Cardiovascular Disorders Unit 4

End Systolic Vol is dependant on 3 variables

• Preload

• Contractility

• After-Load

BP = CO xTPR avg values

• SV = 70ml

• HR: 72 BPM

• CO: 5000ml/min

TPR

• Degree of constriction/Dilation of peripheral vessels

• Can be affected by atherosclerosis and Catecholamines

MAP (Avg between SBP and DBP)

• MAP = DBP + 1/3 PP

• Normally 90-100mmHg

• 40mmHg for adequate cerebral perfusion

Vasomotor Centre medulla

• Controls peripheral vasoconstriction and dilation

• Effects TPR and BP

Baroreceptors in Aortic Arch and Carotid Bodies (peripheral) and Medulla (Central)

Stretch receptors send messages to cardiac center in medulla to (+) or (-) HR and FOC (SV) and triggers vasomotor center

Chemoreceptors in Aortic Arch, Carotid Bodies (peripheral) and Medulla (central)

• Monitor (+) or (-) in CO2 and O2 levels in blood to trigger vasomotor cennter to vasodilate/constrict vessels to direct blood flow where needed

• Alters BP

Preload

• Degree of fiber stretch prior to contraction

• Ventricle stretching is from venous return

• Increased venous return, filling of heart, stretch and FOC

• Elastic nature of myocardium allows for stretch (passive action no O2 required)

Starlings Law of the Heart

Greater the stretch of the ventricle the greater force of contraction (FOC) independent of contractility

(no O2 required)

Contractility

• Ability of myocardial cells to use O2 to form cross bridges and shorten the fibres causing muscle contraction independant of stretch

• Contractility is a factor of Ca and catecholamines

• Acidosis and hypoxia will decrease contractility

After Load

• Amount of tension L ventricle must develop during contraction to open semi-lunar valve and eject bld

• Myocardium has to incr FOC to overcome resistance

• Can lead to hypertrophy ( (-) chamber vol) of L ventricle and Heart Failure

R. Ventricle Ventricular Ejection Fraction

• (-) Ejection fraction

• (+) End-systolic vol

• (+) pressure in R. Ventricle + Atria

• (+) pressure in IVC + SVC

• (+) pressure in venous system

• Leads to peripheral edema, ascites, and JVD

L. Ventricle Ventricular Ejection Fraction

• (-) ejection fraction

• (+) End-Systolic Vol

• (+) pressure in L Ventricle + Atria

• (+) pressure in pulmonary vein

• (+) pressure in capillary bed

• Leads to pulmonary edema

Atrial Kick

• Up to 25% decrease in cardiac output die to incomplete contraction + emptying of Atria

• Caused by atrial Dysrrhythmia + Atrial Fibrillation

• Causes thrombosis in atria

• Pt may feel weak + dizzy + Syncopal episodes

Ventricular Filling occurs through

1. Blood flowing directly from vena cava through atria + open valves into ventricles

2. Blood accumulated in atria is contracted into ventricle but if atrial kick is lost there is not proper contraction of atria resulting incomplete emptying of atria into ventricle so they don’t fill completely

Atherosclerosis

• A disease syndrome resulting in thickening and hardening of the arteries

• Atherosclerosis is the most common type of ateriosclerosis in the coronary, carotid, peripheral, arteries and aorta

• Called CAD when in coronary artery

Atherosclerosis Problems

• Unable to dialate past full size (5-6x normal size)

• Anginal Chest pain (blood flow reduced by > 75%)

• If <75% they will not implant a stent but encourage lifestyle changes

Ateriolarsclerosis

Arteriosclerosis found in renal arteries

3 Stages to pathophysiology of arteriosclerosis Development

1. Fatty Streak development

2. Fibrous Plaque Development

3. Development of complication plaque

Arteriosclerosis Causes

• Smoking

• HTN

• (+) LDL, Diabetes, (-) HD

Arteriosclerosis Etiology

• Injured cells become inflammed

• Macrophages stick to injured cells

• Causes oxidation of LDL which is engulfed by FOAM CELLS

• Move into intima of vessel

• Fatty streak develops from Foam cells

Complicated Plaque

• Plaque becomes unstable and prone to rupture or ulceration

• Lesion exposed to blood flow where platelets adhere + form a thrombus to occlude the artery resulting in ischemia and infarction

Complicated Plaque Manifetations

• Thrombosis

• Plaque hemorrhage

• Embolytic Showeres

• Aneurysm Formation

Hypertension (HTN)

• Sustained SBP >140 + DBP >90mmHg

• 2 types:

• Primary or essential

• Secondary (10% HTN Causes)

Primary HTN

• Most common type of HTN

• Cannot pinpoint exact cause of HTN

• May be generic, baroreceptors set too high, Hypersensitive SNS

Secondary HTN

• Indentifiable cause

• #1 cause is renal impairment

HTN Causes

• (-) distensibility of atrerial wall

• (+) TPR

• Hypervolemia

HTN Psychophysiology

• (+) laer pressure against vessel walls causes degenerative cahgne to walls

• Walls become harder + (-) elasticity causing further (+) resistance to blood flow, heart work harder (+) FOC can lead to

• Heart failure

• Vessels in Kidneys harden (renal failure)

• CVA

HTN Patients

• 25-35% of Pt’s with HTN will die of CHF

• 20% from renal failure

• 15% from CVA

HTN Manifestations

• Headaches

• Dizziness

• Epistaxis

• Visual Disturbances

• Fatigue

• Pulmonary Edema

• Peripheral Edema

Angina

• Myocardial Ischemia due to (-) perfusion to myocardial cells

• Caused by atherosclerosis

Stable Angina

• Pt knows circumstances when pain will occur

• Exertion = no change in plaque

• Relieved by nitro and rest

Stable Angina Pain

• Dull Pain (compressing, squeezing, crushing)

• Substernal

• Radiates to Jaw or Left Arm

• Last 15-30 mins

Unstable Angina (pre-infarction)

• Pain more severe than before

• Unstable plaque = small thrombi

• Cause of pain becomes unpredictable and less exertion is required

• Last longer and not relieved as predictably

• Not relived by nitro

Printzmetals Angina

• Can happen with or without atherosclerosis

• Occurs during night while sleeping (at rest - not exertion)

• Localized spasm of coronary artery wakens Pt

Angina Pathophysiology

• (-) lumen size due to artherosclerosis

• (+) O2 demand, HR, FOC

• O2 demand cant be met = myocardial ischemia

• Lactic acid is produced = Acidosis + Hypoxia

• (-) FOC + CO

• BP Elevated due to (+) catecholamines to compensate for (-) CO

• BP drops during pain event = (-) FOC

Angina Vitals

• (+) HR

• (+) BP

• (+) RR with dyspnea

• p/c/d

Angina Treatment

• ASA

• Nitro

• Rest

• O2 based on SpO2

Angina Pain

• Substernal Chest Pain (heaving, crushing, pressure)

• Radiate to left arm/left jaw pain

• Nausea (SNS response)

• Lasts 10-30 mins

Myocardial Infarction

Necrosis of myocardial cells due to prolonged lack of perfusion

MI Pathophysiology

1. Atherosclerosis of Coronary Arteries

2. Rupture of plaque inside of coronary arteries

3. Platelets aggreate to heal “damaged tissues”

4. Thrombus forms which occludes coronary artery

5. Cells distal to occlusion become ischemic and produce lactic acid

6. ischemia lasts >30 mins and cellular necrosis occurs = MI

Zones of MI

1. Zone of Infarction

2. Zone of Injury

3. Zone of Ischemia

Zone of Infarction

Cells have been without O2 for prolonged time and necrosed to cause irreversible damage

Layers of MI

1. Transmural MI

2. Subendocardial MI

Transmural MI

• Most common type of MI and effects the full thickness of myocardium to suffer from necrosis

• Seen when one coronary artery becomes significantly blocked

• Results in STEMI in ECG

Subendocardial MI

• Inner half of the myocardium and endocardium is involved, but less common

• Usually due to several severely narrowed coronary arteries

• No ST segment elevation seen so called non-ST myocardial infarction (NSTEMI)

Anterior MI

• Front side of L. Ventricle

• Occluded Artery: L ant. descending Coronary Artery

Inferior MI

R. Ventricle

• Occluded Artery: R. Coronary Artery

Lateral MI

• L side of L. Ventricle

• Occluded Artery: L Circumflex Branch

Posterior MI

• Back side of L. Ventricle

• Occluded Artery: L. Circumflex Branch

Septal MI

• Septum between L & R Ventricles

• Occluded Artery: L ant. descending branch

Cardiac Enzymes

• Myoglobin seen within 1hr of MI

• Creatine Kinase seen within 4hrs of MI

• Troponin I (TnI) and T (TnT) seen with 3hrs specific to heart

Diagnosis ECG Changes

• ST elevation

• Inverted T-waves

• Pathological Q Waves

Post-Infarction Recovery

• Cellular Changes

• Degree of Impairment Post MI

Cellular Changes

• 24hrs = cardiac enzymes appear + Edema in heart tissue

• 2-3 days = MI necrotic cells begin to be removed

• 10 days = Fibrous tissue being laid down

• 3rd week = scar formation begins

• 6th week = Scar formation complete

Complications Post MI

• CHF

• Cardio Shock (within 48hrs)

• Dysrhythmias

• Ventricular-Septal defect (may rupture)

• Hypotension

• Mitral Valve regurgitation

• Ventricular Aneurysm

• Pericarditis (outer layer inflammation)

Degree of Impairment Size

• Necrosed myocardium cannot contract

• Larger the MI = smaller ejection fraction

• MI involving 40% of L. Ventricle usually results in cardiogenic shock and death within 48hrs of MI

Degree of Impairment Location

Anterior MI is the worst greatly effecting CO

Degree of Impairment Old Infarcts

Cause cumulative damage each infarct

Degree of Impairment Presence of Collateral Circulation

• More a muscle is exercised needs more O2

• forms more collateral vessels to supply O2

• More exercise = smaller infarct

• Cardiac rehab post MI builds new collateral vessels to supply O2

Degree of Impairment Strength of Compensating Mechanisms

• How well cells are able to (+) FOC and compensate for cells lost

• Cells that work harder will fail losing their ability to compensate and cause CHF

MI Manifestations

• Chest pain

• 30-40 min gradual crescendo-type substernal, left arm, left jaw pain

• Tachycardia (compensating) slow weak pulse (failing)

• Tachypnea + SOB

• P/C/D

• Hypertensive then Hypotensive

MI Treatment

• Rest and reassure

• ASA

• Nitro

• O2 based on SpO2

• Consider STEMI bypass and prepare of Cardiac Arrest

Doctor prescribed medications post-MI regardless of BP

• Betablockers to (-) HR (-) SA node firing

• Anit-Cholesterol Drugs to (-) TPR

• ACE Inhibitors to (-) Vasoconstriction

• Anti-coagulant (if stent inserted)

ASA (Aspirin)

• Platelet Aggregate Inhibitor

• Analgesic + anti-pyretic + Anti-inflammatory NSAID

• Anti-prostaglandin

ASA Actions

• Prevents current thrombus from growing larger and more from forming

• Given in 1st few hrs of MI to reduce mortality up to 30%

ASA Onset

• 30 mins

• Lasts 24hrs

ASA Side Effects

• Nausea + Vomiting

• Indigestion

• GI bleeding

Types of NSAIDS

• Arthrotec

• Celebrex

• Ibuprofen

• Indocin

• Meloxicam

• Naproxen

Nitroglycerin Class

Nitrate

Nitro Actions

• Vascular smooth muscle relaxant of peripheral blood vessels

• (+) Venous capacitance

• (-) Venous return

• (-) Preload + (-) TPR = (-) After load, (-) workload, (-) O2 demand of myocardium

• Dialates Coronary Artery to (+) Myocardium Perfusion

Nitro Onset

• 1-4 mins

• Duration = 30mins

Nitro Side effects

• Hypotension

• Headache

• Dizziness

• Tachycardia

Nitro Considerations

• If Vitals fall outside of parameters but return don’t give nitro

If chest pain goes away then returns (Nitro)

Treat as new episode and give nitro NO ASA

Phosphodiesterase

• Viagra/Revatio for pulmonary HTN

• Tadalfil (Cialis)

• Udenafil (Zydena)

• Avanafil (Stendra)

• Vardenafil (Levitra)

Before every subsequent nitro administration what should one do?

Ask if they still have chest pain and vitals within parameters. If there’s still chest pain give nitro. No chest pain = No Nitro

Angioplasty

• A wire is inserted into the coronary artery and a mesh stent is inserted to maintain patency

• Post-PCI pts are put on anti-coagulants for 3 months

• Can be given ASA + Anti meds

Valvular Sternosis

• Tissue forming valve leaflets become stiff causing the opening to narrow so less blood can flow through

Valvular Sternosis Pathophysiology

• Narrowing of opening = incomplete opening

• Not all blood can flow through

• (+) pressure in chamber before valve

Valvular Regurgitation

• Failure of the leaflets to dose completely, so blood flows backwards (regurgitant flow) when ventricle contracts into chamber before valve

Valvuular Disorders Causes

• Congential

• Post-MI complication

• Atherosclerosis of valve

• Rheumatic Fever

Rheumatic Fever

Caused by streptococcus bacteria that causes endocardits and scars valve

Valvular Disorders Manifestations

• Heart murmur

• Pulmonary Edema

• Hypertrophy of atria or ventricle

Cardiomyopathy

• Disease of the heart muscle that’s not related to CAD, HTN or other abnormalities

• 3 types

• Dialated

• Hypertrophic

• Restrictive

Dialated Cardiomyopathy

• Usually from viral infection and characterized by grossily dialated/stretched ventricle

• Poor contraction of chambers

• High incidence of thrombi formation in chambers

• Prognosis is poor without transplant (develops CHF)

Hypertrophic Cardiomyopathy

• Possibly a genetic predisposition

• Characterized by thickening of myocardium esp in interventricular septum

• Results in stiffening reduced compliance and filling of ventricle

• Prognosis is not as poor but MI may occur is O2 demand is not met

• May be able to surgically remove some of the myocardium

• Disease of young adulthood (sudden death in teens)

Restrictive Cardiomyopathy

• Least common type

• Found in africa india and asia

• Caused by endocardial infiltrations

• Excessive rigidity of ventricular walls restricts ventricular filling

Congestive Heart Failure (CHF)

• Heart failure with congestion of body tissues

• caused by low cardiac output (impaired ejection or filling)

• 4 stages

Causes of CHF

• MI

• Valve disorders

• Cardiomyopathy

• Arrythmias

Pathophysiology of CHF

REFER TO NOTES AND DO FLOWCHART

CHF Manifestations

• Exertional Dyspnea

• Orthopnea

• Paroxysmal Nocturnal Dyspnea

• Chronic Dry Cough

• Hemoptysis

• (+) Skin Turgor

• Severe Edema

• Cyanosis

CHF Treatment

• Reduce preload + afterload

• Nitroglycerin

• Rx = diuretics

Acute Cardiogenic Pulmonary Edema (ACPE)

Acute episode of excess fluid in interstitial space + alveoli of lungs due to a problem in the heart

ACPE Manifestations

• Dyspnea

• Bilateral fine crackles (can rise up to nipple scapula line)

• Fulminating Pulmonary Edema

• Tachypnea/Orthopneic positioning

• Bilateral wheezing

• Hemoptysis

• Pale, cyanotic (-) SpO2

• Normal PCO2 + pH

• (-) PO2 (-) O2 in blood + Cardiac Cells

Non-Cardiogenic Pulmonary Edema

• Near downing

• Aspiration pneumonitis

• Renal Failure

• Smoke inhalation

Continuous Positive Airway Pressure (CPAP)

• Easily initiated, discontinued or interrupted compared to traditional mechanical ventilation

• Good CPAP = (+) Surface area

• Bad CPAP = (-) SA

• Used to splint soft palate open to prevent collapse during obstructive sleep apnea

CPAP Benefits

• Non Invasive

• Low mortality

• Less potential for infection

• Less skill required

• No sedation required

• Less traumatic

• (-) hospital stay compared to intubation

5 Medical Benefits of CPAP

1. Distends Alveoli to splint them open and push fluid out, narrow distance between capillary + Alveoli = better diffusion

2. (+) Alveoli surface area = (+) potential for gas exchange

3. (-) workload of heart by (+) oxygenation of blood

4. Alerters pressure gradient which is reflected in PaO2

5. (-) any V/Q imbalances by improving O2 levels in alveoli

CPAP affects on Pressure Gradient

• Changes from 160mmHg to 110mmHg

• (+) pressures so there’s a greated gradient difference between alveoli + capillary = more gas diffusion