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Year 3: Clinical Medicine and Pathophysiology > Lecture 7: CV infectious diseases and other conditions > Flashcards

Lecture 7: CV infectious diseases and other conditions Flashcards

1
Q

what is pericarditis

A

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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2
Q

clinical presentation of pericarditis

A

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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3
Q

imaging or labs for pericarditis

A

echo
cardiac MRI/CT
leukocytosis/other inflammatory markers

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4
Q

treatment of pericarditis

A

antibiotics

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

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5
Q

what is myocarditis + causes

A

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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6
Q

clinical presentation of myocarditis

A

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

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7
Q

imaging/labs for myocarditis

A

ECG
echo
myocardial biopsy
cardiac MRI/CT
elevated troponins

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8
Q

treatment for myocarditis

A

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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9
Q

what is endocarditis

A

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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10
Q

causes of endocarditis

A

staphylococcus
streptococcus
enterococcus
IVDU
dental procedures
infected indwelling vascular devices

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11
Q

clinical presentation of endocarditis

A

sepsis
fever
leukocytosis
malaise

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

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12
Q

imaging/labs for endocarditis

A

echo (TEE especially)

blood cultures to match antibiotic treatments

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13
Q

treatment of endocarditis

A

> /= 6 weeks IV antibiotics

pharm management of resulting cardiac dysfunction

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14
Q

describe the dental/oral connection to the heart

A

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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15
Q

what is pericardial effusion

A

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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16
Q

what is cardiac tamponade

A

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

17
Q

what does the general term “shock” mean

A

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

life threatening lack of O2 supply

18
Q

what is cardiogenic shock

A

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

19
Q

describe hypovolemic shock

A

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

20
Q

describe septic shock

A

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

21
Q

describe pulmonary artery hypertension

A

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

22
Q

how is PAH diagnosed

A

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

23
Q

describe group 1 PAH

A

inherited/genetic causes

connective tissue disorders, congenital heart deformities

can also be idiopathic with no known genetic component

24
Q

describe group 2 PAH

A

caused by L sided HF

impaired LV filling deficit causes back up of pressure into lungs

25
Q

describe group 3 PAH

A

caused by chronic lung disease

lung dysfunction results in changes to pulmonary vasculature

26
Q

describe group 4 PAH

A

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

27
Q

symptoms of PAH

A

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

28
Q

WHO class 1 of PAH

A

no functional limits

ordinary activity doesn’t result in symptoms

29
Q

WHO class 2 of PAH

A

slight functional limits

comfortable at rest

ordinary activity results in S&S

30
Q

WHO class 3 of PAH

A

marked functional limits

comfortable at rest

minimal activity results in S&S

31
Q

WHO class 4 of PAH

A

inability to carry out normal functional activities

signs of PAH and R HF present at rest and worse with activity

32
Q

management of PAH

A

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

33
Q

PT management of PAH

A

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

34
Q

what is postural orthostatic tachycardia syndrome (POTS)

A

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

35
Q

symptoms of POTS

A

tachycardia/palpations
dizziness
pre-syncope/syncope
SOB
diaphoresis
AMS

to diagnose, there has to be an absence of anything else that could explain tachycardia

36
Q

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

A

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

37
Q

POTS management

A

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

38
Q

LE compression garments for POTS recommendation

A

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

Year 3: Clinical Medicine and Pathophysiology (8 decks)

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