Pathophysiology Exam 3 Flashcards
BP =
CO x SVR
MAP
mean arterial pressure
MAP =
DBP + 1/3 (SBP-DBP)
Pulse pressure
SBP-DBP
Minimum MAP
60 mmHg
Vasodilation
decrease SVR
Vasoconstriction
increase SVR
CO =
SV x HR
What influences SV?
BV & contractility
low BP
hypotension
Hypotension parameters
BP < 90/60 mm
Only treat hypotension if it is what?
symptomatic
In Cardiogenic hypotension what is impacted?
Cardiac output (CO)
How is cardiogenic hypotension treated?
increase CO
- Epi/dobutamine
Epi/dobutamine are what?
(+) inotropes
(+) inotropes do what?
increase contractility
drug that raises blood pressure
- many are vasoconstrictors
pressor agent
Hypotension caused by Sepsis
vasodilation (decreases SVR)
How is sepsis hypotension treated?
Increase SVR
- NE/Vasopressin (ADH)/Epi/Phenylephrine
NE/Vasopressing (ADH)/Epi/Phenylephrine are all what?
vasoconstrictors (pressor agents)
Hypovolemia
decrease BV
How to treat hypotension caused by hypovalemia
increase IV fluids -> increase BV -> increase SV -> increase CO
high BP
hypertension (HTN)
Stage 1 hypertension
- systolic 130-139
OR - diastolic 80-89
Stage 2 hypertension
- systolic >/= 140
OR - diastolic >/= 90
Resistance heart pumping against
afterload
hypertension caused by what?
increased heart workload
effect of heart having to pump against increase resistance (effect of HTN)
ventricular hypertrophy.
ventricular hypertrophy
ventricular layer thickens
- ventricle holds less blood & pumps less blood
How to treat hypertension
decrease CO, decrease SVR or both
how to decrease CO
decrease SV by either decreasing BV or contractility
how to decrease SVR
vasodilation
Drugs that decrease CO
- diuretics (thiazide - HCTZ)
- Beta blockers
- ACE inhibitors/ARBs/Renin inhibitors
- Calcium channel blockers (CCBs)
Drugs that decrease SVR (vasodilators)
- ACE inhibitors/ ARBs/ Renin inhibitors
- CAlcium channel blockers
Drugs that are (-) inotropes and (-) chronotropes
Beta blockers & Calcium channel blockers. (CCBs)
Vasodilations decreases SVR and what?
LV afterload
atherosclerotic plaque
Coronary artery disease
chest pain caused by myocardial ischemia
Angina pectoris
angina with exertion; relieved with rest
- increase demand (exertion)
- decrease demand (at rest)
Stable Angina
Angina at rest
- decrease supply
Unstable Angina
CAD -> Myocardial ischemia -> ?
Myocardial Infarction (MI) = heart attack
- Unstable angina
- MI
Acute Coronary Syndrome (ACS)
MI’s can be _ or _
STEMI or non- STEMI
Immediate compensatory response for MI
increase SNS activity (bororeceptor reflex)
- heart: increase HR & CTX -> increase CO
- Blood Vessels: Vasoconstriction -> increase SVR
Slower compensatory response for MI
increase fluid retention -> increase BP
Cardiac enzymes (MI markers)
Troponins ( not detected till 3 hrs after MI)
CO inadequate to meet metabolic demand
Congestive heart failure (CHF)
Compensatory responses:
- increased preload caused by fluid retention
- increased afterload caused by increase SNS activity
Overall, increases myocardial workload
Congestive heart failure
“stretch” on ventricle wall
preload
“Resistance” ventricle must pump against
afterload
A failing heart _ than a non failing heart
works harder
decrease CO below normal
low output failure
loss of contractility
systolic
filling problem - small, “stiff” ventricle
Diastolic
- increase myocardial workload
- increase preload
- increase afterload
- dilated heart
systolic CHF
Systolic CHF treatment
- increase contraction with (+) inotropes
- decrease workload with beta blockers
- decrease preload with diuretics (decrease BV)
- decrease afterload with vasodilators (ARBs, Renin inhibitors, ACE inhibitors)
Dilated heart =
cardiomegaly
decrease SNS effect
- (-) inotropes
- (-) chronotropes
- used to decrease workload
beta blockers
- often caused by poorly controlled HTN
- increase afterload
Diastolic CHF
Diastolic CHF treatment
- increase ventricle filling time by decreases HR with CCBs
- decrease workload with CCBs
Heart failure with reduced ejection fraction (HFrEF)
Systolic failure
Heart failure with preserved ejection fraction (HFpEF)
Diastolic factor
Ejection factor (EF) =
SV (stroke volume) /EDV (end diastolic volume)
normal EF
50-60%
normal SV
70 mL
normal EDV
120 mL
Ejection fraction is not the same as what?
CO
LV failure ->
pulmonary edema -> increased pulmonary hydrostatic pressure -> fluid retention -> increased BV
low RBC count or low Hgb or low hematocrit
Anemia
% of blood that is RBC
hematocrit
What do you rule out first with Anemia?
blood loss
What do you rule out next with Anemia?
- decreased RBC production (bone marrow)
- increased RBC destruction (sickle cell anemia, hemolytic anemia)
What is the typical presentation of Anemia?
- fatigue (less O2 transport)
- pallor
more pale than normal
Pallor
Whats the anemia test?
H/H test = hemoglobin/hematocrit
Normal RBC size
80-100 fL
RBC may indicate what?
cause of anemia
micrositic anemia
<80 fL
- iron deficiency / Hgb deficiency
macrositic anemia
> 100 fL
- B12 deficiency
high WBCs (>10,000)
leukocytosis
Normal WBC count
5k-10k / uL
Potential causes of a WBC count of 15k
- infection present (rule out 1st)
- inflammation
Potential cause of a WBC count of 100k
Leukemia
- WBC are not function -> increased infection risk
low WBCs
Leukocytopenia or Leukopenia
WBC count of 1k has an increased what?
infection risk
low platelet count
thrombocytopenia
Normal platelet count
150k - 400k
Platelet count of 30k
increased bleeding risk
Platelet count of 15k
severe - may bleed spontaneously
Thrombosis
Deep vein thrombosis (DVT)
clot that has detached from the wall; now in circulation
thromboembolus
DVT -> thromboembolus ->
pulmonary embolus -> circulatory collapse
Virchow’s triad
3 risk factors for DVT
What are Virchow’s triad?
1) Hypercoaguability - blood clots easier
- pregnancy/OC (birth control)/cancer
2) Venous stasis - slow venous blood flow
- immobility/A-fib
3) Vessel wall damage (endothelial injury)
- smoking/ HTN
- life threatening
- cellular/tissue hypoxia
- If caught early, reversible
- If allowed to rapidly progress, irreversible
- most common presentation = hypotension
Circulatory shock
4 types of circulatory shock
- Distributive
- Cardiogenic
- Hypovolemia
- Obstructive
severe peripheral vasodilation
- septic, anaphylactic, neurogenic, toxic shock
Distributive circulatory shock
intracardiac cause of pump failure
- MI, CHF
cardiogenic circulatory shock
Low BV
- hemorrhagic vs non-hemorrhagic
Hypovalemia circulatory shock
extracardiac cause of pump failure
- PE
Obstructive circulatory shock
circulatory shock can lead to what?
Multiple Organ failure (MOF)