Patho2-Cardiac

Preload (load = work)

• Volume of blood in ventricles at END of diastole/End diastolic ventricular pressure 

  • Diastolic = RE=elaxation

  • Blood ENTERING heart BEFORE contraction

  • Venous Return/Blood entering the right atrium

• Increased in

  • Hypervolemia

  • Regurgitation of cardiac valves

  • Heart failure

Afterload (load=work)

Resistance left ventricle must overcome to circulate blood

• Force required to eject left ventricle volume

Increased in

• Hypertension

• Vasoconstriction

Inc afterload = inc cardiac workload

PVR= peripheral vascular resistance which affects afterload

Contractility + SV

Contractility = ability of myocardium to stretch and contract in response to filling of heart with blood////hearts ability to contract and pump blood effectively

SV = amount of blood ejected from ventricles with each contraction

Preload, Afterload, Contractility, and SV

• Increased pre = Increased contractility + SV

• Increased afterload = DECREASED SV + contractility

  • Weaking of heart muscle due to EXCESSIVE afterload

Left ventricular ejection fraction (LEVF)

Percentage of blood leaving the LV each time it contracts

• Healthy = 60-70

• Lower than 40= heart failure

Vol blood ejected/ Vol blood in LV

Inotropic + Chronotropic function

Ino: Force of contraction of cardiac muscle

Chrono = Heart rate

Blood Pressure

BP = CO x PVR

• Refers to PRESSURE IN PERIPHERAL ART SYSTEM

CO = volume of blood pumped/min (ml/min)

PVR = systemic vascular resistance

• Vasoconstrict = inc pvr

• Vasodilate = decreased pvr

Cardiac Outfput

• Volume of blood pumped/min (ml/min)

• CO = SV x HR

  • Avg SV = 70ml

  • Avg = 70 ish

  • Avg CO = 5ml/min

Total BP Equation

BP = (SV x HR) x PVR

• CO = SV x HR

BP regulation (3)

• Sympathetic nervous system

• Antidiuretic hormone (ADH)

• Renin-angiotensin-aldosterone system (RAAS)

• PLEASE KNOW EFFECTS ON EQUATION

Sympathetic Nervous System (BP Regulation)

Steps

• Decrease BP

• Baroreceptor activation + signal send

• Activates SNS

  • B1 activation

    • =HR

    • =CO

  • A1 activation

    • Vasocontriction

    • =PVR

AHD (BP Regulation)

Steps

• Low BP

• ADH secretion by pituitary gland

• Reabsorption of water at kidney

• Increase extracellular water volume

• Increase Blood volume

  • Increases venous return

  • Increases SV = increase CO

RAAS (BP Regulation)

Steps

• Decrease BP or Decrease extracellar fluid (due to decreased Na)

• Kidney

  • release Renin

• Liver

  • Renin causes liver to change angiotensinogen to angiotensin I

• Lung

  • ACE enzyme converts Angio 1 to Angio 2

• 2 responses (to angio2 in body)

  • 1

    • Adrenal cortex release aldosterone

    • Causes sodium reabsorption at kidney + water reabsorption = SV increase

    • Increase volume + arterial blood pressure

  • 2

    • Causes direct vasoconstriction of system arterioles = PVR increase

    • Increases arterial blood pressure

Endothelial damage

Caused by:

• Hypertension

• Hypercholesterolemia (high blood cholesterol)- LDL

• Smoking

• Uncontrolled diabetes mellitus

Uncontrolled endothelial injury leads to ATHEROSCLEROSIS (plaque buildup)

Atherosclerosis Steps (3 main)

1. Inflammation occurring in blood vessels due to endothelial cell damage

   1. WBC arrive + Platelets

   2. WBC margination

   3. Endothelial layer becomes permeable + Leucocytes/WBC adhere + roll

   4. WBCs transmigrate into tunica intima

2. WBC become “FOAM CELL” (wbc filled with LDL)

   1. Macrophage engulf LDL at inflammation cite

3. Bad

   1. Adherence + entry of leukocytes

   2. Adherence + aggregation of platelets

   3. Foam cell formation continue (Inside tunica intima

   4. Smooth muscle migration occurs

   5. Release of toxic oxygen species

4. Fibrous cap formation + Necrotic core

   1. Macrophage + foam cel + lymphocyte + collagen accumulate

   2. Necrotic core formation in center

   3. Smooth muscle migrates to top later to create a “Fibrous cap”

5. IF FIBROUS CAP OPENS

   1. Tissue factor released by necrotic core

   2. Clotting cascade activated

   3. Blockage of blood vessel occurs

Atherosclerotic Plaques + Fatty Streaks

• Fibrous cap =

  • Top “Cap” layer = endothelial cell

  • Macrophage

  • Soft muscle cells

  • Lymphocytes

  • SHOULDER = les reinforced side portion

• Fatty streaks = collection of foam cells

Highest risk locations of athersclerosis

1. Abdominal aorta + iliac arteries

2. Proximal coronary arteries

3. Thoracic aorta, femoral, and popliteal arteries

4. Internal carotid arteries

5. Vertebral, basilar, and middle cerebral arteries

1st = HIGHEST RISK

CHEST/ ABD comes first, then the mroe peripheral brain is the last lukily

Peripheral Arterial Disease (PAD)

• ALSO known as Peripheral arterial “occlusive” disease (PAOD)

• Increased atherosclerosis = Increased chance for PAD

  • Atherosclerosis plaque obstructs blood flow to a LOWER extremity

  • Acute vs chronic

• Risk factors

  • Age

  • HTN

  • DM
    Smoking

  • High fat/LDL diet

  • Sedentary lifestyle

  • Obesity = increase LDL

  • Family history

  • Hyperlipidemia

PAD Steps

• Occlusion of arterial blood flow (due to athero)

• Reduciton in arterial blood flow

• Decrease tissue oxygen supply = hypoxic damage

• Ischemia(dec bloodflow and O2 to an are) AND anaerobic metabolism

• Sx

  • Pain

    • Pain with exertion (due to lwo O2), less pain when resting

  • Pallor + coolness

  • Weak pulses

  • paresthesia- tingling and numbness

Ankle, Brachial Index

• Comparison of BP in leg vs BP in arm

  • BP in leg/ BP in arm

• Normal ratio is OVER 1 (higher BP in ankles than brachial)

• SEVERE PAD = less than 0.5

Arterial vs Venous Disease

• Arterial = PAD

  • No pulse

  • Color = pale to necrotic blue

  • Sharp VERY painful

  • Paresthesia (numbness or tingling)

  • Paralysis

• Venous Disease = PUD

  • Pulse

  • Pink warm dark red - stasis dermatitis

  • NOT as painful, achy instead

  • Edema congestion (blood can’t move back to heart well)

  • Ulcer development

Hypertension

Damaging force on endothelial linings of arteries - leads to atherosclerosis

• High resistance = inc aferload = cardiac hypertrophy = heart failure

• HTN = inflammation = atheroslcerosis

• High BP = High afterload

• Systole = contarction

• Diastole = relaxation

Know hypertension ranges??

Aneurysms

• Weakening in artery wall causing local BULGING + DILATION

  • Susceptible to RUPTURE = internal hemorrhage

• Lead to turbulent blood flow: Erratic blood movement and velocity changes rather than “smooth parallel movement”

• Risk factor:

  • HTN

  • Athero

  • Smoking

• S/Sx: vary based on severity, size, locaiton

  • Asymptomatic UNTIL RUPTURE

  • Bruits = indicative of turbulent blood flow

  • Diminshed pulse

• Common

  • Aorta and cerebral arteries

Laminar vs Turbulent Bloodflow

• Laminar = straight, smooth, parallel blood flow

• Turbulent = winding, erratic speed, erratic overall

Aneurysm types

• AAA/ fusiform = buldge of an artery

• Saccular = sac coming off of blood vessel

Aortic Dissection

• Tear in arterial lining between tunica intima and media

• Forms HEMATOMA in blood wall

• S/sx

  • Pain in chest or back (sharp, ripping pain_

  • BP difference in arms

    • Due to tear being in aorta, effects blood flow to body depending on where (LOOK AT PICTURE)

  • WIDE pulse pressure

Hypercholesterolemia

• More HLD is GOOD, More LDL is BAD

• LDL = low density lipoprotein

  • Less protein, more cholesterol

  • Transports cholesterol FROM LIVER to CELLS

  • Can be oxidized + Despotized onto artery walls = athero

• HDL = high density

  • More protein, less cholestorl

  • Transports cholesterol FROM CELLS TO LIVER

    • CLEAN UP/ regulates LDL storage + promoted excretion

Smoking

• Causes endothelial damage + initiate athero

• Nicotine

  • Potent vasoconstrictor, ESPECIALLY in coronary arteries

Diabetes

• Uncontrolled diabetes intiates athero

• WHY? idk its not in the slides

Coronary Artery Orifice

• How blood gets to heart muscle

• Anterior view

  • Aortic valve sits between LV and aorta

  • Just above valve = aortic sinuses

    • Right AS - goes to right coronary art

    • Left AS- goes to left cornoar art

    • Posterior sinus

      • Aortic sinus = catch blood when valve closes

  • Systole/ valve open

    • Coronary arteries DONT get much blood here

      • Valve leaflets block opening to coronary arteries

  • Diastole/ valve closed

    • Blodo flows backward slightly into aortic sinuses

    • Blood flow in sinuses = blood enter coronary arteries which FEEDS myocardium

IMPORTANT

• Perfusion happens in diastole

  • Shorten diastole (like tachy) = REDUCED coronary blood flow

  • Aortic valve malformation = impact perfusion

  • Etc.

Coronary Art Disease (CAD)/ Coronary heart disease CHD/ Ather erotic heart Ds.

• Disease from impaired blood flow

  • Leads to chronic ischemic heart ds

    • Stable angina, silent ischemia

      • Ischemia = schemia is a condition characterized by insufficient blood flow to a part of the body, leading to a shortage of oxygen and nutrients necessary for cellular metabolism.

      • Angina = pain or pressure

  • Leads to Acute Coronary Syndrome

    • Unstable angina, possible MI

Atherosclerosis leads to CAD

• Steps Stable angina

  • Asymp atherosclerotic plaque buildup

  • Larger, stable atherosclerotic plaque (stable fibrous capsule) = dec blood flow = stable angina

• Steps acute coronary syndromes

  • Unstable plaque buildup, plaque disruption + platelet aggregation (sudden onset, more painful, bigger risk)

  • CAN LEAD TO

    • Non - ST segment elevation MI

      • Minor thrombus in blood vessel = minor blockage

    • ST- segment elevation MI

      • MAJOR

      • Full blockage thrombus

Chronic Ischemia Heart Disease

• Ischemia = imbalance between myocardial oxygen supply + demand

• Sx:

  • PAINFUL, very

  • Stable angina better than unstable angina// stable acts up when exerted du eo diffeirng emands, wheras unstable will hrut EVEN at rest

Atherosclerosis

• Asymptomatic when O2 demand = O2 supply

• Symptomatic when O2 demand is higher than supply

• 2 types:

  • Partial occlude = reduced blow flow

    • When supply less than demand = symptomatic

    • Like with exertion

  • Fully occlude

    • ALWAYS symptomatic

    • Supply ALWAYS less than demand

Stable angina

Chest pain at times of increased myocardial O2 deamnd

• Relieved by: Rest or NITROGLYC (vasodilator)

Due to fixed atherosclerotic plaque = ischemia

VERY COMMON, initial presentation for many people with CAD

Acute coronary syndrome

Acute results of CAD that are most often disruption of unstable plaques

• Unstable angina = minor atherosclerotic plaque rupture

• Myocardial infarction = major rupture atherosclerotic plaque 

  • Necrosis or death of myocardial tissue (due to lack of blood/O2)

Severity: determined by ECG + lab results

EKG Changes of Acute Coronary Syndrome (ACS)

• ST seg elevation

• T wave inversion

• Development of Q wave

T wave + ST seg, ventricular repolarization USUALLY first affected by myocardial ischemia + infarction

Serum Biomarkers/ Cardiac Enzymes

• Increased cardiac enzymes = increased cardiac myocyte damage

  • Troponin I, troponin T, and creatinine kinase, and myoglobin

• Biomarker timelineORDER = MTC

  • Myoglobin elevated 1 hour after myocardial cell death (peak 4-8 hr)

  • Troponins rise 3 hours after onset of MI (stay 7-10 day)

  • CK-MB elevate 4-8 hours after myocardial injury (stay 2-3 day)

Unstable angina/ NSTEMI (partial blockage)

NSTEMI = Non St seg elevation MI

Chest pain:

• At rest

• Minimal exertion

• Worse chest pain than before

NO ST seg elevation

• Can involve infarction, but with NO ST seg changes

• MUST look at serum biomarkers with NSTEMI

STEMI

ST elevated + Full blockage

Necrosis of myocardial tissue, causing SEVERE pain

• Tranmural infarction = full thickness of ventricular wall (EKG + labs needed)

• Prolonged, nitroglycerin does NOT help

• Jaw pain, arm pain, GI complaints (NV)

Consequences of major plaque rupture

Complication

• Replacement by fibrous tissue (less elastic_

• = decreased contractility of heart

• Can develop rupture of papillary muscles, heart wall rupture (bc cant strech)

STEMI S/Sx

Ischemia/infarction

• Severe pain

• Pale,cool skin

• Nausea, vomiting

• Dyspnea

Organ dysfunction (heart)

• Fatigue

• Pale,cool skin

• Dyspnea

• Hypotension

Compensatory mechanism/ SNS

• Tachycardia

Heat sounds

S1

• Tricuspid + mitral valve closure

• These are AV valves

• LUB

S2

• Pulmonary + aortic valve closure

• SL

• DUB

Heart Murmur

• Sounds caused by TURBULENT BLOOD FLOW thru heart or great vessels

  • Commonly due to valve deformities, dysfunction, or defects in heart wall (ASD, VSD)

• OR by backflow of blood

Valve Defects (2)

• Stenosis

  • Valve wont open all the way

  • HARDER to force blood = inc afterload??

  • Murmur of blood shotting through narrow opening

• Regurgitation (insufficiency)

  • Valve NOT CLOSE all the way

  • Leaks

  • Murmur of blood leaking

Valvular disorders (4, 2 for each valve)

1. Mitral stenosis

2. Mitral insufficiency/prolapse

3. Aortic stenosis

4. Aortic insuffiency

Mitral Stenosis (2 pathways)

Narrow MV, does NOT eject enough blood in LV during DIASTOLE

2 part impacts

• Blood congestion in LA (2 parts)

  • Blood backup

    • = increase in hydrostatic pressure

    • = edema in lungs

    • = dyspnea, cough orthopnea

  • Dilated LA

    • = overstretched myocardium

    • = atrial fibrillation

    • = thrombus formation in LA

    • = Ischemic stroke

• Less output to LV

  • Decreased SV and CO

  • Ischemic heart

Mitral Insufficiency (2 pathways)

MV doesn’t close completely = leaking blood in LA during systole

• Blood congestion in LA (2 parts)

  • Pulmonary congestion

    • Blood flows back in LA from LV

    • LA congestion

    • Pulmonary vein congestion

    • Inc hydrostatic pressure

    • Pulmonary congestion + edema

    • Dyspnea, cough, orthopnea

  • Overstretched LA

    • Atrial fibrillation (take blood thinners to prevent thrombus)

    • Thrombus formation (bc blood pools up and cant move)

• Less output output LV

  • Decreased SV CO

  • Chest pain + faitgue

Aortic stenosis (2 pathways)

Narrowed Aortic valve opening does NOT enject enough into aorta during systole

• Blood backup into LV

  • LV congstion

  • LA congestion

  • Pulm vein congestion

  • Pulm edema

  • Pulm congestion

  • Exertion dyspnea

• Forward (2 things)

  • Less output to aorta

    • Dec SV,CO

    • Ischemic chest pain, MI

  • Inc afterload

    • LVH, LVF

Aortic Insufficiency

Aortic valve does NOT close completely

• Leaks blood into LV during diastole

2 pathways

• Backup

  • Blood backups into LV

  • Blood backups into LA

  • Pulmonary congestion

  • Exertional dyspnea

• Forward

  • Less output to LV (BC ITS ALREADY FULL??)

  • Decreased SV, CO

  • Chest pain, fatigue, syncope

Heart Failure (3 types)

• Weakened ventricular muscle CANNOT pump blood into arterial circulation well enough

  • Most common cause of hospitalization

• 3 types

  • Right side vs left side heart failure

  • Systolic vs diastolic dysfunction

  • Backward vs forward failure

Systolic vs Diastolic

• Systolic = NOT ENOUGH OUT

  • Weak ventricle cant pump enough out

  • Dec empty = Dec CO + SV

  • Blood accumulation + backup into atrium = INCREASED PRELOAD ?? why, not blood coming in its the total blood

• Diastolic = NOT ENOUGH BLOOD IN

  • Stiff ventricle is less elastic = cant accept enough blood

  • Dec EDLVV = Dec CO + SV

    • EDLVV (end diastolic left ventricular volume)

Backward vs Foward effects

• Backward 

  • Backup of blood into atriums + pulmonary vessels

  • LVF backup = pulmonary edema/congestion (MAKE SURE TO KNOW PROCESS FROM PREVIOUS SLIDES WILL BE ON EXAM)

  • =Dyspnea, cough, orthopnea SHORT OF BREATH LYING DOWN, paroxysmal (sudden) nocturnal dyspnea

• Forward

  • Cant pump blood out

  • LVF = Dec SV, CO

  • Neurohormonal responses (RAAS, ADH, SNS)

    • Body thinks BP low due to some stuff and tries to compensate

  • Fluid retention + weight gain

Orthopnea

• LVF patients = difficulty breathing when lying flat (dyspnea)

  • Fluid congestion in lung tissue

  • Pt must sleep upward

  • When propped up, fluid in lungs remain in bases = easier to breathe

Paroxysmal Nocturnal Dyspnea (PND)

• Patient with HF awake in middle of night SUDDENLY

  • Due to pulmonary fluid buildup = hypoxia while sleep

  • = Smothering feeling or nightmare

Forward vs backward effects of LVF

Backward LVF = pulmonary congestion pathway

Forward LVF Steps

• Cant pump enough blood into aorta

• Decreased systemic arterial pressure

• Renin, ADH, and SNS stuff activate from earlier

  • Causes fluid retention, increased BP, Incrase HR, Increase Vasoconstrict, etc.

Right Ventricular Failure (RVF)

• Blood backup into RA, SVC (sup vena cava) and IVC

• Leads to

  • Jugular venous distension (Bulging jugular vein)

  • Ascites (crackles)

  • Hepatomegaly (hepatic venous congestion)

  • Splenomegaly (splenic venous congestion)

  • Ankle or sacral edema

• Backward effects are MOST apparent on physical examination (edema and distension, ascites, etc.)

HF compensatory mechanisms (5)

1. Frank starling

2. SNS

3. RAAS

4. ADH

5. Myocardial remodeling/muscle building

Frank Starling Mechanism (HF Comp)

• Increasing SV through increase in end diastolic volume/preload

  • As SV + CP increase, Preload inc (VICE VERSA)

• Increased filling = increased force of next contraction

SNS (HF Comp)

Steps

• Dec Bp

• Baroreceptor activate

• SNS activate

• Vasoconstriction

• Increased HR?

Look back at old slide

RAAS (HF Comp)

• Same as before 

ADH (HF Comp)

Same as before

Myocardial Remodeling

• Heart becomes hypertrophic due to increased demands

• Then decreased imated ???due to systolic heart failure

Heart Failure Signs and Symptoms

Hemodynamic measuremnt changes in HF

1. Central venous pressure (pressure in vena cava)

2. Cardiac output decrease

3. Increase pulmonary capiallry pressure

4. Left ventricular ejection fraction (vol ejected/vol in LV)

5. Systemic BP Decrease (dec BP = dec CO)

Pharmacological treatment of HF (5)

1. ACE inhibitors/ angiotensin receptor blockers = vasodilation = dec afterload

2. Beta blockers = dec HR

3. Diuretics = inc excretino = low blood vol = low preload = low workload

4. Digitalis = inotrophic = supports contractility

5. Nitrates = vasodilation = dec afterload

Shock/ circulator failure

• Failure of circulatory system to supply O2 and nutrients = cellular hypoxia

  • Decreased CO, hypotension, hypoperfusion

4 types of shock

1. Hypovolemic = loss of intravascular volume

2. Cardiogenic = pump fialure

3. Obstructive shock = mechanical obstrucitn of blood flow through central circulation

4. Distributive shock = massive vasodilation

BE FAMILAR WITH EACH, LOOK AT PICTURE

Shock Compensation (3 types)

Shock = dec intravascular volume, heart fails to pump blood, or extensive vasodilation

• Causes dec CO, SV, and BP

1. SNS: Vasoconstriction = Inc HR + contractility

2. RAAS = angiotensin II + aldosterone (what these do again)

3. ADH: what do again