Lecture 7: CV infectious diseases and other conditions Flashcards by Braden Talbert

what is pericarditis

inflammation of pericardial sac

can be acute, chronic, or recurrent

causes:
- common complication of lupus
- certain malignancies or chemo
- systemic bacterial or viral infections
- open heart sx

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clinical presentation of pericarditis

pain with deep inspiration (pericardium is highly innervated)

pain relieved by particular positions (anything that takes pressure or friction off of pericardium)

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imaging or labs for pericarditis

echo
cardiac MRI/CT
leukocytosis/other inflammatory markers

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treatment of pericarditis

antibiotics

pericardiocentesis if needed (removal of excess fluid from around the heart)

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what is myocarditis + causes

inflammation of the myocardium

inflammatory cellular material or the immune response itself can damage myocytes

causes
- bacterial or viral infection
- autoimmune diseases
- toxins/environmental exposure

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clinical presentation of myocarditis

chest pain
tachyarrhythmias
cardiac arrest
malaise
fatigue
flue like S&S

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imaging/labs for myocarditis

ECG
echo
myocardial biopsy
cardiac MRI/CT
elevated troponins

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treatment for myocarditis

medical management of HR/arrhythmias
supplemental O2
fluid resuscitation
MCS if needed for adequate CO

extreme/chronic cases may require heart transplant

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what is endocarditis

bacterial infection of the inner lining of the heart that often involves valves

bacterial vegetations on valve leaflets result in valve dysfunction

vegetations can break off and travel to brain/body (called septic emboli)

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causes of endocarditis

staphylococcus
streptococcus
enterococcus
IVDU
dental procedures
infected indwelling vascular devices

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clinical presentation of endocarditis

sepsis
fever
leukocytosis
malaise

S&S of valve dysfunction:
- angina
- SOB
- dizziness
- fatigue
- pedal edema
- arrhythmias
- syncope

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imaging/labs for endocarditis

echo (TEE especially)

blood cultures to match antibiotic treatments

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treatment of endocarditis

> /= 6 weeks IV antibiotics

pharm management of resulting cardiac dysfunction

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describe the dental/oral connection to the heart

bacteria present in gum disease or oral infections can enter the bloodstream and cause endocarditis

higher risk for oral bacteria to affect pts with artificial heart valves

oral disease exposes vasculature to bacteria that would otherwise be protected by healthy gum tissue and teeth

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what is pericardial effusion

build up of fluid in the pericardial space

fluid can be infectious or malignant depending on the clinical situation

treatment = fluid removal via pericardiocentesis

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what is cardiac tamponade

build up of fluid that exerts pressure in the heart and prevents normal ventricular expansion resulting in rapid loss of CO

medical emergency that needs to be addressed rapidly

what does the general term “shock” mean

sudden lack of CO that results in decreased O2 perfusion an organ dysfunction

life threatening lack of O2 supply

what is cardiogenic shock

adequate intravascular volume but no effective way to deliver to tissue

frequently caused by cardiac ischemia ( L anterior MI), HF/CM, cardiac tamponade, severe and sudden valve regurgitation

compensation via increased HR and peripheral vasoconstriction to maintain O2 supply to essential organs only increases after load and O2 demands

S&S:
-tachycardia (rapid weak pulse)
- no urine output
- skin discoloration
- AMS
- +LOC

describe hypovolemic shock

inadequate intravascular volume reduces preload which impairs CO

nothing wrong with the mechanisms that move blood around body, but no blood to move

acute and massive blood loss results in hypovolemic shock

describe septic shock

inadequate tissue perfusion, metabolic changes, and vascular collapse in response to systemic infection

degree of infection makes it chemically impossible for body to keep up with O2 demand

describe pulmonary artery hypertension

elevated pressure in pulmonary arteries

creates increased after load for RV to eject blood against

higher workload on RV

decreased blood volume to the lungs = less volume than can exchange CO2 for O2 at alveolar membrane

L side of heart affected over time by PAH and increased RV workload
- decreased preload returning to LA = decreased blood available for LV to eject

how is PAH diagnosed

all other differential diagnoses ruled out

R heart cardiac Cath measures chamber and vessel pressures

Pulmonary aa pressure
- BP of pulmonary artery
- normal = 8-20 mmHg
- PAH>20 mmHg

describe group 1 PAH

inherited/genetic causes

connective tissue disorders, congenital heart deformities

can also be idiopathic with no known genetic component

describe group 2 PAH

caused by L sided HF

impaired LV filling deficit causes back up of pressure into lungs

describe group 3 PAH

caused by chronic lung disease lung dysfunction results in changes to pulmonary vasculature

describe group 4 PAH

caused by chronic or severe clot burden from PE or other obstructions PTS after severe PE can result in the same, even after clot burden is removed

symptoms of PAH

SOB fatigue angina pre-syncope/syncope failure to increase CO during exercise faster exercise desaturation hyperventilation to compensate for lack of blood flow available for gas exchange earlier VT2

WHO class 1 of PAH

no functional limits ordinary activity doesn't result in symptoms

WHO class 2 of PAH

slight functional limits comfortable at rest ordinary activity results in S&S

WHO class 3 of PAH

marked functional limits comfortable at rest minimal activity results in S&S

WHO class 4 of PAH

inability to carry out normal functional activities signs of PAH and R HF present at rest and worse with activity

management of PAH

meds to Lowe the pressure in pulmonary aa lowering the after load reduces pressure on RV pulmonary vasodilators - decrease after load in lungs, vascular smooth mm relaxation - i.e. flolan or remodulin phosphodiesterase inhibitors - allows lungs to make more of their natural vasodilators -i.e sildenafil or tadalafil

PT management of PAH

increased risk for abnormal response to exercise dependent on severity of disease symptom limited high degree of energy conservation strategies, learning to live with impairments can require creativity to work around limits

what is postural orthostatic tachycardia syndrome (POTS)

autonomic dysfunction that causes abnormal HR response with position changes sustained tachycardia of >120 bpm or increase > 30 mom within 10 min of standing orthostatic hypotension NOT present symptoms triggered by a standing position and improve after returning to supine

symptoms of POTS

tachycardia/palpations dizziness pre-syncope/syncope SOB diaphoresis AMS to diagnose, there has to be an absence of anything else that could explain tachycardia

normal postural CV response and what is different about it with POTS

500-800 mL blood is displaced to abdomen and legs when we stand, changing direction of blood flow baroreceptors in aortic arch detect change in volume and pressure and signals ANS to respond ANS responds to maintain CO via increased HR and SVR mm activation helps facilitate venous return takes ~4 cardiac cycles to adjust to the fluid shift that occurs with a change in position POTS = this response does not occur naturally

POTS management

non pharm management = more effective gradual habituation; sleep with HOB elevated 4-6" gradual, graded, supported aerobic exercise training; recumbent to semi-recumbent to upright hydration and electrolyte replacement - 16 oz cold water 30 min before exercise - 2-3 L water per day with 8-12g sodium per day avoid du=iuretics with caffeine avoid emotional stress avoid warm/humid environments eat small, frequent meals to avoid excessive intestinal blood shifting during digestion process

LE compression garments for POTS recommendation

10 mmHg for abdomen 30-40 mmHg for legs compression leggings more effective than socks reduces venous pooling use combo that works for pt to improve symptoms and vitals some research suggests abdominal compression is more successful than BLE compression stockings, but use combo that works best for pt