Cardiovascular Test Plan (18%)

 Acute coronary syndromes/unstable

angina

 Acute myocardial infarction &

ischemia/papillary muscle rupture

 Acute peripheral vascular insufficiency

(e.g., carotid artery stenosis,

endarterectomy,

Fem-pop bypass, peripheral stents)

 Acute pulmonary edema

 Arterial venous occlusion

 Cardiac Catheterization (diagnostic &

interventional)

 Cardiogenic shock

 Cardiomyopathies (e.g., dilated,

hypertrophic, idiopathic, restrictive)

 Dysrhythmias

 Heart failure

 Hypertensive crisis

 Myocardial conduction system

defects

 Structural heart defects (acquired &

congenital, including valvular

disease)

 Ruptured or dissecting aneurysm

(e.g., thoracic, abdominal, thoracoabdominal)

Both the right & left coronary

arteries arise at the base of

the aorta (Sinus of Valsalva)

 Immediately above the aortic

valve

 Coronary arteries are

perfused during…? Filling (Diastole)

Heart Sound Locations

Aortic Valve

Pulmonic Valve

Tricuspid Valve

Mitral Valve

 Aortic valve: Right, 2nd ICS

 Pulmonic valve: Left, 2nd ICS

 Tricuspid valve: 4-5th ICS, LSB

 Mitral valve: 5th ICS, MCL

 S1 “LUB”

-closure of the mitral & tricuspid valves

-Loudest over mitral area

 S2 “DUB”

-closure of pulmonic & aortic valve

-Loudest over aortic area

-2nd ICS

S1 systole is 1/3

of the cardiac cycle 

S2

diastole is 2/3

of the cardiac cycle

S1-S2-S3, S1-S2-S3 (Ken-tuck-y) or “I Be-lieve”

 Fluid overload

 Auscultated when preload is ↑

 Normal in kids,

high cardiac output,

3rd trimester of pregnancy

S4-S1 -S2, S4-S1 -S2 (Ten-ne-ssee) or “Believe me”

 Sound caused by vibration of atria ejecting into noncompliant

ventricles

 Auscultated during ischemia (increased resistance to

ventricular filling)

 Other causes: Ischemia, HTN, pulm stenosis, CAD, Aortic

stenosis, LVH

When 1 valve closes later than the other

**best heard during inspiration

 Split S1-Mitral closes before tricuspid valve

RBBB or PVC

 Split S2-Aortic closes before pulmonic valve

Overfilled right ventricle

Atrial septal defect (ASD)

Acute Coronary Syndrome (ACS)

ST Elevation MI ( STEMI ) VS Non-Stemi (NSTEMI)

ST Elevation MI (STEMI):

• Q wave MI

• Non-Q wave MI

Non-ST Elevation (NSTEMI):

• Unstable Angina

• Non-ST Elevation MI

- Non-Q wave MI or

- Q wave MI

Pathophysiology: Progressive atherosclerosis with plaque rupture leading to an imbalance of

O2 supply & demand

Oxygen Supply vs Demand

Definitions

Supply:

 Coronary arteries

 Diastolic filling time

 Cardiac output

 Hemoglobin

 SaO2

Demand:

 Heart rate

 Contractility

 Preload

 Afterload

Cardiac Risk Factors

Modifiable Vs Non Modifiable

Non-modifiable:

 Age

 Gender

 Family history

 Race

Modifiable:

 Smoking

 Cholesterol/Lipids

 Overweight/Obesity

 Diabetes mellitus

 Diet

 Physical inactivity

 HTN

Chest pain assessment

 Onset

 Location

 Duration

 Characteristics

 Associated s/s

 Relieving factors

 Treatment

 Stable

 Exertional

 Unstable

 Increasing frequency, time, duration

 10-20% have a MI

 Variant (Prinzmetal’s)

 Sudden pain caused from coronary

vasospasm

 Occurs at rest or when sleeping

 Treat with NTG, Ca Ch blockers

 Get 12 Lead ECG with & without pain!

NSTEMI

Partial occlusion of coronary artery

 Pain occurs at rest

 Hallmark sign** pain with ↑ frequency, heaviness or

pressure

 Chest pain > 20 min.

 12 lead ECG: ST depression/T wave inversion

 Cardiac biomarkers elevated

 Treatment: Early PCI if high risk

 Early PCI if not high risk is also acceptable\

Cardiab Biomarkers

Enzyme / Origination/ Normal Limit Level/ Rises/ Peaks

Return to Normal Limit

CK-Total

CK-MB

Myoglobin

Troponin I

Troponin T

LDH

LDH1

CK Total

Origination

Heart & skeletal muscle, Brain tissue  

NL(Normal Limit) Level

Men : 55-170 u/L

Women: 30-135 u/L

Rises 4-6 hrs.

Peaks 24 hrs.

Return to NL 3-4 days

CK-MB

Origination

Heart & skeletal muscle, Brain tissue  

NL(Normal Limit) Level

0 or >3% total

Rises 4-8 hrs.

Peaks 12-24 hrs.

Return to NL 2-3 days

Myoglobin

Origination

Heart & skeletal muscle, Brain tissue  

NL(Normal Limit) Level

<85 mcg/L

Rises

1-4 hrs.

Peaks

6-7 hrs

Return to NL

1-2 days

Troponin I

Origination

Myocardium

NL(Normal Limit) Level

<1.5 mcg/L

Rises

3-6 hrs

Peaks

12-20 hrs

Return to NL

1-2 weeks

Troponin T

Origination

Myocardium & Skeletal Muscle

NL(Normal Limit) Level

<0.1mcg/ml

Rises

3-4 hrs

Peaks

12-24 hrs.

Return to NL

2-3 weeks

LDH

NL(Normal Limit) Level

90-200 u/L

Rises

24-48 hrs.

Peaks

72 hrs

Return to NL

8-14 days

LDH1

NL(Normal Limit) Level

17-25% of total LDH

Rises

8-24 hrs

Peaks

72 hrs

Return to NL

8-14 days

• Platelets aggregate to the

atherosclerotic site

• Occlusive thrombus formation

• ~70% occlusion of arterial lumen

before s/s

ST Segments in MI

Elevation vs depresison

ST elevation: Injury

 ≥1mm (inferior) or

 ≥2 mm (anterior) and/or

 New Left BBB

ST depression: Ischemia

 NSTEMI – 8 or more leads

with ST depression

 Elevation in AVR

ST elevation

 ≥1mm (Inferior) or

 ≥2 mm (Anterior) and/or

 New Left BBB

 Hallmark signs*** Chest pain > 20min.

SOB, diaphoresis

 + Cardiac biomarkers

 Complete occlusion

 Treatment:

Reperfusion - PCI or fibrinolytics

Emergent STEMI Treatment

Aspirin

 162 mg – 325 mg PO

load

 Nitroglycerin

 0.4 mg SL Q 5min x 3

 Monitor for hypotension

 Avoid in right ventricular

infarction

 May use IV if continued

chest discomfort

 Supplemental O2 if sats

< 94%

 Hyperoxemia lends to

oxidative stress

 Morphine

 2 – 8 mg IV Q 5 -15 min

if CP unrelieved by NTG

 Beta Blockers

 within 24°

 Hold if hypotension or

signs of

hypoperfusion/shock

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 81mg daily

 Onset of action 1 – 7.5 min

 Potent vasodilator

 Reduces preload & ventricular wall tension

 Decreases myocardial O2 consumption

 Sublingual, spray or intravenous

 Monitor for hypotension

 Do NOT give to patients with

right ventricular infarction

 Not needed for patients without evidence of

respiratory distress (2013 AHA guideline)

 Use if oxyhemoglobin saturation is ≤ 94%

 Hyperoxemia perpetuates oxidative injury after MI

 Use as adjunct therapy to NTG

 Potent analgesic & anxiolytic

 Causes venodilation & reduces preload

 Decreases workload of heart

 Use cautiously in UA & NSTEMI!!

 Increased mortality in a large registry

 More research needed

 Avoid in right ventricular MI

Beta Blockers: “-olols”

 Metoprolol & carvedilol

 Blocks catecholamines

 Decreases HR & contractility

 Decreases myocardial O2 consumption

 Long term, decreases morbidity & mortality

 Administered within 24 hours, continued indefinitely

 Gold standard for ST elevation MI: Revascularization

 Cardiac Cath Lab

 Fibrinolytics

Fibrinolytic Therapy

 TNKase (tenecteplase)* - new fast rapid bolus

 tPA (Activase)

 Bolus followed by infusion

 Will still need to go to the cath lab

Indications:

Pain < 6 hours

ST elevation > 1mm in 2 or more leads

Contraindications:

Active bleeding, hx. hemorrhagic stroke, AVM,

BP>200/120, prolonged CPR

Fibrinolytic Contraindications:

Absolute:

 Intracranial hemorrhage (0.9%)

 Known cerebral vascular lesion

 Ischemic stroke in last 6 mos.

(except acute CVA within 3

hours)

 Malignant intracranial

neoplasm

 Suspected aortic dissection

 Active bleeding

 Closed head or facial trauma

within 3 mos.

Relative:

 Chronic, severe, poorly tolerated

HTN

 SBP >180 mm Hg or DBP > 110

mm Hg

 Ischemic CVA > 3mos.

 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

 Frequent neurological assessment

 Avoid punctures

 Monitor urine output & BUN/creatinine

 Avoid invasive devices

 Avoid compressive devices

 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

 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)

Post-MI therapy

 Dual anti-platelet therapy

 Beta blockers

 Statins

 Nitrates - pain control

 Balancing myocardial O2 supply and demand

 ACE inhibitors-prevent cardiac remodeling

 EF < 40%, new HF

 Complication management

 Groin site management

 Renal function (secondary to dye load)

Long Term & Secondary Prevention

MI

 Beta-blocker – “olol”

 Metoprolol (Lopressor,

Toprol XL)

 Carvedilol

 ACE-Inhibitor – “pril”

 Ramapril (Altace)

 Lisinopril (Zestril, Prinivil)

 Enalapril (Vasotec)

 Captopril (Capoten)

 Statins – Lipid lowering

 Atorvastatin (Lipitor)

 Rosuvastatin (Crestor)

 Simvastatin (Zocor)

 Dual Anti-platelet

 Aspirin – 81 mg

 Clopidogrel (Plavix) or

 Prasugrel (Effient)

 Ticagrelor (Brillinta)

Statins (HMG CoA Reductase Inhibitors)

 Why?

  cholesterol levels by interfering with body’s ability to

produce cholesterol

  inflammatory response that theoretically may be

responsible for atherosclerotic process

 Who?

 Recommended for all patients with

LDL cholesterol > 100

 Atovastatin (Lipitor), Rosuvastatin (Crestor),

Lovastatin (Mevacor), Simvastatin (Lipitor)

 Give at night

 Myopathies & Myocitis

 Don’t drink!

 Don’t smoke!

 Exercise

 Lose weight

 Eat right!

 Lower cholesterol

 Reduce stress

 Take meds

 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

Q-waves

Considered pathologic if:

 Width > 30 ms

 Width ≥ 25% of the height of the R wave

 If present in contiguous leads, indicative of

myocardial necrosis

Q waves – Old MI/Injury

 May or may not be present

Inferior II, III, aVF I, aVL RCA in 65%

L circumflex

Right sided ECG assess

V2R-V4R

Septal V1-V2 II, III, aVF LAD

Anterior V2-V4 II, III, aVF LAD/L main

Lateral I, aVL, V5-V6 L circumflex

LAD

Posterior Posterior leads V7-9 V1-2 L circumflex

RCA

Tall upright R wave

Right ventricle V2R-V4R Proximal RCA

Bradycardia

AV heart block - may need temp. pacer

Hypotension

N/V

Diaphoresis

Changes noted in

Leads II, III & AVF

¨ If suspected RCA

occlusion- Lead III

preferred

¨ Reciprocal changes in

Leads I & AVL

¨ Monitor for RV failure

¤ Tachycardia

¤ Hypotension

Associated with Proximal RCA occlusion & inferior wall MI

Symptoms:

¨ Tachycardia

¨ Hypotension

¨ + JVD (with clear lungs)

Treatment:

¨ **IV fluids**

¨ + Inotrope (increase contractility)

Avoid medications that lower preload:

¨ Nitrates, Morphine,

¨ Beta Blockers, Diuretics

¨ Changes noted in V1 - V4

¨ Reciprocal changes in II, III, AVF

¨ Loss of R wave progression

¨ LAD/L main occlusion

¨ Symptoms: L ventricular failure,

shock

Monitor for:

¨ Heart failure

¨ Heart block

¨ Bundle branch block

¨ loud murmur à suspect

ventricular septal rupture

-Occurs below the AV node

-Can progress to CHB

-Constant PR interval

-2:1 difficult to diagnose

-Place a trancutaneous pacer

-Prepare for transvenous pacer

Complete Heart Block/Third Degree AV Block

-No atrial impulses pass through

the AV node

-Ventricles generate their own

rhythm

¨ Changes in V5, V6, I, AVL

¨ Occlusion of the left

circumflex

¨ Associated with other MI

locations (inferior, anterior)

¨ Changes in V1-V2

¨ Tall, broad R wave

(>0.04) & ST depression

(reciprocal change)

¨ Posterior leads V7 - V9

¨ Associated with

inferior/lateral wall MI

¨ Occlusion of RCA or left

circumflex

Assess posterior leads V7 – V9

for ST elevation

¨ Inflammation of the pericardial sac

¨ Acute or chronic

¨ Chest pain – sharp, stabbing, or dull & achy

¤ Pain improved when sit-up, lean forward

¤ Left sided radiation

¤ Pain worse with cough, positional changes & inspiration

¨ Pericardial friction rub

¨ Treatment:

¤ NSAIDS – high dose Ibuprofen

¤ Antibiotic if bacterial, antifungal if fungus

Clinical signs:

¨ Hemodynamic

instability

¨ LOUD systolic murmur

¨ MITRAL REGURG!!!

Treatment:

¨ Mechanical support

¨ Hemodynamic support

¨ Surgical repair/valve

Left ventricle replacement

¨ Oxygen rich blood shunts to

the right side of the heart

¨ Risk: Anterior wall MI

Symptoms: Acute SOB

¨ S3

¨ Crackles

¨ Holosystolic murmur

PA catheter insertion:

¨ Increased C.O.

¤ falsely elevated on PA cath

¨ Increased SVO2

¨ Large “v” waves

 ABG – Mixed respiratory acidosis, metabolic acidosis;

hypoxemia

 Lactic acidosis

 CXR: pulmonary congestion

 Echo: decreased wall motion

Supportive Treatment:

 Vasopressors/ + Inotrope

 Diuretics (as perfusion allows)

 Afterload reduction / venous vasodilators (i.e. NTG)

 Mechanical support (ie. IABP, Impella)

 Fluid in the alveolus

 Impaired gas

exchange

 Hypoxemia

 Cardiogenic vs. noncardiogenic

Treatment

Diuretics

- Classified as a catecholamine

- Acts on the SNS

‐ ↑HR, ↑BP

‐ Avoid extravasation

‐ Stimulates beta1 & some beta2, alpha

Dosing:

¨ 0.5 - 3 mcg/kg/min – dopaminergic receptors

¨ 3 - 10 mcg/kg/min – beta effects

¨ >10 mcg/kg/min – alpha effects

¨ Max. 20 mcg/kg/min

¨ Effect: ↑ BP, ↑HR

¨ Alpha, Beta 1, some beta 2

¨ Adverse effects: tachycardia, dysrhythmias, chest

pain

¨ Dosing: 2‐10 mcg/min – titrate to effect

¨ Monitor closely for extravasation

¨ Hyperglycemia

¨ Effect: ↑ BP

¨ Alpha

¨ Adverse effects: Reflex bradycardia, dysrhythmias,

HTN, chest pain

¨ Dosing: 2‐10 mcg/kg/min

¨ Monitor for extravasation

Antihypertensive of nitrate origin

Dosing:

0.5 – 8 mcg/kg/min

Closely monitor for:

¨ Hypotension (check BP Q 1-2 min until BP is stabilized)

¨ Arterial line preferred

¨ Hypoxia (from intrapulmonary shunt)

¨ Increased HR (Stimulation of baroreceptors)

¨ Thiocyanate poisoning (esp. > 72 hrs.)

¨ Methemoglobinemia (Hgb can get converted)

Coronary Artery Bypass Graft

(CABG) Where Veins are Harvested

55

Cardiac Surgery

Coronary Artery Bypass Graft

(CABG)

**Longer pump time = increased risk of bleeding

Monitor:

¨ BP (↑ BP = risk for bleeding)

¨ Pain

¨ Electrolytes

¨ Bleeding

¨ Post op ischemia

¨ Dysrhythmias/blocks

¨ Signs of infection

¨ Weight gain

¨ Diet (Na/cholesterol restrictions)

¨ Activity/Exercise

¨ Smoking cessation

¨ Medications

¨ Sternal precautions

Compression of the heart due to fluid accumulation within the pericardium

The pericardial space

normally contains

20 - 50ml fluid

2 layers of

pericardium:

Parietal (outer)

Visceral (inner)

DX imaging : Xray

Clinical signs/symptoms

**Beck’s Triad**:

1) Elevated CVP w/JVD

2) Hypotension

3) Muffled heart sounds

¨ Sudden drop in chest tube output

¨ Narrowed pulse pressure

¨ Tachycardia

¨ Pulsus paradoxus

(>10 mm Hg during insp.)

¨ Pulseless Electrical Activity (PEA)

Treatment

¨ Pericardiocentesis

¨ Risk: Laceration of

coronary artery

¨ Thoracotomy

¨ Median sternotomy

¨ Goal: Locate & control

source of bleeding

Risk factors for developing Afib/aflutter:

 CABG

 Valvular disease

 MI

 Atherosclerosis

 Rheumatic Heart Disease

 Lung Disease

Rates can vary:

<100

>100 “Rapid ventricular

response”

Lose atrial kick

↓ in CO by up to 20-25%

Management:

Rate control vs. conversion

Cardioversion if unstable

Digoxin

Beta blockers*

Ca channel blockers*

Amiodarone

Anticoagulation

*Use cautiously in pts with reduced EF

 AKA: “Congestive Heart Failure”

 Acute Decompensated HF

 Heart Failure with preserved EF (HFpEF)

 Diastolic Heart Failure

 Ejection Fraction ≥ 50%

 Borderline EF 41 – 49%

 Heart Failure with reduced EF (HFrEF)

 Systolic Heart Failure

 Ejection Fraction ≤ 40%

Ventricular failure

Left Sided Failure

Y Tachypnea

Y Tachycardia

Y S3

Y Mitral regurg

Y Displaced PMI

Y Crackles, wheezes

Y Cough, frothy sputum

Y ↑ PA pressures

Y ↓CO/CI

Ventricular Failure

Right Sided Failure

Y JVD

Y Hepatojugular reflux

Y Peripheral edema

Y Hepatomegaly

Y Anorexia, N/V

Y Ascites

Y Tricuspid regurg

Y ↑CVP

Y ↑Liver enzymes

PMI (Point of maximum impulse)

 Normally palpated:

5th ICS, MCL

@ apex

Causes of PMI shifting:

 LVH

 Heart failure

 Right pneumothorax

 Right pleural effusion

Measuring JVD

 Supine position, HOB 30º

 Measure from right side

 Turn head slightly to left

 Observe for pulsations

 Note highest point

 Measure distance between the

pulsation and sternal angle

 4 cm above sternal angle is NL

HFrEF - Reduced EF (Dilated)

-Damage to

myofibrils

BNP Levels

 Hormone secreted by ventricles in response to stretch

 Allows for rapid diagnosis of heart failure

 Levels:

<100 no heart failure

100-300 heart failure is present

>300 mild heart failure

>600 moderate heart failure

>900 severe heart failure

-Reference: Cleveland Clinic

The Breathing Not Properly study

(Level > 100 pg/mL 90% sensitivity 76% specificity to predict HF)

Treatment Strategies

Medical management

VS

Long Term

 ACE inhibitor OR

 Angiotensin Receptor Blocker

(ARB)

 Beta-blocker

 Aldosterone antagonist (i.e.

spironolactone)

 Alpha/beta blocker (i.e.

Carvedilol)

 Vasodilators (nitrates)

 Diuretics (usually loop)

 Cardiac glycosides (i.e.

digoxin)

Long term

 Biventricular pacing

 Cardiac Assist Devices

 Cardiac transplant

 Inotropes (i.e. dobutamine) -

palliative

Renin Angiotensin Aldosterone Stystem (RAAS)

↓ Renal Blood Flow/SNS

Release of Renin

↓

(Beta Blockers "Olols")

Angiotensin >>>>>>>>> Angiotensin I

                        ↓

(Ace inhibitors "prils)  ↓

Angiotensin II

↓                                         ↓

Vasoconstriciton          Aldosterone Release

(Aldosterone Antagonist spironolactone)

NA & h2o Rentension

Increased BP

(Hydralazine & Isosorbide Dinitrate, digoxin, anticoag (afib))

Dobutamine (Dobutrex)

 Stimulates beta receptors, ß1 (some alpha)

 Improves contractility & cardiac output

 Also used in cardiac surgery & septic shock

 Dosing:

2.5 – 20 mcg/kg/min IV (up to 40 mcg/kg/min)

 Onset 1‐2 minutes, up to 10 min.

 Plasma half life 2 min.

 Monitor for:

tachycardia, hypertension, ectopy, hypokalemia

Milrinone (Primacor)

 Phosphodiesterase (PDE) inhibitor

 Increases myocardial contractility

 Vasodilator

 Dosing:

Bolus 50 mcg/kg over 10 min.

Maintenance: 0.375 – 0.75 mcg/kg/min

 Long half life!!!!

 Bridge to transplant

 Effects:

↑CO, ↓paop & SVR, no change in HR

Nesiritide (Natrecor)

 Acute decompensated HF without cardiogenic shock

 Potent vasodilator

 Dilates arteries and ↓SVR, ↓paop, ↑ C.O.

 Inhibits the renin‐angiotensin‐aldosterone system

 Dosing:

Bolus 2 mcg/kg over 1 minute

Maintenance: 0.01 mcg/kg/min

Short half life (~18 minutes)

 Monitor for:

hypotension

Ventricular Assist Device

VADs:

-Left, right or both

-Short term:

Bridge to transplant

-Long term: Destination

therapy

Cardiac transplantation

 Vagal nerve is severed

 Atropine will not work if bradycardia

develops

 Immunosuppression to prevent rejection

Effect of Bi-ventricular Pacing on QRS

Duration

 Prolonged QRS

before therapy

Bi-ventricular

pacing resulting in

shortening of QRS

duration

Goals:

Complement medical therapy

Improve quality of life

Give hope to those who are suffering with moderate to severe heart failure

Cardiac Resynchronization Therapy

Benefits:

-Synchronized ventricular

contraction

-Increased EF/CO

-Symptom improvement

-Increased QOL

Cardiomyopathy management:

Optimize heart function:

 Preload

 Afterload

 Contractility

 Beta blocker, ACE inhibitor

 ARB - Angiotensin

Receptor Blocker (ie.

Losartan, valsartan)

 Diuretics

 VAD-bridge to transplant

 Transplant

 Patient education!!!

Diagnostics:

 12 Lead ECG

 CXR

 ECHO

 TEE

 Heart cath

 Myocardial biopsy

(restrictive

Discharge care

 Medication adherence

 Activity

 Weight (Daily)

 Diet (Sodium restricted*)

 Smoking (and other health habits – quit smoking,

limit alcohol intake, lose weight)

 Prevent infection – flu & pneumococcal vaccines

*Na & fluid restriction debateable;

fluid restrict if hyponatremic, Na if congestion

Hypertrophic Cardiomyopathy

 HOCM (Hypertrophic Obstructive CM)

 IHSS (Idiopathic Hypertrophic Subaortic Stenosis)

Physiologic changes:

 Thickened septum

 Diastolic dysfunction

 Decreased compliance & outflow obstruction

 Many present with sudden cardiac death

Hypertrophic CM con’t:

 Assessment: S4, Murmur, displaced PMI,

 Treatment: beta blockers, calcium channel blockers

 Prolong diastole & filling time!

 Avoid inotropes!!! (i.e. Digoxin/Dobutamine)

 Surgical: Percutaneous transluminal septal myocardial

ablation (PTSMA)

 Myomectomy

Murmurs

2 causes:

Forward flow of blood through stenotic open valves

Backward flow through

incompletely closed

valves

Murmurs are high pitched

**except aortic stenosis

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 Stenosis Diastolic 5th ICS, MCL

Mitral Regurg Systolic 5th ICS, MCL

Aortic Stenosis Systolic 2nd ICS, RSB

Aortic Regurg Diastolic 2nd ICS, RSB

Mitral insufficiency/regurgitation

 Causes:

MI

ruptured chordae tendineae

severe L heart failure

hypertrophic

cardiomyopathy

MV prolapse

Rheumatic fever

Symptoms:

Orthopnea/dyspnea

Fatigue

Angina

Left heart failure

Right heart failure

Systolic murmur

Prone to afib

Mitral Stenosis

 Occurs when the mitral valve is OPEN

 Diastolic murmur

 Pinkish cheeks

 Pulmonary edema

 Prone to afib

Causes: RHD

Treatment:

 Medical mgmt

 Surgical replacement

 Balloon Valvuloplasty

Aortic Insufficiency

 Occurs when the valve doesn’t close completely

 Results in a backflow of blood & reduced diastolic

pressure

Causes:

 HTN

 Rheumatic fever

 Endocarditis

 Syphilis

 Idiopathic

Signs:

 head bobbing

 Brisk carotid upstroke

 Wide pulse pressure - >40 mmHg

 “Water-hammer” pulse – rapid upstroke &

downstroke with a shortened peak

Associated with:

Marfan’s syndrome

Ventricular septal defect (VSD)

Aortic Stenosis

 Systolic ejection is

impeded

 Pressure gradient between

LV & aorta

 50% 2-year mortality if

HF develops

 Symptoms: Heart failure

 Treatment: Valve

replacement

 Echocardiogram

 Cardiac catheterization

(↑LVEDP, ↑atrial

pressure, ↑paop, ↓CO)

 12 lead ECG: left atrial

& ventricular

hypertrophy

 Chest x-ray: left atrial

& ventricular

enlargement, pulm

venous congestion

 Treat heart failure if

present: ACE inhibitor,

diuretics, digoxin, Na

restriction

 Beta blocker if EF>25%

 Afterload reduction

 Valve

repair/replacement

Myocarditis

 Focal or diffuse inflammation of the

myocardium

 Viral or bacterial infection

 Clinical signs: fever, chest pain,

heart failure, dysrhythmias, sudden

cardiac death

 May be accompanied by

pericarditis

 Treatment: Antibiotics

(if bacterial), NSAIDs, diuretics,

inotropes, ACE inhibitor

Pericarditis

 Inflammation of the pericardial sac

 Constrictive: fibrous deposits on the pericardium

 Restrictive: effusions into the pericardial sac

 Causes: Acute MI, post-CABG, connective tissue

disease, infection

 Dressler’s syndrome 2-12 weeks after MI caused

from an autoimmune response or viral infection

Pericarditis con’t

 10-15% develop this 2-7 days after AMI

 Fever

 Chest pain worse with deep breath, relieved by

leaning forward

 Non-specific ST segment changed in the precordial

leads

Pericardial Rubs

 Scratching, grating, squeaking leather quality… LLSB,

leaning forward or lying supine in deep expiration…

high frequency… diaphragm

 3 sounds are present

 One systolic – occurs anywhere in systole

 Two diastolic – occurs w/ ventricular stretch at early and late

diastole

 MI, pericarditis, autoimmune, trauma, s/p cardiac

surgery, autoimmune

Endocarditis

 Infection of the

endocardium or valve

 Damaged leaflets

 Causes: trauma, bacteria

from other sources

 @ Risk: cardiac surgery,

rheumatic heart disease,

dental procedures, IV

drug abuse

Endocarditis Symptoms:

 Stabbing, sharp pain (worse

on inspiration)

 SOB

 cough

 JVD

 pulsus paradoxus

 friction rub

 ST elevations

 narrowed pulse pressure

 Elevated WBC, ESR

Endocarditis common organisms

 Streptococcus

 Staphylococcus

 Gram negative bacilli

 Fungi (ie candida)

 Administer appropriate antibiotics

Pulses

 Pulsus Paradoxus

 decrease in systolic pressure during inspiration>

10 mmHg caused by cardiac tamponade,

pleural effusion, pericarditis or dehydration

 Pulsus Alternans

 Every other beat is weak, indicating advanced

LV failure

Pulsus Paradoxus

Treatment Goals

 Prevent/relieve symptoms (lean forward)

 NSAIDs (ASA or indomethacin)

 Treat infection

 Corticosteroids

 Chronic: partial pericardiectomy

-window is created allowing fluids to drain into

pleural space

Constrictive pericarditis: total pericardiectomy

Cardiac Arrest

 Early CPR with minimal

interruptions

 Compressions of good quality

 AT LEAST 100 per minute

 2 inch depth

 Early defibrillation

 Post-arrest care

 Optimize hemodynamics

 Reperfusion

 Targeted Temperature Management

Ventricular fibrillation

 Shock (if readily available); Repeat Q 2 min.

 CPR for 2 min

 Rhythm check-shock if warranted

 Epi 1mg IV/IO Q 3-5 min or

Vasopressin 40 units IV/IO instead of 1st or 2nd Epi

 Amiodorone 300 mg IV/IO; repeat bolus 150 mg IV/IO

in 3-5 min if still in VF/VT

 Medications (other): Lidocaine1.0-1.5 mg/kg IV/IO, MR X 2, q5-10 min.

0.5-0.75 mg/kg, (3mg/kg max. loading dose) if VF/PVT persists

SCREAM

If pulseless V-Tach,

same treatment as V-fib

Torsades de pointes

 Shift in axis

 Caused by hypomagnesemia, prolonged QT, multiple

medications

 Also caused by Methadone & some quinolones

 Treatment: Magnesium Sulfate 1-2 grams IV/IO

(diluted)

 Magnesium antagonist: Calcium Chloride

PEA (pulseless electrical activity)

Pump: Start compressions

Epinephrine 1mg IV Q3-5 min or

Vasopressin 40 units IV instead of

1st or 2nd Epi

Assess: Differential diagnosis

5 H’s:

Hypovolemia

Hypoxia

Hypo/Hyperkalemia

H+ ion (acidosis)

Hypothermia

5 T’s:

Thrombus: MI

PE

Tension pneumothorax

Tamponade

Toxicology (Drug OD)

Asystole

No cardiac output

Pump (Same as PEA)

Epinephrine 1 mg IV/IO Q 3-5 min

Assess differential diagnosis

Consider termination

Capnography during resuscitation

 Used as a marker of perfusion

 Goal >10 mm HG

 Normal PETCO2 > 40 mm HG

 If less than 10, improve quality of compressions

 If rapid increase in PETCO2, may be a sign of

ROSC

 If consistently < 10 in the setting of adequate

compressions, discuss termination of resuscitation

efforts

Tachycardia – Narrow complex

 Stable vs. unstable

 Unstable: Prepare for cardioversion!

 Stable? Narrow & regular complex?

Vagal maneuvers

Adenosine 6 mg IV-Rapid!!!

(Repeat 12 mg x 2, q 1-2 min)

Diltiazem IV

Tachycardia – Wide complex

 QRS > 0.12 sec.: consult an expert

 Amiodarone 150 mg IV over 10 min.

 Can also use Lidocaine for monomorphic wide

complex tachycardia

 New in 2010 guidelines:

Adenosine 6 mg IV          

May repeat

Antidysrhythmic Medications:

Class IA

Medication Quinidine (Cardioquin)*

Procainamide (Pronestyl)*

Effect Prolongs

repolarization

Uses Atrial dys.

Vent tach

Class IB

Medication Lidocaine (Xylocaine)*

Tocainamide (Tonocard)

Mexiletin (Mexitil)

Effect Shortens action

potential duration

Uses Ventricular

Dysrhythmias

Class IC

Medication Flecainamide (Tambocor)

Propafenone (Rhythmol)

Effect Blocks Na channels

Uses Ventricular

Dysrhythmias

Class II

Medication Propanolol (Inderal)

Esmolol (Brevibloc)*

Effect Decreases HR & SA

node automat.

Uses Atrial dys. & SVT

Class III

Medication Amiodarone (Cordarone)**

Bretylium (Bretylol)

Sotalol (Betapace

Effect Blocks K+ channels,

slows conduction

Uses Ventricular

Dysrhythmias

Class IV

Medication Verapamil (Calan)*

Diltiazem (Cardizem)*

Effect Ca channel antagonist

Uses Atrial tachycardia &

atrial flutter

Class Other

Medication Digoxin (Lanoxin)*

Adenosine (Adenocard)*

Effect Slows AV node

conduction, depresses

SA node

Uses Afib, Aflutter & SVT

Wolfe-Parkinson-White (WPW)

 Pre-excitation

 Abnormal conduction

pathway between the

atria & ventricles

 Accessory pathways

conduct faster than the

AV node

 PR interval <0.12

 Delta wave

Pacemaker Review

 Permanent or temporary

 Indications: Symptomatic bradycardia, 2nd Degree

AV Block (Mobitz II), Third Degree AV Block

 Patients admitted with “Syncope”

Will require f/u EP study

 Modes: Synchronous or Asynchronous

 Temporary:

Transcutaneous, transvenous, epicardial

 Pad placement

 Anterior – posterior

 Anterior – lateral

 Settings

 Demand (synchronous)

 Fixed (asynchronous)

 More energy required vs. transvenous (start @ 50 mA

& increase until capture)

Temporary – Transvenous/Epicardial

 Pacemaker codes:

 First: Chamber paced (A or V)

 Second: Chamber sensed (A or V)

 Third: Response to sensing

I-Inhibits pacing if QRS is sensed, demand

D-Triggers & inhibits pacing

O-None

Examples: VVI, DVI, DDD

 D D D

 V V I

 A A I

 V V O

 D D D

Atria/Ventricle paced, Atria/ventricle sensed, pacing inhibited with

intrinsic rhythm/beat

 V V I

Ventricle paced, ventricle sensed, pacing inhibited with intrinsic

rhythm/beat

 A A I

Atria paced, Atria sensed, pacing inhibited with intrinsic rhythm/beat

 V V O

Ventricle paced, ventricle sensed, will pace regardless of intrinsic

rhythm/beat (dangerous!!! – possible R on T)

Failure to capture

Causes:

 Improper position

 Low voltage

 Battery failure

 Inadequate connection

 Fibrosis of catheter tip

Trouble-shooting:

 Check connections

 Increase mA (energy)

Failure to capture

Causes:

 Improper position

 Low voltage

 Battery failure

 Inadequate connection

 Fibrosis of catheter tip

Trouble-shooting:

 Check connections

 Increase mA (energy)

Failure to pace

Causes:

 Battery failure

 Lead dislodgement

Troubleshooting:

 Assess leads & connections

 Assess labs

 Change battery

 Prepare for TCP

Failure to sense

Common Causes:

 Position of the lead

 Battery failure

 Improper settings

Troubleshooting:

 Assess thresholds

Magnet Operation with Pacers

 Magnet over pacemaker causes asynchronous

pacing at a designated “magnet” rate

 Over an ICD, inhibits defibrillation

Cardiac trauma: blunt vs. penetrating

Penetrating trauma

 Injury to:

Chamber of the heart

Right ventricle

Pericardium

Great vessels/coronary

arteries

Blunt trauma

 Causes:

-MVC/Steering wheel to chest

-Direct blow to chest

-Fall

 Stunned or contused myocardium

 Ventricular rupture

 Acceleration/deceleration injury: vessel damage

 Direct transfer mechanics

Blunt Cardiac Injury

 Formerly called “Cardiac

contusion”

 Right atrium & ventricle

most at risk

Monitor for:

 Dysrhythmias

 Heart block/R BBB

Medical mgmt:

 Prevent complications

 Antidysrhythmics

 Heart failure

 Temporary pacing

Diagnosis:

 Echo

 12 Lead ECG

 CXR

 CT Scan

 MRI

 Trans Esophageal Echo

 Cardiac enzymes

 Other labs: Coags,

electrolytes, CBC

Category SBP / DBP

Optimal <120 <80

Pre-hypertension 120-139 80-89

Stage 1 HTN 140-159 90-99

Stage 2 HTN >160 >/= 100

*HYPERTENSIVE CRISIS

Usually > 240/140

Acute elevation associated with organ damage:

Kidney: decreased blood flow, hematuria, proteinuria

Brain: hypertensive encephalopathy

Heart: LVH, LVF, MI

Eyes: retinal hemorrhages

Vascular system: vessel damage

Long term BP Goals:

≥ 60 years of age:

 SBP < 150 mmHg and DBP < 90 mmHg

≤ 60 years of age:

 SBP < 140 mmHg and DBP < 90 mmHg

4 Types of medications recommended:

Thiazide diuretic

Calcium Channel Blocker

ACE Inhibitor

Angiotensin Receptor Blocker (ARB)

Treatment: Hypertensive Crisis

 BP in both arms (r/o

aneurysm or steal

syndrome)

 Consider 12 Lead

ECG

 Decrease BP by 25%

in 1-2 hrs

 IV anti-hypertensives

(vasodilators, diuretics,

etc)

 Nitroprusside

 Labetolol

 Esmolol

 Nicardipine

Aneurysms

 Thoracic (TAA)

 Abdominal (AAA)

 Aortic dissection

 Rupture

 Definition: permanent localized dilation of aorta

1.5 times diameter

 Patients will describe “ripping” chest pain radiating

to the back

 > 6 cm associated with increased risk of rupture

 At risk: HTN, smoking,

 Dilatation of the aorta >50% of

its normal diameter

 Goal: Prevent rupture or dissection

 Treatment: BP control/HR

reduction

 Surgical repair

BP control

 Esmolol (Brevibloc)- short acting, beta blocker

Initial dose: 250-500 mcg/kg IV over 1 min

Maintenance dose:

 Labetalol (Trandate)- Blocks alpha, B1 & B2

Initial dose: 20 mg IV over 2 min;

follow with 20-80 mg IV q10-15min until BP is controlled

Maintenance dose: 2 mg/min IV continuous infusion; titrate up to 5-20 mg/min; not to

exceed total dose of 300 mg

 Metoprolol

Dose: 5 mg IV q 2min, up to 3 times

 Nitroprusside (Nipride)

Arteriolar & venous vasodilation

0.5-3 mcg/kg/min IV

 Nicardipine (Cardene)

 Calcium channel blocker

 5 – 15 mg/hr

Aortic Dissection