CCRN cardiology

What valves OPEN during DIASTOLE and CLOSE during SYSTOLE

AV valves ( mitral and tricuspid)

What valves OPEN during SYSTOLE and CLOSE during DIASTOLE

Semilunar valves (Aortic and Pulmonic)

Posterior wall perfused by

90% RCA and 10% CRFX

Inferior wall perfused by

RCA

Right atrium/ventricle

SA/AV node

back of septum

Septal and Anterior wall perfused by

LAD

front and bottom of left ventricle

front of septum

Lateral Wall wall perfused by

Circumflex

Left atrium

Back of left ventricle

What is Coronary Sinus

Both the right & left coronary arteries arise at the base of the aorta (Sinus of Valsalva)

Immediately above the Aortic Valve

What should be avoided w/ pt who have Coronary sinus

Tachycardia

- this will decrease overall CO and stroke volume

Since coronary arteries are perfused during Diastole- shorten diastolic filling time

What is Preload

The initial stretching of the myocardium

prior to contraction; therefore, it is related to the

sarcomere length at the end of diastole.

Fluid and volume filled before contraction

How does high/low preload equate to volume status

High preload = Fluid overload

Low preload = Fluid deficit

How do we measure preload on each side of the heart

Right side of the heart as "CVP"

Left side of the heart as "PAOP"

What is afterload?

resistance the ventricles must overcome to circulate blood

What does high/low after load equate to

High afterload = Vasoconstriction

Low afterload = Vasodilation

How do we measure after load on each side of the heart

Right side of the heart as "Pulmonary Vascular

Resistance" (PVR)

Left side of the heart as "Systemic Vascular

Resistance" (SVR)

Auscultation for aortic valve

Right, 2nd ICS

auscultation for pulmonic valve

Left, 2nd ICS

Auscultation for Tricuspid valve

4 - 5th ICS, LSB

Auscultation for Mitral valve

5th ICS, MCL

S1 sound indicates what valves closing

Atrioventricular valves close

(tricuspid & mitral) at the onset of

systole

S2 sound indicates what valves closing

Semilunar valves close

(pulmonic & aortic) at the onset of

diastole

Normal Heart sounds

S1- Lub - loudest over mitral - systole

S2 Dub - Loudest over Aortic - diastole

Systole is 1/3 of cardiac cycle

Diastole is 2/3 of cardia cycle

S3 - Ventricular Gallop

FLUID OVERLOAD

Auscultated when preload is ↑ HIGH

Normal in kids, high cardiac output, 3rd trimester of pregnancy

S4- Atrial Gallop (pre-systolic)

Sound caused by vibration of atria ejecting into non-

compliant ventricles

Auscultated during ischemia (increased resistance to

ventricular filling)

Other causes: Ischemia, HTN, pulmonary stenosis, CAD,

Aortic stenosis, left ventricular hypertrophy

Split Heart sounds

When 1 valve closes later than the other

**best heard during inspiration

Split S1

Mitral closes before tricuspid valve

Right BBB, V-Paced rhythms, PVCs

Split S2

Aortic closes before pulmonic valve Overfilled right ventricle

Atrial septal defect (ASD)

Av valves

Right - Tricuspid

Left - Mitral

Semilunar Valves

Right - Pulmonic

Left - Aortic

Chordae Tendinae & Papillary Muscle

"Heart strings"

Attached to AV valves(Tricuspid & Mitral)

Papillary muscles contract to prevent the leaflets from

prolapsing into the atria

Patients can infarct the

papillary muscle - common in Rv infarct

Stenosis murmurs

Forward flow of blood through NARROW

stenotic OPEN VALVES ONLY

usually chronic

Insufficiency/regurgitation murmurs

Backward flow through incompetently CLOSED VALVES ONLY

usually acute! - needs surgical repair and or mechanical support

Systolic Murmurs

Between S1 and S2 (during systole)

Mitral & tricuspid valves are closed Insufficiency

Aortic & pulmonic valves are open stenosis

S1- murmur - S2

Diastolic murmurs

After S2 (during diastole)

Mitral & tricuspid valves are open stenosis

Aortic & pulmonic valves are closed Insufficiency

S1- S2- murmur

Mitral insufficiency (regurgitation)

Murmur auscultated with the valve is closed!

Mitral valve closed during: SYSTOLE!!!

What are the causes of Mitral regurgitation

MI

Ruptured chordae tendineae

Severe left heart failure ◼ Dilated CM

Hypertrophic cardiomyopathy

Left ventricular hypertrophy

MV prolapse

Myxomatous degeneration

Rheumatic fever

Endocarditis

Symptoms of mitral regurgitation

Symptoms:

SYSTOLIC murmur ( holosystolic)

Orthopnea/dyspnea

Fatigue

Angina

Increased left atrial pressure

Right heart failure

Prone to atrial fibrillation d/t

left atrial enlargement

Left heart failure

Mitral Stenosis

Occurs when the mitral

valve is OPEN

DIASTOLIC murmur

Coarse rough sound - acquired over multiple years

Causes for Mitral stenosis

Pulmonary edema

Prone to atrial fibrillation d/t left atrial enlargement

May have right sided heart & pulmonary congestion issues:

Pulmonary HTN

Increased atrial & PA

pressures

Over time the opening narrows d/t excess tissue/plaque/calcification buildup

Treatment for Mitral Stenosis

Medical management - Usually treating the cause such as Afib, pulm edema etc

Surgical replacement

Balloon Valvuloplasty

(commissurotomy)

Mitral Valve replacement types

Biologic vs Mechanical

Biologic

- Last 8-10 yrs

- no anticoagulant required

No click

Mechanical

- last >20 + yrs

- Lifelong anticoagulant

Loud click audible

Post op consideration after mitral valve replacement

May need + inotrope: Dobutamine or Milrinone

Monitor for atrial fibrillation

Monitor for heart blocks

- damage Bundle of His

Be prepared to pace!

Mitral valve is very close to electrical conductivity- is irritation occurred during procedure- high chance to develop various arrhythmias

Post op Mitral stenosis Valve replacement

Monitor for RV failure -increasing RAP, ↑ PVR

Will need adequate filling pressures to maintain CO

Watch CVP closely!

Increasing CVP may be a sign of right heart failure

Diuretics, may need +inotrope

Post op Mitral Regurgitation Valve replacement

May have increase LV resistance (↑ SVR)

Can lead to ↓ C.O.

Use vasodilators

Monitor for right heart

failure - seen w/ increase in CVP

May need + inotrope

Monitor for heart block

Aortic Regurgitation

Occurs when the valve doesn't close completely

Results in a backflow of blood & reduced diastolic

pressure

- Left ventricular Hypertrophy !!!! RISK

Causes of Aortic Insufficiencies

Causes:

HTN

Rheumatic fever

Endocarditis

Syphilis

Idiopathic

Signs of Aortic Insufficiency

Signs:

DeMusset Sign - head bobbing

Brisk carotid upstroke

Wide pulse pressure - >40 mm Hg

"Water-hammer" pulse - rapid upstroke & down

stroke with a shortened peak

Associated with:

• Marfan's syndrome

• Ventricular septal

defect (VSD)

Aortic Stenosis

Back flow of blood while aortic valve is open, increase LV pressure

Systolic ejection is impeded

Pressure gradient between

LV & aorta

50% 2-year mortality if HF

develops

Left ventricular Hypertrophy !!!! RISK

Symptoms of Aortic Stenosis

Left ventricular hypertrophy

High SVR

Heart failure

How to diagnose Aortic Stenosis

***Echocardiogram

Cardiac catheterization

(↑LVEDP, ↑atrial

pressure, ↑paop, ↓CO)

12 lead ECG: left atrial & ventricular

hypertrophy

Chest x-ray: left atrial

& ventricular

enlargement, pulmonary

venous congestion

management for Aortic Stenosis

ACE inhibitor or ARB

Diuretics

Beta Blocker

Afterload reduction

Valve repair/replacement urgent in the setting of heart

failure

Post op aortic valve replacement for aortic stenosis

Manage BP & avoid

hypertension

Hyperdynamic left ventricle

d/t drop in SVR

Avoid (or careful with) +

inotropes

Ensure adequate preload

Monitor for heart block

Post op aortic valve replacement for aortic regurgitation

May be hypertensive

May need + inotrope

Dobutamine or Milrinone to

improve forward flow & LV

emptying/IABP

Monitor SVR:

↑SVR - vasodilators

↓SVR - vasopressor

Monitor heart block

Monitor for a-fib, likely won't

tolerate it

TAVR - Transcatheter Aortic Valve Replacement

High risk patients, replace aortic valve while heart is

still beating

Post-procedure:

Monitor insertion site for bleeding, hematoma

Femoral access (most common)

Trans-carotid access

Trans-axillary access

Signs of stroke

Bradycardia/Heart Block

STEMI

*Infarction with complete

obstruction of blood flow

• Q wave MI

• Non-Q wave MI

NSTEMI

*Ischemia with partial obstruction of

blood flow

• Unstable Angina

• Non-ST Elevation MI

- Non-Q wave MI or

- Q wave MI

Acute Coronary Syndrome

Pathophysiology: Progressive atherosclerosis often with plaque

rupture leading to an imbalance of O2 supply & demand

What supplies O2

Supply:

Coronary arteries

Diastolic filling time

Cardiac output

Hemoglobin

SaO2

What demand O2

Demand:

Heart rate

Contractility

Preload

Afterload

Non modifiable Cardiac Risk Factor

Non-modifiable:

Age

Gender

Family history

Race

Modifiable Cardiac Risk Factor

Modifiable:

Smoking

Cholesterol/Lipids

Overweight/Obesity

Diabetes mellitus

Diet

Physical inactivity

HTN

Chest pain/symptom assessment

Onset

Location

Duration

Characteristics

Associated s/s

Relieving factors

Treatment

Stable Angina

Exertional

Stop activity, symptoms stop

Fixed vessel stenosis, demand ischemia

Unstable Angina

Sign/precursor to a myocardial infarction

Blood flow is restored

Increasing frequency, time, duration

10 - 20% have a Myocardial Infarction

Variant (Prinzmetal's) Angina

Sudden pain caused from coronary vasospasm

Younger population

> 60% have some mild underlying atherosclerosis

Occurs at rest or when sleeping

Treatment for variant angina

Treat with NTG, Calcium Channel Blockers

Get 12 Lead ECG with

& without pain!

ECG changes noted with pain/symptoms!

Nstemi

Partial occlusion of coronary artery

Pain occurs at rest

Hallmark sign** pain with ↑ frequency, heaviness or

pressure

NSTEMI ekg labs

Chest pain/symptoms > 20 min.

12 lead ECG: ST dep./T wave inversion

Often 8 or more leads

Elevation in aVR

Cardiac biomarkers elevated ( trops!)

Treatment for nstemi

Treatment: Early PCI if high risk

Early PCI if not high risk is also acceptable

"Ischemia-guided strategy"

Cause for MI

• Plaque rupture with clot formation

• Vessel dissection

• Fixed atherosclerotic lesion

• Coronary Artery Vasospasm

• Cocaine

• INFLAMMATION!

• Platelets aggregate to the atherosclerotic site

• Occlusive thrombus formation

• ~70% occlusion of arterial lumen before s/s

STEMI hallmark signs

ST elevation

≥ 1 mm (Limb Leads) or

≥ 2 mm (Precordial Leads) and/or

New Left BBB

Hallmark signs*** Symptoms > 20 min. TSOB, diaphoresis

+ Cardiac biomarkers

Complete occlusion

Treatment for STEMI

Reperfusion - PCI or fibrinolytics door to balloon 90 mins

Emergent STEMI Treatment

Aspirin

81 mg - 325 mg PO load

Nitroglycerin

0.4 mg SL Q 5min x 3

Monitor for hypotension

Caution with inferior wall MI (Avoid in right ventricular

infarction) ( check v1/ V4R)

May use IV if continued chest discomfort

Morphine

1 - 2 mg IV Q 5 -15 min

if CP unrelieved by NTG

Consider load with

P2Y12 inhibitor

Clopidogrel, Ticagrelor

Anti-platelet therapy

ASA

Used indefinitely post MI

Inhibits cyclooxygenase-1 within platelets →

prevents formation of thromboxane A2

Disables platelet aggregation

Monitor for intolerance

Dose at least 81 mg daily

Onset of action 1 - 7.5 min

Nitroglycerin

Potent vasodilator

Reduces preload & ventricular wall tension

Decreases myocardial O2 consumption

Sublingual, spray or intravenous (Tridil)

Monitor for hypotension

Headache common

Do NOT give to patients with

right ventricular infarction or use of other

phosphodiesterase (PDE) inhibitors

Oxygen

Not needed for patients without evidence of

respiratory distress (AHA guideline)

Use if oxyhemoglobin saturation is ≤ 94%

Hyperoxemia perpetuates oxidative injury after MI

Morphine

Use as adjunct therapy to Nitroglycerin

Small incremental doses!

Potent analgesic & anxiolytic

Causes venodilation & reduces preload, mild

afterload reduction

Decreases workload of heart

Use cautiously in inferior wall MI

Avoid in right ventricular MI

Increased mortality in a large registry

More research needed

Radial Approach for PCI

Advantages

Less bleeding - easily

compressible artery

More comfortable for patients

Short bedrest time and LOS

Fewer access site complications

Disadvantages

Technically more difficult -

steep learning curve

Smaller artery - can't

accommodate larger catheters

or devices

Prone to spasm

Femoral artery approach for PCI

Advantages

Large artery can accommodate

larger catheters and devices

Easier to perform

Disadvantages

More bleeding - harder to get

hemostasis

Uncomfortable for patients

Longer bedrest times

More access site complications

(pseudoaneurysms, AV fistula,

retroperitoneal bleed)

Retroperitoneal Bleed & Hematoma (RBH) S/S

usually caused from Femoral approach either from puncture bleed or hematoma development at the site

Signs:

Tachycardia

May not see this d/t beta blockers

Hypotension

Back pain, groin pain, flank ecchymosis (late sign)

Retroperitoneal Bleed & Hematoma (RBH) Treatment

Medically manage or surgical repair (< 10%)

Percutaneous intervention with balloon tamponade

Fluids, prepare to transfuse

Fibrinolytic Therapy

TNKase (tenecteplase)*

5 second bolus; no infusion or 2nd bolus

Weight based dose, no more than 50 mg

rtPA (Activase)

Bolus followed by infusion

Will still need to go to the cath lab

Indications:

Pain < 6 hours

ST elevation > 1 mm in 2 or more leads

Fibrinolytic contraindication absolute NO

Active internal bleeding

History of CVA or hemorrhagic

stroke

Arterial-Venous Malformation

(AVM)

Malignant intracranial

neoplasm

Suspected aortic dissection

Aneurysm

Trauma within 2 months

Severe uncontrolled

hypertension

Fibrinolytic contraindication relative ( case by case)

Chronic, severe, poorly tolerated

HTN

SBP >180 mm Hg or DBP > 110

mm Hg

Ischemic CVA > 3 mos.

Dementia

Traumatic or prolonged CPR

(> 10 min.)

Major surgery (< 3 weeks)

Internal bleeding (within 2-4

weeks)

Pregnancy

Active peptic ulcer disease

Current use of anticoagulants

Nursing considerations with fibrinolytics:

**Bleeding is the most common side effect

If bleeding occurs, discontinue all anticoagulants

Monitor PT/INR/aPTT - prolongs both

Monitor fibrinogen - decreased fibrinogen for up to 24˚

Reversal - Cryoprecipitate & platelets

Frequent neurological assessment

Avoid punctures

Monitor urine output & BUN/creatinine

Avoid invasive devices

Avoid compressive devices

Post PCI: Anti-Platelet Therapy

Thienopyridines (P2 Y12 Inhibitors) - DES or BMS:

Plavix (Clopidogrel) 300 - 600 mg load; continue 75 mg daily

for 12 months or

Effient (Prasugrel) 60 mg load; continue 10 mg for 12 months or

Ticagreolor (Brilinta) 180 mg load; 90 mg BID

Optional per Cardiologist (high risk thrombosis):

Unfractionated Heparin (UFH) or

Bivalirudin (Angiomax) - during PCI; finish in cath lab

GP IIb/IIIa Inhibitors (at time of PCI)

Abciximab (Reopro)

Eptifibatide (Integrilin)

Tirofiban (Aggrastat) **Monitor platelet count!

The "Big 5" Discharge Medications Following ACS

ASA (indefinitely)

P2Y12 Receptor Blocker (at least 12 months)

Beta Blocker (indefinitely)

ACE-I (or ARB) (indefinitely)

Statin (high intensity indefinitely)

Continuing dual antiplatelet therapy for one year is critical - important for patient education

Post-MI therapy

Dual anti-platelet therapy (ASA + P2Y12 Inhibitor)

Beta blockers (lifetime)

Statins (lifetime)

ACE inhibitors-prevent cardiac remodeling

EF < 40%, new HF or anterior wall MI

Nitrates - pain control

Balancing myocardial O2 supply and demand

Complication management

Groin or radial site management

Renal function (secondary to dye load)

Beta Blockers: "-olols"

▪ Metoprolol tartrate or carvedilol

▪ Cardio-protective!

▪ Blocks catecholamine, blunts the sympathetic nervous

system!

▪ Decreases HR & contractility

▪ Decreases myocardial O2 consumption

▪ Long term, decreases morbidity & mortality

▪ Administered within 24 hours, continued indefinitely

▪ Warn patients they may feel exhausted for a few

months after starting!

Myocardial Effects of Beta Blockers

↓ Heart rate

↓ Contractility

↓ AV node conduction

↓ Automaticity

↓O2 Consumption

Metoprolol tartrate

Used post MI + HTN+ Angina

Arrythmia protection

Immediate-release tablet,

liquid form or IV

PO dosing: 100 - 400 mg

daily

IV dosing: full dose 15

mg

Metoprolol succinate

Heart failure + HTN + Angina

Extended-release tablet

taken daily

PO dosing 25 - 100 mg

daily

If tolerated, max 200

mg PO

Effects of Beta Blockers

Lungs

Prevent bronchodilation; may induce bronchospasm

Caution in asthmatics & COPD!

Blood vessels

Prevent vasodilation in arterioles & veins

Blocks the "Fight or Flight" response

Blocks receptor sites for endogenous catecholamine

Epinephrine & norepinephrine

Kidneys

Renin production

Statin use

cholesterol levels by interfering with body's ability to

produce cholesterol

inflammatory response that theoretically may be

responsible for atherosclerotic process

Inhibit enzyme needed to produce cholesterol

Recommended for all patients with MI

LDL cholesterol > 100

Cardio-protective

High dose if tolerated

Decrease risk of MI & stroke

Decreased recurrence by ~ 40%!!!!

Decreases risk of cardiac death by 25 - 35%

Statin Side Effects:

Muscle weakness - thought to be a "nocebo" effect

≤ 5% risk vs. placebo

~ 30% stopped because of muscle aches even when they were

taking a placebo

Myositis - inflammation of the muscles

◼ Statin + fibrate = increased risk!

◼ < 1 in 10K taking statins

Increased LFTs (rarely becomes a problem)

Rhabdomyolysis - extremely rare

Increased glucose or Type 2 Diabetes

Memory loss or confusion

Mental "fuzziness"

Digestive issues

MI education

Medication compliance

Don't drink!

Don't smoke!

Exercise

Manage weight

Heart healthy diet

Lower cholesterol / lipids

Reduce stress

ECG: What do the waves represent?

P wave:

Atrial depolarization

PR interval:

AV conduction time (0.12 - 0.20)

QRS:

Ventricular depolarization (0.06 - 0.10)

T wave:

Ventricular repolarization

QT Interval

Ventricular repolarization time

Q waves - Old MI/Injury

If present in contiguous

leads, indicative of

myocardial necrosis

Considered pathologic if:

Width > 30 ms

Depth ≥ 25% of the

height of the R wave

Inferior Wall MI

Changes noted in Leads II, III & aVF

If suspected RCA occlusion, monitoring

Lead III preferred

Reciprocal changes in Leads I & aVL

Monitor for RV failure

Tachycardia

Hypotension

+ JVD

With inferior MIs, always look for

posterior or RV infarction!

•RV infarction - ST↑ V1

•Posterior MI - ST ↓ V1 - V3

Inferior wall MI symptoms

Bradycardia

Hypotension

Nausea/vomiting

Diaphoresis

High grade AV blocks

Sinus Bradycardia

First degree AV Block

Second degree Type I

May need temporary

pacer

• Occurs high in

the AV node

• Lengthening PR

interval

• Rarely progresses

to CHB

Right Ventricular Infarction s/s

Associated with Proximal RCA occlusion & inferior wall MI

Symptoms:

Tachycardia

Hypotension

+ JVD (with clear lungs)