Cardiovascular Flashcards
Describe Sx associated with myocardial ischemia
Visceral pain
Dull, aching, tight
Sometimes “burning”
Poorly localized
Signs of pleuritis
Increased pain with inspiration and cough
Important life threatening causes of chest pain (3)
Myocardial ischemia
Pulmonary embolus
Aortic dissection
Risk factors for CHD (6)
Diabetes mellitus Smoking HTN Dyslipidemia Fam Hx Abdominal obesity
Also: age, cocaine use
Pain in pericarditis
Pleuritic
Relieved by sitting forward
Can radiate to shoulder/trap due to diaphragmatic irritation
Worrisome features in angina (2)
More than 20 min of pain
Pain at rest => UNSTABLE!
Characteristics of aortic dissection (3)
Abrupt and Most intense at onset
Tearing pain
Radiates to back
Unequal BP between arms
Use transesophageal ECG to detect at bedside
Chest pain DDx (8)
HEART:
Angina => worse with emotion or exercise, relieved by NO/rest, retrosternal pressure like pain
MI
Pericarditis => Sx pleuritic and positional, pericardial rub
Aortic dissection => Sx abrupt, most intense at start, radiates to back
LUNGS:
Pneumothorax => tachypnea, hyperresonant, tracheal deviation
PE => Sx pleurisy and dyspnea
ESOPHAGUS:
Gastrointestinal disease => GERD, esophag spasm
MSK:
MSK => worse on movement/palpation
NEURO:
Neuropathic => VZV
ECG findings - ST depression >1mm
Ischemia!
ECG findings - ST elevation
Acute MI => only in area of infarction
Perdicarditis => ALL leads involved, may have PR depression
ECG findings - RBBB
Right heart strain! => ex. In PE
ECG findings - LBBB
Underlying heart disease such as ischemia or HTN
Causes of low CO in cardiogenic shock (3)
Right heart failure => pulmonary embolism
Decreased venous filling of heart => tension pneumothorax
Obstruction of outflow => cardiac tamponade
Causes of distributive shock (3)
Low SVR resulting from: sepsis, adrenal insufficiency, anaphylaxis
Definition of shock
Decreased perfusion and oxygen delivery to body
SBP < 60mmHg
May manifest as organ failure => renal, CNS, lactic acidosis
Pulsus paradoxus is associated with….
Cardiac tamponade
Definition: On inspiration, a drop in systemic arterial pressure greater than 10mmHg.
In states in which the ventricle cannot expand outward (e.g. tamponade) or in which the drop in intrathoracic pressure with inspiration is profound (e.g. status asthmaticus), the septal shift is exaggerated and the difference in BP is larger.
Hypovolemic shock: CO, SVR, JVP
Cardiogenic shock
Distributive shock
Hypovolemic shock: decrease CO, increase SVR, decrease JVP
Cardiogenic shock: decrease CO, increase SVR, increase JVP
Distributive shock: increase CO, decrease SVR, decrease JVP
Causes of cardiogenic shock (7)
MI, cardiomyopathy, tamponade => pump failure
Arrhythmia
Valve failure
Tension pneumothorax, massive PE => Obstructed outflow
Causes of hypovolemic shock (4)
Hemorrhage
Diarrhea
Heat stroke
Third spacing
Causes of distributive shock (4)
Sepsis
Anaphylaxis
Adrenal crisis
Myxedema coma
Treatment of shock
Decreased JVP => hypovolemic OR distributive shock => IV fluids => NS/RL
Anaphylaxis => epinephrine
Adrenal insuff (hyponat, hyperkal, hypogly, abdo pain, eosinophilia, mild hypercal)=> ACTH stim test => IV steroids
Sepsis => blood and urine cultures => empirical ABx
Myxedema => “hypo” syndrome (hypotherm, hypogly, hyponat, hypovent) => TSH/T4 => exogenous thyroid hormone
Increased JVP => cardiogenic shock => CXR (PE, cardiomyopathy, tamponade, pneumothorax) + ECG (PE=> RBBB, MI => ST dep or elevation) + echocardiogram
Pneumothorax => insert chest tube => midclav 2nd intercostal space
Swan-Ganz pulmonary artery catheter => L atrial filling pressure
Rx:
Vasopressors
Dobutamine => beta 1 agonist => increase cardiac contractility
Norepinephrine => alpha and beta 1 => distributive and cardiogenic
Phenylephrine => pure alpha 1 agonist => increase SVR w/o increasing CO
Three stages of atherosclerotic plaque formation
- Endothelial dysfunction => fatty streak= smooth muscle cells in intima and accumulation of lipid
- LDL enters endothelium => oxidized => macrophages come and recruit fibroblasts and other inflamm cells
- Smooth muscle + CT + lipids incorporated into plaque => fibrous cap formation => narrow artery lumen
Plaques can rupture and lead to thrombosis
Characteristics of unstable angina
- angina that occurs AT REST
- significant change in the pattern of existing chronic angina
Symptoms to look for in atypical angina
Jaw pain
Dyspnea
=> think diabetes
Other PE findings of atherosclerosis (7)
Arteriovenous nicking Copper wire changes in retinal vaculature Third heart sound Fourth heart sound Arterial bruits Diminished peripheral pulses Xanthomas
S4
It occurs just after atrial contraction and immediately before the systolic S1
caused by the atria contracting forcefully in an effort to overcome an abnormally stiff (decreased compliance of ischemic myocardium) or hypertrophic ventricle
S3
occurs soon after the normal two “lub-dub” heart sounds (S1 and S2). The S3 is associated with heart failure.
Reasons for stopping an exercise stress test (used to Dx CHD)
Mod/severe chest pain Dyspnea Dizziness >2mm ST segment depression => test = positive of ST segment depression >1mm Fall in SBP >10mmHg Sustained ventricular tachycardia
Causes of false positive ST depression on exercise stress test (4)
LBBB
LVH
WPW syndrome
Digoxin
Tools to Dx CHD (5)
- Exercise stress test (look at ECG for ST depression >1mm)
- Radiolabeled tracers such as sestamibi to determine regional myocardial perfusion
- Pharmacological stress test with selective vasodilators such as dipyridamole, adenosine => blood shunted away from atherosclerotic vessels
- Dobutamine stress echocardiography to look for wall motion abnormalities
- Coronary angiography => GOLD STANDARD
Treatment of stable angina (ABCDEs)
A: aspirin, ACE inhibitors, antianginals (Beta blockers, calcium channel blockers, Nitro)
B: beta-blockers and BP control
C: cholesterol and smoking cessation, CABG (if severe), coronary stents (percutaneous coronary intervention)
D: diet and diabetes control
E: education and exercise
Side effects of beta blockers (4)
Fatigue
Impotence
Bradycardia
Worsening of CHF
When to consider CABG over medical management of CHD
Left main disease OR LAD + proximal left circumflex
Three vessel disease w/ reduced EF
Severe proximal LAD stenosis
Survivors of sudden cardiac death/ V.tach/fib
Complete occlusion of the coronary artery often results in ……. (ECG)
STEMI!
Leads to necrosis of the myocardium
May occur throughout entire thickness => pathological Q waves
Mechanisms that compromise coronary blood flow/oxygen supply (8)
Atherosclerotic plaque rupture
Demand ischemia => tachycardia, hypotension, severe hypoxia
Coronary artery dissection
Coronary vasospasm => drugs, Prinzmetal angina
In situ thrombus formation => hypercoagulable
Coronary embolism
Vasculitis => Kawasaki
CO poisoning
Complications leading to death from AMI (5)
Arrhythmias => heart block, V.tach/fib Heart failure => cardiogenic shock Ventricular rupture => usually within 3-5 days Ventricular septal defects Mitral papillary rupture Reinfarction (>1 month later)
Prognostic factors for UA or NSTEMI (7)
TIMI risk score (/7) Age >65 At least 3 risk factors for CAD Known CAD with at least 50% stenosis ST segment changes At least 2 episodes of angina in past 24 hrs Aspirin use in past week Elevated CPK-MB or troponin
Tx of a patient with possible MI
- Rapid clinical assessment => vitals, Hx, P/E, 12 lead ECG
- Give OXYGEN
- Give 162-325mg ASPIRIN
- Give SL NITROGLYCERIN (0.4mg every 5 min x 3) => beware hypotension
- Consider IV morphine for pain and pain-related sympathetic drive
- Give IV beta blockers to control HR and relieve myocardial demand
- Treat with a statin, oral ACE inhibitors,
Thrombolytic therapy agents
Streptokinase
Alteplase
Tenecteplase
Reteplase
Absolute contraindications for thrombolysis (6)
Previous intracranial hemorrhage Significant closed head injury within past 3 mo Stroke within 1 yr Intracranial malignant neoplasms Aortic dissection Active bleeding
Relative contraindications include: uncontrolled HTN, distant Hx stroke, recent trauma/surgery, pregnancy, current use of anticoagulants
STEMI vs. NSTEMI
STEMI = full thickness damage to myocardium, complete occlusion of major coronary artery, complications are more common
NSTEMI = partial thickness, complete occlusion of minor artery or partial occlusion of major artery, milder elevations in troponin and CPK-MB compared to STEMI, may see T wave inversions on ECG, thrombolytic Tx is harmful (i.e. NO streptokinase)
Major risk factors for congestive heart failure (5)
Coronary heart disease Hypertension Diabetes Valvular heart disease Cardiomyopathy => amyloid, drug-related, idiopathic
BP is determined by SVR and CO. CO is in turn determined by _________, _________, and ____________.
Preload, contractility and afterload
Frank Starling law of the heart
As preload is increased, the stroke work or contractility (inotropy) of the heart is also increased.
The relationship between increasing preload and CO, in a heart with decreased contractility/ejection fraction….i.e. Post MI etc.
Causes of high output heart failure (rare)
Hyperthyroidism
beri beri => thiamine deficiency
Arteriovenous malformation
=> increased metabolic demands!
DDx dyspnea + dilated cardiomyopathy (7)
Post MI HTN Valvular Toxic (Rx, cocaine etc) Viral (coxsackie!!) Hemochromatosis Hypothyroidism
Tx acute pulmonary edema in CHF
LMNO
Lasix (decrease preload)
Morphine (venodiltor and anxiolytic)
Nitroglycerin (arterial and venous dilator AND coronary vasodilator)
Oxygen (decrease pulmonary vasoconstriction)
Tx CHF caused by systolic dysfunction
ACE inhibitors ARBs Beta blockers Diuretics Fluid and salt restriction Cardiac glycosides (ex. Digoxin) Inotrope infusions Ventricular assist devices
Causes of absent P waves
Failure of SA node to fire => sinus arrest => Sick Sinus Syndrome
Failure of SA node to excite atria => sinus exit block
Also atrial fibrillation => no organized atrial activity
Difference between first, second and third degree AV block
Both cause a prolongation of the PR interval (>200msec)
First degree: generally no Sx or significant bradycardia
Second degree: leads to a blocked beat => QRS fails to follow a P wave
Third: COMPLETE heart block, no relationship between P waves and QRS complex (variable PR interval), P waves fail to conduct to ventricles => slower pacemaker takes over
Difference between Type 1 and Type 2 second degree AV blocks
Type 1 Wenkebach => PR intervals progressively lengthen until a P wave fails to conduct (i.e. A P wave that is NOT followed by a QRS), AV nodal disease
Type 2 => dropped beat occurs suddenly, infranodal disease, higher risk of progressing to complete heart block
Indications for permanent pacemaker (3)
Complete heart block w Sx
Sinus node dysfunction w Sx
Bifasicular block with intermittent type 2 second degree AV block
Type 2 second degree AV block after an MI
Approach to tachycardia
Look at HR => >100
Look at QRS complex => wide (supraventricular OR ventricular) or narrow (always supraventricular)?
Narrow? => regular or irregular
look at P waves => Present? Absent? Sawtooth? P waves before QRS?
Wide? => look at morphology => variable vs. uniform
Tx for hemodynamically stable SVT (i.e. How to block the AV node)(5)
Vagal maneuvers (valsalva/ carotid sinus massage) Adenosine Beta blockers Calcium channel blockers Digoxin
Three main Tx concerns in Atrial Fibrillation
Rate control
Rhythm control
Anticoagulation
Causes of prolonged QT interval (4)
Medications => type 1A and III antiarrhythmics, phenothiazines, tricyclic antidepressants
Electrolyte disorders => hypokalemia, hypomagnesemia, hypocalcemia
Congential
Ischemia
Major causes of secondary HTN (10)
Renovascular disease Intrinsic kidney disease Primary aldosteronism Pheochromocytoma Cushing syndrome Hyper AND hypoyroidism Obstructive sleep apnea Coarctation of the aorta Drugs (ex. OCP, alcohol)
The 7 “Ps” of pheochromocytoma
Pounding headache Perspiration Palpitations Pallor Pyrexia Pressure (BP) elevations Postural Sx
Usually lasting 10-60min
Signs of target organ damage in HTN
LV heave S4 Edema (pulmonary and peripheral) Carotid bruits Neurological deficits Diminished pulses Aneurysms Arteriovenous nicking, papilledema, hemorrhages Renal bruits
The six Ps of acute peripheral arterial occlusion
Pulselessness Pallor Poikilothermia (temperature varies with ambient temp) Pain Paralysis Paresthesias
