of acute MI
syncope arrythmia LHF cardiogenic shock sudden death
Describe the heart pain in an acute MI
30 mis to several hour of chest pain
pain radiates to arm, neck, jaw
MI ECG changes
ST elevation
ST elevation means
the vessel has been 100% occulded (by thrombus)
locations of ST elevation on ECG determines _____
location of MI on heart
as myocytes die the secrete enzymes….
CK
SGOT
LDH
troponin
_____ is a predictor of ischemic event
troponin
more than 1 p wave for every QRS
heart block (casues arrhythmia?)
Tx of heart block
pacemaker
ventricualr fibrillation
know ECG for it
complication of MI
myocardial rupture
-blow hole in wall of ventricle, IV septum, papilary muscle
fluid in lungs due do abnormal accumulation of Na and H2O
HF (fluid in alveoli)
What to do when person has MI and there is no cath lab
get rid of clot to reperfuse
-streptokinase
treateent of choice for a pt with ST elevation MI
put in mesh balloon/stent at area of occlusion = angioplasty
take veins from leg, anastomose to proximal aorta and anastomose to area distal to CA blockage
bypass surgery
What has a positive effect on SV?
Negative?
positive:
- inc length of myocardial fibers by increasing preload (EDV)
negative:
- inc afterload decreases the contractility (dialated left ventricle); inc systolic BP
Formula to calculate ejection fraction
SV / EDV
arthlerosclerotic plaque narrown lumen –> ruptures–>
- increased constriction/resistance
- thrombotic state in which blood clots form at area of rupture
ACS
How are heart pains (in chronic stable angina) distinguished from other pains?
longer than 5 mins and less than 30mins
make a person alter their activities
T or F: in ACS the coronary artery is 100% occluded
False, not 100%
This is why the EKG is unremarkable*
