Chapter 2 - Cardio Flashcards
Physical exam findings of Ruptured AAA
1) Consider in pt with CP, abdo pain or flank pain especially with hematuria
2) abdo distension and/or pulsatile mass
3) periumbilical and flank ecchymoses
4) Melena and hematemesis
5) Signs of heart failure
Size of thoracic aortic aneurysm
defined on CXR as thoracic aorta >4.5cm. Risk of rupture is high when >6cm
Risk factors for aortic dissection
1) Uncontrolled HTN
2) Age
3) Connective tissue disorder
4) Congential heart disease (bicuspid aortic valve)
5) Family History
6) Stimulant abuse
Type AAA dissection symptoms
1) mostly HTN, but can be hypotensive if tamponade or complete rupture.
2) upper extremity BP difference
3) altered mental status
4) stroke symptoms (due to carotid or vertebral artery dissection)
Type B AAA dissection symptoms
asymmetric BP in upper and lower limbs
mesenteric ischemia
refractory HTN (2/2 renin secretion if renal artery involvement)
paraparesis
Peripheral neuropathy (anterior spinal artery involvement)
CXR findings in AAA dissection
abnormal in 85% of patients:
1) widened mediastinum
2) loss of aortic knotch
3) “calcium sign” aortic shadow extension >5mm from an aortic calcification
AAA dissection treatment
Aim to reduce sympathetic tone via pain control, SBP 100-120 and heart rate <60
6Ps of acute arterial occlusion
Pain Pallor Pulseless Paralysis Paresthesia Polar (cold)
PE CXR signs
Hampton hump -> wedge shaped density
Westermark sign -> decreased vessel marking distal to embolus
PE treatment
1) anticoagulation with heparin (if contraindicated then use fonda)
2) thrombolysis if massive PE (hypotension, severe hypoxia, cardiac arrest, evidence of R heart strain on ecg). Tpa 100mg over 2 hours
3) Embolectomy -> beneficial if large embolism not resolved with thrombolysis
4) IVC filter
RBBB ecg findings
QRS >120
RSR’ in V1-V3 with appropriately discordant T wave
Wide slurred S wave in V5-6
Causes of RBBB
Can be normal variant
Can be due to pulmonary HTN, COPD, PE, cariomyopathy
LBBB ecg
QRS >120
Dominant S wave in V1 (deep)
Broad monophasic R wave in lateral leads
Prolonged R wave peak time V5-6 (may be M shape)
Due to depolarization issues there will always be repolarization issues: normal to have ST elevation in leads V1-3, ST depression in lateral and V4, Inverted T waves
Scarbosa-Smith criteria
- STe >1mm in any lead with positive QRS (V4-6, avL, 1)
- STd >1mm in V1-3
- Abnormal/excessive discordance (T wave opposite to QRS with depth >25% of preceding S wave)
Total >3 points for 20-36% sensitivity and 90-98% specificity
Hyper K ecg findings
P wave flattening PR prolonged QRS widened Peaked T waves Sine wave pattern
HypoK ecg findings
Flattening T waves
Prominent U waves
ST depression at low levels
electrolytes leading to long QT
hypoK
hypoCa
hypoMg
Heart Failure Treatment
Lasix Morphine Nitrates (nitroglycerine and nitroprusside) Oxygen Positioning
If hypotensive: correct underlying hypovolemia with fluid challenge first and give norepi (temporary rescue strategy, will increase myocardial demand)
Types of cardiomyopathy
- Dilated -> EtOH, pregnancy, HTN, myocarditis. Treat like CHF and mortality benefit from ACE/ARB
- Restrictive -> least common, restricted filling but preserved systolic function. Caused by amyloidosis, srcoid, hemochromatosis etc. Important to differentiate from constrictive pericarditis
- Hypertrophic -> often autosomal dominant, average age 30-40 with exertional syncope
- Arrhytmogenic R ventricular dysplasia -> autosomal dominant disorder with RV replaced with fibrofatty tissue. Sudden cardiac death or ventricular dysrhythmia. May see RBBB
- Unclassified -> Takotsubo, stress cardiomyopathy
Causes of myocarditis
Viral (Coxsackie, Adeno, Hep B and C, HIV)
Chagas (parasite)
Bacterial (B-hemolytic strep, mycoplasma pneumoniae, diptheria, lyme)
Autoimmune (Kawasaki, SLE, sarcoidosis etc)
Myocarditis symptoms
flu-like symptoms are common (fever, fatigue, myalgias, GI upset)
Retrosternal CP, dyspnea, palpitations, syncope
Signs of heart failure/CHF
Myocarditis treatment
Address infectious symptoms
Treat heart failure (ACEi, B-blockers, diuresis)
MI treatment
Morphine: 0.05-0.1mg/kg IV
Oxygen >90%
NTG 0.4mg SL q5min PRN x3 then IV drip if symptoms persist (contraindicated in hypotension, RV infarct, PDE inhibitors)
ASA + other antiplatlet (clopidogrel 300mg or ticagrelor 180mg)
heparin 60U/kg
PCI with cath lab
Fibrinolysis (TNK or tpa)
Pericarditis causes
majority are idiopathic systemic diseases: SLE, rheumatic fever Peri-infarct (1-7 days post MI) Malignancy Uremia Post-trauma
Pericarditis signs/symptoms
retrosternal, pleuritic, sharp CP relieved by leaning forward.
May hear pericardial friction rub
PR depression is specific
Pericarditis treatment
NSAIDs and colchicine
Beck Triad (tamponade)
Hypotension
JVP
Muffled heart sounds
Tamponade ecg and echo findings
ecg: low QRS voltage, alternans
Echo: R ventricular collapse during diastole
HTN emergency treatment
reduce MAP by 10-20% in 30-60min or reduction in diastolic pressure to about 110 with additional reduction of MAP by 5-15% over next 23 hours. Use IV meds.
Don’t reduce by too much or too fast due to risk of end-organ ischemia 2/2 relative hypotension
Triad for symptomatic AS
angina
syncope
chf
Infective endocarditis pathogens
- Staph aureus -> new prosthetic valve or IDU (usually R sided)
- Strep -> native valve (usually L sided)
- Staph epidermidis -> pacemaker or implantable device
Endocarditis symptoms
Fever/malaise Regurg murmur Osler nodes/Roth spots Arterial emboli/septic pulmonary emboi Janeway lesions Duke Criteria for diagnosis
Infective Endocarditis
Vancomycin +/- gentamicin
Risk factors when presenting with syncope
- Increasing age
- Hx of ventricular dysrhythmia
- History of CHF
- Abnormal ecg
