Pathophysiology Exam #3

Blood Pressure Formula

BP= CO x SVR

T/F:

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If BP is increased, so is CO and/or SVR, and vice versa?

True

Cardiac Output Formula

CO= SV x HR

What is Stroke Volume (SV) directly correlated to?

Blood Volume (BV) and contractility

What is blood volume?

BV is how much blood is pumped out each beat

What is contractility?

Contractility determines how much blood is being pumped out

MAP formula

(Mean Arterial Pressure)

MAP= DBP + 1/3 (SBP - DBP)

OR

MAP= DBP + 1/3 (PP)

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PP or Pulse Pressure = (SBP-DBP)

Minimum MAP

60 mmHg

Vasodilation (arterial)

(increases or decreases) SVR?

decreases SVR

Vasoconstriction (arterial)

(increases or decreases) SVR?

increases SVR

Hypotension

Low Blood Pressure

Hypotension values

BP < 90/60 mmHg

Symptoms of Hypotension

* lightheadedness
* low energy

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* sometimes may be asymptomatic
* only treat it, normally, if symptomatic

Drugs for cardiogenic (heart problem) cause of hypotension

* epinephrine or dobutamine
* both increase CO, increase contractility

\+ inotropes

drugs that increase (↑) contractility

\- inotropes

drugs that decrease (↓)contractility

What does increasing contractility do to BP?

↑ contractility, ↑ CO, ↑ BP

Drugs for Sepsis cause of Hypotension

* patients typically undergo significant vasodilation (↓ SVR)

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* give drugs that cause vasoconstriction (↑ SVR)
* Pressor Agents (drugs that ↑ BP); vasoconstrictors
* Norepinephrine (NE); also called Levophed (Levo), Vasopressin (also called ADH), Epinephrine, Phenylephrine

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* all vasoconstrictors; these are given to constrict the vessels and reverse the vasodilation (↓ SVR) causing the hypotension

Hypovolemic (Low Blood Volume)

* significantly dehydrated or profusely bleeding
* treat by giving IV Fluide (dehydration) or blood transfusion (bleeding)

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* giving the fluids/blood will ↑ BV, which ↑ SVR, which ↑ CO, which ↑ BP

Hypertension (HTN)

high blood pressure

Stage 1 HTN

* systolic value between 130-139 and/or
* diastolic value between 80-89

Stage 2 HTN

* systolic value of 140 or higher and/or
* diastolic value of 90 or higher

T/F:

The patient should be treated even if they are not feeling the effects of the hypertension.

True

HTN effects on the heart

* Ventricular Hypertrophy
* ventricular myocardium (left ventricle) begins to enlarge over time as a compensatory response to the ↑ workload
* If poorly controlled, over time, the patient can develop diastolic heart failure

Afterload

resistance the heart is pumping blood against

HTN Treatment:

Drugs that lower CO

* Diuretics (thiazide - HCTZ)
* increases urine output, lowering BV, which lowers SV and CO
* Beta Blockers
* reduces SNS effects on the heart
* lowers HR, lowers contractility/SV, lowers CO
* ACE inhibitors/ ARBs/ Renin inhibitors
* lower CO by lowering aldosterone
* lowering aldosterone lowers BV which lowers CO
* Calcium Channel Blockers (CCBs)
* lower CO by lowering SV and HR
* SV is lowered by contractility being lowered which lowers HR, therefore, lowering CO

Beta Blockers and CCBs are (+/-) inotropes and (+/- chronetropes)?

\- inotropes

\- chronetropes

\- chronetropes

drugs that decrease heart rate

HTN Treatment:

Drugs that lower SVR

* SVR is lowered through vasodilation

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* ACE inhibitors/ ARBs/ Renin inhibitors
* block R.A.A.P. at various points and the pathway doesn’t come to completion- causes vasodilation which lowers SVR
* Calcium Channel Blockers (CCBs)
* vasodilation and SVR is lowered
* tells vascular smooth muscle to relax

What affects would vasodilators have on LV afterload?

Reduces it because the heart has less resistance to pump against

Coronary Artery Diease

* atherosclerotic plaque formation
* specifically in the arteries
* plaque reduces the lumenal diameter thus reducing the flow of blood through the artery; platelet plugs can form and further occlude the artery
* results in ischemia
* reduced blood flow

Risk Factors for CAD

* Diabetes Mellitus (DM)
* accelerates plaque formation
* Smoking
* High fat/cholesterol diets
* sedentary lifestyle
* obesity
* hypercholesterolemia

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* many risk factors can coincide together which accelerates it even further; however, many are considered modifiable risk factors (habits/behaviors can be changed to reduce the risk of CAD)

What can CAD lead to?

Myocardial Ischemia

What is Myocardial Ischemia?

reduced blood flow to the myocardium

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* myocardium= muscle tissue of the heart

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Mild Myocardial Ischemia can be silent; not present any visible symptoms

What can Myocardial Ischemia lead to?

Angina Pectoris

* stable or unstable

Stable Angina

* angina with exertion
* relieved with rest and or specific medications

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* increased demand from the heart working harder that is placed on a limited supply of blood flow due to reduced lumenal diameter/ smaller space for blood to flow
* with rest, the demand will go back down and the arteries can now keep up with the needs of the heart

Unstable Angina

* angina at rest (ominous sign; impending potential heart attack)
* reduced supply at rest; demand is still the same but supply was reduced
* must be intervened upon

Myocardial Infarction (MI)

* death of myocardium
* substernal chest pain that radiates to the left shoulder or angle of the mandible

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* CO drops and tries to go back up to normal (compensatory response) BP drops because CO drops

Immediate compensatory responses after MI

* increased SNS activity (baroreceptor reflex)
* detects changes in BP and tries to do something about it
* SNS effect on the heart
* increased HR
* increased contractility
* Heart is maxed out after about 15-30 seconds for SNS response on the heart
* SNS effect on blood vessels
* vasoconstriction (↑SVR), ↑BP

Slower Compensatory Response after MI

* ↑ fluid retention
* ↑ BV to ↑ CO to ↑ BP
* CO drops during MI (less blood is flowing; specifically kidneys (urine output goes down and fluid retains) but also to other organs
* This is all increasing the BV (good response) but this also means the heart is being given more blood to pump thus working harder (not good response)

Treatments for MI

Test to run to confirm heart attacks

* Cardiac Enzyme (MI markers)
* Troponins: aren’t detected until about 3 hours after
* Enzymes get released after MI because tissue died and cells get released

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* Don’t order just an EKG but not troponin levels; do as much as possible to be proactive

Congestive Heart Failure

* CO inadequate to meet metabolic demand
* ↑ preload by fluid retention
* preload: “stretch” on the ventricle wall
* ↑ afterload cause by ↑ SNS activity
* afterload: “resistance” ventricle must pump against

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* Both of these increase myocardial workload (O2 demand)
* Preload, Afterload, and Workload are all directly correlated

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* Left Ventricular Failure

T/F: A failing heart works harder than a non-failing heart?

True

Systole

Diastole

Systole: contracting: pumping of blood

Diastole: resting/relaxing; refilling with blood

Low Output Failure

* Most Common


* ↓↓ CO (below normal)
* Categorized as Systolic or Diastolic
* Systolic: loss of contractility; not contracting as forcefully therefore not pumping out as much blood
* Diastolic: filling problem; small, stiff ventricle; common cause: left ventricular hypertrophy from poorly controlled hypertension

Systolic Failure

* loss of contractility
* ↑ myocardial workload
* Treatment: try to ↑ contractility or ↓ workload
* ↑ contractility by giving + inotropes
* ↓ workload by ↓ preload and afterload
* ↓ preload by ↓ BV by giving diuretics (LASIX: loop diuretic)
* ↓ afterload by giving vasodilators (↓ SVR); ACE inhibitors, ARBs, Renin inhibitors

Diastolic Failure

* some form of LV hypertrophy
* Goal of Treatment: ↑ ventricular filling time and ↓ workload
* ↑ ventricular filling time by ↓ HR - CCBs
* CCBs: (-) chronetropes to ↓ HR
* ↓ workload by giving CCBs
* trying to overcome ↑ afterload; CCBs will vasodilate
* overtime, the hypertrophy can slightly be reduced (not back to its original)

Normal Ejection Fraction (EF)

Formula for EF

Normal= \~ 50-60%

Formula: EF= SV / EDV

Stroke Volume (SV)

Ejection Fraction (EF)

End Diastolic Volume (EDV)

SV: the volume of blood that gets ejected per contraction; Normal=70mL

EF: the % of blood in the ventricle that gets ejected

EDV: volume of blood in the ventricle when ventricle is fully relaxed; Normal=120mL

Ejection Fraction

* Systolic Failure (HHrEF; Heart Failure with reduced Ejection Fraction)
* less than 40%
* Diastolic Failure (HFpEF: Heart Failure with preserved Ejection Fraction)
* normal to high %

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* EF is not the same as CO; it can influence CO
* You can have low EF but normal CO: indicates the extra work being put on the heart

Manifestations of Systolic and Diastolic Failure (Left Ventricular Failure)

LV failure --------→ Pulmonary Edema

* Pulmonary Edema: accumulation of fluid in the interstitial space of the lungs and in the alveoli
* interstitial space: respiratory membrane; where O2 is moved from alveoli to the bloodstream and CO2 is moved from the bloodstream to alveoli
* fluid accumulates and is expanding that space causing the oxygen to have to travel a greater distance

Pulmonary Edema

* fluid retention --→ ↑ BV
* ↑ pulmonary capillary hydrostatic pressure
* increased LV pressure with causes ↑ LAP and everything else behind that
* described as back pressure
* Pulmonary Edema further injures the heart and continues to reduce CO and a multitude of other things; reduces oxygen to the heart which makes the heart work harder

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* Treatment: Diuretics (reduced workload); decreases fluid retention and allows fluid to decrease in the lungs and therefore allows patients to breathe better

Anemia

* Low RBC count or low Hgb or low hematocrit

( 4-6 mil/mL) (12-17 g/dL). (35-55%)
* Normal ranges ↑
* Hematocrit: % of blood occupied by RBCs
* Can have just one, two or all factors; but even just one factor= anemia

Causes of Anemia

* Blood loss - Rule out first!!!


* make sure they aren’t bleeding out
* typically ↓↓ RBC


* ↓ RBC production (something affecting bone marrow)
* Leukemia; drugs that suppress bone marrow functionality
* Anything that ↑ destruction
* sickle cell anemia (abnormally shaped RBC; body removes them)
* hemolytic anemia (RBC being targeted and destroyed)

Typical Presentation for Anemia

Tests for Anemia

Presentation: Fatigue (can’t transport O2 well), Pallor (pale appearance)

Tests: H/H (Hemoglobin / Hematocrit)

White Blood Cell Abnormalities

WBC = Leukocytes

Normal Ranges

Normal Ranges: 5-10k μL

Fights infections

* Leukocytosis - high WBC ( >10k)
* EX: 15k
* infection present?
* inflammation? Non-infectious leukocytosis
* EX: 100k
* not infectious cause for the elevation; typical range/ceiling for infectious cause is 40-50k
* more indicative of leukemia; cancers
* increases infection risk
* lots of immature types of WBC

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* Lekocytopenia - low WBC (

Platelets (Thrombocytes) Abnormalities

Normal Count: 150-400k

Plays a role in clotting

* Thrombocytopenia (More Common)
* Low platelet count
* 30k - significant
* increased bleeding risk
* 15k or less - dramatic; can just randomly start bleeding internally or externally
* Can give platelets; transfusions

Thrombus

clot; stationary; stuck to vessel wall; superficial or deep

Thrombosis

abnormal clot developments

deep vein thrombosis (DVT)

* most concerned about deep DVT from knee down

Thromboembolus

* detached clot (DVT) from a wall and now in circulation
* can lead to Pulmonary embolism (PE); in pulmonary circulation
* can be large enough to block path and have a pulmonary circulation collapse
* almost certainly lethal if the PE blocks the bifurcation of Pulmonary trunk and shuts off flow; complete circulatory collapse

Virchow’s Triad: 3 underlying risk factors for DVTs

1. Hypercoaguability


1. blood clots more easily
2. can be caused in pregnancy, oral contraceptive use, cancer patients
2. Venous Stasis


1. stagnant blood flow
2. cause by immobility, A-Fib (LA: stroke problem, RA: PE problem)
3. Vessel Wall Damage


1. damage triggers clotting cascade
2. risk factors: smoking, hypertension, atherosclerotic plaque formation

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* Risk goes up when one or multiple factors is acquired

Circulatory Shock

* life threatening


* Inadequate blood supply that leads to cellular or tissue hypoxia
* early on in shock: if caught and treated, effects can be reversed
* rapid intervention
* Most commonly: rapidly progressing = irreversible state; over the course of minutes to less than an hour
* Manifestations:
* hypotensive (most of the time, not always; could be HTN or normotensive)

Types of Circulatory Shock

Most common types of Circulatory Shock:

* Distributive
* severe peripheral vasodilation (systemic vascular resistance and flow reduced significantly;y; pressure plummets)
* Septic (most common), anaphylactic, neurogenic (associated with TBIs), drug-induced, toxic shock
* have trouble distributing blood throughout
* Cardiogenic
* intracardiac cause of pump failure; something intrinsically wrong with the heart and can’t provide enough blood flow (primary pump problem)
* MI, CHF
* Hypovolemic
* low BV, tissue cellular hypoxia
* Hemorrhagic: excessive bleeding
* Non-hemorrhagic: dehydrated, vomiting
* not enough volume to pump
* Obstructive
* extracardiac cause of pump failure; somewhere else in the body (secondary pump problem)
* PE; right ventricular failure

Multiple Organ Failure (MOF)

* can / will develop after any of the types of circulatory shock
* neurologic, cardiac, renal malfunction = most lethal

T/F: You can quickly go from the reversible state to the irreversible state and once in the irreversible state, there is nothing that can be done to get back to normal. You can stabilize the patient but eventually they will begin to decline further.

True