caring for pts w/ cardiac conditions

what are the different diagnostic tests to diagnose a heart problem

- echo (TEE or TTE)

- ECG

- CXR: gauges size of heart

- cardiac cath: helps visualize internal structures

- exercise tolerance test

- multigated blood pool scanning: used to detect ventricular wall motion and the ejection fraction (velocity and amount of blood ejected)

- invasive hemodynamic monitoring: takes direct measurement of CO, pressure in heart; invasive

echo

• TEE - very invasive → takes probe thru esophagus to look at blood flow thru the heart from a view behind the heart 

• TTE - less invasive (ultrasound) → gold standard → helps evaluate ejection fraction, heart size, left ventricles, how valves are opening/closing, any fusion, etc

what are the different lab tests for diagnosing heart problems

- electrolytes

- BUN and creatinine

- Hct and Hgb

- BNP: produced and released by the ventricles as they stretch (>100) in response to fluid overload

- UA: looking out for microalbuminuria (early warning sign of HF related to damage to the endothelium → poor contraction and refilling of the heart

- ABGs

what is heart failure

• progressive condition in which the heart can no longer pump enough blood to provide for the metabolic needs of the body

• acute or chronic (chronic has acute exacerbations)

• always end up with decreased CO

HF is r/t dysfunction of

• Mechanical Pump - can’t move volume in, can’t move volume out, or heart isn’t strong enough to squeeze

  • a direct problem with CO: preload, afterload, contractility

• Electrical Conduction - something wrong with cardiac path conduction; automaticity (heart can’t generate a beat), dysrhythmia

• Plumbing (coronary arteries) - clotting, occlusion, narrowing?

when the heart is failing, what is the first thing it starts doing

activates compensatory mechanisms: increase HR and BP

what happens when the compensatory mechanisms in the heart start failing

• loss of cardiac reserve - the difference between the rate at which the heart is pumping at and its maximum ability to pump at any given time

• decompensation - extreme results of HF → cariogenic shock & cardiogenic pulmonary edema

what are the different types of HF

- left sided/ CHF

- right sided

- high output

what are the different types of left sided HF/ CHF

- systolic aka HF with reduced EF (HFrEF)

- diastolic aka HF with preserved EF (HFpEF)

what is high output HF

the heart is working hard to pump out enough blood, but it is still not enough to adequately perfuse the body given the disease process

what are the different causes of HF

• HTN

• CAD

• sepsis

• valvular disease

• cardiomyopathy

• NSAIDs

• dysrhythmias

Compensatory mechanism - SNS activation

when we have a drop in CO and BP, our body reacts by stimulating SNS → release catecholamines → heart starts pumping faster to try and increase CO

Compensatory mechanism - RAAS activation

when CO drops, the kidneys aren’t being perfused adequately → activates RAAS → vasoconstriction and retention of sodium and water to try to hold onto volume

Compensatory Mechanism - Frank-Starling Mechanism

the heart’s ability to change the force of contraction (stroke volume) in response to the changes in venous return → however much blood comes in has to be pumped out → can be maxed out 

what are some other compensatory mechanisms of the heart

- when there is a decrease in cerebral perfusion, ADH gets released from posterior pituitary to increase BP and CO via vasoconstriction and fluid retention

- endothelin is secreted when the endothelial cells of the ventricles stretch, which causes vasoconstriction and an increase in peripheral resistance which will cause hypertension and increased CO

what is a complication of long term compensatory mechanisms of the heart

ventricular adaptation

what is ventricular adaptation

myocardium is going to start hypertrophying (grows thicker) to produce stronger contractions but this in turn stiffens and dilates the heart and deprives the muscles of oxygen

when the heart starts using compensatory mechanisms, what should you focus on tx

the underlying problem

what is class 1 of HF characterized by

• no limitations

• activity doesn’t cause s/s

• lot of risk factors

what is class II of HF (according to the AHA) characterized by

• slight limitations

• comfortable at rest

• ordinary physical activity causes s/s

what is class III of HF characterized by

• marked limitations

• comfortable at rest

• most activity causes s/s

• symptomatic HF

what is class IV of HF characterized by

• severe limitations

• s/s present at rest

LHF: left ventricular dysfunction

• decreased CO

• loss of myocardial cells - ventricle is getting weak → losing myocardial cells

• pulm congestion - if left side isn’t working → volume backs into lungs

systolic failure LHF

decreased contractility = low forward flow (heart can’t contract forcefully enough during systole to eject adequate amt of blood to maintain CO)

what does systolic left sided HF cause

- increased preload and afterload due to peripheral resistance (hypertension)

- decreased ejection fraction (<40%)

- develop S3 gallop due to increased volume in ventricles (early sign); sloshing in

what is considered normal EF

50-70%

what EF is considered a high risk for sudden cardiac death

<30%

if someone has a decreased EF, what should be considered

use of an implanted cardio defibrillator (ICD)

what causes diastolic left sided HF

decreased ability of left ventricle to relax bc too thick

what does diastolic left sided HF cause

- stiffened left ventricle

- decreases the amount of blood that can fill into the ventricle

- normal EF but has increased pressure

- develop S4 Gallop due to decrease in ventricular compliance

pulmonary congestion s/s in LHF

- hacking cough, worse at night

- dyspnea/ SOA

- crackles or wheezes

- frothy, pink tinged sputum

- tachypnea

- S3/ S4

what are the s/s of decreased CO in left sided HF

- fatigue

- weakness

- oliguria during the day (nocturia at night)

- angina

- confusion, restlessness

- dizziness

- tachycardia, palpitations

- pallor/ ash gray skin

- weak peripheral pulses

- cool extremities

what is a major complication of left sided HF

cardiogenic pulmonary edema

what is cardiogenic pulmonary edema

• fluid accumulation in the alveoli and interstitial lung tissue: no gas exchange can occur

• pts going to experience tissue hypoxia bc of a ventilation diffusion mismatch → blood flowing around alveoli, but bc its so full of fluid, O2 and CO2 can’t exchange → shunting

what are the different phases of cardiogenic pulmonary edema

gradual or acute (flash pulmonary edema → MEDICAL EMERGENCY)

what are the s/s of cardiogenic pulmonary edema

- crackles

- dyspnea at rest

- disorientation/ acute confusion (esp in older adults as early symptom)

- tachycardia

- hypertension or hypotension

- reduced urinary output

- cough with frothy, pink tinged sputum

- anxiety, restlessness

- lethargy

what is the priority nursing action if someone is experiencing cardiogenic pulmonary edema

administer O2

what is a nonpharmacological intervention for cardiogenic pulmonary edema

place patient in upright position with legs dangling if their BP is good

what are some pharmacological interventions for cardiogenic pulmonary edema

- IV diuretics

- IV or SQ nitroglycerine: vasodilator

- IV morphine: vasodilator

- HF meds (such as positive inotropes)- makes heart pump stronger to move fluid

- ultrafiltration - removes sodium and water if pt isn’t responding to diuretics

what is right heart failure

• right ventricle fails

• blood accumulates in the systemic system

what can be some causes of right sided HF

- lung disease: would then be considered cor pulmonale

- LHF: would have s/s of both failures

what are the s/s of right sided HF

- dependent pitting edema (legs and sacrum)

- JVD

- hepatomegaly, ascites, splenomegaly

- swollen hands/ fingers

- distended abdomen/ increased abdominal girth: pts feel full faster (malnourishment)

- anorexia, n/v

- polyuria at night (nocturia)

- weight gain: 4 to 7 L fluid gain (10 to 15 lbs)

- BP changes (increased then decrease)

what are some additional complications of HF

- pleural effusion due to increased pressure

- dysrhythmias: due to conduction abnormalities

- cardiorenal syndrome: development of renal failure and HF (hearts pumping less blood to kidneys, so kidneys try to compensate by holding onto volume and promoting vasoconstriction, but the kidneys are actually depriving themselves of blood they need)

• Anemia - secondary to chronic kidney disease, which worsens state of HF bc less oxygen being transported now

what are some nonpharmacological ways to increase gas exchange

- monitor respiratory status

- administer supplemental O2 to maintain SpO2 >90%

- consider CPAP: esp with sleep apnea

- have pt turn, cough, and deep breath and use there IS

- can position pt in high fowlers if they do not have hypertension

increasing perfusion: reducing after load

• need to lower vascular resistance to make it easier for heart to pum

• ACE Inhibitors (Lisinopril) & AR Blockers (Losartan (Cozaar))

  • help promote dilation which helps increase stroke volume

  • prevent sodium and water retention -> decreasing fluid overload

  • decreasing BP -> easier to move blood out of heart

  • not good for pts who are dehydrated, volume depleted, HOTN; may not be as effective for African-Americans

  • monitor potassium bc of rx for hyperkalemia

• ARNI

  • used in place of ACEI or ARB (Sacubitril/Valsartan (Entresto))

  • have to be at stage II and have decreased ejection fraction

  • can’t be on ACEI or ARB w/ this

increasing perfusion: reducing preload

goal: by decreasing the volume of blood stretching the heart → lowers ventricular wall tension and improves heart’s ability to fill and pump

• Nutrition therapy

  • Sodium restriction to 2-3 g daily

  • Fluid restriction to 2 L daily → try sodium first then fluid

• Diuretics (Furosemide (Lasix), Spironolactone (Aldactone))

  • Added when restrictions ineffective.

  • First choice for FO.

  • Furosemide is more effective for acute phases → high rx for hypokalemia (ventricular dysrhythmias) → monitor.

  • Spironolactone good for HF pts that stay symptomatic even if on ACEI/beta blocker → potassium sparing so don’t have to worry about rx as much → block effect of aldosterone → decrease sodium and water retention

• Vasodilators

  • For persistent dyspnea → more for acute uses

  • Nitrates (reserved for pt progressed to later stage of HF)

  • reduce afterload bc reduces BP

  • PO vasodilator can be good alternative for African-Americans

increasing perfusion: enhance contractility

• Positive inotropic drugs - Digoxin

  • promotes better contraction, improves atrial kick, lower HR, slows conduction through AV node

  • Monitor for digitoxity!

  • Be cautious for older adults and pts w/ renal impairments

  • monitor for hypokalemia, anorexia, fatigue, blurred vision, change in mental status, dysrhythmias)

• Dobutamine, Milrinone - Acute HF for sicker pts

increasing perfusion: additional meds

• Beta Blockers

  • For chronic HF

  • helps reduce SNS stimulation

  • slow ventricular response to help us get better contraction.

  • Ex: Metoprolol succinate (Toprol XL), Carvedilol (Coreg)

• HCN Channel Blocker

  • For HF patients with EF < 35% & SR > 70 bpm at rest.

  • Ex: Ivabradine (Corlanor)

• SGLT2i drugs

  • Improves renal function with HF.

  • Ex: Canagliflozin, Empagliflozin

increasing perfusion: non-surg options

• CPAP - used to try to control the electrical conduction

• Cardiac resynchronization therapy

• CardioMEMS Implant - monitors pulmonary artery pressure

• Investigative gene therapy

  • injecting growth factor in to replace damaged genes

  • good for pts progressed to later stages, but not yet a transplant candidate

increaseing perfusion: surg options

• Heart transplant

  • curative option

  • high rx, esp w/ infection

  • if progress to certain stage of HF, might be only option to prevent progression to terminal illness

• Ventricular assist device - short/long term; help make heart pump more effectively

• Ventricular reconstruction - reduce the ventricle by removing some actual heart muscle and tissue so that it can beat more effectively

what acronym do you need to teach pts with HF

MAWDS

MAWDS

• medications - take as prescribed, don’t run out, avoid NSAIDs

• activity - stay active → don’t overdo it → manage fatigue by balancing rest and activity → pt BP/Hr >20 w/activty, chest pain, or dyspnea w/ activity indicate activity intolerance → if BP/HR falls, then sign of no cardiac reserve

• weight - weight everyday → same scale, clothes, time of day → weight gain of 2.2 lbs = 1L of fluid

• diet - limit sodium to 2-3 g and fluids to 2L

• signs and symptoms

what s/s should you teach a pt with HF to report immediately (MAWDS)

- rapid weight gain (5 lbs in 1 wk or 2 -3 lbs in 24 hrs)

- decreased exercise tolerance lasting 2-3 days

- cold s/s (cough) lasting more than 3-5 days (esp at night)

- nocturia

- development of dyspnea or angina at rest, or worsening angina

- any new or worsening s/s (ex: increased dependent swelling)

heart failure core measures

- beta blocker prescribed at dc

- follow up w/in 7 days after discharge

- record of care transmitted to the next level of care w/in 7 days of discharge

- documentation of advance care planning (advance directives) discussion with a health care provider

- documentation of advance directives within the medical record

- follow up discharge evaluation of pt status and tx adherence w/in 72 hrs of discharge

what are the different problems that occur within valvular heart disease

stenosis and regurgitation

what is stenosis

impeded or obstructed forward flow due to a diseased valve that has become narrowed or rigid (can’t open)

what is regurgitation/ insufficiency

backflow of blood due to incomplete closure of the diseased valve (can’t close)

what are the different types of valvular heart disease

- mitral stenosis

- mitral regurgitation

- mitral valve prolapse

- aortic stenosis

- aortic regurgitation

what is mitral stenosis

• mitral valve fuses, stiffens, and narrows → mitral valve doesn’t open correctly

  • increased L atrium pressure (if valve can’t open and is narrow → L atrium has to work harder to push blood thru) → pulm congestion & HTN 

  • decreased forward flow (not getting enough blood into left ventricle) → decreased SV → decreased CO

• secondary to rheumatic carditis from rheumatic fever → damages valve

• diastolic prob

what are the s/s of mitral stenosis

- fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis

- if progresses to RHF → hepatomegaly, JVD, pitting edema

- a fib, rumbling apical diastolic murmur (best heard at apex)

mitral regurgitation

• incomplete valve closure during systole →  backflow of blood into LA when LV contracts

  • → increased LA volume → heart works harder → hypertrophy of LA and LV (they dilate to accommodate the increased volume → LA is dilating to accommodate the blood from the ventricle and the new blood → LV is dilating and then thickening to accommodate the new increased preload)

• has a slow progression

• can lead to decreased SV and CO

• systolic prob

what are the primary causes of mitral regurgitation

- mitral valve prolapse

- rheumatic heart disease

- heart attack

- infective endocarditis

- dilated cardiomyopathy

what are the s/s of mitral regurgitation

- fatigue, chronic weakness, dyspnea, orthopnea

- atypical chest pain, palpitations, a fib

- S3 (sign of severe regurgitation)

- hepatomegaly, JVD, pitting edema

- high pitched holosystolic murmur (heard through all of systole; best heard at apex)

mitral valve prolapse

• MV leaflets enlarge and MV prolapse into LA during systole → blood is flowing back into valve itself and goes back in LA as well

• severe/worse form of mitral regurgitation

• associated w/ congenital heart defect

what are the s/s of mitral valve prolapse

- asymptomatic

- may report atypical chest pain (sharp pain in left chest), palpitations, exercise intolerance

- midsystolic click and late systolic murmur (best heard at apex)

aortic stenosis

• most comm valve dysfunction

• “wear and tear” disease → pts have atherosclerosis and degenerative calcification of valves that occur throughout lifetime

• secondary to congenital heart disease &/or hx of rheumatic disease

• systolic prob

patio of aortic stenosis

• Narrow opening and stiff aortic valve (aortic valve should be opened during systole bc that is when left ventricle contracts and moves blood into aorta)

  • Increased pressure in LV → LV hypertrophy → increased pressure in the LA → Pulmonary congestions and HTN → RHF

  • Decreased forward flow:  ↓ SV →  ↓ CO

what are the s/s of aortic stenosis

- angina, syncope on exertion

- late signs: marked fatigue/ debilitation, peripheral cyanosis, narrowed pulse pressure

- harsh systolic crescendo to decrescendo murmur (best heard at second right intercostal space)

aortic regurgitation

• Usually secondary to infective endocarditis, congenital defect, HTN, Marfan syndrome

• incomplete closure of aortic valve during diastole → valve leaflet becomes dilated

  • → Backflow of blood from aorta to LV → LV hypertrophy → progression to LV failure → ↓ SV and ↓ CO

• diastolic prob

what are the s/s of aortic regurgitation

- asymptomatic

- w/ progression: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, palpitations, nocturnal angina/ diaphoresis, widened pulse pressure

- blowing, decrescendo diastolic murmur (best heard at the left sternal border around the 3rd and 4th intercostal space)

non-surg mgmt for valvular heart disease

• drug therapy

• balance rest and exercise

• balloon valvuloplasty

• transcatheter aortic valve replacement 

drug therapy for valvular heart disease

• Treat HF and a-fib (important to manage bc w/ a-fib you don’t have good coordinated atrial contractions, and lose atrial kick → causing a decrease in CO)

• Prophylactic antibiotics prior to invasive dental/oral procedures

balloon valvuloplasty for valvular heart disease

• feed catheter through femoral artery to deploy balloon into valve to widen so it opens → creates a little regurgitation by doing this procedure

• For stenotic valves - more comm w/ mitral valves than aortic (typically only effective for around 6 mths); isn’t permanent fix for mitral valves either

• Monitor bleeding at site, heart sounds, BP, cardiac rhythm, s/s LHF (since messed w/; decreased CO and pulmonary congestion)

transcatheter aortic valve replacement

• For aortic stenosis

• Requires hybrid operating room - bc of risk of complications, may have to convert to open heart surg → have to be prepared

• Transfemoral or transapical route 

• New valve placed around a balloon and deployed into aortic valve - pushing old valve aside

• Requires lifelong antiplatelet therapy - recommend Clopidogryl for 1st 6 months, then lifelong daily aspirin

surgical mgmt for valvular heart disease

• repair - direct commisuortomy or mitral valve annuloplasty

• replacement - open heart surgery → biologic valve or mechanical valve

direct (open) commissuortomy

• pt placed on cardiopulmonary bypass & surgeon opens chest and to valve

• remove any clots they can

• can incise the fused leaves leaflets, remove calcium deposits, widen the valves

mitral valve annuloplasty

• go in and repair the valve

• put a little supportive ring in to make valve smaller

• elongated leaflets can be shortened by lengthening the core that binds them in place

• can patch any perforated leaflets with synthetic grafts

pre-op for open heart surgery

∙ Education on expectations

∙ Pre-dental work-up - bc risk of infective endocarditis

∙ Stop oral anticoagulants – at least 72 hours prior bc of risk of bleeding

post-op for open heart surgery

∙ Critical Care Unit

∙ Aortic valve: high risk for hemorrhage

∙ Mitral valve: high risk for pulmonary complications

∙ Monitor CO, S/S of HF, surgical incision

biologic valve replacement

• uses actual tissue to replace a valve in the heart

• Xenograft: porcine/bovine 

• Homograft: cadaver/transplant

• Low risk of thrombus formation

• No long-term anticoagulants 

• Less durable (replaced q 7-10 years)

mechanical valve replacement

∙ Durability

∙ Indicated for aortic valve replacement 

∙ Audible click as valve opens and closes

∙ Lifetime anticoagulation - greater rx for clot formation

∙ Avoid MRI - depends on material

∙ Medic alert bracelet - if pt has mechanical valve; shows information clearly

what should you teach a pt with valvular heart disease

- notify all your PCP that you have a defective heart valve

- remind the PCP of your valvular problem when you have any invasive dental work

- request abx prophylaxis before and after dental procedures if the PCP does not offer it

- clean all wounds and apply abx ointment to prevent infection

- notify your PCP immediately if you experience fever, petechiae (pinpoint red dots on your skin), or shortness of breath

what should you teach a pt with valvular replacement

- prophylactic abx therapy

- avoid vitamin K foods (if on anticoagulants)

- avoid BUE heavy activity for 3 to 6 mths

- avoid MRI (mechanical valve)

what are the different layers of the heart going from most outside to least outside

- pericardium

- myocardium

- endocardium

what are the different layers in the pericardium going from the most outside layer to least outside one

- fibrous pericardium

- parietal layer of serous pericardium

- pericardial cavity

- epicardium (visceral layer of serous pericardium)

infective endocarditis 

• Microbial infection of the endocardium commonly secondary to Staph aureus or Strep viridans

• High mortality rate - most serious

• Obtain cultures → if positive, then can do an echocardiogram to assess for involvement of endocardium)

what are the risk factors for infective endocarditis

- IV drug abuse

- valve replacements

- structural defects

- systemic infections

what are the s/s of infective endocarditis

- fever → can be associated w/ chills, night sweat, fatigue, anorexia

- cardiac murmur (newly developed or change in existing)

- petechiae

- splinter hemorrhages

- osler nodes

- janeway lesions

- roth spots

what is Osler nodes

Red spots on palms and soles of feet

what are laneway lesions

Flatter and more reddened spots on hands and feet

what are splinter hemorrhage

Tiny streaks of blood underneath nails r/t microemboli

what are Roth spots 

• hemorrhagic lesions that appear as round/oval spots on retina

• can’t observe w/out a scope

how do you manage/ tx infective endocarditis

- IV antimicrobials 4 to 6 weeks: penicillin or cephalosporins

- activities balanced with rest

- tx HF s/s

- remove/ repair/ replace valve

- drain abscesses

∙ Prophylactic antibiotics for invasive dental procedures

what are the complications of infective endocarditis

- HF

- arterial embolization due to bacteria emboli (anticoagulants are not effective in this disease)

- sepsis

pericarditis

• inflammation or alteration of the pericardium

• acute or chronic

what causes acute pericarditis

- infection

- post MI

- post cardiac surgery

- connective tissue disease

what causes chronic pericarditis

- TB

- radiation

- trauma

- renal failure

- metastatic cancer

what are the s/s of pericarditis

- pericardial chest pain ("sharp, stabbing"): aggravated by breathing and coughing

- fever, elevated WBC

- pericardial friction rub

- new ST elevation in all ECG leads (resolves)

- chronic constrictive → signs of RHF, fatigue, and dyspnea

what actions should you take when txing someone with pericarditis

- NSAIDS

- colchicine for inflammation

- abx (if bacterial)

- consider corticosteroids (last resort)

- comfort positions: tripod

- chronic constrictive= pericardial window (remove portion of pericardium to allow it to better expand) or pericardiectomy (remove damaged pericardium)

- monitor for pericardial effusion (>50 mL)

what is a complication of pericarditis

cardiac tamponade