PATHO - Exam 2 Review

Tissue Perfusion

• PaO2

• O2 Sat

• Hgb (hemoglobin) - oxygen carrying compacity of the blood 

• Arterial

• O2 delivery

• Cardiac output - how effective your heart is with pumping blood where it needs to go 

• SVR

  • MAP (average pressure in arteries)

• Stroke volume/heart rate 

  • SV - how much blood is pumped out per heart beat

    • Can be adjusted by increased contractability (by SNS) 

  • HR - how fast/slow your heart is beating 

• Preload - amount of blood in heart before contraction 

• Contractability

• Afterload - how much force the heart has pump against to get the blood out to the body 

---

• Problem with arteries: downstream 

• Problem with veins: upstream 

• Cardiac issues can affect the whole body 

SVR

• Systemic vascular resistance (also called peripheral vascular resistance)

• Increase resistance down the pipeline:

  • Diameter of the blood vessels (vasoconstriction and vasodilation)

  • “Clogged tube" in atherosclerosis 

MAP

• Difference between systolic and diastolic blood pressure

• Tells us how much oxygen is getting to organs (perfusion) 

• Needs to be about 70, over 60 to perfuse adequately 

Contractility

Forcefulness of heart’s contraction

Blood Pressure

• Hydrostatic pressure + blood pressure (pressure of blood exerts on walls)

• Laminar flow

  • Plasma on outside, cells on the inside

  • Stimulates prostaglandins and nitric oxide (dilates blood vessels)

• Turbulent flow

  • More pressure required to move blood forward

  • Damage epithelium

  • Heart has to pump harder to move blood

  • EX: increased velocity, decreased vessel diameter, low blood viscosity

*Arteries = take blood to extremities (high pressure) 

*Veins = bring blood back to the heart (low pressure) 

Components of Blood Pressure

• Cardiac “pump”

  • Heart failure = pump failure

• Vascular system “pipes”

  • Vascular tone

  • Vascular resistance

• Blood volume “fluid”

• Too little = shock

  • Cardiogenic shock

  • Vasodilation = Blood volume leaks out of capillaries (distributive)

  • Hypovolemic shock = decrease in blood volume

• Too much fluid/vasoconstriction = hypertension

Blood Pressure + Resistance

• Pressure differences drive blood flow: high to low (RA)

• What generates driving pressure on arterial side of circulation?

  • Pump - muscle becomes pump 

    • Veins can stretch and have valves 

  • Lowest circulatory pressure in body = right atrium (2-7 mmHg) - where blood comes back to heart

  • Pressure in veins lower than arteries 

• Pressure = cardiac output (HR x SV) x resistance

  • SV = amount of blood ejected during contraction

  • Cardiac output in one minute

  • Resistance = opposition blood encounters in blood vessels

• Ohm’s law: flow (CO) = pressure/resistance

  • Resistance increases, pressure constant = flow decreases

  • Pressure increases, resistance constant = flow increases

• Factors affecting resistance:

  • Blood viscosity = overproduction of RBCs (thicker blood)

  • Vessel length = hypertension (more blood vessels heart needs to pump to, more pressure to pump against)

  • Vessel diameter = vasoconstriction and vasodilation

Hypertension

• Sustained elevation of arterial blood pressure (causes endothelial and silent target organ damage)

• Silent killer 

• Primary risk factor for cardiovascular disease

• If pressure = CO x resistance, then:

  • What could raise blood pressure?

    • RAAS system 

    • Vasoconstriction

    • High heart rate 

    • Hypervolemia: indicate something is wrong with pump (high BP)  

    • Thick blood 

    • SAD diet: high processed food 

      • Too much salt = hold on to more water = hypervolemic = high BP 

• Systole = arterial pressure during contraction

• Diastole = arterial pressure during relaxation (filling)

• Healthy = <120/80

Primary Hypertension

• Increased BP (heart has to pump even harder each heart beat - get extra muscle - can be pathologic in nature) due to 1+ of these factors:

  • Increased HR

    • To much thyroid hormone in blood = tachycardia

  • Increased myocardial contractility

  • Increased vasoconstriction

    • Too much renin

  • Increased blood volume

    • Increased blood volume due to high sodium diet

• SNS, Baroreceptors, RAAS, plasma volume (controlled by kidneys) all determine blood pressure

• Dysregulation from:

  • Ineffective communication/collaboration between organs responsible for regulating blood volume, vascular tone, and cardiac performance

  • Renal artery stenosis - kidneys not perfused well with blood, RAAS, blood pressure goes up

Risk Factors of Hypertension

• Nonmodifiable

  • Age

    • BP gets higher with age (blood vessels loose elasticity, forcing heart to pump harder)

    • Kidneys can’t secrete sodium, blood volume higher

    • Older adults have low grade inflammatory response

    • Older biological males

      • Females catch up after menopause and they lose the protection of estrogen

  • Assigned sex at birth

    • Male = higher rate of hypertension earlier (based on hormones)

    • Women after menopause (loose estrogen) = heart attack becomes equal with men

  • Family history/genetics

    • Ethnicity = AA have more symptomatic problems with hypertension

    • Family history contributes 50% increase in susceptibility

  • Race

    • More bad outcomes in black populations then white

• Modifiable

  • Diet

    • SAD diet = processed foods (sodium, sugar, trans fats, low in plants)

    • Blue zone diet:

      • 100% whole grains: farro, quinoa, brown rice, oatmeal, bulgur, cornmeal

      • Nuts and seeds: a handful a day

      • Beans, legumes, pulses: a cup of cooked beans/pulses per day

      • Fruits and vegetables: 5-10 servings per day

  • Blood lipid levels

    • Increased LDL levels, low HDL levels = fatty plaques in arteries

  • Tobacco/alcohol consumption

    • Toxins enter bloodstream from tobacco and damages endothelium

    • More than one drink a day = LDL cholesterol builds up

  • Activity/fitness level

    • Lowers stress

    • Lowers resting heart rate 

  • Weight

    • 1 pound of weight loss = 1 mmHg lost

  • Blood glucose levels

    • Damages endothelial lining of blood vessels if high for a long time 

    • Glucose has osmotic pull, increases blood volume

  • Allostatic load

    • Chronic stress not able to be resolved

    • Minority populations

    • Poverty

Physiologic Systems Contributing to Hypertension (HTN)

• RAAS

  • Kidneys not perfused = increased renin = vasoconstriction = increased blood pressure = aldosterone = sodium retention by kidney = increased blood volume and pressure = HTN 

  • Thirst center (hypothalamus and ADH - retains water = increased BP)

• SNS

  • Baroreceptors

  • Cardiac output increased = heart rate increased

  • Resistance increased = SNS (vasoconstriction)

• Endothelial dysfunction

  • Reduced nitric oxide (NO) production - endothelium produces this, helps blood vessels relax

    • in HTN = the production of NO is reduced = vasodilation = vasoconstriction = can’t regulate inflammation 

  • Oxidative stress - high BP increases oxidative stress, which damages endothelial cells and further reduces NO availability 

  • Inflammation - chronic inflammation in HTN = endothelial cells become dysfunctional = pro-inflammatory and pro-thrombotic state  

Creation of Hypertension

Obesity = adipocytokines = constant inflammatory state = hypertension

Blood Pressure and Vascular Damage

• Blood pressure exerts shearing force (parallel movement) on blood vessels

  • Inner lining: endothelium (important for cardiovascular health - platelet formation, blood clotting, controlling resistance and blood flow, stops things from sitting to blood vessel wall, vasodilation)

    • NO promotes vasodilation 

    • HTN = endothelium damaged due to turbulent flow = cholesterol particles are pulled under endothelium by immune system to be stored 

• Over time, hypertension damages blood vessels leading to chronic inflammatory process

• Arteriosclerosis (hardening of vessels)

• Atherosclerosis (fatty plaques in blood vessels)

  • Arteries with greatest shear force most effected (aorta, coronary arteries, branched arteries)

    • Bigger the artery = the stronger the force

    • Branching = strong shear force

  • What most heart disease is caused by

Atherosclerosis

Creation of Atherosclerosis

• 1) Things stick to damaged endothelium = release growth factors = becomes permeable = LDL go through and accumulate = macrophages eat LDL and become foam cells = foam cells release cytokines = more macrophages come to site

  • Lots of inflammation

• 2) Fatty streak process begins

  • Macrophages filled with LDL = foam cells = accumulation of foam cells (macrophages and T cells and T lymphocytes = release growth factors = collagen and smooth muscle cells form cap over fatty cap = artery becomes closed off

  • Patients becomes symptoms when 60-70% of blood vessel is closed off (ischemia - lack of blood flow to organs)

    • Angina (chest pain due to ischemia)

  • Fibrous cap can become eroded due to shear force = platelet form clot = blood flow shut off

    • Carotid artery = storke

    • Cornary arteries = heart attack

Atherosclerosis + Angina

• Coronary artery disease (CAD) - atherosclerosis in coronary arteries

  • Acute (ACS)

    • Myocardial infarction (MI) - blood flow is completely blocked (tissue with undergo necrosis and die) servere

      • Chest pain, SOB, sweating (SNS), decreased BP, nausea/vomiting (ANS), pale, LOC, pain in back/stomach, left arm pain, jaw pain 

    • Unstable - angina (chest pain due to decreased oxygen to heart) randomly appears (plaque in heart in so much that angina is unpredictable such as during rest)

      • Emergency

  • Chronic

    • Stable (can lead to unstable) - know when angina (chest pain) will occur such as with exercise (blood vessels vasoconstriction and plaque restricts blood flow to portion of the heart = chest pain)

    • Asymptomatic - no sides of symptoms but disease is still present

• Peripheral artery disease (PAD) - atherosclerosis in legs (clotication - causes inadequate blood flow in peripheral due to plaque in arteries (which can cause increased pressure on arteries))

*CAD or PAD ultimately leads to tissue death of the heart muscle 

Effects of Cigarette Smoke on Cardiovascular System 

• Increased sympathetic response

  • Increased systolic and diastolic pressure 

  • Increased HR, CO, and coronary flow 

• Blood vessels vasoconstriction

• More likely for aortic aneurysm - weakens vessels walls

• Effects favoring thrombosis increases:

  • Platelet aggression

  • Platelet adhesiveness (more sticky, form blood clots (MI, stroke))

  • Plasma fibrinogen (protein involved in clot formation = thrombosis)

  • Blood viscosity (endothelial wall damage = no vasodilation, more blood cells = more likely to clot)

  • Decreased clotting time

*Daily aspirin helps

Heart Anatomy

Pathway of Red Blood Cell Through the Heart

Deoxygenated vena cava = RA = tricuspid = LV = pulmonic = pulmonic arteries = lungs = oxygenated pulmonary veins = LA = mitral = LV = aortic valve = body

Heart as a Two-Sided Pump

• Left side = to the body as systemic circulation

  • LV wall is thicker against RV (pumps against bodies systemic pressure)

• Right side = to the lungs

  • Less muscle since only pumping to lungs

• Pathway of blood:

  • Muscles

  • Kidneys

  • Digestive tract

    • Liver is gatekeeper for everything we digest (first pass effect - liver detoxifies, takes out of systemic circulation)

  • Brain

  • Other systemic organs

• Congestive heart failure

  • LV can’t pump to body, backs up into LA into lungs

    • Increases hydrostatic pressure, lungs fill with fluid = pulmonary edema (difficulty breathing, fatigue, frothy sputum)

  • RV fails = blood backs up in RA and into vena cava and then systemic circulation = jugular venous distention = increases hydrostatic pressure = edema (peripheral edema - seen in legs due to gravity)

    • Back up into liver = hepatomegaly (enlarged liver)

      • Liver failure

    • Back up in slpeen = splenomegaly

Function vs. Dysfunction of Heart 

• Diastole: ventricles relax

  • Dysfunction: ineffective filling

  • EX: cardiac tamponade (abnormal amount of fluid in pericardial sac around the heart - third spacing - compresses ventricle, decrease in CO, can’t fill = complication in heart surgery)

• Systole: ventricle contract

  • Determines stroke volume (how much blood is being ejected from ventricle with each contraction)

  • Dysfunction: ineffective pumping

  • EX: aortic stenosis (aortic vavle doesn’t fully open = blood in ventricle can’t be pumped out fully)

• Which valves are open

  • During systole: Pulmonic and aortic

  • During diastole: Tricuspid and mitral

Preload vs. Afterload (NOT OPPOSITES) 

• Preload

  • End-diastolic pressure: the amount of stretch on the ventricle wall at the end of diastole (ventricle filling) BEFORE VENTRICLE CONTRACT

    • Frank Starling Mechanism = the greater the stretch on myocardium, the stronger the contraction (like a rubber band)

    • Increased by having more fluid

      • Increase fluid volume (IV)

      • Increase venous return through vasoconstriction (blood coming back to heart) - SNS and RAAS system

    • Decrease…

      • Vasodilation (not as much blood back to heart)

      • Bad = too much fluid in interstitial space, less blood in blood vessels

      • Diuretics that eliminate excess fluid volume

  • Hypervolemia would increase

  • Frank-Starling Mechanism - the greater the stretch, the stronger the recoil

• Afterload 

  • Work (or force) required of LV to move (eject) blood into the aorta

    • Higher pressure in aorta the heart has to overcome= higher the afterload

      • Blowing up a ballon (think resistance)

      • Increased = vasoconstriction, hypertension

      • Decreased = vasodilation

    • Increases ventricular wall tension, over time can eject blood (and impact ejection fraction)  

• Shock = drop in blood volume = less blood to heart (preload decreases) = blood pressure drops (afterload decreases) 

• Volume overload (hypervolemic) = preload increases (more blood volume to heart) = afterload increases = increases blood pressure

• Decreasing work of heart (MI) = nitroglycerin = dilates blood vessels = decreases BP = decreases afterload and preload

• Heart failure = ventricles hold more blood = preload increases = heart works harder to move more fluid

Cardiac Output 

• CO = the heart’s pumping output (L/min) normal = 5-6 L/min

  • CO = SV x HR

• Stroke volume = how much the heart beats out in each beat (mL/beat)

  • Preload - initial stretch, fullness before contraction

    • End-systolic volume = whats left after systole

    • Venous return = amount of blood back to body

    • How much in ventricle

    • Increased preload = increases stroke volume

    • Vasodilation = decreases preload

    • Hypervolemia increases 

  • Afterload - resistance (hypertension, vasoconstriction) heart overcome to eject blood to body

    • Total peripheral resistance

    • Aortic pressure

      • Aortic stenosis can increases

    • Increases cardiac workload 

    • Increases ventricular wall tension (impact ejection fraction) 

  • Contractility = how strong the heart beats

    • End-diastolic volume = whats left after diastole

    • Sympathetic stimulation (more forceful)

    • Myocardial oxygen supply (more O2 = more force)

• Heart rate - beats per minute

  • CNS - pons and medulla regulate the rate and rhyth,

  • ANS = SNS (raises HR) and PNS (lowers HR)

  • Neural reflexes = startle reflex (jump in heart rate)

  • Barorecptors = increased stretch = PNS = decreases heart rate = vasodilation

  • Atrial receptors = stretch receptors = speed up heart rate to prevent pooling

  • Hormones

    • Epipinephrine

    • Thyroid = too much = tachycardic 

You are taking care of a patient who has been diagnosed with atrial fibrillation. You are doing your morning assessment and notice their heart rate has increased to 200 bpm. Blood pressure has decreased from 110/78 to 88/60. 

1. Using the CO = SV x HR, what should the HR in the case do to cardiac output 

2. Why is BP low? 

• Ventricles aren’t filling due to high HR, have less time to fill (diastole shortened, systole doesn’t change) = smaller SV (less volume in ventricles)

• Atrial fibrillation = atria quivering, not pump

  • HR increases = diastolic filling time drops = CO decreased = low BP

• Needs cardioversion to jolt heart into normal rhythm

End Diastolic Volume (EDV)

• Amount of blood in heart chamber at end of diastole 

• Determine preload

• 120 mL

• Weak heart = EDV increases

• Small aortic opening = increased EDV

• Preload increases EDV, increases SV

End Systolic Volume (ESV)

• Amount of blood remaining in ventricle after systole

• Heart does not empty completely with each beat

• Weak heart = increased ESV

• Small aortic opening = increased ESV

Stroke Volume (SV)

• Amount of blood ejected from chamber with each beat

• EDV - ESV

• Weak heart = decreased SV

• Small aortic opening = decreased SV

• If stroke volume goes up + heart rate goes up = cardiac output goes up 

• Influenced by the amount of blood that returns to right atrium from venous circulation (RIGHT SIDE) and left atrium (LEFT SIDE) from pulmonary veins

  • Higher SV increases workload of the heart…typically due to too much VOLUME

  • Tachycardia INCREASES cardiac oxygen demands, workload, and DECREASES stroke volume because there is less time for the ventricles to fill

  • Goal of medication therapy with any cardiac patient is to DECREASE cardiac workload through manipulating SV, HR, preload, afterload, and contractility

Ejection Fraction (EF) 

• Percentage of EDV ejected from heart with each beat 

• 55-75%

• Left side of heart

• Weak heart = EF decreased

• Small aortic opening = decreased EF 

• Increased TPR = decreases SV - hard to pump blood out of heart 

• Heart failure: An MI kills heart muscle and affects its ability to pump effectively (decreases contractility)

• Heart failure decreases ejection fraction and increases our left ventricular end diastolic volume, which increases our preload - which will lead to renal failure 

• OR we decrease our renal perfusion, which triggers our RAAS system and increases our blood pressure (increasing afterload and causes HTN)

• Low EF = systolic HF

• Low EDV = diastolic HF

• Increase in preload = increase in blood return to heart

---

• EX: 100 ml of blood in the LV at end of diastole (EDV), and 60 mL of blood pumped with each beat during systole (SV), EF = 60% 

  • EDV around 120 mL

  • ESV around 50 mL

  • SV would be 70 mL

  • EF = 59%

EF (%) = ?

(SV/EDV) x 100

Heart 

• “Plumber”

• "Electrician”

• How many sub-specialties?

  • Coronary artery disease

  • Heart failure

  • Rhythm disorders

  • Valvular disease

Normal Heart vs. Heart Failure 

What are the functions of the cardiovascular system? 

• Delivery of oxygen and nutrients needed for metabolic processes to the periphery, and removal of wastes 

• Circulates hormones 

• Controls body temperature 

Pathophysiology of HTN

• Diagnosed over a series of office visits and/or with continuous blood pressure monitoring

• Increased risk for

  • Cardiovascular disorders

  • Ischemic heart disease and stroke

  • Peripheral arterial disease

  • Renal disease

  • Heart failure

• Stiffening of arteries with age can cause, as well as sodium retention that occurs with age

Complications of Persistent HTN 

Risk Factors of Atherosclerosis

• Hypercholesterolemia 

• Elevated LDL

• Age

• Family history 

• Biological males

• Smoking 

  • Vasoconstriction

  • Damages endothelial lining

• Obesity 

• Hypertension 

• Diabetes 

---

• Atherosclerosis:

  • Cellular injury in smooth endothelial wall

  • Inflammatory cells are attracted to the area and gather

  • Causes gathering of lipids and smooth muscle tissue that begin to collect

  • Lipids/smooth muscle form a hard plaque in the vessel

Progression of Atherosclerosis

• Thrombosis is the formation of the clot, the thrombus is the clot and the embolism is the clot on the move

• Can be slowed or reversed 

• >75% = symptoms 

Heart Anatomy

Pathway of Blood Through the Heart 

• AV and SL valves close and open at the same time 

• Left side of heart failures:

  • Blood backs up = wet lungs

Cardiac Cycle

• Systole: ventricles contracting (pumping)

  • Top number for blood pressure

  • Atria and ventricles contract at same time

    • Atria stay open

  • Takes same amount of time

• Diastole: ventricles are relaxed (filling with blood)

  • Bottom number for blood pressure

  • Lost due to to:

    • Stiff ventricles

    • Dysfunction of valves and veins

    • Heart rate

      • Over 180 = pass out

  • Time can change (atheltes have more time of filling)

Frank Starling Relationship 

More preload = contraction is stronger 

• HF = overstretch = lose elasticity of heart muscle 

• Inotropic = strength of contraction 

• Cronotropic = how fast heart is beating 

You are taking care of a patient who has been diagnosed with atrial fibrillation. You are doing your morning assessment and notice their heart rate has increased to 200 BPM. Blood pressure has decreased from 110/78 to 88/60.

• Using the CO = SV x HR, what should the HR in this case do to cardiac output?

• Why is BP low?

• HR increase should increase CO 

• Not enough time for the ventricles to fill

How does hypertension affect afterload? What would be the consequences for the heart? Why might someone with long-standing hypertension develop heart failure?

Afterload is the resistance the heart must overcome to eject blood from a given chamber. Hypertension increases afterload in the ventricle because the heart must generate more force to overcome the elevated blood pressure and eject blood from the chamber. This could create afterload in the left ventricle (if it is systemic hypertension/elevated blood pressure in the aorta) or the right ventricle (if it is pulmonary hypertension/elevated blood pressure in the pulmonary artery leading to the lungs). Another example of a process that could increase afterload would be valve stenosis. For example, in aortic stenosis, the heart must generate more pressure to push blood through the narrowed heart valve.

If the heart has to continually work against high blood pressure, the cardiomyocytes (heart muscle cells) will hypertrophy to compensate, just like any other muscle that has to work against increased resistance. Unfortunately, the hypertrophy of cardiomyocytes is pathologic and leads to ventricular wall thickening and stiffness which decreases the chamber size. Both of these factors can contribute to diastolic dysfunction (the ventricle has a filling issue) and leads to heart failure.

A patient has been diagnosed with left sided heart failure and an ejection fraction of 33%.  What is the significance of this EF? How would this patient's left ventricular end-systolic volume (ESV) compare to someone with a healthy heart? Would the ESV be increased or decreased? Explain your answer.

Ejection fraction tells us what percentage of the EDV is pumped out of the heart with each beat. Thus, ejection fraction is very much related to cardiac output. A normal EF is somewhere between 55%-70%. So a person with a normal EF who starts with an EDV of 100 mL will pump out between 55 and 70 mL of blood during systole. A person with an EF of 33% has systolic dysfunction. If they start with 100 mL of blood, then they only pump out 33 mL of blood during systole, which results in a subsequent drop in cardiac output.

ESV in the left ventricle would be increased because more blood would be remaining in the ventricle at the end of systole. When the heart relaxes during diastole, the heart will continue to fill as normal, and the blood entering from the atria during diastole is added to the excess blood already in the ventricle. This will lead to increased ventricular pressures, which cause excessive stretch of the ventricle. The increased stretch of the myocardium will lead the atria and ventricles to release ANP and BNP respectively, which increases sodium (and therefore water) excretion in the kidneys.

Coronary Arteries

• RCA = SA node, AV node pacemakers of the heart

• Myocardial infarction = clot on plaque

• Cardiomyocytes starved of oxygen = angina

• Originate in aorta (blood high to low - aorta has highest pressure)

• Blockage affects things downstream (higher up the worst)

• Left CA blockage = widowmaker (supplies smaller amount of oxygen to heart)

Supply vs. Demand

• Lack of oxygen and then tissue death, you get chest pain even at rest

• Angina = chest pain, substernal, radiate to left arm or jaw

• MI = clot on plaque

Goals of Heart Related Symptoms 

• Decrease platelet aggregation - give aspirin 

• Decrease preload and afterload - give nitrates 

• Decrease oxygen demand - give oxygen 

• Decrease SNS involvement and pain - give morphine 

Progression of Coronary Artery Disease

• May get complete obstruction of the vessel, cutting off the oxygen supply (STEMI)

• Troponin being released in bloodstream is key in diagnosing MI

---

• Asymptomatic CAD = no symptoms, but have disease = coronary calcium score = tells us of the plaque in arteries since calcium stabilizes clots 

• Stable angina = chest pain with activity, goes away with rest = oxygen demand high, but supply low 

• With unstable angina, symptoms may occur at rest; become more frequent, severe, or prolonged than the usual pattern of angina; change from the usual pattern of angina; or not respond to rest or nitroglycerin (chest pain at rest shows myocardial ischemia) = no calcium

• NSTEMI - partial blockage = troponins present

• STEMi - complete blockage = ST elevation on EKG troponins present = worse

Acute Coronary Syndrome

• Progression to complete blockage of blood flow to the heart muscle causing tissue death

• Unstable angina = no positive troponin

• NSTEMI - non ST elevated myocardial infarction (unstable angina, with elevated cardiac enzymes)

• STEMI - ST segment elevation myocardial infarction (tombstone) = positive troponin, full thickness damage

Radiation of Cardiac Ischemia 

• Ischemia causes pain, typically radiating to these areas 

• “Crushing, vice like pain” 

• DM< females, older adults more likley to have different sex, fatigue 

Symptoms of Myocardial Infarction

• Myocardial infarction - tissue death of the cardiac muscle due to blockage of blood vessels of the heart

• No oxygen = no contraction = no CO

• Diaphoresis = sweating

Acute MI

• Diagnosis based on 3 findings:

  • Clinical presentation

  • Serial 12-lead ECG’s

    • Earliest findings in areas of ECG representing repolarization

  • Lab findings: cardiac enzymes

• Heart attack is suspects - reperfution (best within 90 mins+)

• Troponin = heart attack

12 Lead ECG 

• Deploarization and repolarization of the atria and ventricles 

• “Organization of the squeeze” of the cardiac muscle 

• Atrial depolarization = p wave

• Ventricle depolarization = big bump

• Ventricle repolarization = last part 

Labs of Cardiac Enzymes

Troponin is the main indicator

Complications of Myocardial Infarction

• Tissue necrosis = death of heart tissue

• Irreversible tissue damage 

• Acute MI = contractility decreases = blockage can form = stroke

• Papillary muscle = controls mitral valve 

• What would happen to…

  • SV

  • CO

  • UOP

Valve Disorders 

• Stenosis - not enough blood passes through, hardened, narrowed artery (hypertrophy, afterload increases)

• Regurgitation - blood leaks backwards (RV lowest pressure, high to low, preload high and EDV)

• AV valves - mitral and tricuspid (“tri” to be right)

  • Tricuspid = prone to damage from IV drug use 

• Semilunar valves - aortic and pulmonary

• Murmur during systole (ventricular contraction) = aortic/pulmonic stenosis, mitral/tricuspid regurgitation

• Murmur during diastole (ventricular relaxation) = aortic/pulmonic regurgitation, mitral/tricuspid stenosis

Valve Disorders - Stenosis 

• Aortic and mitral valve most common

  • On same side of heart (left) = muscular, more friction, force, wear and tear

  • Scar from rheumatic fever (from untreated strep throat) - can destroy valves

  • Wear and tear

  • Congenital anomalies - babies born with heart abnormalities 

• Valve doesn’t open completely

• Tricuspid valve disorders - drug abuse (first that blood encouters, unproper use of needles)

• Young women - mitral valve regurgitation 

• High pressure - treatment 

• Where does blood back up into? What would these patients present with?

  • Aortic stenosis = left ventricle, LV ESV increased (afterload increased), chest pain, fatigue, syncope, dyspnea (no pulmonary edema), can eventually cause LVH

  • Mitral stenosis = left atrium, EDV decreased (preload decreased), can cause pulmonary congestion

  • Pulomonic stenosis = right ventricle, EV EDV increased (RV afterload increased), can cause RVH

    • Would this increase or decrease blood flow to the lung?

    • What would happen to LV preload?

  • Tricuspid stenosis = right ventricle, RV ESV increased, abdominal distention, fluttering discomfort in the neck (why??)

Stenosis Signs + Symptoms 

• Mitral Valve 

  • Pulmonary congestion (would you hear crackles on examination?)

  • Orthopnea

  • Nocturnal paroxysmal dyspnea

  • Palpitations

  • Fatigue

• Aortic Valve 

  • Angina

  • Syncope (LOC - valve replaced immediately)

  • Easily tired

  • Dyspnea

  • Peripheral cyanosis

  • Poor perfusion

Valve Disorders - Regurgitant 

• “Closing disorder”

• Can be caused by:

  • Mitral valve prolapse

  • Damaged tissue cords

  • Rheumatic fever

  • Endocarditis

  • Heart attack

  • Abnormality of the heart muscle (cardiomyopathy)

  • Trauma

  • Congenital heart defects

• Where does the blood back into? What would these patients present with?

  • AR = LV preload/EDV? LV ESV?

  • MR = retrograde flow from LV to LA during systole, LV preload? (increased(

  • Increased EDV!

• Endocarditis = vegetations

Regurgitation Signs and Symptoms

• Mitral Valve 

  • Don’t develop symptoms for years 

  • Pulmonary congestion 

  • Dyspnea on exertion 

  • Orthopnea 

• Aortic Valve

  • Exertional dyspnea 

  • Orthopnea

  • Drop in diastolic pressure (blood is getting out, but diastolic is low)

  • Widening arterial pulse pressure 

Systolic Murmurs

• Problems occurs during ventricular squeeze:

  • Aortic stenosis (think as pair) - systolic (only when contracts, aortic valve doesn’t open)

  • Mitral regurgitation (doesn’t close)

  • Pulmonic stenosis (doesn’t open)

  • Tricuspid regurgitation (doesn’t close)

• Heard after S1

*Know when valves are open and closed during systole 

Diastolic Murmurs

• Problem occurs during ventricular filling:

  • Aortic regurgitation (open)

  • Mitral stenosis (not opening)

  • Pulmonic regurgitation (open)

  • Tricuspid stenosis (not opening)

• Hear murmur during diastolic (after lub dub)

*Know when valves are open and closed during systole 

Heart Failure 

Progressive and often fatal mortality resulting from decreased cardiac output and tissue perfusion and increased fluid retention (peripheral edema/SOB/exercise intolerance) 

• Caused by heart attack, high (chronic) BP

  • After load high = hypertrophy

• Diastolic (preserved EF) HFpEF (HF with perserved EF)

  • Stiff and thick chambers

  • Heart can’t fill, not a lot of blood goes out with contraction

  • Stronger LV - pump to whole body 

  • Hypertrophy (can’t fill properly) = due to tachycardia, high BP, obesity (increased after load due to more peripheral vascular resistance) 

• Systolic (reduced EF) HFrEF (HF with reduced EF)

  • Stretched and thin chambers 

  • Heart can’t pump (not strong enough)

  • Severe heart attack (damage to myocytes) = weak heart muscle 

  • Have blood in ventricle, just can’t squeeze it out

• Can be right sided, left sided, or both!

  • Diastolic-systolic HF (whole heart)

How does the body compensate for the decrease in cardiac output that occurs during heart failure?

• Cardiac remodeling: dilating ventricles (systolic) and increasing wall thickness (diastolic) 

• Increased fluid and Na+ retention: (increasing BP)

  • RAAS

  • Causes more afterload with increased BP (process of HF is ongoing) 

• Activating the SNS: +inotropic (contractility, or force of heartbeat) and +chronotropic (heart rate)

• Often begins asymptomatically

*Body is great at short term surivivial (long term harmful)

*A slow process 

Main Consequences of Heart Failure Compensation - Hypertrophy 

• Diastolic HF (can’t fill/rest = hypertrophy = increase in oxygen demand = supply of oxygen can’t meet demands) 

  • More muscle = more oxygen/calories 

• Increase in muscle mass and cardiac wall thickness in response to chronic dilation, resulting in… 

  • Impaired filling

  • Higher O2 needs

  • Poor coronary artery circulation

  • Risk for ventricular dysrhythmias

• Chronic HTN + increase systemic afterload = LVH

Main Consequences of Heart Failure Compensation - Dilation 

• Enlargement of the chamber of the heart that occurs when pressure in the left ventricle is elevated (systolic)

• Initially an adaptive mechanism

  • Frank-Sterling Law

    • More stretch, stronger contraction 

      • If preload is increased, a greater quantity of blood is ejected during systole due to increased stretch of the myocardium and larger amount of circulating blood volume present

      • Only up to a maximal point, greatest force of contraction is when the muscle fibers are stretched 2.5 times their normal length

      • Overstretch of cardiac muscle is like an overstretched rubber band; it will decrease cardiac contractility and efficient over time

        • Why an enlarged heart is not good!

• Eventually this mechanism becomes inadequate, and CO decreases

*EF decreases (SV/EDV) = filling a lot, SV small, EDV big 

*Diastolic EF = don’t need, look clinically 

Heart Failure + Cardiac Output

• Heart Failure 

  • 4-5 meds to combat these mechanisms 

• Baroreceptor response 

  • Detect decrease in volume + pressure

• RAAS activation, decreased GFR 

  • Decreased CO = increases fluid retention = increases BP = increases preload (more fluid back to heart) 

• Increased ventricular wall tension

  • Helps at first 

  • Hypertrophy = abnormal/ineffective 

*ALL mechanisms are short term, harmful long term (HF) 

What are two ways of viewing heart failure?

• Right vs. Left Sided Heart Failure

  • Heart is two pumps

  • Either pump or both could fail

  • Useful for understanding clinical presentation, and isolated left or right failure does happen

    • Right: JVD, sacrum + scrotum + lower extremity edema, liver + spleen enlargement (where blood back up), abdominal distentsion

      • Back up to the body

      • Pump to lung 

    • Left: SOB, coughing, crackles/wheezing, PND (Paroxysmal nocturnal dyspnea - SOB at night since fluid backs up into lungs), increased work of breathing, orthopnea (can breath laying down, have to prop themselves up)

      • Back up to lung 

      • Pumo to body 

  • Most patients present with failure of both sides

• Systolic (decreased EF, weak) vs. Diastolic (normal EF, stiff) Dysfunction

  • More recent way of viewing heart failure

  • Compromised pumping (systolic failure)

  • Compromised filling leading to underfilling (diastolic failure)

  • Reduced ejection fraction vs. preserved ejection fraction

  • Systolic = can’t pump

  • Diastolic = can’t relax/fill

*SL and SV valves work together at the same time 

Characteristics of Heart Failure

• Right or left?

  • Enlarged liver (R) 

  • JVD (R)

  • SOB (L)

  • Venous congestion/edema (R)

  • Crackles on exam (L)

  • Orthopnea (L)

  • Cough (L)

  • Pulmonary edema (L)

  • Cool, clammy extremities (R) 

  • Hypoxia - not enough oxygen to tissues (BOTH)

Left Sided Heart Failure 

• Systolic: coronary artery disease, MI, dilated cardiomyopathy, myocarditis, acidosis, hyperkalemia, aortic valve stenosis and regurgitation, hypervolemia 

• Diastolic: restrict cardiomyopathy, LVH, pericarditis, tamponade, mitral stenosis (all increase ESV and pressure, back up blood flow into pulmonary circulation)

• #1 cause of LHF = CAD/MI

• Common cause of RHF (blood backs up to heart) = symptoms of everything 

  • Left side failed, back up into lungs, eventually into right side

Right Sided Heart Failure

• Fluid backed up into peripheral circulation

  • Is it leaving body? Why not?

• Systolic dysfunction: cardiomyopathy, myocardits, weak heart muscle due to MI, ischemia, heart disease, pulmonary embolism, chronic pulmonary disease, hypervolemia, tricuspid stenosis (all increase RA ESV and pressure)

• Diastolic dysfunction: cardiomyopathy with right ventricular hypertrophy, cardiac tamponade or pericarditis

• In this case blood backs up into the peripheral circulation (organ distention - hempatomegaly, splenomegaly, peripheral edema, JVD)

• #1 cause of RHF = LHF and pulmonary HTN

• Cor pulmonale = chronic pulmonary HTN (due to lung disease - left side if fine, caused by lungs) that causes RHF/enlargment “pulmonary heart”

Clinical Manifestations of Acute Decompensated HF 

• When HF becomes severe enough to cause symptoms requiring immediate treatment

• Manifests as pulmonary edema and poor organ perfusion 

  • Lungs alveoli become filled with fluid 

• Signs and symptoms of pulmonary edema: 

  • Symptoms of low CO (body not perfused) = pale, weak, LOC, low blood pressure, low oxygen staturation, syncope 

  • Anxious

  • Pale, possibly cyanotic

  • Skin is clammy and cold

  • Severe dyspnea

  • Wheezing, coughing, frothy/blood-tinged sputum

  • Crackles, wheezes, rhonchi

  • HR rapid, BP variable

• Causes: off meds, too much salt/water intake, alcohol use, pregnancy, infection/illness, arrythmia, ACS/MI

• Tests ordered = echo (might shown low EF) 

  • <25% severe 

  • <40% abnormal 

• Treatment

  • Diurectic = decrease preload 

  • If BP elevated = decreade afterload + inotropic meds

*Worse! EMERGENCY!

Signs and Symptoms of Decompensated HF

• Like an elephant sitting on their chest - fluid, stress, sodium

• Cyanosis - bluish discoloration - too much desaturated hemoglobin (poorly oxygenated blood) - need oxygen!

  • Best monitored in lips/mucus membranes

• Why the pallor/pale skin color?

  • Reflex vasoconstriction - shunting blood flow to increase the peripheral vascular resistance

• Can be due to MI

• Symptoms of both sides of HF 

Right Sided Heart Failure

Left Sided Heart Failure

Patho of Ventricular HF - Systolic

• Decreased ability to pump due to increased afterload, impaired contractile function, cardiomyopathy, or mechanical abnormalities

• Heart muscle is damaged and nor contracting as it should to move blood flow forward

• LV loses its ability to generate enough pressure to eject blood forward through the aorta

• Hallmark = decrease in ventricular ejection fraction (EF)

• Leads to low-output failure, because the heart isn’t pumping as it should - cardiomyopathy or damage from MI

• Reduced EF

• Systemic vasoconstriction, cold, pale, cyanosis in extremities

• EF = <30% (very severe)

Patho of Ventricular HF - Diastolic 

• Inability of the ventricles to relax and fill during diastole

• Normal EF

• Leads to decreased SV + CO

• Leads to venous engorgement in pulmonary and systemic vascular systems 

• Diagnosis: pulmonary congestion, pulmonary HTN, ventricular hypertrophy, normal EF

• Fluid backs up into lungs

Heart Sounds in HF - S3

• Early diastolic sound

• Blood is not moving forward enough

• Thin and weak

• Low pitched

• Suggest poor systolic function and/or volume overload

• After systole, there is too much blood in the ventricle 

• Occurs when mitral valve opens and blood enters overfilled ventricle

• Blood coming from the atria hit the overfilling and causes turbulence - S3

• Happens when AV valves first open at the beginning of diastole (fluid overload)

*Systolic = 3 syllables 

*Abnormal = occur in HF 

---

• Lub - ventricles contract (AV valves close)

• Dub - ventricles relax (SL valves close)

Heart Sounds in HF - S4

• Late diastolic sound (before S1) 

• Stiff as a board

• Caused by atrial kick 

• Low pitched

• Suggest poor diastolic function

• Occurs from atrial kick squeezing blood into stiff ventricle

• When atrial squeeze and push blood forward, that still and small ventricle can’t accept the blood 

• When atrial squeeze to force it in is squeezes it in and makes that sound 

• Poor diastolic dysfunction

*Diastolic = 4 syllables

*Abnormal = occur in HF 

Systolic vs Diastolic Dysfunction Summary

• Systolic is a pump problem (clot on plaque)

• What impacts pump: pump impacts EF and drops it 

• Diastolic is a filling problem (glass too small)

  • From chronic issues like HTN, obesity 

• What impacts filling: heart swollen and too big, pressure within the pericardial sac (like tamponade)

Natriuretic Peptides

• Blood tests for HF 

• Natural substances released by the heart (for increased stretch - fluid overload) 

  • ANP (atrial natriuretic peptide) - secreted from atria 

  • BNP (B-natriuretic peptide) - secreted from ventricles, elevated in decompensated HF

    • More common 

    • Increased stretch of heart ventricle = BNP released 

    • Inhibits compensatory mechanisms 

• Higher levels may indicate a heart is stretched too much and releasing high levels of these substances (HF) 

Natriuretic Peptide Labs

• Monitoring the circulating BNP levels is an important indicator of cardiac health

• High BNP = poor cardiac health (lower chance of survival, fluid overload) 

• Low BNP = better cardiac health/survival rate 

• Increased preload (ventricle stretch) = increased BNP

Vicious Cycle of HF

• HF = tachycardia (SNS stimulated)

• Decreased BP = decreased afterload (direct relationship) 

• Vasodilation = decreased afterload = decreased BP 

• Vasoconstriction = increased afterload = increased BP 

Patho of Heart Failure

• Lifetime risk of HF ≈ 20% for patients >40 yrs.
• Most common causes: long-standing hypertension, multiple myocardial infarctions, diabetes mellitus.
• Categories:
   - By side: Left Ventricular Failure (LVF) vs Right Ventricular Failure (RVF).
   - By function: Systolic dysfunction (HFrEF = reduced EF) vs Diastolic dysfunction (HFpEF = preserved EF).

Left Ventricular Failure (LVF)

Main problem: Backup into lungs → pulmonary symptoms.
Symptoms/Signs:
- Dyspnea on exertion
- Cough, orthopnea, paroxysmal nocturnal dyspnea (PND)
- Cyanosis
- Crackles on auscultation
- Pulmonary edema → pink frothy sputum + coarse crackles

Compensatory mechanisms:
- RAAS activation → ↑ blood volume, ↑ BP, ↑ resistance (afterload).
- Sympathetic stimulation → ↑ HR, ↑ strain on heart.

Diagnostics:
- BNP to distinguish cardiac vs pulmonary cause of dyspnea.
- LVEF <40% = Heart failure.

Right Ventricular Failure (LVF)

Main problem: Backup into systemic venous circulation.
Symptoms/Signs:
- Jugular venous distension (JVD)
- Ascites
- Hepatomegaly & splenomegaly
- Peripheral edema (ankle, sacral)

Key Clinical Findings of HF

• S3 gallop rhythm common in HF.
• Preload = blood returning to right atrium.
• Afterload = resistance against ventricle (aortic pressure).

Management of HF

Lifestyle modifications: diet, exercise, fluid/salt restriction.

Pharmacologic therapy:
- ACE inhibitors / ARBs
- Beta blockers
- Diuretics
- Nitrates, vasodilators
- Ivabradine
- Neprilysin inhibitors
- Digitalis (digoxin)
- Spironolactone (aldosterone antagonist)

Devices/Procedures:
- ICD: prevents sudden cardiac death.
- LVAD: bridge to transplant or destination therapy.
- Intra-aortic balloon pump: temporary support in end-stage HF.
- Transplantation in severe/end-stage cases.

Left vs. Right HF

Category	Left Ventricular Failure (LVF)	Right Ventricular Failure (RVF)
Main cause	Often HTN, MI, DM	Often secondary to LVF or lung disease
Primary backup	Lungs	Systemic veins
Symptoms	Dyspnea, orthopnea, PND, pulmonary edema, crackles, pink frothy sputum	JVD, ascites, hepatomegaly, splenomegaly, peripheral edema
Diagnostics	↓ LVEF, BNP elevated	Clinical exam findings

Heart Failure - Study Tips

• Remember: LVF = Lungs; RVF = Rest of body.
• HFrEF = reduced EF (<40%), HFpEF = preserved EF but stiff ventricle.
• BNP helps distinguish HF-related dyspnea from pulmonary disease.
• S3 heart sound = classic for HF.

How could myocardial infarction lead to low blood pressure and shock? What signs and symptoms might you see and why would they be present?

Myocardial infarction is death of a portion of the myocardium (those myocardiocytes) due to blockage of a coronary artery. When part of the myocardium dies, this can lead to acute systolic dysfunction of the heart (an acute pumping problem), as the heart can no longer pump effectively. The heart's reduced pumping ability leads to a drop in stroke volume, and can lead to inadequate cardiac output. Remember, cardiac output = stroke volume x heart rate. If the cardiac output drops too much, then blood pressure will drop due to a decrease in the overall circulating blood volume. (Remember, blood pressure has 3 main components; the blood, the blood vessels, and the cardiac pump). To compensate, the heart can increase the heart rate, so we may see tachycardia. The sympathetic nervous system causes vasoconstriction and attempts to shunt blood from the extremities back to the core organs (the heart and the brain). Thus we may see pale or ashen skin and the skin would likely feel cool to the touch. This is because we have a drop in the blood flow to the skin, much like we saw with hypovolemic shock. The kidneys would begin retaining more sodium and water from the urine in an effort to increase blood volume even though the heart can not effectively pump blood forward.  So patients will have reduced urinary output as well.  

How could a pulmonary embolism lead to right-sided heart failure?

The right ventricle pumps deoxygenated blood through the pulmonary semilunar valve into the pulmonary artery and into the lungs. A pulmonary embolism is a blockage in one of the pulmonary arteries of the lungs.  That blockage can thus cause blood to back up into the right ventricle.  The right ventricle then has to pump harder to overcome the increased afterload in pulmonary circulation. However, if the PE is large enough, the pressure may become too great for the RV to overcome, and it can lead to sudden, acute right ventricular failure. It can be a rapidly developing situation that requires emergency care to prevent cardiac arrest and respiratory failure. 

What is the difference between valve stenosis and valve regurgitation (incompetence)? How could these valve disorders lead to heart failure? 

Valve stenosis is a thickened, stiff, scarred, or malformed valve that does not open fully. Regurgitation is an "incompetent" valve that does not close fully (it can't make an effective seal when it is closed). Both of these disrupt the normal one-way route of blood flow through the heart, leading to congestion in the chambers and structures before the valve.

The last sentence is very important! For example, mitral stenosis or regurgitation will lead to congestion in the left atria. This causes left atrial hypertrophy and an increase in the left atrial ESV. The left ventricle, however, will have a decreased ESV. Why does the left ventricle have a reduced ESV? Here is why:

1. With mitral stenosis, less blood makes it into the left ventricle during filling, which decreases end diastolic volume. If you start with less blood at the beginning of systole, you will have less at the end of systole as well.

2. Mitral regurgitation reduces left ventricular afterload. How? Because you essentially now have two "doors" out of which blood can escape during systole (both the aortic valve and the mitral valve are now allowing blood out during systole). Since blood is escaping out of both valves, more blood is pumped out during systole, leading to a lower left ventricular ESV.

Heart failure will eventually happen in valve stenosis/regurgitation because of blood back up. For example:

Aortic stenosis --> blood backs up in to left ventricle--> ventricle dilates and hypertrophies to compensate --> compensatory mechanisms eventually are inadequate (remodeling of heart becomes pathologic) --> blood backs up into left atria --> blood backs up into lungs, potentially leading to pulmonary edema and to signs of inadequate organ perfusion (dizziness, possible fainting, chest pain, low urine output, diminished pulses, etc.)

Like the preceding example, you could chart a backward course of blood congestion and heart failure for each of the valves!

Which of these conditions would likely lead to diastolic heart failure? Select All That Apply

a. Left ventricular aneurysm
b. Cardiac hypertrophy from long-standing hypertension
c. Cardiac tamponade
d. Aortic regurgitation
e. Restrictive cardiomyopathy
f. Dilated cardiomyopathy
g. Long-standing anorexia nervosa

a. Left ventricular aneurysm. This would be a systolic function. Ventricular aneurysm is a large outpouching in the ventricle. Filling isn't compromised, but pumping is. Thus, this is a systolic issue. 
b. Cardiac hypertrophy from long-standing hypertension  - CORRECT. The ventricle becomes bulky, stiff, and non-compliant. This compromises filling (a diastolic problem)
c. Cardiac tamponade- CORRECT. When fluid accumulates in the pericardial sac it will impede ventricular filling (It is "squeezing the heart). This is a diastolic issue.
d. Aortic regurgitation- Blood moves backward during diastole, which overfills the ventricle. This results in a loss of SV and a reduction in ejection fraction (the blood initially moves out during systole, but then some of it travels backward back to the ventricle). This overfills the ventricle and causes an overall reduction in the ejection fraction. This would be a systolic issue. 
e. Restrictive cardiomyopathy- CORRECT. A restrictive cardiomyopathy is when the heart becomes stiff from infiltrative connective tissue. This impedes the heart's ability to relax and fill, which is a diastolic issue. 
f. Dilated cardiomyopathy- In dilated cardiomyopathy the ventricular chamber is large (dilated) and the muscle is reduced in size. This leads to problems pumping, which is a systolic issue.
g. Long-standing anorexia nervosa- Long standing anorexia can cause heart muscle fibers to degenerate because of lack of nutrients to maintain healthy cardiac muscle. This leads to a weak cardiac pump, which is a systolic issue.

Mr. Alwyn is a 53-year-old man who began experiencing chest pain while playing tennis with his friend. He described the pain as crushing and vice-like. The pain radiated up into his left jaw and down his left arm. He noticed that his heart was racing as well. He sat down in the shade and the pain subsided after 10 minutes. He went home and had no further problems. He decided that it was probably due to the large breakfast he had before the game and so did not seek medical treatment.

1. What information in the scenario suggests that this is cardiac-related pain?

2. Why did the pain go away after he sat down?

3. Could the large breakfast that Mr. Alwyn ate play a role in his chest pain?

1. What information in the scenario suggests that this is cardiac-related pain?

   1. Chest pain (angina) that radiates, tachycardia 

2. Why did the pain go away after he sat down?

   1. Stable angina - pain only occurs with exertion (less demand of oxygen with rest = adequate supply of oxygen to heart)

3. Could the large breakfast that Mr. Alwyn ate play a role in his chest pain?

   1. Yes - body will shunt blood away from other organs to ones that are doing more work (digestive organs)

      1. Not enough blood/oxygen to the heart

   2. MI mostly happen between 4 am - 10 am (breakfast time)

Mr. Alwyn has the following medical history:

      HTN, diagnosed 12 years ago

      Type 2 DM, diagnosed 5 years ago

      Hypercholesterolemia

      BPH (biegnin prostatic hypertrophy) , diagnosed 2 years ago

 

Mr. Alwyn has the following family/social history

      Father had history of DM, died of an MI at age 55

      Mother died from breast cancer at age 79

      Brother has hypertension

      Occasional alcohol use, reports drinking 2-3 beers a week

      Grandparents “may have had heart disease”

 

1. What are Mr. Alwyn’s most significant risk factors for coronary artery disease?

   1. How do each of these risk factors contribute to the pathogenesis of CAD?

2. Which risk factors would you want to target as a nurse?

3. Mr. Alwyn is prescribed sublingual nitroglycerin PRN for his chest pain.

4. Nitroglycerin is a potent vasodilator. How could this help alleviate chest pain in patients with angina?

1. What are Mr. Alwyn’s most significant risk factors for coronary artery disease? How do each of these risk factors contribute to the pathogenesis of CAD?

   1. HTN - turbulent blood flow that damages walls of blood vessels, inflammatory response, increased after load (pressure for heart to pump against), plaque formation and rupturing increased, risk for heart attack

   2. DM - inflammatory to blood vessels (increased cytokine release), increased risk for plaque rupture

   3. Hypercholesterolemia - LDL forms plaques 

2. Which risk factors would you want to target as a nurse?

   1. HTN - treated to decrease workload of heart

   2. Hypercholesterolemia - want to decrease cholesterol to decrease plaques

   3. Controlling blood glucose levels to decrease inflammation in the body

3. Mr. Alwyn is prescribed sublingual nitroglycerin PRN for his chest pain. Nitroglycerin is a potent vasodilator. How could this help alleviate chest pain in patients with angina?

   1. Decreases preload (amount of blood coming back to heart)

   2. Dilates arteries - decreased blood pressure and after load

Mr. Alwyn wakes up at 3:00 in the morning with crushing, substernal chest pain. He takes three doses of his nitroglycerin, but the chest pain is unremitting. He is nauseous, diaphoretic, and extremely anxious. He tells his wife “I think I’m dying”. His wife notices that he is cold and clammy. She calls 911 and he is brought to the emergency department. The paramedics transmit a 12-lead ECG to the ED physician along the way. They also give Mr. Alwyn an aspirin, which they tell him to chew. At the ED, Mr. Alwyn presents as follows:

Vital Signs
BP 156/88 mmHG, right arm sitting	Temp   98.3 F
HR  105	HT    70”
RR   26	WT    83.5 kg

Skin	Cool, diaphoretic, pale without cyanosis
Chest	Slight bibasilar inspiratory crackles with auscultation. No wheezes or friction rubs
Cardiac	Tachycardia with occasional premature beats. Normal S1 and S2. No S3, soft S4
Abdomen	Soft, nontender, hypoactive bowel sounds present in all quadrants.
MSK	Normal range of motion throughout, Pulses 2+, distinct bruit over the femoral artery, no pedal edema
Neuro	Cognition, sensation, gait, DTR in normal limits. Anxious and restless

 

1. Describe the physiologic mechanisms behind Mr. Alwyn’s abnormal vital signs.

2. Describe the physiologic mechanisms behind Mr. Alwyn’s clinical presentation.

1. Describe the physiologic mechanisms behind Mr. Alwyn’s abnormal vital signs.

   1. High blood pressure (systolic noted) 

   2. High heart rate 

   3. High respiratory rate - pain, panic 

   4. Temperature - normal 

   5. Height + weight not significant at the moment 

2. Describe the physiologic mechanisms behind Mr. Alwyn’s clinical presentation.

   1. Blood being shunted away from body - core blood to vital organs by SNS 

   2. Sweaty - SNS 

   3. Crackles - fluid backing up into lungs

   4. S4 - always pathologic (diastolic issue - filling problem)

   5. Not as much function in bowel sounds - blood in vital organs 

   6. Bruit - turbulent blood flow 

   7. Anxious - SNS

*SNS - body uses too much oxygen (give morphine which decreases oxygen intake)

Ms. Duquette is admitted to the ICU with a right-sided MI due to occlusion of the right coronary artery. Heart rate is 45 BPM, blood pressure is 86/40 mmHg.

1. Why might this patient have a low HR and a low BP?

2. The physician has prescribed the following medications that are often given to patients in the acute phase on MI:

   1. Nitorglycerin (vasodilator)

   2. Beta blocker (negative inotropy and negative chronotropy).

Considering Ms. Duquette presentation, you might want to:

A. Administer the nitroglycerin and hold the beta blocker

B. Administer the beta blocker and hold the nitroglycerin

C. Administer both medications

D. Hold both medications

1. Why might this patient have a low HR and a low BP?

   1. Right-sided MI 

   2. RCA - perfuses SA and AV nodes (pacemakers of the heart) 

      1. SA node is killed, AV node takes over - around 40 bpm (bradycardia)

   3. Low HR = low BP (drop in CO)

   4. Dizziness and syncope (LOC)

      1. Brain not perfused - fall risk

2. The physician has prescribed the following medications that are often given to patients in the acute phase on MI:

   1. Nitroglycerin (vasodilator)

   2. Beta blocker (negative inotropy and negative chronotropy)

      1. Slow contractility, HR 

Considering Ms. Duquette presentation, you might want to:

A. Administer the nitroglycerin and hold the beta blocker

B. Administer the beta blocker and hold the nitroglycerin

C. Administer both medications

D. Hold both medications - vasodilator will drop her BP

Thanks to an amazing health care team and the support of his wife and children, Mr. Alwyn survives his MI and returns from the cath lab after two stents are placed in his LAD artery. On day two, the nurse notices that Mr. Alwyn is becoming more short of breath. Course, bilateral crackles are auscultated in the mid and lower lobes. The nurse also notices that there is both and S3 and and S4 heart sound present. His heart rate is elevated again (102 BPM) and his blood pressure is at 100/64 mmHg.

 

1. Explain Mr. Alwyn’s respiratory symptoms

2. Why would Mr. Alwyn be hypotensive?

3. You would expect Mr. Alwyn’s ESV to be:

   1. Increased

   2. Decreased

   3. Within normal limits

4. You would expect Mr. Alwyn’s LVEDV to be:

   1. Increased

   2. Decreased

   3. Within normal limits

5. You would expect Mr. Alwyn’s pulmonary pressures to be:

   1. Increased

   2. Decreased

 

 

1. Explain Mr. Alwyn’s respiratory symptoms

   1. Crackles - fluid in lungs (pulmonary edema)

   2. HF a complication of MI = heart not pumped blood forward, backing up into lungs (left side of heart not pumping effectively)

2. Why would Mr. Alwyn be hypotensive?

   1. Reduced CO

   2. Blood is backed up into lungs

   3. Blood not leaving heart = low BP

3. You would expect Mr. Alwyn’s ESV to be:

   1. Increased - more blood left in V after systolic

   2. Decreased

   3. Within normal limits

4. You would expect Mr. Alwyn’s LV EDV to be:

   1. Increased - more blood staying in ventricle

   2. Decreased

   3. Within normal limits

5. You would expect Mr. Alwyn’s pulmonary pressures to be:

   1. Increased - pulmonary congestion, right side has a lot of pressure to push against 

   2. Decreased

Mr. Norrell has experienced increasing fatigue and shortness of breath over the past few months. He developed a dry cough and his legs swell by the end of the day. He reports that he has to prop his head up on four pillows at night and that he goes to the bathroom to urinate 4-5 times during the night (orthopnea - fluid in lungs when laying fluid, nocturia - laying flat = edema comes back into vessels = goes to kidneys). His past medical history includes diabetes (type II), hyperlipidemia, and peripheral arterial disease. An echocardiogram reveals an ejection fraction of 33% (systolic HF) and a BNP (brain-type natriuretic peptide) level is 750 pg/mL (normal range: < 100 pg/mL). His vital signs upon presentation are: HR 94 bpm, BP: 160/94, RR: 22/minute, Temp: 97.4 oral, O2 saturation: 94% on room air. Mr. Norrell is diagnosed with heart failure.

1. Based on the preceding information, Mr. Norrell likely has:

   1. Systolic dysfunction

   2. Diastolic dysfunction

1. BNP would most likely indicate:

   1. Increased EDV

   2. Decreased ESV

   3. Decreased ventricular filling pressures

   4. A and B

   5. A, B, and C

1. Based on the scenario, Mr. Norrell is likely experiencing:

   1. Left ventricular dysfunction

   2. Right ventricular dysfunction

   3. Biventricular dysfunction

2. True or False: Left ventricular afterload appears to be severely decreased.

3. True or False: From a clinical standpoint, we probably need to focus on interventions that will increase Mr. Norrell’s preload so that we can increase cardiac output.

1. Based on the preceding information, Mr. Norrell likely has:

   1. Systolic dysfunction - heart is pumping blood out (pumping problem) = EF < 40%

   2. Diastolic dysfunction

      1. Filling problem

1. BNP would most likely indicate:

   1. Increased EDV - too much stretch

   2. Decreased ESV

   3. Decreased ventricular filling pressures

   4. A and B

   5. A, B, and C

1. Based on the scenario, Mr. Norrell is likely experiencing:

   1. Left ventricular dysfunction

   2. Right ventricular dysfunction

   3. Biventricular dysfunction - edema (right sided issue, blood backs up in RA, body, JVD), orthopnea, cough, pulmonary symptoms - all left side

2. True or False: Left ventricular afterload appears to be severely decreased.

   1. BP is elevated

3. True or False: From a clinical standpoint, we probably need to focus on interventions that will increase Mr. Norrell’s preload so that we can increase cardiac output.

   1. Don’t want to increase if there is a pumping problem

   2. High BNP - already too much preload (want to decrease)

Ms. Terry has been diagnosed with mitral stenosis r/t rheumatic fever. Based on this diagnosis, answer the following questions:

  

1. True or False: You would expect Ms. Terry to present with a systolic heart murmur.

2. What type of hypersensitivity reaction led to her condition?

   1. Type I

   2. Type II

   3. Type III

   4. Type IV 

3. What type of antibodies are primarily responsible for this type of hypersensitivity?

4. Which chamber in the heart will most likely undergo pathologic remodeling first?

   1. Left ventricle

   2. Left atria

   3. Right ventricle

   4. Right atria

5. Based on her condition, you would expect left ventricular end-diastolic volume to be:

   1. Increased

   2. Decreased

6. True or false: The ESV of her left ventricle will likely be increased

7. True or false: Ms. Terry’s condition would likely contribute to increased fluid formation in the pulmonary interstitial space.

8. True or false: Over time, the right ventricle is likely to hypertrophy.

1. True or False: You would expect Ms. Terry to present with a systolic heart murmur.

   1. Stenosis - problem with opening

   2. Mitral opens during diastolic

2. What type of hypersensitivity reaction led to her condition?

   1. Type I

   2. Type II - IgM + IgG

   3. Type III

   4. Type IV 

3. What type of antibodies are primarily responsible for this type of hypersensitivity?

   1. IgG and IgM (type II hypersensitivity) 

4. Which chamber in the heart will most likely undergo pathologic remodeling first?

   1. Left ventricle

   2. Left atria

   3. Right ventricle

   4. Right atria

5. Based on her condition, you would expect left ventricular end-diastolic volume to be:

   1. Increased

   2. Decreased - not enough blood in ventricle due to stenosis mitral valve

6. True or false: The ESV of her left ventricle will likely be increased

   1. Not filling enough (not enough EDV) = less ESV

7. True or false: Ms. Terry’s condition would likely contribute to increased fluid formation in the pulmonary interstitial space.

   1. Blood back flows into the lungs = pulmonary edema 

8. True or false: Over time, the right ventricle is likely to hypertrophy.

   1. Pulmonary edema = increases right side pressure to push against