Patho Exam 3 – Anemia; Hypertension, Coronary Artery Disease (CAD), Angina Pectoris / Myocardial Ischemia, Myocardial Infarction (MI), Heart Failure

formula for blood pressure

BP = CO x SVR

blood pressure = cardiac output x systemic vasucalar resistance

Cardiac Output

how much blood the heart pumps per minute

Systemic Vascular Resistance (SVR)

how tight or constricted the blood vessels are

formula for cardiac output

CO = SV X HR

cardiac output = stroke volume x heart rate

Vasoconstriction

raises systemic vascular resistance (SVR)

Vasodilation

lowers systemic vascular resistance (SVR)

Stroke volume is directly influenced by:

blood volume & contractility

Mean Arterial Pressure (MAP)

The average blood pressure in a person's arteries.

Minimum MAP

60 mmHg

*This is important for adequate perfusion

MAP formula (mean arterial pressure)

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

Hypotension

low blood pressure

<90/60

Treatment for hypotension

The goal is to raise BP

*To do this, you must raise CO and SVR

Pressors

drugs that raise BP

common pressors

vasopression, EPI, NE (Levophed)

hypertension (HTN)

high blood pressure

Stage 1 hypertension

SBP 130-139 or DBP 80-89

Stage 2 hypertension

SBP >140 or DBP >90

treatment for hypertension

the goal is to bring BP down

*to do this you must lower CO & SVR

angina pectoris

chest pain caused by myocardia ischemia

stable angina pectoris

initiated by increased demand (activity) and relieved with the reduction of that demand (rest).

*high demand

Unstable Angina Pectoris

initiated at rest

*low supply

acute coronary syndrome (ACS)

sudden symptoms of insufficient blood supply to the heart, indicating unstable angina or acute myocardial infarction

Compensatory Mechanisms

The body's response to maintain cardiac output/ blood pressure in heart failure.

rapid/immediate compensatory mechanisms

increase the sympathetic nervous system through the baroreceptor reflex

*This will raise HR, contractility, and SVR

Slower compensatory mechanisms

increase fluid retention

*This will raise BV

myocardial infarction (MI)

heart attack; cardiac muscle death

What is a common symptom of classic myocardial infarction?

Angina

What type of chest pain is associated with classic myocardial infarction?

Substernal chest pain or pressure

*feels like someone is sitting on the chest

What gastrointestinal symptom may occur during a classic myocardial infarction?

Nausea

Where does the pain typically radiate during a classic myocardial infarction?

To the left shoulder, jaw, or left elbow

What skin condition may be present during a classic myocardial infarction?

Cool, clammy skin

What is a visible sign of distress in a patient experiencing a classic myocardial infarction?

Palor (pale skin)

What psychological symptom may accompany a classic myocardial infarction?

Sense of impending doom

Symptoms of nausea, clammy skin, and pale skin are classic symptoms of myocardial infarction because of:

an increase in the SNS

LV congestive heart failure (CHF)

The left ventricle (responsible for pumping blood to the body) fails to function properly

Systolic LV congestive heart failure

loss of contractility

-It has enough blood, but it can't contract

Diastolic LV congestive heart failure

filling problem

-can contract, but it doesn't have enough blood

What do you typically see in systolic LV CHF?

-cardiomegaly (enlarged heart)

-increase in preload and LV afterload - leads to an increase in myocardial workload

2 problems with systolic LV CHF

-loss of contractility

-increase in workload

What are the solutions to the problems with systolic LV CHF?

-increase contractility

-decrease workload

Inotropes

Drugs that affect contractility, the force of contraction of the heart.

Positive inotropes

increase contractility

negative inotropes

decrease contractility

Chronotropes

drugs that affect the heart rate

Positive chronotropes

increase heart rate

Negative chronotropes

decrease heart rate

treatment of systolic LV CHF

-increase contractility using positive inotropes

-decrease workload using beta-blockers

treatment of diastolic LV CHF

-increase filling by lowering HR

-decrease workload by vasodilating

LV failure leads to:

pulmonary edema and dyspnea (shortness of breath)

The common cause of RV failure is

LV failure

Ejection fraction

stroke volume/end diastolic volume

(sv/edv)

normal ejection fraction

50-60%

systolic heart failure =

heart failure reduced ejection fraction

*HFrEF

diastolic heart failure =

heart failure preserved ejection fraction

*HFpEF

dilated cardiomyopathy

increased edv

decreased EF

hypertrophic cardiomyopathy

decreased edv

increased EF

circulatory shock

life-threatening condition of circulatory failure

Circulatory shock produces

cellular hypoxia (low cell 02)

Circulatory shock is initially reversible, but

It rapidly becomes irreversible, leading to multiorgan failure

With circulatory shock, most patients have

hypotension, but may be normaltensive or hypertensive

cardiogenic shock

Shock caused by inadequate function of the heart, or pump failure (myocardial infarction)

*The problem originated from the heart

distributive shock

severe peripheral vasodilation

4 types of distributive shock

septic, neurogenic, anaphylactic, toxic/drug induced

obstructive shock

pulmonary embolism problem

*the problem originated outside the heart the led to a heart problem

hypovolemic shock

shock resulting from blood loss

The most common types of shock are

cardiogenic and distributive

CAD

atherosclerosis plaque formation of the coronary arteries

myocardial ischemia

decreased blood flow to the heart

preload

"stretch" on ventricular wall

determined by BV

Afterload

"Resistance" heart must pump against to overcome to allow perfusion and circulation

determined by SVR and BP

Complications of Heart Failure?

fluid retention (increases BV, leads to increased preload) increased SNS activity (increase HR & SVR, increased afterload)