Internal Med - Cardio Flashcards
1
Q
Stable angina sx
A
Stable angina is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia predictably (versus unstable angina which doesn’t follow a pattern) exacerbated by physical activity and relieved by rest or sublingual nitroglycerin
Myocardial ischemia is often experienced as a sensation of discomfort lasting 5-15 minutes, described as dull, aching or pressure
2
Q
Stable angina workup
A
> 70 % stenosis
Normal troponin and CK-MB
Resting ECG is normal
During anginal episode abnormal ECG with greater than 1 mm ST depression +/- T wave
3
Q
Stable angina tx
A
Treatment may include aspirin, nitrates, β-blockers, Ca channel blockers, ACE inhibitors, statins, and coronary angioplasty or coronary artery bypass graft surgery
4
Q
Unstable angina sx
A
- Angina at rest (most common)
- New onset of angina symptoms
- Increasing pattern of pain in previously stable patient
Unstable angina is suspected when the pain is less responsive to NTG, lasts longer, and occurs at rest or with less exertion than previous episodes of angina. Such changes are termed unstable angina and require prompt evaluation and treatment
5
Q
Unstable angina dx
A
Gold std= Angio
EKG - Can be normal
Stress test - If a patient has a normal resting ECG and can exercise, exercise stress testing with ECG is done
6
Q
Angina tx
A
Modification of risk factors (smoking, BP, lipids)
- Antiplatelet drugs (aspirin and/or clopidogrel or ticagrelor)
- β-Blockers
- Nitroglycerin and Ca channel blockers for symptom control
- Revascularization if symptoms persist despite medical therapy
- ACE inhibitors and statins
7
Q
Prinzmetal variant angina
A
Cardiac chest pain (angina), that occurs at rest and usually happens at night or early morning hours
- Prinzmetal variant angina: Transient coronary artery vasospasms within normal coronary anatomy or at site of atherosclerotic plaque
- Variant angina is characterized by a transient, abrupt, marked reduction in the luminal diameter of a coronary artery which leads to symptomatic myocardial ischemia
8
Q
Biggest RF of prinzmetal angina
A
Smoking #1, substance abuse, cocaine
9
Q
Dx of prinzmetal anginga
A
Angiography
10
Q
Tx of Prinzmetal Variant Angina
A
itrates and calcium channel blockers.
- Calcium channel blockers are effective prophylactically to treat coronary vasospasm associated with variant or Prinzmetal’s angina.
Use of a beta-blocker such as propranolol is contraindicated in Prinzmetal’s angina
11
Q
Afib presents as
A
low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of narrow QRS complexes.
Palpitations
13
Q
Tx of Afib
A
Rate control - below 110 beats per minute
Calcium channel blocker (diltiazem, verapamil) or beta-blocker (metoprolol)
Rhythm control
Duration of Afib < 48 hours- cardioversion, amiodarone (obtain transesophageal echo (TEE) to determine if a clot is present prior to cardioversion)
- Duration > 48 hours - anticoagulate for 21 days prior to cardioversion
- Unstable Patient with rapid ventricular rate = synchronized cardioversion
Anticoagulation is determined by CHA2DS2-VASc
Direct oral anticoagulants or DOAC (eg, dabigatran, rivaroxaban, apixaban, or edoxaban) rather than warfarin for most patients in whom oral anticoagulant therapy is chosen
- Warfarin for mechanical heart valves, mitral stenosis, unacceptable increase in cost, EGFR < 30 ml/min, on certain medications (phenytoin or certain antiretroviral therapy)
- Adjusted-dose warfarin target INR is 2.5 (range 2–3)
14
Q
Sx of sick sinus syndrome
A
dysfunction in the sinus node’s automaticity and impulse generation
- Sinus bradycardia: Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
- Sinus pause: pause
- Sinus arrest: pause > 3 seconds
- Tachy-Brady Syndrome: Episodes of alternating sinus tachycardia and bradycardia
15
Q
MCC of sick sinus syndrome
A
Idiopathic SA node fibrosis ; Other causes → Drugs or inflammatory/infiltrative disorders
15
Q
MCC of sick sinus syndrome
A
Idiopathic SA node fibrosis ; Other causes → Drugs or inflammatory/infiltrative disorders
16
Q
Tx of Sick Sinus Syndrome
A
Pacemaker
17
Q
MC type of cardiomyopathy
A
Dilated
18
Q
What heart sound is associated with dilated cardiomyopathy?
A
S3
19
Q
MCC of dilated cardiomyopathy
A
- Causes include viral infections, genetic abnormalities (25% to 30%), hypertension, excessive alcohol consumption, postpartum state, chemotherapy toxicity, endocrinopathies, and myocarditis; it may also be idiopathic
- Dilated cardiomyopathy is characterized by a reduced strength of contraction and systolic dysfunction. The result is right and/or left ventricular enlargement and progressive heart failure with increased risk for sudden cardiac death
20
Q
Dx of dilated cardiomyopathy
A
Echo = Most definitive
EKG = nonspecific ST/T wave changes
CXR = Balloon - like heart, cardiomegaly, pulmonary congestion
21
Q
Tx of dilated cardiomyopathy
A
Tx like systolic heart failure → Bblockers + Ace + Loop Diuretic
*Add Digitalis to increase contractility
22
Q
What will increase murmur intensity associated with HCOM?
A
The murmur associated with HCM is worsened by conditions that cause reduced ventricular volumes such as the Valsalva maneuver, sudden standing, and tachycardia
23
Q
MCC of HCOM
A
Hypertrophic cardiomyopathy (HCM) is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction
- Myocardium gets sick, heavy, and hypercontractile
24
MC sudden death in young athletes
HCOM
25
What heart sound and what kind of murmur is heart with HCOM
[**S4 gallop**](https://youtu.be/KcMF8rJDTIk) **and apical lift with a thick, stiff left ventricle**
**medium-pitched, mid-systolic crescendo-decrescendo murmur** that **decreases with squatting** and **increases with standing or Valsalva**
26
How do you dx HCOM
Echo or MRI; EKG will show left ventricular hypertrophy
27
Tx for HCOM
**β-blockers (metoprolol)** and/or **rate-limiting Ca channel blockers** (usually verapamil) to **decrease myocardial contractility** and **slow the heart rate** and thus prolong diastolic filling and **decrease outflow obstruction**
* **Avoid nitrates** and other **drugs that decrease preload** (eg, **diuretics**, ACE inhibitors, angiotensin II receptor blockers) because these decrease LV size and worsen LV function
* **Digoxin** is **contraindicated** since it increases the force of contraction which can increase the obstruction
* Consider an **implantable cardioverter-defibrillator** for patients with syncope or sudden cardiac arrest
28
MCC of Restrictive cardiomyopathy
**History of an infiltrative process** ⇒ caused by deposition into or between myocardial cells ⇒ **amyloidosis, hemochromatosis, sarcoidosis, scleroderma, fibrosis, radiation and chemotherapy**
29
What heart sounds are heart with restrictive cardiomyopathy?
* **Think diastolic heart failure: S4 and thick stiff ventricle**
30
Dx of restrictive cardiomyopathy
Echo + cardio cath
31
Tx of restrictive cardiomyopathy
Tx underlying cause
Diuretics ; ACE/ARB;CCB
32
NY heart failure classification for congestive heart failure
* **Class 1:** no limitation of physical activity
* **Class 2:** slight limitation physical activity; comfortable at rest
* **Class 3:** marked physical limitation; comfortable at rest
* **Class 4:** can’t carry on physical activity; anginal syndrome at rest
33
MCC of congestive heart failure
MC cause: CAD, HTN, MI, DM – LV remodeling ⇒ dilation, thinning, mitral valve incompetence, RV remodeling
34
Sx of congestive heart failure
* exertional dyspnea ⇒ rest, chronic nonproductive cough, fatigue, orthopnea, nocturnal dyspnea, nocturia
* Signs: Cheyne-stokes breathing, edema, rales, S4 (diastolic HF, preserved EF); S3 (systolic; reduced EF); JVD \>8cm, cyanosis, hepatomegaly, jaundice
35
Dx of CHF
**ECHO** → Most useful imaging (EF determines prognosis)
**CXR** → Kerley B lines, cardiomegaly, pleural effusion, pulmonary edema
BNP**\>100 = CHF is likely**
36
Tx of CHF
**Systolic left heart failure:** Treat with Ace Inhibitor + βblocker + **Loop Diuretic**
**Diastolic heart failure:** Ace inhibitor + βblocker or CCB (do not use diuretics in stable chronic diastolic failure)
**ACEI** need to be used ASAP **/decrease comorbidity** and **mortality**
**Three specific beta-1 selective** drugs in reducing mortality from heart failure:
* bisoprolol
* carvedilol
* metoprolol succinate
37
#1 killer in the US and worldwide
Coronary artery dz (Stemi + Nstemi)
38
Most sensitive and specific cardiac marker
TROPONIN; **Appears at 4-8hours peaks 12-24 hours and lasts for 7-10 days**
* **CK/CK-MB appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days**
* Myoglobin (Mb): appears **at 1-4 hours, the peak is 12 hours, and returns to baseline levels within 24 hours.**
39
Tx of NSTEMI
**Obtain EKG within first 10 minutes**
1. **Morphine (IV iw pain not relieved by NTG)**
2. **Oxygen (4L/min)**
3. **Nitroglycerine (sublingual)**
4. **Aspirin (160-325 mg)**
40
Tx of STEMI
**Reperfusion therapy is the mainstay of treatment in STEMI** especially within 12 hours of symptom onset
1. PCI (Percutaneous Coronary Intervention) GOLD STANDARD - best if within 3 hours of sx onset (especially 90 minutes) PCI is superior to thrombolytics
2. Thrombolytic therapy - Done if no access to cath lab or surgery is contraindicated
1. TPA
1. Streptokinase
41
Primary prevention of CAD
**Smoking cessation, lifestyle (BP, LDL/HDL, obesity)**
* **Primary prevention = platelet inhibitors (Aspirin, etc.) = cornerstone**
* Secondary prevention = aspirin, β-blockers, ACE-I/ARB, statins; nitro if symptomatic
42
What is the MOA for atherosclerotic dz
* **Foam cells are macrophages that gobble up lipids in the wall; it then dies off and stays there and becomes a foam cell; when it dies it releases cytokines that attract more macrophages to the area ⇒ plaque clot**
* Fibrous plaque forms over lipid core: Complete clot – ST-elevation MI; Incomplete clot – unstable angina/NSTEMI
* Vulnerable plaque is easy to rupture; thick plaque is stable
* Adhesion, activation, aggregation, propagation of clot, platelet adherence
43
What are the bugs associated with Acute, Subacute, IVDU, and Prosthetic valve endocarditis
**Acute bacterial endocarditis:** Infection of normal valves with a virulent organism (S. aureus)
## Footnote
**Subacute bacterial endocarditis:** Indolent infection of abnormal valves with less virulent organisms (S. viridans)
**Endocarditis with intravenous drug users** - Staphylococcus aureus
**Prosthetic valve endocarditis** - Staphylococcus epidermidis
44
MC bug of endocarditits
Strep Viridans
45
Sx of endocarditis
* **Splinter hemorrhages** in fingernail beds
* Osler nodes **painful lesions** on fleshy portions of extremities
* “**Roth spots”** retinal hemorrhages
* **Janeway lesions** (cutaneous evidence of septic emboli)
* Palatal or conjunctival petechiae
* Splenomegaly
* hematuria (due to emboli or glomerulonephritis)
46
Dx of endocarditis
Duke Criteria - **Major** = 2 positive blood cultures, positive echo (will show vegetations), new murmur (valve regurge)
Duke Criteria - **Minor** = **Fever,** predisposing heart condition, vascular phenomena, immunological phenomena
**TEE = Gold Standard**
47
Tx of Endocarditis
* Empiric treatment: **IV vancomycin or ampicillin/sulbactam PLUS aminoglycoside**
* Prosthetic valve: Add rifampin
* High-Risk patients prophylaxis for procedures: **Amoxicillin -** 2 g 30-60 minutes before the procedure
48
Diastolic Heart Murmurs
Ass rim, pussy rim, makes sexy tits sweat
Aortic Rergurg
Pulmonic Regurg
`Mitral Stenosis
Tricupsid stenosis
49
harsh systolic ejection crescendo-decrescendo at the right upper sternal border with radiation to neck and apex
Aortic Stenosis
50
blowing holosystolic murmur at the apex with split S2 radiating to the left axilla
Mitral regurgitation
51
midsystolic ejection click heard best at the apex
Mitral Valve Prolapse
52
Four groups most likely to benefit from Statin therapy
* **Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)**
* Patients with primary **LDL-C** levels of **190 mg per dL** or greater
* **Patients WITH diabetes mellitus**, 40 to 75 years of age, **with LDL-C levels of 70 to 189 mg per dL**
* **Patients WITHOUT diabetes,** 40 to 75 years of age, with an **estimated 10-year ASCVD risk ≥ 7.5%**
53
Optimal lipid goals
**LDL \< 100 optimal**
**TOTAL\< 200 desirable**
**HDL\> 60 protective**
54
Primary HTN is defined as
rimary hypertension is defined as a resting **systolic BP ≥ 130** or **diastolic BP ≥ 80** on at least **two readings** on at least **two separate visits** with **no identifiable cause**
55
What is the target BP for pts with comorbities
* **Targets for patients with comorbidities: \< 130/80**
56
For **NON-BLACK** patients, including those with **diabetes:** Initial treatment should be with either:
* **ACE** inhibitor or **ARB**
* Long-acting **calcium channel blockers** (most often a dihydropyridine such as **amlodipine**)
* or a **thiazide-like diuretic** (**chlorthalidone** or indapamide)
**For stage 2 HTN:** the recommendation → **2 BP-lowering medications** of **different classes**
57
For **BLACK adults** **2 or more medications are recommended** to achieve a target of less than 130/80 mm Hg
**Thiazide-type diuretics** and/or **calcium channel blockers** are more effective in black adults at lowering BP alone or in multidrug regimens
58
Amlodipine is what class of antihypertensive?
CCB
59
Which CCB are used for rate control?
**erapamil** and **diltiazem**
60
Which CCB are used for rate control?
**erapamil** and **diltiazem**
61
Which class of antihypertensive is used for HTN and BPH?
a-blockers (-zosin drugs)
62
What classifies htn urgency vs emergency?
**Hypertensive emergency:**
* BP usually **\>180/120 WITH** impending or progressing **end-organ damage**
**Hypertensive Urgency:**
* BP usually **\> 180/120** **WITHOUT** signs of **end-organ damage**
63
Tx of htn emergency
**sodium nitroprusside (drug of choice)**
64
Tx of htn urgency
**clonidine (drug of choice)**
65
MCC of myocarditis
**viral infection →** etiologies: bacterial, parasitic, cardiotoxin, systemic disorders, radiation, hypersensitivity
66
Sx of myocarditis
Symptoms include fatigue, fever, chest discomfort, dyspnea, palpitations, **tachycardia** disproportionate to fever or discomfort
## Footnote
\*\* A severe case can weaken the heart, which can lead to **heart failure**, abnormal heartbeat, and sudden death
67
Dx of myocarditis
**endomyocardial biopsy = gold standard**; clinical presentation, cardiovascular MRI; echo = decreased ventricular EF with hypokinesis
68
Tx of myocarditis
supportive, heart failure treatment prn, antidysrhythmic prn
69
MCC of pericarditis
SLE, uremia, coxsackievirus, TB, RA, neoplasm, drug, radiation, scleroderma, MI, open-heart surgery, radiotherapy
70
MOA of pericarditis
inflammation of pericardial sac; often ⇒ pericardial effusion
71
Sx of pericarditis
* Chest pain that is **relieved by sitting and/or leaning forward**
* [**A pericardial friction rub**](https://smartypance.com/wp-content/uploads/2016/11/Pericarditis-Friction-Rub.mp3) is heard best with patient **upright and leaning forward:**
* **Worse** when the patient is **supine** and **during inspiration**
* **Alleviated** when the **patient leans forward**
72
What is Dresslers syndrome?
pericarditis 2-5 days after an acute myocardial infarctions
73
Which virus is MCC of pericarditis
Coxsackie virsu
74
Dx of pericarditis
**EKG** will demonstrate **diffuse, ST-segment elevations in the precordial leads**
* **Echo** may show **pericardial effusion/tamponade**
75
Tx of pericarditis
Tx underlying dz
* **NSAIDs** 7-14 days; **steroids** if sx \> 48 hrs; abx to treat bacterial endocarditis; pericardiocentesis; head at 45 degrees
* Dressler’s syndrome: pericarditis 2-5 days after acute MI
76
6 Ps of peripheral vascular dz
pain, pulselessness, pallor, paresthesias, poikilothermia (inability to regulate temperature), paralysis
Caused by acute arterial embolism
77
Ulcers from arterial insufficiency are painless or painful?
Painful
78
Peripheral artery dz sx
* Lower extremity atherosclerotic PAD is **initially asymptomatic** but typically progresses to **claudication, ischemia,** and **pain with exercise**
79
Sx of peripheral artery disease
* Femoral and distal **pulses will be weak or absent;** an aortic, iliac, or femoral bruit may be present.
* **Skin changes** to the lower extremity include loss of hair, **shiny atrophic skin**, and pallor with **dependent rubor**
* Severe, chronic disease results in numbness, tingling, and ischemic ulcerations, which may lead to gangrene.
* Acute arterial occlusion threatens limb viability and results in the “6 Ps”: pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis
80
Dx of intermittent claudication
**An ankle-brachial index (ABI),** which uses Doppler measurements to compare the **BP** in the **upper** and **lower extremitie**s, is a highly sensitive and specific test
## Footnote
\*\* An **ABI of ≤ 0.9** indicates significant disease
**Angiography** remains the **gold standard** study
81
Tx of intermittent claudication
**Stop smoking first line**
## Footnote
Graduated exercise - walk to point of claudication, rest, then continue walking
Control HTN, DM, weight
ASA + clopidogrel (plavix → blood thinner)
**Cilostazol → Vasodilator via platelet inhibition**
Surgery → Angioplasty; Bypass grafting
82
PE sign with phlebitis
**Homan's sign (calf pain w foot dorsiflexion)**
83
MCC rheumatic fever
Inflammatory reaction to strep throat infection
**inflammatory immune response to Group A Strep**, with the formation of **antistreptolysin antibodies** which **react with proteins on the synovium, heart muscle,** and **heart valves**
84
Dx of rheumatic fever
2 major criteria or 1 major and 2 minor **Jones criteria** are required, along with evidence of preceding GAS infection
**MAJOR:**
Carditis
Chorea
Erythema marginatum
Polyarthritis
Subcutaneous nodules
**MINOR:**
Arthralgia
Elevated ESR or C-reactive protein
Fever
Prolonged PR interval (on ECG)
85
Major vs Minor Jones criteria for Rheumatic Fever
Major = Carditis, chorea, erythema marginatum, polyarthritis, subcutaneous nodules
Minor = Arthralgia, elevated ESR/CRP, fever, prolonged PR on ECG
86
Rheumatic fever MC affects which valve
Mitral valve
87
**Major: J♥NES**
**J** oints **-** polyarthritis; ♥ - carditis; **N** odules (subcutaneous); **E** rythema marginatum; **S** ydenham's chorea
88
Tx of Rheumatic fever
* Aspirin or another NSAID
* Sometimes corticosteroids
* Antibiotics
89
Prophy against recurrent strep A infections
Pen G; alternatives → Pen V, Sulfadiazine; Erythromycin for PCN allergies
90
Etiology of rheumatic heart disease
**consequence of rheumatic fever** characterized by **inflammation and scarring of the heart valves**
* Most commonly affects the **mitral valve** \> aortic valve \> tricuspid valve
* Etiology → at least 1 episode of **acute rheumatic fever** from **group A streptococci**
91
Dx of rheumatic heart dz
* **Echocardiography** → valvular abnormalities, including regurgitation or stenosis
* Labs: **↑ anti-streptolysin O (ASO) titers**
* Histology: Aschoff bodies (granulomas with giant cells) on heart valves
92
Tx of rheumatic heart dz
* All patients with rheumatic heart disease should undergo **prophylaxis with penicillin** for the specified time period below
* **No evidence of carditis** ⇒ 5 years or until age 21 (whichever is longer)
* **Evidence of carditis without valvular abnormalities** ⇒ 10 years or until age 21 (whichever is longer)
* **Evidence of carditis and valvular abnormalities** ⇒ 10 years or until age 40 (whichever is longer)
93
Tx of aortic aneurysm
immediate surgical repair if \>5.5cm or expands \>0.5cm per year;
monitor annual if \>3cm, q6mo \>4cm; beta-blocker
94
Tx of aortic dissection
ascending aorta = surgical emergency; descending: beta-blocker
95
spontaneous / after trauma or IV/PICC lines – dull pain, erythema, induration of vein, **palpable cord**
Phlebitis/thrombitis
96
Sx of Endocarditis
97
PE findings in restrictive cardiomyopathy
Increased JVP, pericardial knock, **Kussmaul sign,** pulsus paradoxsus
98
JNC 8 recommendations for BP goals for pts \< 60 years or those with diabetes
Age \< 60 years or those with diabetes: 140/90 mm Hg
99
Ankle-brachial index (ABI) of \<0.4 indicates
**Ischemia**
\<0.9 indicates 50% stenosis
**Hanging the foot over the side of the bed** relieves pain in individuals with PAD because they are increasing the amount of blood flow and pressure to their lower legs by means of gravity.
100
PE shows **↓ breath sounds** + **dull percussion** + **↓ tactile fremitus**
Pleural effusion
CXR will show **blunting of the costophrenic angle**
* Can also use CT or US to diagnose
* **Most common causes**
* **Transudate: heart failure**
* **Exudate: infection \> malignancy, PE**
101
MCC of pleural effusions
* **Most common causes**
* **Transudate: heart failure**
* **Exudate: infection \> malignancy, PE**
102
How is orthostatic hypotension diagnosed?
* Decrease in **systolic blood pressure of 20 mm Hg**
* Decrease in **diastolic blood pressure of 10 mm Hg**
* Inadequate physiologic response to postural changes
103
Dx of Sarcoidoisis
* Labs will show hypercalcemia and **elevated serum ACE**
* CXR will show **bilateral hilar adenopathy**
* Biopsy will show **noncaseating** granulomas
104
Anterior vs Lateral MI locations
**Anterior wall myocardial infarction** is characterized by **ST elevation in leads V1–V4**, **with reciprocal changes in the inferior leads (III** and **aVF)**
105
Polymorphic ventricular tachycardia is dx by
Prolonged QT interval → QTc interval **\> 480 ms with a syncopal episode, or \> 500 ms** in the absence of symptoms
106
Cardiac electrical conduction system (how electricity goes through the heart)
SA node → AV node → bundle of His → bundle branches → Purkinje fibers
107
At what age is statin therapy recommended if family hx of premature ASCVD
* Age 20–39
* Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk
* Consider statin if family Hx of premature ASCVD and LDL-C ≥ 160 mg/dL
108
ECG findings in Wolff-Parkinson White Syndrome
ECG will show short PR, delta wave, wide QRS
109
Definitive tx of WPW syndrome
Radiofrequency ablation
110
MCC of WPW syndrome
Accessory pathway (bundle of kent) connecting atria to ventricles, bypassing AV node
111
PE findings of constrictive pericarditis
pericardial knock, kussmaul sign, pulsus paradoxus
112
Sx of Aortic stenosis
RF: Advancing age, DM, HTN
Sx → Dyspnea, chest pain, syncope
113
PE findings of Aortic Stenosis
PE: Cresendo-decresendo systolic mumur radiating to carotids paradoxically split s2, s4 gallop; Murmur decreases with Valsava
114
Soft S1 and a loud blowing holosystolic murmur
Mitral Valve Regurge
115
The **PR interval is longer than 0.2 seconds** or one block on EKG.
First Degree AV Block
116
**progressive lengthening of PR** interval then **missed QRS complex**
Type I Second Degree (Wenckebach)
117
**fixed PR interval** with occasional **dropped QRS complexes**
Type II Second Degree (Mobitz)
118
R and R’ (upward bunny ears) in **V4-V6**
Left bundle branch block
119
R and R’ (upward bunny ears) in **V1-V3**
Right bundle branch block
120
Heart unable to pump normally → blood flow through chambers obstructed → cardiac output decreases → hypotension → lower tissue perfusion → heart rate increase
Cardiac tamponade
121
2 main causes of cardiac tamponade
* **Acute onset:** trauma, myocardial infarction, aortic dissection, pericardial effusion
* **Slow onset:** cancer, chronic inflammation, uremic pericarditis, hypothyroidism, connective tissue disease
122
3 D's in Becks Triad
**Cardiac Tamponade**
**The 3 D's: D** istant heart sounds**, D** istended jugular veins**,** and **D** ecreased arterial pressure **= Beck's triad**
**Beck’s triad:**
1. Hypotension
2. muffled heart sounds
3. elevated neck veins (JVD)
